■ii|iiiiiP!.lii,:. 3tt;aca. N»tn ^nrk THE CHARLES EDWARD VANCLEEF MEMORIAL LIBRARY BOUGHT WITH THE INCOME OF A FUND GIVEN FOR THE USE OF THE [THACA DIVISION OF THE CORNELL UNIVERSITY MEDICAL COLLEGE BY MYNDERSE VAN CLEEF CLASS OF 1B74 1921 Cornell University Library RC 387.E11 Brain abscess, its surgical patliology and 3 1924 003 490 541 Cornell University Library The original of tiiis book is in tine Cornell University Library. There are no known copyright restrictions in the United States on the use of the text. http://www.archive.org/details/cu31924003490541 BRAIN ABSCESS ITS SURGICAL PATHOLOGY AND OPERATIVE TECHNIC THE MACMILLAN COMPANY NEW YORK • BOSTON • CHICAGO • DAIXAS ATLANTA • SAN FRANCISCO MACMILLAN & CO., Limited LONDON • BOMBAY ■ CALCUTTA MELBOURNE THE MACMILLAN CO. OP CANADA, Ltd. TORONTO Fig. 1. — Frontispiece. The Osteoplastic Flap fur Exploration for Abscess of Middle Fossa. BRAIN ABSCESS IT8 SUBOIGAL PATHOLOGY AND OPERATIVE TEOHNIO BY WELLS P. EAGLETON, M.D. NEWAUK, N. J. M.-Colonel, M. B. C. President of the American Otolo^cal Society — 1931; Medical Director, Newark Eye and Ear Infirmary, Newark, N. J.; Chief of the Division of Head Surgery, Newark City Hospital; Attending Craniolog^t, Newark Presbyterian Hospital; Consulting Cranlolo^st, St. Barnabas Hos- pital and St. Michael's Hospital, Newark, N. J., Muhlenberg Hospital, Plainiield, N. J., Mountainside Hospital, Montclair, N. J.; Chief of the Section of Surgery of Head, Base Hospital, Camp Dix, N. J., 1917-1918. THE MACMILLAN COMPANY 1922 All rights reserved n FBINIXD IN THE UNITED STATES OF AMERICA OorTRiSHT, 1922, bt the macmillan company. Set up and printed. Published July, 1922. Press of J. Little Je Ives Company New Yorlc, U. S. A. To the Memory of My Father who taught me "If all were frankly to record their thoughts and experiences, even of one day, humanity would be advanced centuries," and TO MY WIFE the inspiration of the book. FOEEWOED This monograph, is the result of considerable intradural experi- ence, associated with many bitter disappointments and failures ; some animal experimentation; and of observations during post-mortem examination of cases in which death had resulted from varied intra- cranial lesions. Eecognizing that surgical as well as pathological and diagnostic information is obtainable from post-mortems, a personal effort invariably has been made to obtain an autopsy on all cerebral cases coming under my observation. The fatal cases previously examined or operated upon, on which post-mortems were not performed, are very few. The laity are anxious to assist the surgeon in obtaining whatever knowledge may be derived from an examination of their dead, pro- vided they feel that the surgeon has striven earnestly to assist them, and that the post-mortem will be reverently conducted. Gushing, whose genius has transformed non-suppurative intra- cranial surgery into comparatively safe, delicate, almost bloodless physiological procedures, has long contended that the ordinary surgical technic applicable to other parts of the body is insufficient to combat successfully the unique physiological factors and patho- logical changes presented within the dura; and it is Cushing's tech- nic which the author largely has used in operating for intracranial suppuration. Surgically considered, intracerebral abscess stands in a class by itself, the problems presented in its surgical treatment differing from those of suppuration in other parts of the body and distinct from those encountered in the treatment of non-suppurative lesions of the brain. As many of the technical problems presented still remain far from solution, it is proposed to call attention to some of these physiological factors, their alteration by pathological proc- esses, and the technic which, to the author's mind, most satisfactorily meets them. The success of intradural surgery always will depend upon utilizing every advantage offered by the preventive and reactive efforts of nature, while a single technical error may mean the loss of the patient's life or at least of his subsequent usefulness. vii viii FOREWOED In this monograph, the writer has attempted to correlate the surgical treatment of the different pathological lesions of brain ab- scess, for he believes that, although pathology and treatment usually are dealt with in separate chapters, they are in reality one and should be so considered. Certain it is that if one is to meet with even a moderate degree of success in the treatment of brain abscess, the surgical manipulation in each individual case must be adapted to the exact pathological condition present. With this object in view emphasis is laid upon the pathology and on mechanical changes, and a classification is adopted which is capable of individual clinical recognition, because the author believes that our present knowledge should enable us not only confidently to diagnose the presence of brain abscess, but also in a large pro- portion of the cases to determine its location and whether or not it is surrounded by a capsule. To accomplish this the surgeon must divest himself of certain ideas inherent in the old classification of aural and nasal origins, and must conceive of them not according to their immediate origin, but pathologically, according to the causative lesion of entrance into the central nervous system; that is, whether extension is by direct tissue suppuration or by retrograde thrombophlebitis, for which the author suggests the terms Adjacent (Secondary), and Intercurrent (Tertiary) , when immediately occasioned by a secondary gross lesion such as sinus thrombosis, to differentiate both from abscesses origi- nating from the deposit of infected bacterial virus circulating free in the blood stream, the latter being pathologically metastatic, even though the original focus of infection may be in the ear or the nose. One of the chief objects of this work is to enable the surgeon to apply a pathological nomenclature to the subject and thus approach the treatment of brain abscess in a pathological as well as a technical mental attitude. ITo apologies are offered for the personal character of the book. It is largely an account of experience in more than fifty cases of ad- jacent brain abscess which have come under the author's observation. It has been written because he recognizes that many deaths might have been avoided had he earlier been in possession of the knowledge he has gained by his failures. He has analyzed his cases, making an effort in each particular case to learn why the patient recovered or died. In the chapter on Diagnosis the writer voices many opinions which must be regarded as purely speculative, much of which doubt- less will be demonstrated to be fallacious as our physico-pathological FOREWOED ix understanding of the clinical manifestations of suppurative cerebral lesions increases. For this he offers no eixcuse, believing that a better understanding of disease often may be obtained by speculation, pro- vided the speculation is founded on the available clinical and experi- mental evidence. Nor does he apologize for the minutely detailed technic. He has emphasized the technic, rather, because he has learned from personal experience to regard it as equally important with diagnosis. "While the opinions expressed are his own, he has endeavored whenever possible to substantiate them by reference to recorded opinions and observations. When an unsubstantiated opinion is cited, the author- ity for it is cited in the text. In the preparation of the book the author's thanks are due to Dr. Frederick A. Sutton and Dr. Harrison S. Martland for the pathological examinations and sections; to the staff of the Newark Eye and Ear Infirmary for placing at the author's disposal the records of cases under their care ; to Dr. F. Kobbins for compilation of the cases of frontal and cerebellar abscess and for other valuable cooperation ; to Mr. Edward B. Mead for helpful mechanical aid in the construction of instruments, and to the author's secretary, Miss Catherine Fideles Casey, for indispensable assistance in the prepara- tion of the manuscript. Wells P. Eaglbton. Newark, N. J., January 2, 1922. TABLE OF CONTENTS FAOB FOEEWOBD vii PART I.— GENERAL CONSIDERATIONS IN INTRACRANIAL SUR- GERY. CHAPTER I. PftEFAEATION' 1 Mental Attitude of the Surgeon 1 Importance of Proper History Taking Before Exploration . . 1 History Taking and Complete Neurological Examination Prior to Appearance of Severe Cerebral Symptoms 2 Time of Operation 3 Assistants 4 Anesthesia 4 II. GeWEEAI, STTBGICAL TeCHNIO of INTBACEANIAL OPBaiAIIONS ... 6 Position of Patient 6 Utilization of Gravity 6 Head-rests 7 Elevation of Head 7 Limitation of the Field 7 Control of Hemorrhage 7 Hemorrhage from the Scalp 8 Technic of Controlling Hemorrhage 8 Tourniquets and Compressors 8 Perforation of Skull and Formation of Osteoplastic Flap ... 9 Instruments 9 Sacrifice of bone 9 Control of Moderate Bleeding from the Diploic Vessels' during the Perforation of the Skull 9 Bulging of the Dura into the Perforation Opening .... 10 Technic of Ventricular Puncture 10 Cutting the Osteoplastic Flap 10 instruments 10 Technic 10 Control of Hemorrhage from Interior of Skull before Dura is Opened 10 Control of Hemorrhage from the Dura Itself 11 Control of Hemorrhage from the Pial Vessels 11 Control of Hemorrhage from the Brain Substance .... 12 Closure of Dura 12 Additional References to Operative Technic 12 PART II.— SURGICAL PATHOLOGY AND OPERATIVE TECHNIC OF BRAIN ABSCESS. III. Pathological aisTd Subgical Considbeations 13 Histopathology of Cerebral Tissue 13 xi xii CONTENTS CHAPTER PAGB Factors Peculiar to Cerebral Tissue which Demand Surgical Recognition 13 Acute CEdema from Trauma of Operation; Sudden Increase within Contents of Dural Envelope 15 Summary 15 References 16 General Surgical Classification 17 Surgical Pathology 17 Surgical Classification According to Position and Relationship to the Brain and Encircling Membrane 19 Clinical Classification of Brain Abscess 21 Chronic Brain Abscess 21 Intracerebral Abscess with a Capsule and Stalk .... 22 Intracerebral Abscess without Cortical Involvement Discov- erable Macroscopically 23 Subdural Abscess 24 Metastatic Abscess 25 Traumatic Brain Abscess 25 Meningeal Abscess — ^Intrapiarachnoid 26 General Surgical Principles 27 Surgical Factors 28 General Technic 28 Injury to the Brain from Its Own Pressure 29 Lumbar Puncture; Its Dangers 29 Ventricular Puncture 29 Technic of Incision of the Dura 29 Classification of Brain Abscess According to Location ... 30 IV. Abscess of Middle Fossa 31 Adjacent (Secondary) Abscess of the Middle Fossa — ^Temporo- sphenoidal 31 Location; Pathological and Anatomical Considerations . . 31 Intercurrent (Tertiary) Abscess of the Middle Fossa, Secondary to Thrombosis of the Superior Petrosal Sinus or a Dural Vein 31 Adjacent Meningeal Abscess (Intrapiarachnoid or Subdural) of the Middle Fossa 32 Localized Serous (Protective) Meningitis 32 Clinical Diagnosis 33 Extension of Intrapiarachnoid Abscess 34 Adjacent Intracerebral Abscess of the Temporo-sphenoidal Lobe without Macroscopical Manifestations of Cortical Involvement 36 Temporo-sphenoidal Abscess with a Stalk 36 Considerations Prior to Operation for Adjacent (Secondary) Ab- scess of Middle Fossa 37 Principles of Operative Treatment 40 Exposure 40 Exposure for Suspected Localized Intradural Suppuration of the Middle Fossa 40 The Osteoplastic Flap for Exploration for Abscess of Middle Fossa 41 Inspection of Brain with the Dura 42 CONTENTS xiii OHAPTBR PAGE Herniation of Brain upon Incision of Dura in Temporo- sphenoidal Abscess 42 Obliteration of Homolateral Ventricle 42 Puncture of Opposite Ventricle for the Eeduction of Brain Herniation Sufficient to Admit of Elevation of Brain . . 44 Inspection by Elevation of Brain ; 44 Teclmic of Elevation of Brain 44 Protection of Exposed Piarachnoid Prior to Exploration . . 44 Exploration within Cerebral Substance 45 Site of Adjacent Intracerebral Abscess without Maorosoopical Evidence of Cortical Involvement of Middle Fossa ... 46 Selection of Site for Exploration 46 Chronic' Adjacent Intracerebral Abscess with a Capsule ... 47 Surgical Pathology 47 Surgical Principles Underlying the Intradural Technio in Suspected, Adjacent (Secondary), Abscess of the Middle Fossa (Temporo-sphenoidal) 49 Technic Following Elevation of Brain 50 Surgical Significance of Areas of Adhesive Inflammation of Piarachnoid to Dura 50 Chronic Adjacent Intracerebral Abscess of the Middle Fossa . 51 Surgical Principles and Specific Factors Involved in the Treat- ment of Encapsulated Adjacent Intracerebral Abscess of the Middle Fossa 51 Eradication 51 Drainage 52 Selection of Cases 52 Difficulties of Complete Evacuation 52 Importance of Thorough Primary Evacuation 53 Technio of Surgical Treatment of Chronic Adjacent Intracere- bral Abscess with Capsule 55 Complete Evacuation; Difficulties 55 Cleansing and Obliteration of Cavity of Abscess with Stalk or Near Cortical Surface 56 Drainage 57 Technic of Drainage Following Incomplete Evacuation . . 57 Secondary Compression 58 Principles in Teehnic of Decompression 58 After-treatment 59 Second Abscess, or Double and Secondary Abscess 59 Case of Double Cerebellar Abscess 60 Acute Brain Abscess • 61 Pathology 61 Surgical Pathology 62 Surgical Treatment 62 Closure 65 Additional Eeferences to Double Abscesses 66 V. Mbtastatio Abscesses 68 Classification "° Development Adjacent Abscesses 68 xiv CONTENTS CHAPTER '■*'"' Metastatic Abscesses 69 Metastatic Vascular Occlusion 69 Metastatic Abscesses of Venous Origin 71 Origin of Thrombotic Nidus 71 Frequency , 72 Location 74 Multiple Metastatic Absces"ies 75 Limitation of Metastatic Abscess by Capsule 76 Formation of the Cspsule 76 Case of Metastatic Brain Abscess of Otitic Origin, the Result of an Infective Vascular Occlusion, with Involvement of the Internal Capsule, Clinically Simulating Cerebral Apoplexy and Presenting Unusual Psychic (Toxic Delirium) Phe- nomena; Operation; Recovery 77 Additional References to Metastatic Abscess 82 VI. Cebebellak Abscess 84 Section 1 84 Origin 84 Immediate Occasion 84 Surgical Anatomy of the Posterior Fossa 84 Surgical Classification of Adjacent Cerebellar Abscess .... 85 Surgical Considerations 85 Herniation in Exploration for Cerebellar Abscess; Anatomical and Physiological Factors 86 Pathological Factors . . , 87 Surgical Importance of Direction of Maximum Intracerebellar Pressure 87 Routes of Infection 88 Surgical Importance of Determining the Probable Path of Infec- tion, Whether Through the Petrous Pyramid or the Lateral Sinus 88 Influence of Path of Primary Infection on Situation of Abscess 88 Routes of Invasion of Cerebellum in 125 Cases 89 SBCiroiT II. — ^In the Anterior Portion of the Cerebellum Originating from Infection of the Petrous Pyramid 91 Origin 91 Infection of Cerebellum from Bony Caries or Necrosis ... 91 Frequency of Different Forms of Labyrinthine Suppuration Causing Cerebellar Suppuration 94 Abscess in Lateral Cisterna 95 Secondary Serous Labyrinthitis 95 Clinical Classification 95 Principles of Surgical Treatment 95 Operative Approach to the Cerebellum 95 Exposure of One or Both Lateral Lobes of the Cerebellum, with Exploration and Drainage Behind the Lateral Sinus . . 96 Incision and Evacuation in front of Lateral Sinus .... 96 Destruction of the Labyrinth Followed by Exploration of the Cerebellum in Front of the Sinus: Enlargement of the Dural Opening Following Application of Two Closely Allied CONTENTS XV HAPTSB FAOI Encircling Ligatures to the Sinus and Incision Between Them 96 Primary Exposure of the Lateral Sinus from Behind . . 97 Anatomy of the Lateral Sinus on Cross Section 97 Physiological and Anatomical Factors. Blood Pressure Within the Sinus 98 Surgical Obliteration of the Lateral Sinus 98 Technic Obliteration of the Lateral Sinus by Invulsion of Its Outer Wall into the Lumen 98 Section III. — From Sinus Thrombosis Frequently Situated on One of the Surfaces in the Posterior Two-thirds of the Cerebellar Fossa 101 Irregular Shape of Cerebellar Abscess: Its Surgical Importance 101 Surgical Principles in Treatment of Adjacent Cerebellar Abscess 101 Abscess of Sinus Origin Situated in or on Posterior IVo-thirds of Cerebellum 101 Cerebellar Abscess with Secondary Sinus Thrombosis . . . 102 Intercurrent (Tertiary) Abscess Secondary to Sinus Throm- bosis 102 Traumatic Abscess, Acute or Chronic 103 Metastatic Abscess, Acute or Chronic 103 Treatment of Abscess in or on the Posterior Two-thirds of the Cerebellum Following Thrombosis of the Lateral Sinus and Its Communicating Veins 103 Incision through Inner Sinus Wall 103 Exploration Behind the Sinus over the Lateral Lobe of the Cerebellum 103 Influence of Displacement of the Affected Hemisphere Beyond the Median Line 104 Ventricular Puncture 104 Technic of Exposure Behind the Sinus 104 Situation of Abscess Secondary to Sinus Thrombosis .... 104 Situation of Abscess in Cerebellum in 125 Autopsy Records . . 105 Surgical Requirements for Systematic Exploration and Evacuation 105 Association of Extradural with Cerebellar Abscess 105 VII. Feontai Lobe Abscess , 107 Introductory Note 107 Anatomical and ' Pathological Considerations Peculiar to the Frontal Region; Their Surgical Importance 107 Influence of Trauma 109 Relationship Between Osteomyelitis, Extradural and Intra- dural Abscess 110 Surgical Classiflcation 112 Adjacent Frontal Abscess 112 Occurrence 112 Origin of Infection 114 Paths of Infection 115 Adjacent Frontal Lobe Abscess Associated with Osteomyelitis 117 Types of Adjacent Frontal Lobe Abscess 117 Adjacent Meningeal, Subdural 118 Adjacent Piarachnoid Abscess 119 xvi CONTENTS CHAPTER FAGB Adjacent Abscess with Stalk 119 Adjacent Intracerebral Abscess without Macroscopical Evi- dence of Cortical Involvement 120 Traumatic Frontal Lobe Abscess 121 Immediate Occasion of Adjacent Abscess 121 Situation of Adjacent Frontal Lobe Abscess 122 Presence of Capsule 122 Operative Results in Recorded Cases of Adjacent Abscess . . 122 Treatment 123 Termination 124 Surgical Aims of Operation for Adjacent Abscess of Frontal Lobe 124 Puncture of Dura and Evacuation of Abscess through Posterior Wall of the Frontal Sinus 125 Chronic Encapsulated Frontal Lobe Intracerebral Abscess with Stalk, Following Trauma and Secondary Infection of Frontal Sinus 125 VIII. Heenia Cbbebbi 127 Etiology 127 Circulatory Factors 129 Surgical Pathology and Physiological Factors 131 Surgical Treatment 132 Prevention of Hernia; Site of Dural Defection 182 Protection 133 Reduction of Increased Intracranial Pressure 134 Case of Hernia Cerebri Following Operation for Temporo-sphe- noidal Abscess 135 IX. Peotectivb Mechanism op the Brain 137 Prevention of Infection 137 Pathological Processes in Infection 138 Protective Mechanism of the Brain 139 The Dura 139 The Subdural Space 140 The Subarachnoid Spaces 140 Anatomy of the Cerebro-spinal Fluid System 141 Impregnability to Infection of Cerebro-spinal Fluid System . . 142 Infection of Cerebro-spinal Fluid System from Blood Stream . 144 Brain Abscess from Meningitis 144 Report of Case XXV, Streptococcus Meningitis 144 Elimination of Bacteria from the Subarachnoid Space .... 145 Immunization 145 Susceptibility of Cerebral Tissue to Bacterial Virulence . . . 146 Sensitiveness of Brain to Toixio Influences 147 Protective Mechanism in the Brain Itself 147 Varying D^rees of Sensitiveness to Infection 148 Limitation of Suppuration within the Brain 148 Extension of Infection 148 Removal of Dead Tissue 149 Repair 149 Recrudescence of Latent Infection 149 CONTENTS xvii PAGE Conclusions 150 Relationship between Suppurative Meningitis with Brain Abscess and Protective Meningitis 150 Report of Case XXVI, General Suppurative Meningitis . . . 151 Additional References for Protective Mechanism ..... 153 PART III. SURGICAL DIAGNOSIS. X. Diagnosis of Brain Abscess in Gbneeal 155 Evidences of Cerebral Suppuration 157 Initial Vague Chill 157 Headache 157 Vomiting 157 General Malaise 157 Bisproportion 158 Positive Evidences of Cerebral Suppuration 160 Protective Meningitis 160 Convulsion 161 Subnormal Temperature 163 Absence of Lymphatics; Autolysis 164 Symptoms of Cerebral Compression 165 Specific Symptoms of Compression 166 Slow Pulse 166 Blood Pressure 166 Pulse Pressure 167 Projectile Vomiting 167 Ocular Paralysis 167 Coma 167 Papilloedema 168 Influence of Increased Intracranial Pressure . . . 168 Interference with Venous Return Circulation .... 169 Influence of Location of Lesion 171 Influence of Alterations in Composition of Parenchyma- tous Fluid 172 Intracellular Pathways of Optic Nerve and Retina . . . 172 Induced Stupeur Arterielle 174 Diagnostic Deductions from Presence or Absence of Nerve-Head Changes in Brain Abscess 175 XL Diagnosis of ADJACJafT Tempoeo-sphenoidal Lobe Abscess . . 176 Localizing Symptoms 176 Localizing Value of Primary Focus of Infection 176 Pathognomonic Symptoms in Temporo-Sphenoidal Lobe Abscess . 177 Aphasia 177 Word Deafness 178 Hemianopsia — Transient or Fixed 180 Facial Paralysis of Opposite Side 181 Paralysis of Contralateral Arm '. 181 Contralateral Hemiplegia 181 xviii CONTENTS CHAPTEB TXBH SjTnptoms of Assistance in Diagnosing Temporo-Sphenoidal Lobe Abscess 183 Pain in Teeth 183 Pain Behind the Eye 183 Convulsions — ^Localizing Value 184 Dreamy State 184 Psychic Manifestations of Toxic Delirium 185 Uncinate Symptoms 185 Past Pointing 187 Roentgen Ray Diagnosis 188 XIL Diagnosis op Ceekbhllak Abscess 190 Localizing Value of a Known Iiabyrinthitis or Lateral Sinus Thrombosis 190 Symptoms More or Less Characteristic of Cerebellar Abscess . 191 Classification 191 Manifestations of Impaired Cerebellar Function Exclusive of the Vestibular Tract 192 Partial or Complete Obliteration of a Symptom the Result of Cerebellar Compensation 194 Cerebellar Paralysis 194 Cerebellar Ataxia 194 Hypermetria — Failure of Inhibition 194 Cerebellar Convulsions 195 Forced Cerebellar Attitude 195 Speech Defects 195 Vestibular Manifestations 196 Differential Value of Mode of Onset 196 Spontaneous Nystagmus 197 Lateral Deviation of the Eyes 197 Vertigo, Spontaneous Falling and Spontaneous Past Pointing 197 Induced Abnormal Vestibular Reactions 198 Changing Character of Abnormal Spontaneous or Induced Ves- tibular Manifestations 199 Diagnosis of Increased Intracranial Pressure, Especially of the Posterior Fossa, by Induced Vestibular Reactions . . . 199 Cerebellar Cortical Localization in Relation to Vestibular Reaction 200 Induced Vestibular Manifestation from Pressure upon the Cere- bellar Cortex 200 Local Symptoms from Direct Pressure Presumptive of Cerebellar Origin 201 Pupillary Disturbances 201 General Symptoms Suggestive of Cerebellar Involvement . . . 201 Suboccipital Tenderness 202 Yawning 202 Rapid Loss of Flesh 202 Knee Jerks 202 Vomiting 202 Psychic Disturbances 202 Symptoms Due to an Accompanying Internal Hydrocephalus . 203 CONTENTS xix OHAPTEB PAOB Report of Case XXXI — Cerebellar Abscess with Vagueness of Early Symptoms 203 XIII. Diagnosis op Fbontal Lobe Abscess 206 Orbital Abscess, Osteomyelitis and Extradural Abscess — ^Dispro- portion 206 Symptoms of Cerebral Suppuration 207 Convulsions 207 Diabetes Insipidus 207 Symptoms of Cerebral Compression 207 Coma 207 Papillcedema 208 Post-Neuritic Retrobulbar Neuritis 208 Localizing Symptoms 208 Loss of Smell 208 Aphasia 208 Loss of Abdominal Reflexes of the Same Side 209 Sudden Paralysis of Arm of Contralateral Side 209 Hemiplegia of Contralateral Side 209 Mental Disturbances 209 Change of Disposition 209 Symptoms Due to Association Between Frontal Lobe and Cere- bellum 210 Additional References 210 XIV. Complications and Results 211 Complications after Evacuation 211 Differential Diagnosis 211 After Effects 211 Results 212 Appendix. I. Guide for Detailed Neurological Examination .... 213 Appendix II. Cerebellar Abscess: Analysis of Pathological Condition in Reported Autopsies of 125 Cases 220 Appendix III. Frontal Lobe Abscesses; Analysis of 140 Reported Cases 244 Index of Authors 283 Index of Subjects 289 PART I. GENERAL COlSrSIDERATIONS IN INTEAOEANIAL SURGERY. CHAPTER I. PEEPAEATION. Mental Attitude of the Sttbgeon. In approaclimg the problems involved in localized, intradural suppuration the surgeon must cultivate a peculiar mental attitude which will render him sensitive and attentive to the minute details of diagnosis and of surgical procedure. In no other branch of sur- gery may the advisability of a major operation depend upon such apparently trivial manifestations; in no other part of the body will neglect of slight hemorrhage play so important a part in the recovery or in the future well-being of the patient; in no other branch of surgery is preparedness for operation more important or team work more essential. The surgeon who postpones an operation for brain abscess to suit his personal convenience starts with a handicap that too often results in the death of his patient — a death frequently avoidable. Impoetancb of Pbopeb Histoby Taking Bbfoee Exflobation. Many patients suffering from brain abscess are brought to the hospital in a dazed condition, unable to furnish a reliable account of their illness. The possibility of a brain abscess, then, may rest upon the presence of a purulent discharge from the ear or nose, a bronchiectasis, or the scar of a previous head injury, and the diag- nosis or elimination of such abscess can only be made by the expendi- ture of time and patience in interviewing persons who are in pos- session of accurate information about the patient prior to the appear- ance of pronounced cerebral symptoms. This has been accom- plished many times, and has resulted in the greatest personal satisfaction. The following apparently trivial, yet really important, diagnostic details have thus been ascertained: — The presence and exact date of the initial "vague chiU," from which could be calculated the prob- able duration of the abscess, and whether it was acute without limit- ing membrane, or chronic with limiting membrane ; the occurrence of attacks of uncontrollable vertigo, knowledge of which has largely 3 BEAIN" ABSCESS influenced tlie selection of the cerebellum as the site for exploration ; transient periods of a "dreamy" state; transient or permanent aphasia; complete motor, sensory, or "naming" ataxia; the gradual or sudden onset of hemiplegia — ^the involvement of the hand, leg and face being separated by appreciable intervals; and the presence of an unrecognized hemianopsia. Some or all of these symptoms always occur in the development of an abscess of the brain, and a knowledge of their presence is of incalculable value to the surgeon in making his diagnosis. HiSTOET Taking and Complete Nedbological Examination Peioe to Appbab- ANCE of SevEEE CeEUEBBAI. SYMPTOMS. It is the practice among many surgeons when treating suppura- tive diseases of the ear or nose associated with slight but suspicious symptoms — ^vague chill, headache, dizziness, slight subnormal tem- perature, slow pulse — to await the appearance of outspoken cerebral symptoms before making a complete neurological examination. (See Appendix I, "Guide for Neurological Examination.") This fre- quently results in the performance of an intracranial operation with- out that minute and accurate information, previously obtainable, upon which depends the adoption of the correct exploratory procedure. Examination of the recorded cases ^ of brain abscess shows that a very large proportion had been operated upon previously for mas- toid disease, accessory sinus suppuration, or compound fracture of the skull. The radical mastoid operation has frequently been per- formed for symptoms — ^headache and dizziness — ^the intracranial origin of which was not apparent until some time after the operation. In the presence of a wound or scar from a suppurative lesion of a cranial bone, or any suppurative disease capable of causing meta- static brain abscess, a chill, no matter how vague, followed by a slightly subnormal temperature, demands not only a complete neu- rological examination, but repeated blood cultures ; while slight cere- bral symptoms, such as persistent headache, attacks of dizziness, slow pulse, subnormal temperature and slight psychic changes, call for the removal of the patient to a hospital and the performance of a lumbar puncture, repeated if necessary until a positive diagnosis is obtained. The association of brain abscess and sinus thrombosis demands the early recognition of the blood-stream contamination in order to differentiate between the symptoms due to sinus thrombosis and to intracerebral suppuration. On more than one occasion, in the pres- > See Appendix II and Appendix III, recorded cases of cerebellar and frontal lobe abscess. PEEPAEATION 3 ence of a papilloedema secondary to occlusion of tlie venous return circulation by a thrombus, one positive blood culture was the decid- ing factor against intradural exploration. On the other hand, in a number of instances the operative finding of an occluding sinus thrombosis has caused the author to overlook an abscess of the cere- bellum. In one case, at least, the thrombus was undoubtedly aseptic and secondary to the abscess. Repeated negative blood cultures dur- ing the period of observation would have indicated exploration of the brain. The diagnosis of a secondary "protective" (aseptic) menin- gitis ^' ^' *■ ^' * — a frequent manifestation of the effort of the intra- cranial contents to wall off the suppuration — is of the greatest value in the early recognition of the localized intradural suppuration, while the early diagnosis of a general streptococcic and pneumococcic meningitis, both of which may exist for some time without producing marked symptoms, has frequently prevented a useless exploration. Time for Operation. — Brain abscess, once the diagnosis has been made, permits of no delay or temporizing; it demands the im- mediate sacrifice of all other interests. Two cases illustrate the im- portance of prompt surgical intervention. CASE I, B. F. Cerebellar Abscess. Male, age 34; running ear for fifteen years. Seen at eleven a. m. on the tenth day of illness. Temperature 100°; pulse 54; severe dizziness; intense pain in occiput; occasional vomiting; double optic neuritis. Had been delirious previous night. No tenderness over mastoid; no discharge from ear. Diagnosis. Cerebellar abscess. Ordered to hospital and preparations made for operation. Patient did not report as ordered. Late in the day he arrived in good condition; walked up two flights of stairs, needing only the help of the balustrade because of dizziness. Operation appointed for next day. Less than four hours after admission the patient suddenly became maniacal, had a convul- sion, and expired within a few minutes. The abscess had ruptured. CASE II, C. M. Cerebral Abscess. Girl; chronic discharging ear; headache for several weeks; vague chill; attacks of dreamy state; papilloedema; paresis of external ocular muscle; heminapsia. Wvhen examined in excellent condition, rational and strong. Diagnosis. — Cerebral abscess. Operation advised. Attending physician un- willing to consent without permission of family, who did not regard girl as seriously ill. Delay in obtaining consent. Next morning physician reported that patient was so much better there must be doubt of brain abscess, but family 2 "Meningitis Aseptica" : Eeisehlg; Zeit, f. Ohrenheilkunde, 1913, Bd. 69, p. 78. ' "Meningitis Sympathetica" : Plaut una Schottmiiller ; Leitfaden xur Untersuchung der OerebrospmalfliissigkeU , » "Meningitis Sympathetica" : Strauss, Israel ; Amer. Jour. Med. Soo., November, 1917, Vol. CLIV, No. 5, p. 748. » "Protective Meningitis" : Martland, Harrison S., Personal Communication . • Case XVII, M. D., Metastatic Abscess, Chapter Five, p. 77. 4 BKAIN ABSCESS consented to operation. Afternoon appointed for operation. Suddenly severe rigor and convulsions and patient passed into coma. Strong pulse but respiratory paralysis. Artificial respiration failed to sustain pulse while hasty prepara- tions for operation were being made. Autopsy. Large temporo-occipital lobe abscess with capsule which could have been drained by proposed operation with an excellent chance of recovery. Four other fatal cases have come to the author's attention in which the surgeon allowed external circumstances to occasion a post- ponement of the operation after the diagnosis of brain abscess had been made. In these four cases one abscess was temporo-sphenoidal, one occipital, one frontal and one cerebellar. While it is well recognized that sudden death results from rupture of a cerebellar abscess, it is not sufficiently appreciated that ab- scesses in other parts of the brain frequently cause death without warning. Assistants. — In no branch of surgery is trained team work as necessary as in intradural surgery. In many hospitals the oper- ator is assisted by a house surgeon and a nurse and the anesthetic is administered by a junior house surgeon — a system which frequently results in the neglect of small details on which the success of an intradural operation essentially depends. To be prepared to meet the technical difficulties which may be encountered during any intra- dural operation, a team of not less than four persons trained in brain surgery is required — ^operator, assistant, anesthetist and chief nurse. Furthermore, it is desirable to have two assistants skilled in apply- ing artificial respiration and direct blood transfusion. The first assistant and the chief nurse should have an understanding of the operator's technic, inasmuch as the assistant must anticipate every surgical need. To allow an assistant imperfectly trained in intra- dural surgery to participate actively in the operative work is to invite disaster. I have more than once "lost" an abscess before its complete evacuation because the assistant was not sufficiently trained to respond quickly to the emergency. Likewise, I have had an as- sistant well trained in general surgery but without intradural expe- rience, and consequently not appreciative of the extreme delicacy of the wall of a non-capsulated brain abscess, cause the searching canula which had been placed within the abscess cavity to perforate the delicate wall between the abscess and the adjacent lateral ventricle. Anesthesia. — ^Ether is the anesthetic of choice except when the patient is in such deep coma that no anesthetic is required. The frequency of embarrassed respiration with its associated increased bleeding demands that aU intradural operations be conducted under PEEPAEATION 5 anesthesia/ administered by an expert with an apparatus capable of exact dosage. Horsley^ used a mixture of chloroform and oxygen. The author has not adopted this as it does not appear to him that the hemorrhage would be lessened by this method though theoretically it should be advantageous. Gushing ® advocates a local anesthetic for cranial war injuries and experience with local anes- thesia va. the highly sensitive area of infected mastoids convinces the author that many cases of brain abscess may be explored under local anesthesia. Technic. — The success of local anesthesia in cranial bone surgery depends upon: (1) Systematic infiltration; (2) avoidance of pulling by instruments — retractors, artery clamps, etc.; (3) avoidance of all transmitted shocks — chisel- ing or hammering; (4) performance of all bone work by cutting or biting instru- ments such as electric or hand-driven burrs, rongeurs, gauges, GrigU saws, etc. The dura is not a sensitive structure; it requires only the application of a local anesthetic. The author has frequently slit the dura even without a local anesthetic. The brain tissue itself is non-sensitive. ' Heuer and Dandy : "A Report of Seventy Cases of Brain Tumor" ; Johns Bopkitia Hospital Bulletin, August, 1916, p. 333. » Horsley, V. : "On the Technic of Operations on the Central Nervous System" ; Brit. Med. Jour., 1906, II, p. 411. » Cushlng, H. : "Concerning Operations for the Craniocerebral Wounds of Modern Warfare" ; MiUtary Burgeon, 1916, Vol. 38, p. 601. CHAPTEE II. GENEKAL SUEGIOAL TEOHNIO OE IlfTEACEANIAL OPEEATIONS. GENEEAOii SUEGIOAL TECHNIC. Position of Patient.-^Iii all intradural explorations the field mapped out by the original incision should be horizontal with the operating table and provision should be made for its maintenance without muscular strain on the patient. " Technic. — The table should be flat and covered by a thick mattress with a rubber casing. A sloping table renders impossible the proper position of the iiead. The neck allows a certain degree of latitude by which the head can be rotated from the perpendicular of the body. This position can be maintained by the patient without strain or interference with respiration. The extent of the rotation varies with the individual patient and can be determined only by placing the patient on the table before administering the anesthetic, finding the degree of rotation available, and then adapting the supporting and restraining apparatus to the individual requirements. In a tempororsphenoidal lobe exploration the patient's body lies on the table with the head rotated sufficiently for the occipito-bregmatio line to be exactly horizontal with the plane of the table. The position is maintained by padding with sandbags under the head and neck, thus elevating the shoulders, back and buttocks. While the patient is under the anesthetic occasional slight pressure of the hand of the anesthetist applied to the jaw will prevent the backward rota- tion of the patient's head. In frontal lobe exploration the patient lies prone. In cerebellar abscess, if the exploration is to be behind the sinus, the patient is supported by his abdomen and shoulders with chest and face pointing directly downward, an "outrigger" being used. If the exploration is to be in the anterior portion of the cerebellum one shoulder of the patient is elevated more than the other and the head slightly rotated so that the face points dovraward forty-five degrees from the vertical — Sims' chest position. Utilization of Gravity. — A device permitting the rapid con- version of the operative field to admit of complete evacuation of a brain abscess by gravity is of material assistance. In one case of encapsulated intrapiarachnoid abscess, after the evacuation of as much pus as would flow, the patient, a small child, was elevated by the feet and the operated side turned downward. This was followed by the escape of an additional large quantity of pus. Failure to utilize gravity has resulted in numerous instances in incomplete evacuation, the abscess having been punctured at its uppermost extremity. In 6 GENEEAL SUEGICAL TECHNIC 7 such a condition the elevation of the foot of the table causes a recurrence of the flow of pus after its cessation — always desirable and frequently the deciding factor for success. For complete primary evacuation the table should be equipped with a device to allow of depression and elevation of the head and rotation of the patient to one side or the other. Head-rests. — The author has tried head-rests attachahle to a general operating table hut they have not proved thoroughly satis- factory. F. Krause, of Berlin, while performing an occipital opera- tion, had the patient in a sitting position, the head inclined forward, resting against the chest of an attendant who steadied the patient's head between his hands. For cerebellar operations the "outrigger," with shoulder supports to allow of free respiration, is most satisfactory.^- ^' ^ Elevation of the Head. — Elevation of the patient's head during the operation lessens hemorrhage. Some surgeons operate with the head and shoulders elevated at an angle of about thirty degrees. This, however, necessitates a constrained position for the operator which, especially in a "temperamental" man, seriously interferes with his efficiency, particularly toward the end of a long operation. Technic. — ^The operating table should be at least twelve inches higher than the standard tables used for abdominal operations. The operator and assistants should stand squarely on their feet, without strain, thus enabling them to work for several hours without unnecessary fatigue. Each should attain the height at which he works best, by an individual platform. UMITATION OP THE FIELD: Technic— After marking the proposed incision with a, knife, the head is covered with gauze, the operative field being left exposed and surrounded by toweling pinned to the scalp, a wall of toweling being erected between the anesr thetist and the operator so that it is impossible for the anesthetist's hand to invade the operative field or for the operator to go beyond it.* By pinning the toweling to the skin with delicately constructed clips an area with a margin of one-half inch may be walled off. Control of Hemorrhage. — One of the imperfectly solved prob- lems of cranial surgery is the control of hemorrhage. The number of operations which result fatally, directly or indirectly from bleed- ing, is still large. Many surgeons, chiefly because of failure to con- trol hemorrhage, divide all intradural operations associated with marked increase of the intracranial pressure into two stages — at one » BYazler, C. H. : "Problems and Procedures in Cranial Surgery" ; Jour. Am. Med. Aseoo., June 5, 1909, Vol. 52, p. 1805. " Smitli, H. B. : "An Apparatus for Supporting and Holding the Head and Shoul- ders In Cerebellar and High Spinal Operations"; Jour. Am. -Med. Assoc, Nov. 26, 1910, Vol. 55, p. 1859. ' Cushing, H. : "Tumors of the Nervus Acustleus" ; 1917, W. B. Saunders Co., Phlla. and London, p. 252. * Cushing, Harvey : "Technical Methods of Performing Certain Cranial Opera- tions" ; Burg. Oyn.. and Ois., 1908, March, Vol. 6, No. 3, p. 22T. 8 BRAIN ABSCESS operation turning down tlie osteoplastic flap, and at a later time opening tlie dura. With proper attention to hemostasis this should rarely be necessary. Hemorrhage from the Scalp. — ^In cases with greatly increased intracranial pressure bleeding from the scalp may be very severe. In addition to the many spurting points there is a general oozing which, though temporarily of little moment, may seriously militate against the patient's recovery if allowed to continue. Over both cerebrum and cerebellum the hemorrhage can be controlled by firm manual pressure against the skull and the subsequent reflection of the galea over the cut surface. The excessive general oozing so frequent during operations for brain tumor does not occur during exploration for cerebral or cere- bellar abscess, because in the presence of intradural suppuration, long before the development of the excessive increase of intra- cranial pressure so frequently associated with tumors, the patient has expired. Continued excessive increase of intracranial pressure is not compatible with life in the presence of suppuration. Technic of Controlling Hemorrhage.— The assistant, with the finger tips of both hands, presses the scalp firmly against the bone while the surgeon cuts in the small area between them, checking the hemorrhage by catching the galea with fine artery forceps and reflecting it over the cut surface. The artery forceps controls the hemorrhage, not by actual compression, but by pulling the galea over the vessel. The assistant must not remove the pressure until the hemorrhage is com- pletely controlled. The number of forceps necessary is very large. The clamps are dropped into the open palm of an assistant, for if allowed to hang they will become detached by their own weight or during manipulation. The assistant keeps the forceps absolutely flat and in proper relation to «ach other. Straps of gauze wrapped around or through the handles of bundles of ten or twelve forceps allow the assistant to control a large number. After the application of the forceps a band of flat gauze pulled tightly over the cut surface controls the re- maining ooze and protects the forceps from displacement. Sufficient attention to this simple method prevents loss of blood and shortens the time of operation. The author has attempted ligation of the clamped vessels before closure; but it has been found to consume time and is of very little value. During closure, with the exception of actual spurters, the hemorrhage must be controlled by exact and careful approximation of the cut surfaces by suturing, layer by layer, no dead spaces whatever being allowed to remain. Because of the adhesion of the galea to the pericranium and subcutaneous tissue the soft parts must be pushed, not pulled, together by an assistant, all traction by sutures being avoided. The process is long and tiresome, but it is the only one that is uniformly attended with success. Tourniquets and Compressors. — ^When applicable in abscess well above the floor, metastatic or following trauma, a rubber tourniquet' materially lessens • Gushing, Harvey : "Pneumatic Tourniquets, with Special Beference to their Use in Craniotomies" ; Medical News, Marcli 26, 1904, Vol. 84, p. 577. GENERAL SURGICAL TECHNIC 9 the bleeding. On several occasions, however, the tourniquet interfered with the proper exposure of the abscess which, being subdural, had gravitated down- ward. Removal of the tourniquet with an open dura is associated with annoying bleeding which may be difficult to control. Heuer^s temporo-muscular clamp, a modification of an intestinal clamp, mate- rially lessens the bleeding but in temporo-sphenoidal abscess, as the exposure must be low down, it cannot be employed. The spring clips of Makkas are distinctly useful when respiratory or circu- latory troubles necessitates very rapid exposure. They slip, however, if applied near the edge of the wound rendering closure difficult. They also severely bruise the tissue, frequently causing local necrosis. Heidenhain's method of using deep sutures of heavy silk or silkworm gut passed with a large, full curved needle through skin to bone, one overlapping the other, does not control the hemorrhage but seriously interferes with the closure and is followed by stitch abscesses. Kredel's plates, likewise, have similarly failed. PEKFORATION OF SKTJIL AMD FORMATION OF OSTEOPLASTIC FLAP : Instruments. — Hudson's perforators save time, but it requires a little experi- ence to recognize correctly the sensation when the skull is perforated; otherwise it is possible to injure the dura and damage the brain substance with them. Hartley and Kenyan's perforator," driven by an electric motor, is somewhat dan- gerous, but properly used it makes possible a rapid and safe perforation of the skull. Frazier's electric fraise' neither works rapidly nor allows a proper bevel. SACKIFICE OF BONE: Instruments. — ^When a large area of bone is to be sacrificed, as in cerebellar abscess, the usual gauges and chisels are too small. The author is using more and more very large chisels, rongeurs and heavy hammers. A large chisel properly placed is not so dangerous an instrument as a small one, but it requires a heavier hammer to drive it. Herman Bleyle has made a well-balanced hammer weighing nearly twelve ounces; but the author has not yet found the rongeur strong enough and powerful enough to cut bone as rapidly as is necessary. The French bulldog rongeurs and the long-handled rongeurs devised by Bryant ' are the most satisfactory. contbol of modeeate bleeding from the dlploio vessels dueing the Pebfokation of the Skull. Disregard of moderate bleeding results in unnecessary loss of blood. Moderate hemorrhage can be controlled by cotton or wax until the dural opening is enlarged, when the venous hemorrhage generally ceases entirely. Technic. — Horsley's wax must be of the proper consistency. There is a little knack required for its successful application. It must be WIPED, not pressed, into the bony foramen. The proper pressure to be exerted comes with experience. Attempts to control hemorrhage by all forms of stiff plugs — ^Krause's hooks, ivory " Hartley and Kenyon : Experiences in Cerebral Surgery ; Annals of Surgery, April, 1907, Vol. 45, p. 481. ' Frazier, C. H. : Problems and Procedures in Cranial Surgery ; Journal American iledUsal Aaaodation, June 5, 1909, Vol. 52, p. 1805. • Bryant, William Soliier : An Improved Rongeur for Mastoid Operations ; Journal American Me4ical Association, August 6, 1910, Vol. 55, p. 502. 10 BEAIK ABSCESS or wooden plugs — are useless as they are constructed on a wrong principle, namely, that the bleeding has to be overcome by force whereas in reality it re- quires complete occlusion of the vessels. The slightest pressure completely stops bleeding. A frequent cause of failure is the attempt to wipe wax into a vessel which is still partially outside of the bony foramen. BULGING OF THE DtfBA INTO THE PEEFOKATION 0PBININ6S : If the intracranial pressure is greatly increased on making the initial opening the dura bulges forcibly into the opening and it is with difficulty that a director can be passed from one to the other. The proper use of the dural separators is acquired only after a little experience. A large number of dural separators of different sizes and shapes is required. The instrument should be advanced carefully, by gentle pressure and a to-and-fro movement. The introduction of the protected guide for the Gigli saw is facilitated by bending its tip. The bulging of the dura through the opening can be prevented by the performance of a lumbar puncture. This is frequently attended with severe hemorrhage, which can be completely controlled only after the bone flap has been elevated. TECHNIC OP VENTRICULAR PUNCTURE: A trephine opening is made in the occipital bone about three-quarters of an inch above the transverse sinus and three-fifths of an inch from the median line; the dural opening need only be large enough to admit the searcher. The searcher is passed directly forward; if two or three punctures fail to reach the ventricle the opposite hemisphere should be similarly trephined and punctured, as obliterar tion of one lateral ventricle from pressure is a frequent occurrence. THE CUTTING OF AN OSTEOPLASTIC FLAP OF THE SKULL: Instruments. — The spaces between the openings are cut with a Gigli saw or with a narrow Marentz rongeur. Technic. — The saw should be held tense, with the handles wide apart so that the cutting angle of the saw will be as obtuse as possible. The movements of the saw should be transmitted partially by rotation of the operator's body rather than by a to-and-fro movement of his arms alone. If the arms alone are used the operator is apt to allow his hands to approach each other, thus breaking the saw. Properly used a Gigli saw will out through any skull without difficulty, making H, bevel upon which the flap can rest. It is the best and safest instrument at our command. (See Part II, p. 41.) Control of Hemorrhage feom Interior of Skull Before Duea is Opened. After the elevation of the flap, or sacrifice of the bone, consid- erable blood occasionally comes from beneath the edge of the bone. The crowding into the bleeding area of a very small roll of cotton with a black thread attached generally controls the bleeding. The hemorrhage is frequently quite profuse at first, but later the small compress can be slowly removed, generally without recurrence of the hemorrhage. In hemon-hage from a venous sinus the accurate placing of a piece of fascia lata over the rent — ^the postage-stamp method — will control the bleeding. Its proper application, its unfolding and tuck- ing away with forceps, requires considerable experience. GENBEAL SURGICAL TECHNIC 11 CONTBOL OF HeMOEBHAGE FBOM THE DtJBA ITSELF. In cases of increased intracranial pressure there is a constant oozing from the small vessels of the dura which, while of slight im- portance before opening the dura, is extremely annoying later, and is most difficult to control. Oozing is readily stopped by placing over the oozing points strands of dry cotton, in the meshes of which the blood will coagulate. Upon the removal of the cotton, however, at the end of the operation, the oozing is apt to recur with increased persistence. A properly applied piece of muscle is very effective. It should be placed flat over the bleeding point and the blood pressed from under it. The muscle acts by occlusion and as a chemical hemostatic. Applied blood clot also at times will control a very troublesome oozing. When obtain- able, the application of fibrin paper is of the greatest advantage. *• ^** The larger vessels of the dura are encircled with a needle and ligated in two places, or "double-clipped," before incision. In liga- tion by a needle-passed suture I have frequently injured a pial vessel, with resultant annoying hemorrhage. OONTEOL OF HBMOEKHAGE FBOM THE PlAI, VESSELS. All hemorrhage must be controlled before the closure of the dura, for if a single point is left bleeding at the primary closure it will continue to ooze, with resulting degeneration, the pressure from the brain itself being insufficient to stop the hemorrhage. The pial ves- sels — endothelial tubes — run in the substance of the piarachnoid, which itself hugs the cortex, dipping down into each convolution. The pial vessels anastomose freely with each other, and furnish the superficial vessels of the cortex. They cannot therefore be caught and elevated without tearing the adjacent piarachnoid and injuring the superficial cortical vessels ; they must be encircled without eleva- tion or laterally occluded by pressure. Technic.-^-The application of the finest hemostat only increases the bleeding, since it is impossible to elevate the piarachnoid or pial vessels sufficiently to ligate by the forceps. The pial vessels may be ligated by passing a needle ligature around them, but passing the needle and tying the ligature without tearing the tissue is a most delicate procedure. Cashing "double-clips" all pial vessels and cuts between the dips. Horsley double-ligated all pial vessels before cutting. Hartley stopped bleeding by applying with a slight pressure a thick layer of • Harvey, S. C. : Fibrin Paper as an Hemostatic Agent ; AnncUs of Swgery, 1918, Vol. 63, p. 66. " Cushlng, Harvey : The Control of Bleeding In Operations for Brain Tumors ; ArmaJa of BurgerVi 1911, Vol. 64, p. 1. 13 BRAIN ABSCESS vaseline spread on a piece of gauze. If the gauze is raised the vaseline adheres to the bleeding points and seals them. The use of adrenalin, also, will stop pial bleeding, but the hemorrhage will recur later from the relaxation of the con- striction unless pressure is applied. CiONTEOL OF HEMOKBHAGE FEOM THE BRAIN SUBSTANCE. This is generally slight and is stopped spontaneously hy the sur- rounding tissue. If not, a piece of fascia, or, even better, of temporal muscle, or the fibrin paper plates of Harvey, -"^^ must be smoothly ap- plied to the bleeding surface. The immediate control of hemorrhage by the smooth application of autogenous tissue over the bleeding part is one of the most beautiful and delicate procedures in surgery. It is rarely necessary in operation for brain abscess to destroy the con- tinuity of the brain substance, for, unlike brain tumors, which must be removed from the place where they are embedded in the brain, an abscess is drained from within without disturbing the surrounding tissues. OLOSUKE OF DUEA: Technic— Approximation by catgut suture is most unsatisfactory, but in the presence of suppuration the author uses it. Waxed fine silk gives a much better approximation of the dural edges. In increased intracranial pressure it may be impossible to close the dura with- out injury to the brain substance. Suturing a transplant of fascia lata into the dural defect makes an excellent cerebral covering. Additional References to Operative Teohnio. Bahm, Hans: Die Meohanik der Gehirnerschiitterung; Oentralblatt fUr Ohirurgie, February 14, 1920, No. 7, p. 146. Barany: Die offene imd geschlossene Behandlung der Schussverletzungen des Gehims; ZeitsoJirift fur AerztUche FortWldvng, 1917, Bd. XIV, S. 397. Masland, Harvey C.: Cutting the Boae Flap in Cranial Surgery; Armals of Surgery, October, 1920. Midgeville, Een6: Mnde de Topographie Cranio-Cfirebrale pour la Eecherche des Abcfes Oto-Enc6phalique; 1919, Vigot Frtres, Paris. Di5jerine, Mme. et Landau, M. E.: M^thode de Topographie Cranio-En- cephalique simple et pratique pour prdciser, dans les Blessures du Crane par Pi-ojectileB de Guerre, la partie du Ceirveau 16s6e par le Projectile et le Si^e de ce dernier; Revue Neu/rologique, Mars, 1916, Tome XXIII, No. Ill, pp. 425-447. ^Loo. elt. PAET II. SUEGIOAL PATHOLOGY AND OPERATIVE TECHNIO OF BRAIN ABSCESS. CHAPTEE III. PATHOLOGICAL AND SURGICAL CONSIDERATIONS. HISTOPATHOLOGY OF CEEEBEAL TISSUE. Histologically, cerebral tissue is composed of neurons — the functioning cells of the brain, the most highly specialized tissue in the body. Between the neurons is the supporting tissue of the brain, the neuroglia — ^the glial cells and fibres. The neuroglia plays only an inactive part in the nervous mechanism; with the small amount of connective tissue from the pia and alongside the blood channels it forms a framework, as it were, in which the nerve cells functionate. Under stress, such as infection, certain cells of the neuroglia take on amoeboid activity and are instrumental in the removal of waste products from the brain. ^ Following the law that the more highly specialized the cell the more it depends upon nutrition for its life, and the less able it is to regenerate itself, nerve cells die easily and do not regenerate; glial tissue, on the other hand, while more resistant, regenerates. The re- generation of glial tissue, however, plays no active part in the restora- tion of nerve function. Thus, in traumatic epilepsy, if unrelieved at an early date, a general gliosis, or proliferation of the glial tissue, occurs, in the presence of which any operative procedure for the cure of the epilepsy is useless. FACTOKS PECULIAR TO CEREBRAL TISSUE WHICH DEMAND SURGICAL RECOGOTTION. Upon, opening the dura the following factors peculiar to cerebral tissue are encountered: (1) In the normal state the dural envelope is completely filled by its contents. During pathological processes, inflammatory or traumatic, the bulk of the intradural content is greater than can be contained within the dural envelope without alteration and com- pression. Normally, the intracranial tension, being of circulatory origin and varying with the tension of the cerebral veins and capil- * Alzheimer, Alois : BeltrSge zur Kenntnlss der Fathologtscben Neuroglia tind llirer Beziehungen zu den AbbauTorgSngen im Nervengewebe ; HUtologiache »»d Hitto- pathologische Arbeit Uier QraesMrn/rinie ; Jena, March, 1910. 13 14 BEAm ABSCESS laries, is variable in degree; in the dog tlie brain functions witbin a wide range of intracranial pressure ^ from zero to 50 mm. Hg. In the presence of a localized intracranial suppuration (abscess) addi- tional space within the dural envelope is obtained by (a) obliteration of the venous sinuses; (b) displacement of the cerebral tissue, not only of the affected but also of the unaffected hemisphere; and (c) obliteration of the cerebro-spinal fluid circulatory systean spaces. These factors, by interfering with the delicate circulatory systems — hemic, cerebro-spinal fluid, and intracellular — ^increase the liability to extension of infection even before the appearance of actual com- pression of the cerebral tissue. (2) The over-filling of the dural envelope is partially due to the cerebro-spinal fluid system. In abscess, not only is the amount of the cerebro-spinal fluid increased from the irritation, but there is an associated internal hydrocephalus due to diminished exit off cerebro-spinal fluid by the cortex, and definite obstruction in the main cerebro-spinal fluid circulatory system by displacement of the hemispheres. (3) The blood vessels of the brain are endothelial tubes, easily ruptured. Every drop of blood effused into the cerebral tissue causes shock by over-stimulation of the cerebral cells. The writer has seen paralysis lasting for days and convulsions continuing for hours as the result of small hemorrhages and pressure on the cortex caused by subdural injections of an autogenous serum. (4) Injury to cerebral tissue, no matter how slight, has a deeply depressing effect upon the organism as a whole. (5) Death of ganglionic cells and neurons (the functioning cells of the brain) is not followed by regeneration. (6) Cerebral tissue, the seat of infection, does not tolerate manipulation and injury as well as normal cerebral tissue; the sup- purative process with the associated compression of cerebral tissue so lowers its resistance that slight trauma may occasion extensive oedema or encephalitis. This is of the greatest surgical importance. (7) The micro-organisms of an encapsulated brain abscess gen- erally are of low virulence while within the abscess cavity ; but placed upon the normal piarachnoid they may cause a rapidly fatal sup- purative meningitis. (8) After the evacuation of the brain it must be realized that the piarachnoid and cerebral tissue must be entirely and firmly covered by dura, bone, fascia or skin, as failure to provide a tight • Hill, Leonard : "Physiology and Pathology of the Cerebral Circulation" ; London, 1896. Fig. 2. — Brain, with large tumor, which presented few symptoms for over a year after decompression. Death 2% years after operation. (This case at no time developed a papillcedema.) Fig. 3. — Brain, with large tumor. Spontaneous decompression, followed by marked improvement in symptoms. Fig. 4. — Sections of cerebrum with extensive infiltrating glioma. Decom- pression followed by such relief of symptoms that one year after operation patient, through deception, successfully passed an "inspection" for industrial life insurance. PATHOLOGICAL AND STJEGICAL CONSIDERATIONS 15 covering in the presence even of mild suppuration, witli associated increased intracranial pressure from oedema, frequently is followed by fungating hernia, -whicli almost invariably terminates in a fatal meningitis. (Witness the fungating hernia following a small "leak" from improper closure or stitch abscess, in a subtemporal decom- pression.) AouTE CEdema feom Teaitma op Oeeeahon : Sttdden Inckeasb within Contents OF DuEAL Envelope. Sudden death may result from acute oedema of the brain, with- out marked gross changes, as is frequently shown at post mortem. CASE ni, P. Labyrinthitis. Male, 58 years of age. Undoubtedly serous meningitis, as shown by papilloedema, and excessive pressure of fluid from lumbar puncture, but no micro-organisms in cerebro-spinal fluid. Operation: long chiseling process; re- peated shocks. Death in coma eighteen hours after operation. Autopsy: cortical contents flattened from pressure against skull; excessive amount of cerebro-spinal fluid; no micro-organisms. This case illustrates a condition which is but an exaggeration of the acute oedema of the brain which occurs with acute abscess, or as the result of trauma. Cases are not uncommon in which death rapidly follows a cerebral trauma or hemorrhage into a slowly growing glioma, in which at post-mortem, the amount of the hemorrhagic infiltration into the brain is not sufficient, of itself, to cause death, were it not for the rapidity of its effusion. CASE IV, L. Glioma. Adult male. Always well. Several months previously headache followed by convulsion and irregular attacks of "dreamy state." In intervals apparently perfectly well but listless; later irregular headache for two weeks, followed by convulsions, slight aphasia, loss of memory, slight papilloedema; six weeks later suddenly became unconscious. Death within eighteen hours. Autopsy : Two gliomatous masses in left temporo-sphenoidal lobe. One, old under- going cystic degeneration with evidences of former blood extravasation. Second, filled with recent blood extravasation. In contrast with these cases consider the enormous brain tumors of slow growth, which, when given a vent by decompression, cause' few symptoms because the intracranial contents have time to re- adjust themselves. (See Figs. 2, 3, and 4.) Summary. — The increase in the intracranial contents from sup- puration, and the associated protective meningitis, with the possibility of the blocking of the fluid within the ventricles in cerebellar abscess, are all to be considered in the surgical treatment of brain abscess. 16 BEAIN ABSCESS In brain abscess tbe cerebral tissues, as a result of the toxemia from the suppuration and of the increased intracranial pressure, perform their proper functions with diiBculty. If, in addition to these, trauma, oedema, or hemorrhage into the cerebral tissue from manipulation should occur, a fatality is apt to result, — a fatality for which the surgeon is largely responsible. How frequently have patients who, prior to operation, were in excellent mental condition, immediately following operation passed into deep coma or active delirium ! REFERENCES. {Pathology of Brain Abscess) (1) Miodowski, F. : Beitrage zur Pathogenese und pathologischen Histologie des Hirnabszessen; Arch, fiir Ohrenheilkunde, 1908, B. 77, Case I, S 239. (2) Tylor: In "Pathology of Encephalic Infection in Otitis"; Brain, 1912, Vol. XXXV, p. 109. (3) Homen, B. A.: Experimentelle und Pathologische Beitrage zur Kenntniss der Hirnabazesse; Arbeiten was dem, Patholog. Institut d. Universitat Eelsingfors, 1913, B. I, H. 1-2, S. 1. (4) Friedmann, M. : Der Himabszess (Encephalitis purulenta) ; Handbuoh der Pathol. Anat. des Nervensystems, 1904, B. 1, S. 504. (5) Kolpin: Zur Symptomatologie und pathologischen Anatomic des Hirn- abazesses; Deutsche Zeitschrift fiir Nervenheilkimde, 1903-04, B. XXV, S. 365. (6) Topley, W. C: A Case of Generalized Streptotrychosia with Extensive Lesions in the Central Nervous System; Brain, 1912, Vol. XXXV, p. 26. (7) Korner, Otto: Die Klinischen Erkrankungeu des Hirns, der Hirnhaute und der Blutleiter; 1902. (8) MacEwen, Wm. : Pyogenic Infective Diseases of the Brain and Spinal Cord; 1893, pp. 972-991. (9) Politzer, Adam: Diseases of the Ear; Fifth Edition, p. 636. (10) Wittmaack: Ueber die Beziehungen der pneumatisation Storungen zur Bntwickelung endokranieller Komplikationen; Archiv fiir Ohrenheil- kunde, B. 97, No. 1. (11) Hegener, J.: Labyrinthitis und Himabszess; Passow wnd Sohdfer'a Beir tr&ge zur Anat., Phys., Pathol., und Therap. des Ohres, der Nase und des Balse&, 1909, B. II, S. 359. (12) Hassin, G. B. : Histopathological Studies on Brain Abscess; Medical Record, January 19, 1918. (Gives description of cells and a bibliography.) (13) Westphal, A.: Ueber Gehirnabszesse; Archi/v fiir Psychiatrie, 1900, B. XXXIII, S. 206. (Gives detailed pathological and microscopical report with microscopical illustrations.) (14) Beck, K. ; Zur Entstehung und Ausheilung von otitischen Kleinhirnab- szessen; Zeitschrift fiir Ohrenheillcvmde,^. 64, 1911-12, S. 262. (Gives note on discovering route of infection.) (15) Essick, C. K. : Pathology of Experimental Traumatic Abscess of the Brain; Archives 'Neurology and Psychology, 1919, Vol. I, p. 673. (16) Macklin and Macklin: A Study of Brain Repair in the Eat by the Use of Trypan Blue; Archives of Neurology and Psychiatry, April, 1920, Vol. 3, p. 353. (17) Mayman, L. : Zur Pathologic und Klinik der otogenen Grosshirnabszesse; Munohener med. Woohenschrift, 1913, No. 2-3, S. 65. PATHOLOGICAL AND STJEGICAL CONSIDBEATIONS 17 (18) V. Hibler, E.: Zur Kenntniss der pathogenen Anaeroben. Bin Kleinhirn- abazess bei chroniBcheT eiterig-emsiger Otitis, Sinus Thrombose und Car- cinom-Entwickelung im rechten Felsenbein; Oentralilatt fiir Bakteriol- ogie, 1913, B. 68, S. 257. GENERAL SURGICAL CLASSIFICATION. Brain abscess, from the standpoint of surgical pathology, con- stitutes a group of surgical problems, separate and distinct, yet so intertwined that they pass imperceptibly from one to another, as nature (or the surgeon) undertakes to limit or eradicate the patho- logical process. It is by an appreciation of the fundamental patho- logical differences, by availing himself of favorable conditions, and by the creation of favorable and the avoidance of the creation of unfavorable conditions, that- the surgeon may guide a localized intra- dural suppuration to a successful termination. From a surgical standpoint, brain abscess may be divided into four general classes, each based on pathological and etiological fac- tors, which are utilizable by the surgeon during the operative treat- ment. I — Chronic Adjacent {Secondary) ; (temporo-sphenoidal, frontal, or cerebellar) with a capsule. The abscess is secondary and adjacent to a known focus of extradural suppuration, such as the mastoid or nasal sinuses, while its slow growth has permitted its limitation by a capsule and has facilitated a readjustment of the disturbed intracranial contents. II — Acute Adjacent {Secondary) ; (temporo-sphenoidal, frontal, or cerebellar) without limiting membrane. The rapid formation of the abscess, and its accompanying oedema, have caused a sudden increase in the intracranial contents before the protective mechanism of the brain could have time to erect a macroscopically demonstrable limiting membrane. Ill — Intercurrent {Tertiary) to a gross lesion, namely, sinus thrombosis or progressive osteomyelitis. IV — Metastatic, which includes: (a) Chronic, without a capsule, (b) Chronic, with a capsule, and (c) Acute. V — Traumatic. SURGICAL PATHOLOGY. A large proportion of brain abscesses, (with the exception of the truly traumatic), belong to types I and II, being secondary and adjacent to suppuration within the ear or nose, the infection extend- ing within the dura either by direct continuity of tissue, or what is 18 BEAIN ABSCESS much, more frequent, in my experience, by retrograde thrombo- phlebitis, with or without an intercurrent sinus thrombosis. In my series, excluding all truly traumatic cases, out of the first forty-four brain abscesses, forty, or over ninety per cent., belonged to the secondary adjacent types, chronic or acute. Metastatic abscesses originate from embolic septic occlusion of a cerebral vessel, the primary foci being generally far distant from the brain, the most frequent site being the lungs, from a bronchiectasis. Occasionally, a true embolic septic occlusion originates from an infected mastoid or petrous bone, in which case as the septic embolus has passed freely through the circulation prior to its lodgment in the brain, the cerebral invasion is distinctly apoplectiform in onset, while the brain abscess is not adjacent to the ear, but is lodged either in the frontal or occipital lobes, deep within the cerebral tissue, or in the opposite hemisphere.* An examination of the clinical and post-mortem histories of the recorded cases of brain abscess, not traumatic, whose situation is not adjacent to the site of infection, demonstrates their embolic origin.* Of the author's forty-four brain abscess cases three were meta- static, one from bronchiectasis, one from suppurative endocarditis, and one, while originating from a sinus thrombosis and mastoiditis, was undoubtedly embolic in origin.^ There still remains a small number of so-called "idiopathic" brain abscesses,^' "^ in which the site of the original suppuration is unknown. The demonstration of the fusiform bacillus as the caus- ative micro-organism in certain of these abscesses and in the tonsils has greatly limited the number. (See Metastatic Abscess, p. 68.) In types I and II of intracerebral abscess secondary to adjacent suppuration the pathological process is a nutritional death of cerebral tissue following a retrograde thrombophlebitis. While direct exten- sion of tlie infection through the dura, piarachnoid and brain in the writer's opinion but rarely occasions intracerebral abscess, it is un- doubtedly the causative factor in localizing intrapiarachnoid suppura- tion. • Lombard, Bloch, A., and Moulouguet, A. : TJn cas d'abac6s du lobe frontal du c8t£ oppos€ & une otite suppur£e chronlgue ; Annal dea Maladies de I'Oreille, etc., 1914, Tome 90, p. 749. • Berens, T. P. : Abscess of the Frontal Lobe of the Brain of Otitic Origin ; Trana. Amer. Otol. Soq^ 1913, Vol. 13, p. 66. ' Quimby, Wm. O. G. : Personal Communieation. (Observed at a post-mortem, a temporo-sptaenoldal lobe abscess in the opposite hemisphere to the originating aural suppuration.) " Casamajor, L. : Brain with Double Frontal Abscess ; Medical Record, 1915, Vol. 87, p. 412. (Report of case and exhibition of specimen autopsy findings. New York Neurological Society meeting December 1, 1914.) ' Climenko, H. : A Case of Brain Abscess ; Journal Nervoua and Mental Diseaaea, 1918, Vol. XLVII, P. 444. PATHOLOGICAL AI^D SUEGICAL CONSIDEEATIONS 1? In either case long before the micro-organisms have entered the cerebral tissue, — in one case being confined within the walls of the vessels and in the other because of the continuity of structure — the protective forces of the brain have become active in the affected area. Chief among these, as we have seen, are the leucocytes and endothelial cells from the blood vessels, the cells lining the arachnoid spaces, and the macrophage from the neuroglia, each contributing towards com- batting the invading micro-organisms, and the limitation and subse- quent repair of the inflammatory septic process by the formation of new connective and the removal of dead tissue. The same applies, to a limited extent, in metastatic abscess because of the temporary limitation of the invading organisms within the lumen of the occluded cell.* In traumatic abscess, on the contrary, the immediate death of cerebral tissue from trauma, associated with the transplantation of micro-organisms in unprepared cerebral tissue, furnishes favorable conditions for the rapid extension of the suppurative process before the limiting protective reactions of the brain can be marshalled; while the associated oedema and hemorrhage of extensive trauma so increases the intracranial pressure that the protective reactions of the brain are actually prevented from playing an active part in the limiting process. SUEGICAIi CLASSIFICATION ACCORDING TO POSITION AND RELATION- SHIP TO THE BRAIN AND ENCIRCLING MEMBRANE. Intradural abscess may be divided, surgically, according to its position within the brain or piarachnoid, and its relationship with the encasing dura and piarachnoid, through which its evacuation must be conducted, into: (a.) Intracerebralj without macroscppical evi- dence of cortical involvements (&) Intracerebral, with a cortical "stalk"; (c) Meningeal, either intrapiarachnoid or subdural. (a) Intracerebral abscess without macroscopical evidence of cortical involvement originates from retrograde thrombophlebitis, or from perivasculitis from an adjacent area of suppuration — ^lateral sinus thrombosis, mastoiditis, or sinusitis, — or from the deposit of a septic embolus in metastatic abscess. (6) Intracerebral abscess with a cortical "stalk," probably origi- nates from a combination of direct extension and associated retro- grade thrombophlebitis or perivasculitis from an adjacent suppura- tion. In my opinion the direct extension advances more frequently • See Chapter 9, Protectlye Mechanism. 20 BEAIN ABSCESS outward from the abscess cavity itself toward the dura than inward from the dura to the abscess, the "stalk" being always a late mani- festation. The "staUc" is nature's effort to evacuate spontaneously an encapsulated intracerebral abscess through the original site of iu- fection. The literature contains numerous instances of the spon- taneous evacuation and cure of intracerebral abscess by the develop- ment of a stalk followed by a secondary necrosis of the dura. As the perivascular spaces of the brain contain cerebro-spinal fluid, not lymph, and histologically and embryologically are not lymph channels, the term "perivascular" should be substituted for the frequently employed and incorrect "lymphatic" path of infection in the brain substance." (c) Meningeal Abscess j (either intrapiarachnoid — limited to the meshes of the piarachnoid — or subdural — limited to the subdural space — results from a direct extension from an adjacent infective process — osteitis, phlebitis, extradural abscess or trauma.-'*' As far as the author is aware, subdural and intrapiarachnoid abscess have not previously been differentiated clinically. In a case in which death resulted from leptomeningitis, following the evacua- tion of a temporo-sphenoidal intracerebral abscess, the post-mortem disclosed a large flat collection of pus and organized fibrin, entirely limited to the subdural space; it was very yellow and resembled the exudate frequently seen covering the appendix, the exudate being about half an inch in thickness and apparently undergoing resolu- tion. It was not entirely a reparative process, however, as it ex- tended underneath the whole frontal lobe of the affected side. It was possibly of traumatic origin from infection of the subdural space during evacuation of the intracerebral abscess, although its appearance and the clinical history would point to its having existed prior to the operation. The exact site of an abscess in or on the different lobes of the brain depends largely upon its origin and mode of invasion. If the abscess originates from an adjacent suppuration in the ear or nose, it is situated in or on the temporo-sphenoidal lobe, the cere- bellum, or the frontal lobe. An adjacent abscess is almost invariably single, the multiple abscesses reported being generally of traumatic or embolic origin. • Weed, L. H. : An Anatomical Consideration of the Cerebrospinal Fluid ; jlna- tomtcal Record, May, 1917, Vol. 12, p. 492. " In offering the above claeslflcation the author is fully aware of its pathological imperfections. Exact pathological knowledge of the relative frequency of brain abscess from direct extension, from improperly called "lymphatic" Infection, from thrombophlebitis, and from septic thrombi by occlusion, is not available since but few microscopical examinations to ascertain the exact route of infection into the brain are recorded in the literature. PATHOLOGICAL AND SUEGICAL CONSIDEEATIONS 21 An adjacent abscess may be chronic or acute, witli or -without a distinct limiting membrane, depending upon its age. If the abscess is of metastatic origin, following a vascular occlu- sion by a septic embolus or thrombus freed from a distant focus, it may be situated in any part of the cerebrum or cerebellum. It is apt to be multiple, but not so frequently as is generally believed; it is apt to be subcortical, but may be cortical, never, however, possessed of a true stalk; and it may be meningeal. (See lieport of Case XVI, T. v., Chapter V, Metastatic Abscess, p. 75.) A metastatic abscess is rarely encapsulated, the limiting membrane being thrombotic, not the formation of new connective tissue. If the abscess is traumatic, originating from compound fractures of the skull, or from traumatized and infected cerebral tissue during the exploration and evacuation of an adjacent or metastatic abscess, it may be situated in any part of the brain traumatized, a subcortical "abscess frequently being associated with a meningeal abscess. CLINICAL CLASSIFICATION OF BRAIN ABSCESS. The importance of a thorough understanding of the origin, mode of infection, relationship with the dura and piaraohnoid, and the probable exact site and duration of the intradural suppuration, must be fully appreciated by the surgeon before entering the dura, as each may occasion such variations in the mechanical, pathological and physiological factors as to call for specific surgical reco^ition. Exploration into cerebral substance when the abscess is situated entirely within the meshes of the piarachnoid, may result fatally; while the attempted evacuation of a meningeal abscess through a small dural opening — sufficient in an acute intracerebral abscess — is bound to be followed by failure. If now the surgical types. Chronic {Secondary) Adjacent Abscess with a capsule; Acute Adjacent Abscess without limiting membrane; Metastatic, and Traumatic Abscess; be combined with the specific surgical types: — Intracerehral Abscess without macroscopical evir dence of cortical involvement; Intracerebral with a cortical "stolh/' and Meningeal Abscess ; from the clinical point of view the following varieties in intradural abscess may be recognized surgically, each presenting individual technical problems : — CHBONIO BBAIN ABSCESS: 1 (o), Intracerebral with Capsule, without Macroscopical Evidence of Cortical Involvement; Origin; Adjacent, Metastatic, or Traumatic. Tliis is the most frequent type of adjacent (secondary) abscess, exceptionally of traumatic or metastatic origin. 22 BBAIN ABSCESS 1 (&), Intracerebral without Limiting Membrane; Origin; Metastatic, or Adjacent. To this type belong most of the metastatic abscesses, but a certain proportion of otitic and rhinologic abscesses, although of long dura- tion, have no capsule. 2, Adjacent Intracerebral with Capsule and "Stalk"; Origin; Adjacent (Secondary), or Traumatic. The stalk extending through the cortex and attached to the inner surface of the dura over the site of original infection. In exceptional cases the stalk may extend through the dura. 3, Meningeal; Origin; Adjacent, Traumatic, or Metastatic. ACUTE BEAIN ABSCESS: 1. Intracerebral without Limiting Membrane, but whose fluid contents are distinctly circumscribed: Origin; Adjacent, Metastatic. 2. Meningo-Cerebral, associated with an active surrounding encephalitis: Origin; Traumatic. 3. Meningeal; Origin; Adjacent, Traumatic. Metastatic abscess and abscess originating from sudden vascular occlusion are classified together, and "acute abscess with a stalk" is omitted, the stalk not being macroscopically recognizable and consequently cannot be utilized surgically. INTRACEREBRAL ABSCESS WITH A CAPSULE AND "STALK." In the author's experience abscess with a stalk is not so frequent as intracerebral abscess without maoroscopical cortical involvement, although Komer states that forty-two per cent, of all brain abscesses are from direct extension. However, in the reports of 131 cases of brain abscess analyzed by the author, a sinus leading to the abscess was found in but four. The abscess situated in both the cortex and the subcortical tissue is attached by its stalk to an adjacent area of suppuration in either the temporal bone or the accessory sinuses of the nose. It is a chronic process, the entire abscess and stalk being distinctly encapsulated. There is reason to believe that intracerebral abscess with a stalk is a late stage of intracerebral abscess without maoroscopical evidence of cortical involvement. The stalk develops after the formation of the abscess cavity by a continuation of tissue necrosis from the abscess cavity toward the cortex, following in reverse order the path of in- fection originally taken by the causative thrombophlebitis, the nutri- tional disturbances of the cerebral tissue, plus the pressure of the abscess from above, causing the necrosis. Those who have viewed through a large dural opening throm- bosis of a cortical cerebral artery ; who have seen how distinctly the area of improper blood supply is demarked, and yet how normal it appears until compared with the surrounding cortex, can understand PATHOLOGICAL AND SITEGICAL CONSIDBEATIONS 23 How the area surrotindiiig a retrograde throm'bophle'bitis is the seat of an extension of the suppurative process from the abscess. The writer's reasons for believing that the stalk is frequently a secondary process after the development of the abscess itself are: that abscesses with stalk are much less frequent than intracerebral abscesses without macroscopical evidence of cortical involvement; that the stalk is found only in old abscesses; that post-mortem ex- aminations show a large number of extensive abscesses with a per- fectly normal cortex ; and that there is sometimes seen at post-mortem an area of necrosis of the surface of the cerebral tissue, not extending from the dura. In the abscess with a stalk from direct extension of tissue necrosis, the suppuration having advanced from the adjacent site of infection, firmly uniting the piarachnoid with the inner surface of the dura and extending through the cortex, furnishes a direct route into its interior without injury to the subarachnoid or subdural spaces. During operation, if the dural opening is large the stalk is easily located by the area of adhesions of the piarachnoid to the dura. This type of abscess, if evacuated early, should give a high percent- age of recovery. Many cases of brain abscess have recovered spon- taneously by evacuation through the stalk and the formation of a fistula in the dura. This — Jbfature's method — the establishment of an encapsulated tract through the dura, piarachnoid and cerebral tissue into the abscess cavity — should be one of the first principles to be followed in surgical treatment. In like manner in adjacent abscess the surgeon should attempt to convert an intracerebral abscess with a limiting membrane but without macroscopical evidence of cortical involvement into a cap- sulated abscess with a stalk; i.e.j to convert an acute abscess without limiting membrane into an encapsulated intracerebral abscess. INTRACEREBRAL ABSCESS WITHOUT CORTICAL INVOLVE- MENT DISCOVERABLE MACROSCOPICALLY. This type is generally caused by a retrograde thrombophlebitis of a cerebral vessel.^^ TTpon opening the dura no evidence of dis- ease is discoverable in the piarachnoid or the cortex, the abscess being situated entirely within the cerebral substance at a depth of from one to four centimeters beyond the cortex, but adjacent to the primary infection. Although at operation the cortex usually appears normal, in one " Preysing, H. : Neun Gehirnabszesse im Gefolge von Obren-und Nasenerkrank- nneen ; ArcMv Jilr Ohrenheilkunde, 1900-01, B. 61, S. 262. 24 BEAIN ABSCESS instance in a metastatic abscess secondary to bronchiectasis the writer found a small thrombosed vessel running from the dura through the arachnoid space, the abscess being located directly under the affected vessel. The author is not familiar with a similar observation during life/^ but surgically it suggests a careful inspection of all vessels running from the dura into the brain for surrounding infiltration or thrombosis.-^* The peculiar blood supply of the brain accounts for the formation of the abscess entirely beyond the cortex.^* The blood vessels of the pia run horizontally upon the surface of the cortex and anastomose freely; consequently, thrombosis of a pial vessel but infrequently interferes with the nutrition of the cortex sufficiently to produce extensive local necrosis. On entering the cerebral tissue, however, the blood vessels run vertically and become terminal; infective thrombosis of a cerebral vessel, therefore, is rapidly followed by local nutritional death of cerebral tissue with abscess formation. The cerebral necrosis from lack of proper nutrition, following infective vascular occlusion of a terminal and intracerebral vessel, explains the frequency with which intracerebral abscesses grow in- ward toward the ventricle — rupture into a ventricle being a frequent termination — and the futility of leaving the dura open "so that the pus may follow the line of least resistance," in case of failure to locate an abscess. "The line of least resistance" in nutritional death is really in- ward. If a capsule is not formed the brain offers but little resist- ance until the abscess approaches the ventricle, when, according to Miodowski,^^ the choroid plexus may take on a definite protective action, becoming thickened by several layers of exudate. (This observation has not been confirmed in the writer's experience, although he has repeatedly examined the choroid plexus at post- mortems.) SUBDURAL ABSCESS." Subdural abscess rarely exists except as a traumatic complica- tion of intracerebral abscess. The literature contains but a few ref- " MacEwen, W. : "Pyogenic Infective Disease of the Brain and Spinal Cord" ; 1893, p. 90, Fig. 39. (Depicts a thrombophlebitis over the area of a brain abscess at post- mortem.) " The vessels that normally enter the dura directly from the cerebral cortex are comparatively few and consequently may be rapidly investigated. "Plersol: Textbook of Human Anatomy, III Edition, 1911, p. 1206. ■■ Mlodowski, F. : BeitrSge zur Pathogenese und pathologischen Histologie des Hirnabszesses ; Archie fiir OhrenheUkunde, 1908, B. 77, S. 239. >• There exists confusion in the anatomical nomenclature. Some authors regard the smooth, glistening lining of the dura as the parietal layer of the arachnoid, and consequently would call It the arachnoid instead of the subdural space. (Santfie, H. B. : "Anatomy of the Brain and Spinal Cord," 1915, p. 9.) PATHOLOGICAL AND SUEGICAL CONSIDBEATIONS 25 erences to collections of pus confined to the subdural space.^'^ The author's own experience is limited to the case referred to on page 73, which, it is believed, originated from the exploration and evacuation of an intracerebral abscess through a small dural opening. The frequency of subdural abscess as a complication of eixperi- mentally produced traumatic intracerebral abscess would make it appear that trauma is the usual cause. ^*' ^®' ^^ METASTATIC ABSCESS. This is usually situated within the white substance of the brain, secondary to septic vascular occlusion, the infection having been brought from a distant focus by the circulation. All possess the two characteristics of metastatic abscess — the situation away from the site of original infection, and an apoplectic onset. Metastatic brain abscesses are frequently secondary to bronchiec- stasis, pyemia, and endocarditis, but are rarely associated with aural suppuration, although a personal experience has convinced the writer of their occurrence. ^^' ^^ From an operative standpoint metastatic abscess belongs to the group having no macroscopical cortical involve- ment ; the frequency of multiple metastatic brain abscesses, however, should be recognized. (See Metastatic Abscess, p. 68.) TRAUMATIC BRAIN ABSCESS. Prior to the development of otology and rhinology, and before the recognition of aural and nasal suppuration as the cause of adja- cent brain abscess, trauma was regarded as the most frequent cause of intradural suppuration. Although its importance has been much neglected in recent years, an examination of the recorded cases dem- onstrates that, in the presence of a chronic or acute adjacent suppu- ration, trauma still may be regarded as playing an active part. Many " Strelt, Herman : Weltere Beitrage zur Histologie una Pathologle der Meningitis nnd Slnusthrombosis ; Ardhvo filr Ohrenheilkunde, 1912, Bd. 89, S. 177. (Gives analyses of reported cases.) " Esslek, C. R. : Pathology of Experimental Traumatic Abscess of the Brain ; AffiKi. Neurol, (md Pgychol., 1919, I, p. 673. (States that during the experimental production of brain abscess, "in one-third of the animals the infection entered the subdural space, forming a subdural abscess.") "» Heine, B. : Zur Kenntniss der subduralen Biterungen. Beitrage aur Ohren- heilJcundej Featscti/Hft Lucae, Julius Springer, Berlin, 1905. (Contains an excellent colored illustration of a subdural abscess.) ™ Hinsberg, v. : Ueber dem Infections Mechanismus bei Meningitis und Stlrn- hohleneiterung ; Verhandlungen der Deutsche Otol. Oesenachaft, 1901, S. 191. (Gives microscopical findings of path of invasion by blood vessels and lodgment in subdural space, with microscopical Illustrations.) =1 Jobson, G. B. : Contralateral Otitic Brain Abscess ; Laryngoscope, Vol. 25, 1915, p. 7. >= Bagleton, W. P. : Report of a Case of Brain Abscess Resulting from an Infec- tive Vascular Occlusion of Otitic Origin, with Involvement of the Internal Capsule, clinically Simulating Cerebral Apoplexy, and Presenting Unusual Psychic (toxic de- lirium) Phenomena. Operation — Recovery — Subsequent History. (Reported at the annual meeting of the Medical Society of New Jersey, held at Spring Lake, N. J., June, 1915.) 26 BEAIN ABSCESS oases of clironio otitis first present cerebral symptoms following a blow or fall on the head. (See Case XII, W. K., Chapter IV, page 60.) Likewise, in many recorded cases the first symptoms of brain abscess followed a surgical manipulation, such as a radical operation, on a neighboring bony structure. Such cases are so numerous that the inference is forced that the trauma of the opera- tion was the direct cause of the brain abscess, or lighted into activity a long dormant intracerebral suppuration. (See Analysis of post mortem examination of cerebellar abscess, p. 105.) Traumatic brain abscess may be defined as a collection of pus, the result of death of cerebral tissue in the presence of infection, the tissue death resulting not from the infection, as in secondary adja- cent brain abscess, but from trauma coincident with the infection. Traumatic infective encephalitis passes imperceptibly into trau- matic brain abscess. Infective encephalitis is a diffuse septic process, whereas traumatic brain abscess is a partially- — but only partially — ^limited one. The difficulty of limiting the process is the distin- guishing feature between traumatic and adjacent abscess. In the latter the protective mechanism of the brain has been marshalled, the bulwarks of resistance have been prepared before the actual en- trance of the invading micro-organisms. In the former the trauma, by killing cerebral tissue, has furnished a most favorable medium for the grovTth of micro-organisms before provision for combating them has been made ; and the secondary oedema following the trauma, — ^by blocking the nutrient channels of the brain, by the induction of thrombosis and hemorrhage into its substance, and by increasing the brain's bulk and thus causing compression — ^has established a vicious circle which not only favors extension of the infection, but actually paralyzes all attempts at limitation. These specific factors of traumatic abscess (death of cerebral tissue prior to preparation; secondary oedema with associated hem- orrhage and thrombosis; increase in the brain's bulk, all causing compression with further death of tissue, and paralysis of the brain's protective mechanism) should forewarn the surgeon because an en- capsulated adjacent abscess — which has been fully walled off — may be converted during operation into a traumatic abscess with its associated encephalitis. MENINGEAL ABSCESS. Intrapiarachnoid. — This type, the result of direct infection through the dura, is at first a protective process of the piarachnoid in ^^s^ JCi a^"': ■ ^^ ^ ^■-^ ^^i.'- i^J*^ ^ y^ &^>^' pf-i M 1 ,-^ ^tt tm :?# ■•?^. \, ^S mM¥ ■'►'' K^' »^-- \ :^m m ■' ^a in Fia. 5 (a) Fig. 5 (b Fig. 5 (a) and (1>). — Brain abscess situated In meshes of piaradmoid; super- ficial necrosis from pressure. E.Kpioration .and evacuation tlirougli small open- ing. Death from nreningitis. Autopsy disclosed a further brain necrosis and abscess contiguous to dural opening. Osteoplastic flap and dural incision would have exposed the entire intrapiarachnoid abscess ancl prevented the cutting off by brain pressure of tlie undiscovered portion. PATHOLOGICAL AND SUEGICAL CONSIDBEATIONS 27 its attempt to prevent general infection of the meninges.^' The delicate cells of the piarachnoid take on great activity when ap- p^roached by infection, and offer a very efficient barrier to the inva- sion of micro-organisms from either the dural or the cerebral sur- face. While our knowledge of the function of the cells lining the subarachnoid spaces is still very meagre, they play an active part m the brain's protective mechanism. In the presence of an adja- cent suppuration, a large collection of cerebro-spinal fluid is fre- quently localized around the infected area, which later may become a localized collection of pus. As our present knowledge but rarely admits of a positive differ- ential diagnosis between cortical and subcortical lesions, the surgeon, before exploring the brain substance, should examine the brain sur- face in all directions accessible to the dural opening. If the abscess is situated within the meshes of the piarachnoid, exploration into the brain tissue is not only unnecessary, but may seriously militate against the patient's recovery. In three cases after an unsuccessful exploration of the cerebral substance, the post-mortem disclosed an abscess localized entirely within the meshes of the piarachnoid. In each instance I failed to locate the intrapial abscess because I was working through an insufficient opening. All of these cases, though ending fatally, were favorable cases for recovery, had they been properly treated. (See Fig. 5 a and b.) These experiences con- vince me that exploration through an intact dura, as so frequently practised, is fundamentally wrong. GENERAL SUEGICAL PRINCIPLES. Clinical experience and experimental observation abundantly teach that one of the prime objects in the surgical treatment of intra- cerebral abscess, secondary to adjacent suppuration, is the utilization of the already organized protective reactions of the brain. Surgical manipulations should be so conducted as not to paralyze this protec- tive mechanism. If the operative trauma to the brain is not the minimum necessary to meet the individual requirement — the eradi- cation and obliteration of the abscess in an encapsulated abscess with a stalk — ^the complete or partial evacuation in an encapsulated intracerebral abscess, or simply the partial evacuation of the abscess for the relief of increased intracranial pressure in an acute abscess, (a localized collection of pus — localized either actually if a capsule has been formed, or potentially if the abscess is acute) will convert " Kllppel, D. : Mfinlngites Chroniques : Nouvecm Traiti de Midedne de Thera- pmtigue, 1912. Tome 35, p. 274. 28 BEAIN ABSCESS such abscess into a traumatic abscess, with almost inevitable rapid extension of the infection, cerebral necrosis, and death. Surgical Factors. — The factors to be considered in surgically approaching a brain abscess are: (1) the duration of the cerebral suppuration, (2) the presence or absence of a limiting membrane, and (3) the extent of the disturbances in the brain substance, out- side the abscess. The different pathological processes not only call for variations in the operative technic to be adopted, but markedly influence the possibility of successful surgical intervention. Irrespective of the pathological condition and because of the factors peculiar to cerebral tissue, the surgeon on entering the dura must endeavor to prevent all injury to the brain from its own pres- sure; to lessen, as far as possible, injury to the brain tissue by manipulation thereby converting the abscess into an unlocalized traumatic process; to prevent the spread of the infection to tissues as yet not infected, especially the meshes of the piarachnoid ; to con- trol compression, which of itself favors extension of the suppurative process, and to convert an unfavorable into a favorable type of abscess whenever this is possible. General Technic. — Slow, painstaking work, from tlie first nick in the dura to its complete closure, is of primary importance. The intradural work should be performed with as much delicacy and attention to detail as are required dur- ing the extraction of a cataract. Each drop of blood effused into the piarachnoid or the cerebral tissues, each separate trauma, hemorrhagic or manipulative, lessens the probability of the patient's recovery. Essick " believes that there is experimental evidence that whole blood limits the spread of infection to the meninges. If this is substantiated, it will revolu- tionize our ideas of the treatment of the subarachnoid spaces during the evacua- tion of brain abscess. The experiments of Flexner ^ and Weed,'" however, demonstrate that any disturbance of the protective mechanism of the brain — ^the withdrawal of cerebro- spinal fluid, the production of an aseptic meningitis by the injection of sera, or the infusion of blood within the subarachnoid spaces — greatly predispose to a general infection of the meninges in the presence of a blood stream infected by certain micro-organisms. Of course Essick's experiments approach much nearer to the conditions present during the evacuation of a brain abscess than the induced blood stream infections of Weed and Flexner. The latter, however, dem- onstrate how delicate the protective mechanism of the nervous system is and how easily it is disturbed, while clinical experience teaches that hemorrhage into the subdural spaces in the presence of infection actually facilitated its spread. Until Essick's observation has been amplified, the surgeon must be careful to avoid all effusion of blood within the meninges or brain. " Essick, C. E. : Pathology of Experimental Traumatic Abscess of the Brain ; li^h. Neurol, ana Psychol., 1919, I., p. 673. =' Flexner, S., and Amoss, H. L. : The Relation of the Meninges and Choroid Plexus to Poliomyelltlc Infection ; Jour. Exper. Med., 1917, Vol. XXV, p. 525. 2" Weed, L. H., Wegeforth, P., Ayer, J. B., and Felton, L. D. : Meningitis Pro- duced by Intravenous Inoculation ; Monographa of RooTcefeller Institute Jor Medical Beseareh, No. 12, March 25, 1920, pp. 67-112. PATHOLOGICAL AND SUEGICAL CONSIDEEATIONS 29 Injxjbt to the B&ain fbom Its Own Fbessuse. Upon, opening the dura excessive internal pressure may cause cerebral herniation, with injury to the arachnoid, associated with slight hemorrhage into its substance. In acute abscess, the tension within the dura is always excessive ; consequently, if the dura appears very tense, before opening it a lumbar or ventricular puncture, de- pending upon whether the suppuration is in the cerebrum or in the cerebellum, may be performed, although the early withdrawal of cerebro-spinal fluid is to be avoided if possible. LuMBAB Puncture; Its Dangees: Lumbar puncture, with the withdrawal of a small amount of fluid prior to the incision of the dura in abscess of the cerebrum, will allow the brain, to fall away from the dura so that it can be incised without injury to its contents. The performance of lumbar puncture is not without danger, especially if there be an abscess below the tentorium, as, by the removal of the cushion of the cerebro-spinal fluid from below, the increased pressure above may drive the medulla through the foramen magnum, herniating it, with resulting immediate paralysis of the respiratory centre. I have seen death on the table following a lumbar puncture; while the fluid was still flowing, the patient stopped breathing, and although the heart continued to beat for ^ome time, during which artificial respiration was continuously performed, the patient from the time of the accident gave no evidence of voluntary respiration. VENTEICULAB PUNCTURE: In cerebellar abscess the intracranial pressure is not only increased by the abscess, but also by an internal hydrocephalus, — a usual complication of cere- bellar abscess. (See Appendix, Part IV.) In abscess of the brain, with its complicating internal hydrocephalus, the increased intracranial pressure may obliterate the lumen of the large venous sinuses, the blood, ordinarily carried by the sinuses, leaving the skull by the normally small diploic vessels. Extreme venous obstruction, so frequent in tumors of the posterior fossa, is not encountered, however, during operations for cerebellar abscess, as death will have supervened long before an advanced stage is reached. Sufficient venous obstruction to obliterate the lateral sinus of the affected side, giving rise to a mistaken diagnosis of a sinus thrombosis, has been observed by me during operation. When venous obstruction is present the removal of bone over the cerebellum may be accompanied by considerable hemorrhage, and the opening of the dura without immediate prolapse of the brain and rupture of the piarachnoid will be impossible, especially if only one hemisphere is exposed. If, however, a ventricular puncture is performed before the dura is opened, the sinuses again become patent, the bleeding stops and the cerebellum drops back, permitting dural incision without prolapse of the brain. Technic of Incision of the Dura: To avoid possible injury to the piarachnoid. Gushing originally caught and elevated the dura with two fine silk ligatures, cutting between them. Later he employed a small, sharp, half-curved membranous cataract hook for the primary opening. By either method the dura can be incised without injury to the 30 BEAIN" ABSCESS piarachnoid. When the dura is not excessively tense, it can generally be safely incised by cutting superficially with a knife, scraping a little from side to side, and then cutting a little deeper and scraping again. In several instances, how- ever, I have injured the piarachnoid during this procedure. The small dural opening may be enlarged safely by cutting on a flat brain spatula, the dural vessels being "clipped" by Cuahin^s silver wire" or ligated before incision. CLASSIFICATION OF BEAIW ABSCESS ACCORDING TO LOCATION. The anatomical and physiological relationships of suppuration in the frontal, temporo-sphenoidal, occipital lobes and cerebellum occasion great differences, not only in symptomatology, but in surgi- cal considerations. A useful clinical classification, however, is into : Abscess of the Middle Fossa (Temporo-sphenoidal), Frontal lobe abscess and Cerebellar abscess. The occipital lobe is in such inti- mate relationship with the temporo-sphenoidal lobe that surgically they are considered together, suppuration confined to the occipital lobe alone occurring only in abscess of metastatic or traumatic origin. " Gushing, Harvey : The Control of Bleeding In Operation for Brain Tumor, with the Description of Silver "Clips" for the Occlusion of Vessels Inaccessible to the Ligature ; Trams. Amer. Surg. Assoc, 1911, XXIX, p. 389 ; Annals ot Surgery, 1911, Vol. LIV, pp. 1-19. CHAPTEK IV. ABSCESS OF MIDDLE EOSSA. ADJACENT (sECONDAEt) ABSCESS OF THE MIDDLE FOSSA TEMPOBO-SPHENOrOAL, LOOATIOK; PATHOLOGICAI AND ANATOMICAL CONSIDERATIONS: During the early stages of brain abscess, the symptoms as a rule are so vague tbat they do not warrant a positive diagnosis of intra- cranial suppuration, much less its definite localization. Consequently any operative procedure vrhich may be undertaken at an early stage must be largely exploratory and must be so conducted that in case of failure to locate the suppuration as little damage as possible, im- mediate or remote, wiU be caused by the exploration. The usual sites of intradural suppuration of the middle fossa secondary to aural disease, are, (1) in the meshes of the piaraohnoid, directly above the tegmen of either the antrum or the middle ear; such an abscess is probably preceded by, and results from, an extensive but still localized menin- gitis, a pathological condition which lumbar puncture and post- mortems lead the author to believe is of greater frequency than, is generally recognized :^ (2) in the substance of the temporo-sphenoidal lobe itself, in the second temporo-sphenoidal convolution, or (3) an extension from one or other of the above. INTERCURRENT (TERTIARY) ABSCESS OF THE MIDDLE FOSSA, SECONDARY TO THROMBOSIS OF THE SUPERIOR PETROSAL SINUS OR A DURAL VEIN:' As thrombosis of the lateral sinus is often the immediate mode of transmission to distant portions of the cerebellum, away from tiie petrous, so thrombosis of the superior petrosal is in rare cases the transmitting agent of the temporo-sphenoidal lobe; for it is to be re- >Brleger: In Blau'a EneuelopeeUe der Ohrenheflkimde, 1900, S. 245. ' See Case XXVIII ; Chapter XI, page 182. 31 33 BKAIN ABSCESS membered that one of the main venous efferents of the basal por- tion of the brain — one of the medio-cerebral veins, often called the temporal sinus — empties into the superior petrosal sinus.*' * ADJACENT MENINGEAL ABSCESS (INTBAPIAEACHNOID OE SUB- DUEAL) OF THE MIDDLE FOSSA.' Post-mortem examinations lead the writer to believe that an abscess primarily situated in the meshes of the piarachnoid, the result of direct extension through the tegmen, is apt to remain con- fined to the meshes of the piarachnoid. As it increases in size, the intrapiarachnoid abscess frequently involves the cerebral cortex, by direct pressure causing "superficial brain necrosis," but never re- sulting in an intracerebral abscess. Localized Sebous (PKOTEca^vE) Meiningitis. To this group belong the cases of so-called "serous meningitis," with localizing symptoms, aphasia, paralysis, etc., which recover after the removal of the focus of infection within the temporal bone without opening the dura. Serous meningitis is probably primarily a sterile, localized collection of cerebro-spinal fluid of toxic origin, which later may become easily infected — the primary stage of an intra-piarachnoid or subdural abscess.®' ''• ®' ® The experimental work of Essick, in which the presence of bac- teria in the adjacent tissues without invasion of the subarachnoid space itseH causes a large increase in the amount of cerebro-spinal fluid and leucocytes, explains the frequency of serous meningitis and its operative treatment, viz.; — (a) The removal of the adjacent infected area of the mastoid cells or the petrous pyramid, and (b) , the prevention of compression by decompression through a clean area, lumbar puncture or the evacuation of the fluid by incision of the dura through the infected area. The latter method is frequently successful, but it allows the evacuation of only a small quantity of fluid, with the liability of infection of an uninfected area. « Browning, W. : The Veins of the Brain and Its Envelopes : Their Anatomy and Bearing on the Intracranial Circulation ; Monograph, Brooklyn, 1884. * Whitehead, A. L. : Some Points in the Diagnosis of the Complications of Tem- poral Bone Disease, Based upon a Study of 135 Fatal Cases ; Journal oj Lwryngology, Otolagu and RMnoiogy, 1906, Vol. XXI, p. 269. » See p. 17, Surgical Classification of Brain Abscess. ' Boenninghaus, Georg : "Die Meningitis Serosa Acuta" ; Wiesbaden, Verlag von J. F. Bergman, 1897. (Reviews cases reported prior to 1897.) ' Warrington, W. B. : Intra-cranlal Serous Effusions of Inflammatory Origin, Meningitis, or Ependymitis Serosa; Quarterly Journal of Medicine, January, 1914, Vol. 7, No. 26, p. 98. (Reviews the literature.) ' Knapp, A. : Serous Meningitis ; ArcMves ot Otology, 1906, No. 1, p. 10. » Emerson, Linn : A Case of Serious Meningitis Mistaken for Brain Abscess ; Opera- tion ; Recovery ; Reprint from Laryngoteope, July, 1906. ABSCESS OF MIDDLE FOSSA 33 CASE r, B. B. Sinus Thrombosis. Male. Chronic otitis media, left ear. Frequent attacks of pain and lieadache; chills. Admitted to hospital suffering from mastoiditis, left side. Mastoidectomy done. Sinus thrombosis discovered; jugular not ligated because of condition of patient; thought to be dying. Eecurrence of symptoms. Operation: Ten days after mastoid operation, ligation of jugular. On open- ing vein it was found to contain free pus for a distance of about three inches, running down below the clavicle. The pus was not in the fascia around the vein, but was in the vein itself. Immediately after the second operation the man complained of dizziness. Ten days later chill; violent headache, repeated at regular intervals during the day. Patient gradually became violent from pain, which passed as suddenly as it came. Had two chills. Marked papilloedema of both eyes. Labyrinth dead. Spontaneous deviation of both hands to right. Fell to right. No spontaneous nystagmus. Slight area of anesthesia along third branch of trifacial. One attack of vomiting. Lumbar pimcture revealed cloudy fluid under pressure; cell count 160; increased globulin. Spontaneous deviation to right and falling to right, both away from lesion, pointed to involvement of cerebellum over posterior surface of petrous portion of temporal bone. This was also confirmed by cerebro-spinal fluid, which gave symptoms of protective meningitis. Cerebellum exposed in front of sinus. Incision of dura through sinus region; in front of this evacuated large amount of cerebro-spinal fluid. Diagnosis: Serous meningitis. Uneventful recovery. CASE VI, J. G. Aseptic Meningitis. Male, 26 years of age. Eight ear had been discharging for past three years, with attacks of pain, which, however, were not severe. Never any dizziness except when he had grippe about one year before coming to hospital; but did not think it was associated with any exacerbation of his ear trouble. About three weeks before admission to hospital had an ulcerated tooth; after extraction tlie pain continued for a time and then subsided. At the same time he began having pain in his ear, and dizziness ; pain in ear was not steady — it was sometimes severe and sometimes not. It was associated with pain in the head in the right temporal region, running forward toward the frontal region. During these three weeks he had dizziness — ^ran into things but did not fall. Swayed at times, but could not tell to which side he was inclined to fall. Had two attacks of vomiting, not influenced by food. When first seen had no facial paralysis, but three or four days later was found to have a right-sided facial paralysis, and the discharge in the ear was very much increased. Examination of his ear showed a large mass of polyp coining from roof. Had a slight convergent strabismus; was totally deaf in right ear; complained of chilly sensations; no patella reflexes; no sense of taste. Operation: A radical operation was done, following which the cochlea was opened and the vestibule entered. The external semicircular canal had necrosed through. The dura over the internal auditory meatus was opened, evacuating cerebro-spinal fluid; no increaseji tension. For several weeks patient had con- siderable temperature, pain in his head, stiff neck, and high cell count. Some weeks later patient, discharged sequestra of cochlea. It was then seen that protective meningitis had followed operation. Uneventful recovery. (The case is recorded in The La/rynffosoope, for January, 1922.) Clinical Diagnosis. — ^With a high temperature without chills but with symptoms of compression, such as papilloedema, if repeated 34 BEAIIT ABSCESS blood cultures have been negative or the sinus has been explored and found to be uninfected, or if the infection has been thoroughly elimi- nated, and especially if cytologieally an aseptic meningitis is pres- ent — see Case V, K. B. — ^we are warranted in suspecting an aseptic meningitis of the irritation type. In which case, before exploration within the dura it is justifiable — (1) to thoroughly evacuate all infected areas, mastoid, labyrinth or sinus, and (2) to control the increased intracranial pressure by decompression through a dean area, ventricular puncture or liunbar puncture. The procedure to be adopted for the control of compression depends somewhat upon the site of the suppuration, for it must always be doubtful if an intracerebral abscess is not also present. If the labyrinth and sinus are both intact the decompression should be a subtemporal one, while if either the labyrinth or sinus is known to be involved, and consequently a cerebellar abscess is possibly present, a ventrictilar puncture or a cerebellar decompression should be performed. The danger of a lumbar puncture causing sudden death from respiratory paralysis in cerebellar abscess is so great that it should only be re- sorted to in case a ventricular puncture for some reason is not advisable. Extension or Intrapiabachnoid Abscess. In its growth a localized meningeal collection of pus, starting from just above the tegmen, usually extends externally along the under surface of the temporo-sphenoidal lobe; then upward and for- ward, along the external surface of the temporo-sphenoidal lobe in which direction it may travel a considerable distance. A meningeal abscess so situated is always very shallow, due to the firmness with which the temporo-sphenoidal lobe is held to the floor and sides of the middle fossa by the weight of the brain, the exit of the nerves and vessels toward the median line, and the veins entering the lateral sinus. An abscess so situated is frequently divided into several compartments communicating with each other — the so-caUed "oyster- shaped abscess." Earely the localized meningeal collection of pus extends directly backward, inward and upward, along the upper surface of the ten- torium cerebelli, below the occipital lobe. When the abscess is situ- ated above the tentorium, the purulent collection is apt to be very large in amount but of very thin consistency, being in reality simply a large localized collection of purulent oerebro-spinal fluid, not thick pus. ABSCESS OP MIDDLE FOSSA 35 In evacuating a meningeal abscess on the external surface of tlie temporo-sphenoidal lobe, a part of the abscess may be easily over- looked because the internal pressure of the brain forces it firmly against the edge of the dural flap, thus cutting the abscess in two. In meningeal abscess over the tegmen, a similar accident is not in- frequent, the brain descending before the abscess is completely evacu- ated. This is illustrated by the following case : CASE VII. J. J. o. Brain Abscess. Steam fitter, well developed and nourished, admitted to hos- pital November 18, 1912. Diagnosis: Brain Abscess. Two months previously, patient "got cold in ears" while swimming, and two days later became almost totally deaf first in right, then in left ear. Abscess developed in both ears and broke in right. No discharge from ears. The right ear gradually got better, but pain continued in both ears. About two weeks before admission to hospital pain increased in left ear, and patient became very deaf in that ear. There was never any discharge from either ear. Eight days before the patient was seen, intense pain developed in head and in left ear, with dizziness, and the man was obliged to stop work. Tym.panic membrane lanced. For three days previous to admission had been almost totally deaf in left ear, with intense pain; also had peculiar frontal headache and pain in eyes. He suddenly felt something break in head which soimded in left ear like cannon shot, and since explosion had word deafness; vomiting three days before and during explosion. There was a previous history of pneumonia in childhood, and typhoid 11 or 12 years ago. Use'd neither tobacco nor alcohol. Examination revealed right sided hemianopsia, paresis of right arm, and Wernicke's aphasia. Could recognize family and his own doctor, but could not understand their names. There was word deafness, slight dizziness, absence of right-sided abdominal reflexes, exaggerated knee-jerks, especially the right, exag- gerated plantar reflexes, and tendency to ankle clonus on right side; no Oppen- heim, no Babinski, no nystagmus, but increased P. K. on right side. Tongue very eoateid; no tremors. Left ear: could hear watch on contact; deaf to aerial con- duction. Eight ear: could hear watch at 2 inches. Operation.—^ large flap was made above the left ear and the skull exposed and trephined; mastoid not opened. Some pus was found in the external audi- tory canal. Dura found to be adherent and covered with granulations; no pus in dural cavity. Upon exposing the temporo-sphenoidal area of the brain an oyster-shaped abscess was discovered in posterior portion of lobe, with distinct limiting membrane. Brain surface was irrigated with warm saline, the dura closed and rubber drain inserted. The scalp was closed with interrupted sutures of plain catgut. The following day patient appeared confused, but was able to recognize names of objects shown to him. Temperature 102°. A lumbax puncture was done and about 300 c.c. of fluid withdrawn under tension. Paresis of right arm still present, and probahly hemianopsia of right aide. Patient unable to talk, and upon attempting to read printed numbers tried to make them; usually made them inverted. Nine days later patient had two severe convulsions, lasting about five minutes each. Temporo-sphenoidal region again explored, but no abscess found. Eubber tissue placed over brain and a drain passed through soalp. Patient then turned on abdomen and incision made in median line of neck down to base of skull, bone chiselled away and medulla exposed. Dural and basal cisterns opened and 36 BKAIN ABSCESS rubber drain inserted into the latter. Gauze drain inserted down to base of wound. The next day patient had convulsion which lasted one minute, and on follow- ing day convulsion and chill. The day after, he had convulsion at 2.30 a.m. which lasted one minute, and another at 4.45 p.m., with incontinence. Death occurred at 1.00 a.m., on the thirteenth day after operation. Post-mortem examination showed that this man originally had infection of the left middle ear, which was followed by the extradural abscess disclosed at operation. The abscess was walled off from the dura by firm granulations, and was followed by an intradural, extrapial abscess, which at operation appeared to be intracerebral ; the covering, however, proved to be simply a thick membrane. Patient subsequently developed suppurative meningitis. The infection was evi- dently one of low virulence, as no bacteria were found in the cerebro-spinal fluid or in the pus examined. Local collections of pus at post-mortem exhibited a tendency to recede under the occipital lobe in the position of normal drainage from gravity. Nothing abnormal was found in the ethmoidal, sphenoidal, or lateral sinuses, or in the opposite ear. ADJACENT INTRACEREBRAL ABSCESS OF THE TEMPORO- SPHENOIDAL LOBE WITHOUT MACROSCOPICAL MAN- IFESTATIONS OF CORTICAL INVOLVEMENT. Abscess of the temporo-sphenoidal lobe, without macrosoopical evidence of cortical involvememt is the most frequent variety of brain abscess. It develops either from a retrograde thrombophlebitis, or from direct extension of tissue suppuration from the beginning of the mastoid antrum or of the middle ear. When it originates from a retrograde thrombophlebitis because of the anatomical vascular con- dition, it is situated in or near the second temporo-sphenoidal con- volution, which, being a silent area, produces no outstanding localiz- ing symptoms on the right side in right-handed patients ; but if situ- ated on the left side it frequently produces a "naming" aphasia, which latter may at first be of but transient duration and of im- perfect extent. Adjacent abscess may, however, be situated entirely within the occipital lobe — (H. Knapp) — ^the author having seen one such case where the abscess was secondary to a lateral sinus thrombosis, or thrombosis of the superior petrosal sinus. Its situation may also be entirely removed from the temporo-sphenoidal lobe. This type of abscess may attain great size, having a tendency to extend inward from nutritional disturbances. Rupture into the ventricle is a frequent termination. TEMPORO-SPHENOIDAL ABSCESS WITH A STALK. "Abscess with a stalk" is located almost invariably in the second convolution of the temporo-sphenoidal lobe, directly above the teg- men in the cerebral substance, generally from one-half to one and a haK inches above the tegmen. (Figs. 6 and Y.) The external sur- Fig. 6. — Position of three temporo-splienoidal abscesses with a stalls, above the ■tegmen tympani and antrum, showing uniform position of adjacent abscess. Illustration copied from Preysing drawing in Korner's "Die otitischen Erkran- kungen des Hirns, der Hirnhiiute und der Blutleiter," .3d Edition, 1902. assfiiiUi LA ■ "*n t^l*Manraro MO Fig. 7. — Horizontal section of head with temporo-sphenoidal abscess with stalk, showing uniform position of adjacent abscess within cortex, low down in temporo-sphenoidal lobe, above antrum or middle ear. Illustration copied from Preysing drawing in Korner's "Die otitischen Erkrankungen des Hirns, Hirnhaute und der Blutleiter," 3d Edition, 1902. der ABSCESS OF MIDDLE FOSSA 37 face of tibe dura is frequently adherent to the bone and covered with granulations, and the dural inner surface is always united to the brain. Considerations Pbiob to Operation fob Adjacent (Secondary) Abscess of Middle Fossa. A diagnosis of a probable adjacent (secondary) temporo-sphe- noidal lobe abscess having been made, (based upon the presence or history of an adjacent suppuration within the mastoid or petrous portion of the temporal bone; the general symptomatology of the intracranial suppuration ; localizing symptoms varying between nega- tion and the pathognomic "naming" aphasia; elimination of cere- bellar suppuration), a definite opinion must be formed prior to op- eration, whether the abscess is chronic with a probable capsule, or acute without limiting membrane. This is of prime importance, as the technic to be adopted is fundamentally different, and failure properly to visualize the surroundings of the abscess may lead to an irreparable blunder. The operation must not be simply an effort to find and evacuate pus, irrespective of its surroundings ; it roast be a procedure adapted to existing conditions, the most important being the presence or ab- sence of a limiting membrane. This is in opposition to the dictum that "brain abscess, as pus in other parts of the body, is to be treated by free drainage." Eeviewing my many failures in the light of post-mortem findings, I am convinced that to avail himself of everj' advantage, the surgeon must be fairly sure before he operates whether a capsule does or does not limit the abscess. Histories of two cases of temporo-sphenoidal lobe abscess improp- erly treated because of incorrect diagnosis as to pressure or absence of capsule. CASE vm. Temporo-sphenoidal Lobe Abscess — Chronic. A. M. M. Male. Progressive muscular atrophy of left side, beginning about a year before admission to hos- pital. Four weeks before admission he began to have neuralgia on left aide of face, with pain in teeth, continuing after paracentesis of membrana tympani of left side. Ear continued to discharge. One week before admission became un- able to talk. On admission had typical "naming aphasia." Mild papilloedema of left eye. Occlusion of left aural canal. Slight paralysis of lower portion of right side of face, seen chiefly on emotional movement. Eight-sided hemianopsia; right hand slightly weak; no Babinski; no clonus; apparently deaf in left ear. Cerebration rather slow. Lumbar puncture gave apparently normal fluid; culture revealed microorganisms. Operation: — Believing it to be an acute abscess, temporo-sphenoidal region exposed over an area of an inch and a half in diameter. A small dural incision made through which the brain protruded. Gangrenous. Free pus evacuated 38 BEAIN ABSCESS through small needle. No capsule felt. Following operation slow pulse, patient in good condition, apparently disorientated. Autopsy Findings. — On removing the skullcap by the Washburn method the whole anterior lower inner surface of the anterior fossa between dura and brain was found to be covered with a yellowish exudate which looked like chicken-fat, the thickest portion being several millimeters thick; it was smooth, glistening, and extremely yellow. This covered the whole of the frontal lobe of the left side. The abscess itself was in the temporo-sphenoidal lobe, was about one inch in diameter and had a beginning membrane, the margins of which were becoming sharply defined. Its inner surface was red, undoubtedly from hemorrhages which had undergone absorption. There was no free pus in the abscess. There were many areas of slough or moisture in the abscess which, as a whole, was round with very few pockets. The area around the abscess was yellow, taking on the character of the exudate. There was typical lepto-meningitis in several parts of the brain. The lateral ventricle of the left side was much displaced over and beyond the median line and was slightly distended. The opposite lateral ven- tricle was markedly distended. The left middle ear showed an extensive area of degeneration, bluish-yellow from acute necrosis. The anterior wall of the middle ear was apparently entirely gone, leaving a fistula. The inferior petrosal sinus contained an exudate in the portion before it enters the cavernous sinus; the cavernous sinus was free. The mastoid cells were not markedly involved; the ethmoids and sphenoid not involved. On removing the dura over the tegmen the bone looked bare — ^no communication was seen between the area of the abscess and the tegmen. No adhesions between the dura and the brain. Comment. — In making a small dura! incision and trying to pass a small Whiting's encephaloscope through the small opening nothing was accomplished except to incite a traumatic encephalitis, as was shown afterwards by the gan- grenous hernia. The man had an acute abscess which should have been simply evacuated through a large or a small opening in the dura, but nothing else should have been done. On evacuation the pus was first watery and then floccu- lent. This should have warned us that this was an acute abscess. The opening made was large enough to permit herniation but too small to permit inspection. Three days after operation the pulse was only 88, although the temperature was as high as 104° The patient was restless. Systolic blood pressure was 100. Five days after the operation the pulse was 68, temperature 102°, and the patient apparently better. After operation there was marked papilloedema of both eyes — not present before operation — indicating compression. CASE rx. Temporo-sphenoidal Abscess (Chronic). G. W. Male, seven years of age. Admitted to hospital March 1, 1920. Running ear three months before; mastoid operation February 8, 1920. Operation: Operated on March 3, 1920, for temporo-sphenoidal abscess. Evacuation through a small opening in the dura with a very small needle. No pus was withdrawn, but a large quantity of clear fluid having the appearance of cerebro-spinal fluid evacuated. On introduction of the needle resistance was encountered, but on the assumption that we were dealing with an acute abscess, this was not recognized as due to the capsule of a chronic abscess. Strabismus was noted at this time. The patient did very well for three days following opera- tion. The strabismus almost entirely disappeared, but recurred. Six days after operation paralysis of the rectus of the opposite eye appeared and the patient became sleepy and drowsy, growing gradually worse until the fourteenth day after operation, when death occurred. Autopsy Findings. Very extensive encephalitis surrounded an encapsulated abscess which was adherent over the tegmen. The encephalitic tissue was soft, Fig. 8. — 'Jcinporo-splieuoidiil lobe abscess caA'itj' with displacement of hemi- sphere beyond median line. Showing increase in size of brain bulk. Death from extension of suppurative process and compression after several weeks of apparent freedom from s.Mnptoms. Aljsccss erroneously treated as an acute a,bscess by small opening wlien it was a chronic abscess with capsule. ABSCESS OF MIDDLE FOSSA 39 with numerous hemorrhages. The abscess had approached the cortex in many places, causing gangrenous areas. The capsule was distinct, firm, and in some places several millimeters thick. It was so firm that it was covered with blood vessels and by taking hold of it the whole abscess was lifted out intact. The pus surrounding the capsule was thin, such as is developed from an acute encephalitis, while that inside the capsule was thick, such as is seen in chronic brain abscess. (Fig. 8.) Comment. — From the clinical course after operation and from the autopsy findings this was evidently a case of chronic (encapsulated) brain abscess, which was treated as an acute abscess. The death of the patient was probably the out- come of this failure to differentiate the acute from the chronic condition, and of the traumatizing of the brain tissue in the effort to drain the abscess, the procedure followed being likewise the outcome of this error in diagnosis. At the time of operation, it will be remembered, a large quantity of perfectly clear fluid was drawn away which looked like cerebro-spinal fluid and was found to contain streptococci. At that time it was thought that this might be a large collection of cerebro-spinal fluid outside the brain, the abscess being intra- arachnoid. The clearness of the fluid also suggested that the abscess was acute. It is unfortunate that it was not recognized that the resistance encountered in the efforts to evacuate the abscess was due to the encapsulation of a chronic abscess, and that this encapsulation accounted for the absence of chill after the patient was admitted to the hospital. The chill probably had occurred at the time of the mastoid operation, seven weeks before, at which time, doubtless, the abscess had begun to form. The autopsy showed that the clear fluid drawn off at the time of the abscess operation was probably from the top of the abscess, the pus having settled below. The exploring needle being so small, only the clear fluid could pass through it. When the encapsulation was encountered during the exploration, a larger needle should have been used, on the theory that the abscess was chronic and the pus too thick to pass through a small needle. This case may be contrasted in that respect with that of Mrs. H., Case XIII, Chapter Four, p. 63, in which the abscess was easily evacuated through a small needle. However, the question arises whether, at the time of the operation on the boy, it could have been determined that the abscess was chronic and not acute. In the diagnosis reliance must be placed upon the difference between the symptoms of compression from chronic abscess and those of brain destruction from acute abscess. In an acute abscess there probably is brain destruction going on, with symptoms of sepsis, as shown in Case XIII, Mrs. H., to which reference has just been made. One of the symptoms of compression is slowing of the pulse. The fact that this boy had an irregular pulse should have called attention to the probability of the extension of the process, but not necessarily to compression. The increase in the optic neuritis was also signiflcant. The temperature was of little assistance. A second lumbar puncture might have been of assistance in the diagnosis. An error in technic involved the improper anchorage of the stylet tube in the capsule. The cotton must be placed in pledgets close up to the tube itself, touching it in all its parts, building a pyramid which comes from the side of the apex where the tube is. Over this must be placed a dressing and the bandage must go around the neck. Failure to observe these two essential proceedings caused the tube to become displaced in this case and also in Case XIII. Furthermore, failure to place the drainage tube within the abscess capsule, which, as stated, was not recognized as such at the time of subsequent dressing and exposure of the wound, was an error in technic, giving rise in manipulation to undue traumatization of the tissues and setting up the encephalitis found at autopsy. In other words, this chronic brain abscess was converted into an acute abscess which caused the patient's death. If the compression caused by the 40 BKAIN" ABSCESS chronic abscess had been relieved by a decompression operation, the encephalitis might not have developed, the chronic process would not have been converted into an acute one, and the final outcome of the case might have been very different. Pkinciples of Operauve Trea.tment. Exposure. — Exposure of the under surface of the temporo- sphenoidal lobe through the roof of the tympanum and antrum, fol- lowed by puncture of the dura and brain, and introduction of drain- age material, has resulted in a larger proportion of recorded cures than any other method. Were it possible to make a positive diag- nosis of an encapsulated intracerebral abscess of the temporo-sphe- noidal lobe, with a stalk, this would be the method of election, as the surgeon thus enters the abscess through the walled-off area of primary infection at its nearest approach to the cortex. Such a diagnosis is infrequent except on finding a fistulous tract during or subsequent to mastoid operation. Many such cases are on record. In the greater proportion of cases, if the surgeon is to operate early enough to offer a fair chance of recovery, the operation must be largely explorative. Exposure and exploration through the teg- men has the following objections : (a) It is througb an infected field ; if the abscess is not located, death from meningitis is almost inev- itable, (b) The exposed area is so limited that an intrapiarachnoid abscess may be entirely overlooked ; if exposed, its ramifications are obliterated by the brain pressure, (c) The surgeon, seeing a few drops of pus, cannot know it to be part of an extended, thin layer of extra-cerebral suppuration, but realizing that a larger collection of pus must exist to account for the symptoms, he is tempted to ex- plore the brain substance, creating a traumatic intra-cerebral sup- puration, (d) An intra-cerebral abscess without macroscopical evi- dence of cortical involvement, an abscess with a stalk, and a menin- geal abscess cannot be differentiated, and consequently cannot be differently treated, (e) Compression cannot be provided for except by enlargement of the dural opening into a clean area after an operation in a highly infected area — the reverse of a properly planned surgical procedure. Exposure for Suspected Localized Intrordural Suppuration of the Middle Fossa. — The operative procedure is planned to form an osteoplastic flap sufficiently large to admit of complete inspection and exploration of localized intra-dural suppuration of the cerebrum, without involving the infected middle ear and mastoid, and if an abscess is not located, to allow complete aseptic closure of the dura and replacement of the flap. (See Frontispiece.) If an abscess is Fig. 9. — Outline for formation of osteoplastic llap for exploration for sus- pected abscess of the temporo-splicnoidal lobe. ABSCESS OF MIDDLE EOSSA 41 located, especially one contiguous to tlie middle ear, tlie flap permits of drainage tlirougli the middle ear, tlie primary route of infection. The OsTEX)PiiASTic Flap fob Exploration roB Abscess of Middle Fossa. See Frontispiece. Technic. — ^Preparation. The osteoplastic flap, irregularly trapezoidal in shape, has its base upwards. The limits of the proposed flap are first outlined by a very superficial skin incision; the area is covered by moist gauze, and Lake's semi-circular incision is then made. This incision, which surrounds the upper one-half of the ear, begins posterior to the auricle in the auricular fold in front of the mastoid, hugs the attachment of the cartilage to the skin, and ends anteriorly at the lower level of the epitragus in front of the ear. The incision, carried through the fascia and muscle to the bone, allows of a forcible refiection of the external ear, with an evulsion of the membranous canal downward. A small piece of cotton to which is attached a black string is now placed in the space between the exposed superior auricular bony wall and the reflected canal in order to absorb whatever purulent secretion may be expressed from the middle ear by pressure. After covering with another layer of moist gauze, the reflected aural flap may be held in position downward by a narrow, flexible tourniquet, so placed that its upper edge exposes the superior wall of the external auditory canal, and con- sequently is below the level of that portion of the middle fossa formed by the superior surface of the petrous pyramid. Cushing's canopy is then applied, limiting the operative area. If, as is usual, th« mastoid has previously been opened, the whole procedxire is considerably complicated, as the walling off of the infected area of the previous operation. Lake's incision, the downward reflection, and the fllling of the whole cavity with iodoform gauze, must be treated as an entirely separate procedure preparatory to the aseptic exposure of the brain above. Technic of Formation of Bone Flap." — The skin incision for the lower border is from three and a half to four inches in length. It begins one inch in front of and three-quarters of an inch above the external auditory meatus, on an imagi- nary line perpendicular to the center of the eminentia articularis, runs horizon- tally backward for two inches to an imaginary line perpendicular to the posterior border of the base of the mastoid, and then turns sharply upward at an angle of 30 degrees and runs one and one-half inches to the posterior inferior angle of the parietal bone, just above the parieto-occipital suture. The anterior incision, three and one-half to four inches in length, is at right angles to the anterior section of the inferior border. (Figure 9.) The skull is perforated at both superior angles (Holes 1 and 2) ; then at the center of both anterior and posterior borders (Holes 3 and 4). The superior halves of the anterior and pos- terior borders, (Line "a," between holes 1-3, and Line "b," between holes 2-4), '» See Chapter Two, p. 10. Tbe formation of the flap Is described In detail because, while osteoplastic resections in this region have been frequent (Krause, Surgery of tlie Brain, Vol. 3, p. 900, English edition, 1912), the author is not aware that a replaceable osteoplastic flap has previously been devised which automatically aims at utilizing all available space as near tbe floor of the middle fossa as pos- sible without Injury to the sinus and without entrance into the infected areas of the middle ear and mastoid. During the last few years the author has made many of these bone flaps, and must confess that the majority have become infected when an abscess has been located because of their close proximity to an infected ear. How- ever, In a case in which an abscess is not located the whole flap can generally be saved even if a local area of Infection may have occurred. With this disadvantage the osteoplastic flap has served a most useful purpose and the author believes that with strict observance of technic it will commend itself for all cases of suspected temporo-sphenoidal lobe abscess. 42 BEAIN ABSCESS are then formed by the Gigli saw, making the bevel outward, after which, under the skin, the bone of the base of the flap, (Line "c," between holes 1-2), is par- tially sawed so as to insure the flap breaking properly. The formation of the lower border of the flap, which is three and one-half inches in length, is the most important, the object being to have it reach as near as possible to the floor of the middle fossa, where the principal investigation will be held. The bone of the lower border is perforated, (Hole 5), at the junction of the anterior (horizontal) and posterior (elevated) portions in the squamous portion of the temporal, directly over the root of the mastoid, about one inch behind and three-quarters of an inch above the external auditory meatus, and above and slightly in front of the root of the temporal ridge, which here makes a sharp bend upward. The bone over the anterior inferior angle, (3-5-6), being deep under the temporal muscle, can be sacrificed as well as the bone below it as far as the floor of the middle fossa. The remainder of the anterior border is then cut with a Gigli saw. The posterior half of the inferior border is then elevated to avoid the knee of the lateral sinus, which here rises very high. The posterior inferior angle, (Hole 7), one and one-half inches above Eeid's line, is in the in- ferior angle of the parietal bone, just above the parieto-occipital sutures, two inches behind the end of the horizontal portion of the inferior border of the anterior section. In making the posterior inferior angle, (Angle 4-7-5), hemor- rhage is frequently encountered from external diploic vessels running directly into the sinus, which may necessitate the rapid completion and elevation of the flap to control the hemorrhage. Consequently the perforation at the posterior inferior angle, (Hole 7), and its connection with the anterior sector of the inferior border, (Line "d," between holes 5-7), and the posterior border, (Line "e," between holes 7-4), is left until all other parts of the flap have been made. (Fig. 10, Elevation of Flap.) Inspection of Brain within the Dura. — ^Free incision of the dura exposes the external surface of the temporo-sphenoidal lobe, frequently the site of oyster-shaped localized intra-arachnoid abscess. Hebniatioii of Brain topon Incision of Ddba in Tempobo-sfhenoidai, Absoess. \ While moderate herniation of the brain occurs immediately upon incision of the dura, in my experience the excessive uncontrollable herniation associated with rupture of the piaraohnoid and hemor- rhage, which frequently accompanies exposure of the cerebellum, especially when but one cerebellar hemisphere is exposed, does not occur. Making a large dural opening greatly lessens the chief dan- ger from the herniation, viz., rupture of the piarachnoid. If threat- ened, this calls for reduction of the internal cerebral pressure by lumbar puncture. However, if the abscess is large and so situated that it compresses the ventricles with displacement of the hemi- sphere, lumbar puncture may liberate but a few drops of cerebro- spinal fluid apparently not under tension. Obliteration of Homolateral Ventricle. — ^As the abscess in- creases in size, the lateral ventricle gradually becomes compressed; ■> ''- -T-,-- Fig. 10. — Bone flap elevated. (See Frontispiece.' Fig. 11. — Section of brain in skull, slio\\'ing' tcniporo-spbenoidal hemorrhagic infiltration and l\erniation, with displacement of liomolateral hemisphere beyond the median line and almost complete obliteration of lateral ventricle aldiouoh a large dural opening liad been made. Prior to tlie diiral opening the displace- ment and the oljlitcration must have Ijcen extreme. Figs. 13 (a) and (b). —Acute eerelielhir aliseess in lateral lobe of cerebellum — a frequent position vlien secondary to sinus tlirombosis. During evacuation pus passed over piarachnoid; prior to evacuation a careful exaniinalion of cerebro- spinal lluid gave no evidence of sup- ])urating meningitis; immediately following operation fulminating meningitis. Death within thirty- six hours. Fro. 13 (b) ABSCESS OP MIDDLE FOSSA 43 this is followed by a partial displacement of the cerebral hemispliere beyond the median line, probably with actual obliteration of the aqueduct of Sylvius. Obliteration of the ventricle of the affected side, with displace- ment of the hemisphere beyond the median line by abscess, is a matter of great surgical importance to which attention has not hitherto been directed. Gushing has long recognized that subcortical tumors frequently obliterate the ventricle of the affected side, pre- venting its location by ventricular puncture. Of the frequency of obliteration of the lateral ventricle and partial displacement of the hemisphere the writer has post-mortem evidence in one case of cere- bral abscess (Fig. 11), in two cases of subcortical tumor of the temporo-sphenoidal lobe, and, clinically, by repeated failures to find the ventricle on puncture. ^^ The following case demonstrates obstruction in the main cerebro- spinal fluid channel by cerebral abscess, the compression and dis- placement of the hemisphere probably causing a "block" at the aqueduct of Sylvius and the restoration of the channel by the evacua- tion of the abscess. CASE X, C. H. Temporo-sphenoidal Lobe Abscess. Girl. Diagnosis: Abscess of tem- poro-sphenoidal lobe. On incising dura great herniation of brain. Lumbar punc- ture liberated but a few drops of cerebro-spinal fluid, dropping slowly at inter- vals of several seconds. Exploration within brain by canula; partial evacuation of abscess through canula. Upon relief of excessive pressure cerebro-spinal fluid in large quantities under pressure began to flow from the lumbar puncture canula, the partial evacuation of the abscess having removed an obstruction which prevented the free flow of the cerebro-spinal fluid. ( Of. Case XXIV, Chap- ter VIII, p. 135, Hernia Cerebri Following Temporo-sphenoidal Lobe Abscess.) Failure to locate the lateral ventricle by puncture would seem to indicate that if, during an explorative operation for suspected brain abscess, free incision of the dura is associated with marked herniation, and lumbar puncture fails to reveal the excessive hernia- tion which threatens rupture of the piarachnoid, the surgeon should immediately explore the temporo-sphenoidal lobe and partially evacu- ate the abscess, if located. On several occasions evacuation of abscess has converted an uncontrollable cerebral herniation into an apparent collapse of the affected hemisphere, the brain no longer completely filling the skull. Puncture of the Opposite Ventricle for the Reduction of Brain ^' Reynolds, C. B. : Journal American Medical AasociaUon, 1914, Vol. LXII, p 449, contains illustration showing obliteration of ventricle and displacement of hemisphere beyond median line by a brain abscess. 44 BRAIN ABSCESS Herniation Sufficient to Admit of Elevation of Brain. (See Lum- bar and Ventricular Puncture, p. 29.) The post-mortem and clinical evidence of obliteration of the lateral ventricle vpith displace- ment of the affected hemisphere would indicate that, in the presence of marked herniation, if lumbar puncture liberates but a few drops of cerebrospinal fluid, or cerebral exploration fails to locate the abscess, puncture of the opposite lateral ventricle, through an inde- pendent opening, may reduce the intracranial pressure sufficiently to permit of inspection between the dura and the brain. Inspection by Elevation of Brain. — Inspection of the under surface of the temporo-sphenoidal lobe, as far as the tegmen is de- sirable, because upon the presence or absence of adhesions between the dura and brain will depend the surgical procedure to be adopted. Technic of Elevation of Brain. — On first opening the dura over the external surface of the temporo-spheno-idal lobe, it is generally impossible to inspect the area of limited adhesions about the middle ear by elevation of the brain, as the internal pressure of the brain is so great that it is jammed tightly against the cut edges of the dura. Although a lumbar puncture lessens the herniation, the reduction of the pressure is usually not sufficient to allow of inspection by dis- placement of the brain upwards. Reduction of the intracranial pressure by puncture of the opposite ventricle, or by partial evacuation of an intracerebral abscess, usually permits elevation of the brain in the anterior portion of the flap, allowing inspection of the under surface of the temporo-sphenoidal lobe above the tegmen antri and tympani — the most frequent location of intrapiarachnoid abscess and abscess of the second temporo-sphenoidal convolution "with a stalk." By elevating the brain in the posterior portion of the flap above the hori- zontal portion of the sinus, the upper surface of the tegmen cerebelli, as it rises upward and inward, and the under surface of the occipital lobe, may be inspected. Inspection of this area is difficult, as the margin of the dural opening, and the elevated postero^inferior border of the bony flap are both considerably above the outer limit of the tentorium. Introduction of the spatula between the dura and the brain is accompanied by considerable hemorrhage from injury to the posterior-inferior cerebral veins entering the sinus directly from the tem- poro-sphenoidal region of the brain in the triangle between the superior border of the temporal containing the superior petrosal sinus, the knee of the lateral sinus and the transverse sinus. Protection of Exposed Piarachnoid Prior to Exploration. — In all cases of suspected brain abscess, before exploring the brain substance, the piarachnoid exposed by the dural opening should be covered with wet cotton to protect it from drying and from possible infection dur- ing the sudden liberation of pus through the exploring canula. The piarachnoid is a mesh of endothelial cells and fine blood vessels. It offers great resistance to trauma while moist. The brain, as long as its piarachnoid covering is intact, may be displaced and handled without injury or hemorrhage, except at the comparatively few places where blood vessels run directly from the arachnoid into the Fig. 12. — Uemorrlmgic infiltratioii into substance of piaraclmoid from tear- ing small pial vessels during operative manipulation. Note multiple minute hemorrhages, partially due to surgical manipulation and cerebral herniation. ABSCESS OP MIDDLE EOSSA 45 dura, or outside the cranium.^^ When the piarachnoid becomes dry, however, it tears easily; even the weight of the brain, itself, may cause rupture, and, as the piarachnoid is largely made up of blood vessels, tearing is accompanied by hemorrhage. Hemorrhage into the piarachnoid is largely infiltration into the cortex itself, because of the close adhesions of the pia to the cortex. How frequently do we see the beautiful glistening surface of the cerebral cortex become dry, lustreless, and almost black with hemorrhage, as the surgeon proceeds with his operative manipulations. (See Fig. 12.) Horsley operated within the dura under a stream of warm, weak bichloride solution. Absorbent cotton saturated with warm normal salt solution, as employed by Gushing, is much better, as it may be used to control any slight hemorrhage and, at the same time, to pro- tect the meninges from infection. Many cases of brain abscess, after evacuation, end fatally from meningitis, the otologist frequently giving less consideration to the protection of the piarachnoid from the pus of the abscess than the abdominal surgeon gives to the peritoneum in draining an appen- dicular abscess. As a matter of fact the arachnoid is much more susceptible to infection than is the peritoneum, the peritoneum pass- ing its existence in the neighborhood of infection, whereas tbe arach- noid, normally, is remote from infection. (See Fig. 13, a and b.) Technic. Before searching within the brain, the piarachnoid should be cov- ered Tvith wet cotton, that the first gush of pus from the searcher may not soil it, after which the remainder of the pus should be removed by a suction appa- ratus, as it presents in the searcher." Explwwtion within C&rebrcd Sichstance. — Exploration into the brain substance should be performed with a hollow semi-blunt searcher. This is of the greatest importance. Exploration with a knife is generally associated with hemorrhage from the interior of the brain. The vessels within the cerebral substance run perpendicu- lar to the surface; consequently a blunt searcher passing parallel to a vessel pushes it aside, whereas a knife cuts it. The disadvantage of exploration with a semi-blunt searcher is that the capsule of the abscess may be so dense that penetration by the searcher is impossible (Fig. 18) — a very rare condition. '= In exploring over the temporo-sphenoidal lobe with the spatula, after the brain has been caused to "fall back" by the withdrawal of the cerebrospinal fluid by lumbar or ventricular puncture, one large and one or two small venous communications wiU be seen passing directly into the sinus. Care should be taken not to tear them before the application of "silver clips" ; otherwise, hemorrhage sufficient to interfere seri- ously with further inspection may result. ^ , ^ ^ . ^. ... ... . >" A suction apparatus with the tip at least twice the calibre or the searcher should catch the pus as it presents itself in the searcher, or in the cavity of the encephaloscope. The tip should never, of course, touch the brain tissue itself. 46 BRAlSr ABSCESS In Blake's case" it was one-sixth, and in Knapp's*" one-flfth inch thick, while in a personal case it was so dense it could not be perforated with a sharp chisel.'" The pus may be too thick to run through the lumen of the searcher. The contents in Bacon's case" had "almost the thickness of chewing gum"; in Manasse's"' it was necessary to use a curette to remove it; while in Kopke^s" the abscess cavity was filled with blood. Difficulty in evacuating is encountered only in chronic abscess. Technic: Exploring Instrument. — In abscess of recent formation a smooth, graduated, soft rubber catheter, lubricated, with a well fitted metal stylet, should be employed for exploration. If simple evacuation is decided upon it may, without withdrawal, be utilized as a drainage tube and for the formation of a tract. If a firm capsule is suspected, Cushing's metal searcher should be sub- stituted, as the capsule may be impervious to the rubber searcher. SITE OF ADJACENT INTEACEEEBRAL ABSCESS WITHOUT MACKO- SCOPICAL EVIDENCE OF CORTICAL INVOLVEMENT OF MIDDLE FOSSA: Post-mortem examinations and clinical experience have demon- strated that the vast majority of adjacent intracerebral abscesses originating from the ear are situated primarily in the white sub- stance of the third temporal convolution, directly above the tegmen tympani et antri.^"' ^^ It ia the involvement of this area on the left side, containing as it does the "naming" center of Mills, that gives the localizing symptoms of a pathognomonic "naming aphasia." ^^ From this original site the abscess extends either (1) inward and upward, causing a paresis, first of the lower face, then of the arm, and later of the leg; or (2) downward, towards the cortex over the tegmen. Selection of Site for Exploration. — Because of the uniform appearance of the abscess in the white substance of the third temporal convolution, the site of the exploration should be as low down as possible toward the floor of the middle fossa, just above the tegmen. Otherwise the abscess, if small, may be overlooked; — this occurred to the writer in one of his earlier cases. CASE XI., D. D. Abscess Lovr Down in Middle Fossa. Male, 45 years of age. History; chronic alcoholism; left-sided otitis media of three months' duration; constant pain in head; vague chill for several weeks, with loss of fiesh; coated tongue; » Blake : Lancet, I, March 31, 1900, p. 439. « Knapp, H. : Archives of Otology, Vol. 29, 1900, p. 46. " See Chapter Five, Metastatic Abscess, p. 68. " Bacon : Trema. Amer. Otol. Soc, May, 1900, p. 404. >»Manasse: Arch. Otol., Vol. XXVII, 1898, p. 115. » Ropke : Arch. Otol., 1901, Vol. XX:x, p. 30. " MacEwen : Pyogenic Infective Diseases of the Brain and Spinal Cord ; 1893, p. 72, Fig. 30. "■ MacEweu : Atlas of the Head Sections ; 1893, Plate 8. 2» Mills' Naming Center Is "located In the Inferior temporal gyrus, Just anterior to the middle of the Inferior lateral border of the hemispheres." Santfie : Anatomy of the Brain and Spinal Cord ; 1915, p. 192. ■p''i'. •'. " A. ' t Fig. 14- a ^/■^■Ar';v;' 'W' /' ■':r/ ^'v. .''/:•'. /■;,:,' ,:(,'^ •^■•>.'^' 0-^- '':*ll"'' i('''/( W']ff^^ Fig. 14-B o ' ■vv -"■^ t i J • a^_^ * .- ,', ^ ^^<] V ' > -"> ^ • « »» -" - < •':-- ! ^f * "," * ' ' « Im %. ^^ . • *.«. Ftg. 14-C 4". • Fic 14 A B C ^Micropliotograph made from sections taken from encapsu- lated al.scess'ol brain of 'iV-i months' duration. (Dr. Harrison Martland.) bee '^ A— Inner tliird of abscess capsule; showing shaggy tissue composed of necrotic, sloughing and disintegrating brain tissue containing hemorrhage, fabrm, nus ( poly nucTear leucocytes) and bacteria. „,,,,. j.- = B— Middle third of abscess capsule; showing fibroblastic tissue forming a dense fibrous protecting wall with scattered polynuclear and endothelial leuco- cytes. Fibroblastic proliferation is in this instance due to stimulation of fabro- b'lasts by the presence of fibrin in the disintegTating bram tissue. C— Outer third of abscess capsule; showing endothelial leucocytes around dilated blood-vessels and in the surrounding oedematous brain tissue. JNote absence of polynuclear leucocytes. ABSCESS OF MIDDLE EOSSA 47 indefinite history of inability to name objects, which had entirely disappeared at time of examination. Mastoid Operation: For one week apparently recovering, but headache con- tinued. Later, attacks of transient and incomplete "naming aphasia"; slight paresis of lower portion of right face, only elicited by spontaneous emotional movements, namely, smiling or laughing. Second Operation: Exploration through clean area above the ear; no abscess located. Marked improvement followed operation; patient insisted upon leaving bed; suddenly, a few days after operation fell while walking; became cyanosed; paralysis of respiration, and death. The exploration low down toward the floor of the middle fossa has the advantage that, being adjacent to the infected mastoid area, the piarachnoid is punctured through the area of inflammatory protective changes which are always present. And puncture through a "prepared" area is much less frequently followed by leptomenin- gitis than through one which is "unprepared." CHRONIC ADJACENT INTRACEREBRAL ABSCESS WITH A CAPSULE. Surgical Pathology. — The pathological processes in chronic brain abscess are the same as in abscess formation in other parts of the body, viz., death of tissue and the changes due to the tissues' protective reactions, the latter being governed, however, by the special tissue involved. Microscopically, a chronic braia abscess with a capsule is com- posed of : (1) A cavity filled with detritus and pus (Mg. 14A) the end result of complete death of tissue from bacterial action and nutritional disturbances, and (2) a limiting capsule, formed by the irritation of the bacteria and their toxins on the tissues, and the tissues' protective and reconstructive reactions. The capsule in a general way may be divided into three zones, all closely intermingled, the destructive bacterial action having predominance nearest the cavity, while in the external zones the tissues' reconstructive and protective powers are chiefly manifest; although far beyond the cap- sule, bacterial action can always be demonstrated. Just external to the cavity and projecting into it is (1) the "necrobiotic zone," in which the tissue now dead is undergoing lique- faction from the action of the toxins. To insure the ideal surgical result, namely, the eradication of the infection, the surgeon must remove this zone, as far as possible, using the utmost delicacy. Merg- ing into the necrobiotic zone is (2) the granulation tissue zone, with connective tissue developing from it — the capsule (Fig. 14B) ; and external to both in the otherwise normal brain tissue is (3) a round-, cell infiltration in the perivascular sheath of the vessels, showing that 48 BEAIN ABSCESS the inflammatory or the protective process is still active well beyond the capsule. (See Figs. 140, 15 and 16.) The capsule of connective tissue is the result of two factors — the resistance of the tissues and the virulence of the infection. With a high resistance and a low virulence, nature attempts a complete encapsulation of the abscess by a wall of new connective tissue, which grows denser with time. The connective tissue reaction of the body is simply the attempt of the orgajiism to limit the extent of the inflammatory process. In most parts of the body, subcutaneous, muscular, etc., if the infec- tion is not virulent, an encapsulation rapidly follows, partly because the tissues in general are freely supplied with connective tissue which, being of a low order of cell, rapidly propagates itself. In the brain, however, the formation of a connective tissue capsule is a considerably slower process; partially because practically all the new cells making up the capsule must be brought to it by the newly formed blood vessels. These blood vessels, consisting at first of only an endothelial tube, soon develop an outer connective tissue layer, and from this layer is formed the connective tissue of the capsule. (See Fig. 14B.) The connective tissue of the piarachnoid also plays a part, but the glial cells, the framework of the brain, being highly specialized connective tissue, plays little or no part in the encapsulation. In the formation of a capsule the type of micro-organism is thought by some) to play a large part, Neumann ^* stating that "dip- lococci cause an abundant secretion of fibrin, and so form a capsule, but when anerobio micro-organisms are preseoit, a firm capsule is not formed." While, microscopically, the formation of connective tissue can be demonstrated within a short period, the development of a capsule firm enough to be appreciable macroscopically and consequently of great surgical assistance, is a slow process. Friedmann ^* found microscopically a distinct membrane, composed of two layers, be- tween the eighth and the twelfth day after the cerebral infection. The resistance to the advance of the searcher offered by such a cap- sule would not be appreciable to the surgeon. Westphal ^^ found a delicate encapsulating membrane seventeen days after the onset of the cerebral symptoms. In such a case it is probable that, with very delicate handling of the searcher the surgeon would be aware '^ Neumann, H. : Cerebellar Abscess, Bngllsb Ed., 1907, p. 14 ; Polltzer : A Text- book of Diseases of the Har, 5tb Ed., 1909, p. 66. "' Filedmann : Handbucb der Pathologlechen Anatomle des Nervensystems, 1905. » Westphal : AroMv fUr PaycJdatrie, 1900, Bd. 33, S. 206. v^ Fig. 15. — Section (Dr. Fredk. Sutton) ; low power: through granulation layer of chronic brain abscess of about 14 days' duration. To right, new con- nective tissue: perivascular infiltration. To left, normal brain tissue. Fig. 16. — Same case as Fig. 15. Section; high power: perivascular infil- tration. Fig. 17. — Section through streptococcic brain abscess of 105 days' duration. Firm capsule % to % inch in thickness. (For microphotographs of sections see Fig. 14.) ABSCESS OF MIDDLE EOSSA 49 of a slight resistance at the moment of perforation. Uchermann *' estimated that it probably takes about 24 days to form a capsule of one millimeter thickness; about 38 days for one of two millimeters. The latter condition would offer considerable resistance to a semi- blunt searcher and would be impervious to a blunt instrument. (Fig. 17.) Although several clinical observers ^''' ^®' ^^ contend that a capsule is not formed until between the third and eighth week, the author has recognized the presence of a capsule as early as the seventeenth day.*" After the incision of the piaraehnoid the consistency of the brain tissue is so uniform that, by delicate handling, very slight resistance is appreciable. Stirgicai, Principles Undeelying the Intradubal Technic in Suspected, Adjacent, (Secondaet) Abscess of the Middle Fossa ( Tempoeo-sphenoidal ) . As the diagnosis of brain abscess must of necessity be more or less provisional, and as cortical and subcortical suppuration can rarely be differentiated, all explorations must be conducted through a clean area, and adequate exposure must be provided for. In no field of surgery is it more important that the surgeon keep an open mind. Because of the uncertainties of the diagnosis, he must prepare to assume a "shifting policy," depending upon whether the exploration reveals, in chronic abscess, an intracerebral abscess without macroscopical evidence of cortical involvement, with a stalk, or meningeal; and in acute abscess, an intracerebral or meningeal abscess. He must not adhere to a particular procedure simply because it resulted successfully in a former operation. He must adapt each act of his technic to the condition found, preserving the protective structures erected by nature, and availing himself of their assistance. Compression, because it favors extension of suppuration and paralyzes the protective mechanism, must be controlled or prevented. In the treatment of individual clinical types of abscess (see p. 21), existing pathological conditions and clinical experience both suggest that the surgeon follow the method adopted by nature in its efforts to cure spontaneously an adjacent brain abscess. In encapsulated adjacent abscess with a stalk, as nature has " TJchermann : ZeitacJiHft Jii/r Ohrenheilkunde, 1904, Bd. 46, S. 306. " Lebert : ArcMv fiir Pathol. Anat. und Physiol., 1856, Bd. 10, S. 78. 2» Schott : WUmburg. Med. Zeitschrift, 1861, Bd. 2, S. 462. » Huguenin : Handbuoh der spes. Pathol, und Therap., 1876, Bd. 2, S. 331. '» See further discussion of formation of capsule, Chapter Five, Metastatic Abscess, p. 76. to BEAIN ABSCESS erected a walled-off tract througli the piarachnoid into the cavity of the abscess, the surgeon should utilize this tract for the complete evacuation, cleansing, and obliteration of the abscess and the intro- duction of necessary drainage. In adjacent intracerebral abscess with capsule, but without macroscopical evidence of cortical involve- ment, the abscess should be completely evacuated and an attempt made to form a walled-off area through the piarachnoid, after which it may be completely evacuated, cleansed and obliterated. In acute abscess, as compression is favoring the extension and preventing the limita- tion of the suppuration — as well as being the cause generally of most of the clinical symptoms — the abscess should be evacuated as com- pletely as possible through a small searcher and the dura closed, or at least the brain completely covered. In several instances I have firmly anchored the small searcher to facilitate the formation of a tract. Later, after the formation of the capsule, it niay be treated as an encapsulated intracerebral abscess. A meningeal abscess, chronic or acute, should be fully exposed in all directions, no mat- ter how extensive the sacrifice of bone or dura, the area should be thoroughly cleansed by irrigation, adequate drainage provided at a distance from the dural margin through "stab" wounds, and the brain completely covered. Technic Following Elevation of Brain. — i lumbar or ventricular puncture of the dilated opposite ventricle, or the partial evacuation of the abscess, through the cortex, having caused sufficient "falling back of the brain" to allow an intra- dural inspection over the roof of the tegmen if adhesions are seen above the middle ear, all of the exposed external surface of the temporo-sphenoidal lobe should be covered with wet cotton, the bone rongeured away down to and includ- ing the middle ear and antrum, and the dura opened from below. If the stalk of the abscess is short so that the abscess cavity is separated by only a few millimeters from the under surface of the temporo-sphenoidal lobe, it may be possible to eradicate it, viz., to evacuate, cleanse, obliterate and introduce drainage material through the lower dural opening, in which case the upper dural opening should be tightly closed and the bone flap replaced. In cases in which the protective inflammation is very limited, this area may be increased by placing strips of moist cotton, from the upper wound, between the dura and the brain on as many sides of the adhesive area as possible, before opening from below. Stteoical Significance op Areas of Adhesive Inflammation of plaeachnoid to dura. When elevation of the brain with the spatula discloses, on the under surface of the temporo-sphenoidal lobe, adhesive inflammation uniting the brain with the dura, it may be inferred that if the area of adhesion is extensive, the abscess is probably in the meshes of the piarachnoid ; and that if the adhesions are limited to the tegmen, ABSCESS OF MIDDLE FOSSA 61 the abscess is probably in the brain substance, a "stalk" uniting the abscess with the area of primary infection. Both forms of abscess offer excellent prospects of recovery, for nature has walled off the infected tract from the meshes of the piarachnoid, and established a tract' from the dura to the furthest extremity of the abscess, while the adjacent tissues have become largely immunized during the limitation of the infection. CHRONIC ADJACENT INTRACEREBRAL ABSCESS OF THE MIDDLE FOSSA. It is recognized that a larger proportion of recoveries have fol- lowed evacuation and drainage from below through the middle ear and antrum than through the external surface of the temporo- sphenoidal lobe, because in abscess with a "stalk" the tegmen per- mits entrance into the abscess at its nearest approach to the dura, and through an immunized tract of protective adhesions. Conse- quently, in operating, a definite attempt should be made to evacuate the abscess at its nearest approach to the dura, — the antrum and middle ear,- — and to utilize the area of protective adhesions, — ^for it is through this tract that the abscess may be entered, thoroughly evacuated, and drainage material introduced with the least danger of inciting a suppurative meningitis, or of injuring and infecting the neighboring cerebral tissue, with its accompanying oedema, en- cephalitis and fungating hernia. SUBOICAI. PEINCIPtES AND SPECIFIO FACTOES INVOLVED IN THE TBEATMENT OF Encapsulated Adjacent Intbacebebeal Abscess of the Middle Fossa. In the surgical treatment of encapsulated intracerebral abscess one of two principles is employed: (1) Attempted eradication of the suppuration, and (2) drainage. Drainage, while efficiently controlling suppuration in other parts of the body, is generally inadequate in cerebral suppuration (see p. 57), and may be the direct cause of secondary infection of the meninges, the development of the so-called secondary abscess, and of hernia cerebri. On the oliier hand, an attempt at eradication, except in selected cases, will be associated with cerebral trauma, resulting in the presence of infection in traumatic encephalitis. On the proper selection of the principle to be adopted in each individual case, largely depends the life of the patient. Eradication. — In the treatment of chronic intracerebral abscess with a capsule with a stalk, the surgical aims should be the same as 52 BRAIN ABSCESS in the surgical treatment of low grade infection in other soft tissues, viz.: (1) thoroughly to remove all pus and detritus, thus largely eliminating the infection; (2) to reduce as far as possible the sup- purative surface by the collapse and obliteration of the cavity; (3) to convert the granulating surface of the obliterated cavity into an active reparative process, the subsequent discharge being then largely the discarded products of healing, and not, as formerly, the result of the destruction of tissue. In addition to this the surgeon must endeavor, (4) to accomplish the above without spreading the infection to the susceptible adjacent piarachnoid; and (5) to do so with a minimum of operative trauma. Drainage. — In encapsulated intracerebral abscess without macroscopical evidence of cortical involvement, complete evacuation, cleansing, and obliteration are impossible, because wide entrance into the abscess is apt to be followed by meningitis (there being no area of protective adhesion) and traumatic encephalitis from injury to cerebral tissue. Selection of Cases. — When the falling back of the brain reveals a wide stalk leading into an abscess cavity, an attempt should be made at complete evacuation, cleansing, and obliteration of the cavity. Again, if exploration of the under or lateral surface of the temporo-sphenoidal lobe reveals an encapsu- lated intracerebral abscess without macroscopical evidence of cortical involve- ment, within one or at most two centimeters of the cortex, attempted eradication is justifiable, although vpithout a stalk a systematic effort at complete evacua- tion, cleansing and obliteration, increases the danger from meningitis and traumatic suppuration. With an intracerebral abscess without a stalk, situated beyond two centi- meters from the corteK, an attempt at eradication is associated with great tech- nical difficulties and prohibitory trauma to the brain. The surgical effort should be limited to as complete an evacuation as is possible through the searcher, and the formation of a tract through which the abscess is drained and later, possibly, cleansed. Difficulties of Complete Evacuation. — Certain anatomical and physiological factors peculiar to cerebral tissue make difficult the complete evacuation of the pus and obliteration of the cavity : — (1) the brain substance has a specific gravity of 1036,^^ 78.9 per cent, of it being water; (2) the brain substance is practically a semisolid, homogeneous mass of nerve cells and glial tissue, while the blood vessels within the substance are comparatively small ; ** (3) the brain is largely held in shape by the enveloping piarachnoid — (witness its distortion upon removing the fresh brain from the calvarium and stripping off the piarachnoid). " Santee, H. 3D. : Anatomy of the Brain and Spinal Cord, 1915, p. 49. "Mallory: Principles of Pathology and Histology, 1914, p. 625. ABSCESS OF MIDDLE FOSSA 53 The mechanical factors inherent in the abscess itself which in- fluence the operative procedure and modify the surgical aims, are: (1) the thickness of the enveloping capsule; (2) the distance of its outer wall from the point of puncture on the cortex; and (3) the consistency of the pus. Taken in its entirety, cerebral substance within the piarachnoid is approximately of the consistency of mush contained within a deli- cate gauze bag. If now a raw egg with the shell removed is placed within the mass and an effort is made to remove the entire yolk with little disturbance of the mush, we have a fair model of the mechanical difficulties of thoroughly evacuating an intracerebral abscess with a delicate encapsulation. Puncture through the mush into the egg will cause the liberation of some of the yolk, but col- lapse of the surrounding mush will uniformly prevent the evacua- tion of the larger part of the semi-liquid contents of the enveloping membrane. Upon entering an intracerebral abscess with the searcher, sudden expulsion of a portion of the pus is caused by the tension of the surrounding cerebral substance; but as soon as the tension between the abscess contents and the surrounding cerebral tissue is equalized, further evacuation of the pus is accomplished by gravity, and the weight of the surrounding cerebral tissue. Muscular contraction of surrounding tissue — so powerful a factor in the evacuation of the pus of an abscess in the soft structures — plays no part. The nearer the pus approaches the density of the surrounding cerebral tissue, the greater the mechanical difficulty of complete evacuation. Pus of thin consistency will be much more completely evacuated by the brain than thicker pus. The firmer the envelope, the greater the possibility of entrance into the abscess cavity of an instrument which will insure complete evacuation, cleansing, and obliteration of the cavity. Importance of Thorough Primary Evacuation. — Complete evacuation, cleansing and obliteration of the cavity whenever feasible without trauma to normal cerebral tissue, should be carried out at the time of the primary aperation. In recent years I have realized more and more that, having once located the collection of pus with the exploring searcher, thorough evacuation and obliteration of the cavity greatly lessens the liability of subsequent re-filling, or second- ary abscess from inadequate drainage. The literature of the treatment of chronic brain abscess shows how frequently reliance is placed on partial evacuation, with the in- troduction into the cavity of some form of drainage material to allow 54 BKAIN" ABSCESS of subsequent drainage of pus. I am convinced, towever, that not only is incompleite primary evacuation, preventing obliteration of the cavity, generally followed by inadequate drainage (because of the collapse of the opposing walls shutting off portions of the abscess with the frequent formation of an apparently new cavity), but that the retained pus favors an extension of the encephalitis. Many fail- ures to locate pus at a secondary operation, in which primary incom- plete evacuation had failed to stop the suppurative process, and in which at post-mortem the drainage material was found outside the abscess cavity, have persuaded me that the surgeon, in chronic brain abscess with a capsule, has but one major chance to combat infection, namely, cut the time af the primary operation. The importance of primary complete evacuation is supported by two clinical observations of great prognostic value, which have long been recognized : (1) if following an operation for brain abscess, the disappearance of the symptoms is accompanied by alm,ost com/plete cessation of the discharge, — complete primary evacution — relapse and refilling of the abscess cavity but rarely occurs ; (2) on the other hand, continuation after the first few days of a profuse discharge from the drainage tube — incomplete primary evacuation — ^frequently results in recurrence of the symptoms associated with a sudden cessa- tion of the discharge, cleansing of the tube showing that the ces- sation of the discharge is not due to "plugging" of the tube ; the new area of encephalitis being apparently not connected with the region drained. Evacuation through puncture of the dura is recommended by Lemaitre.^* This gives a large percentage of recoveries because it evacuates the abscess with but a slight ajnount of trauma. How- ever, it has the great disadvantage that a subtemporal and piarach- noid abscess either will be entirely overlooked or imperfectly evacuated. The method fulfills the surgical requirement for the successful treatment of acute brain abscess; it results in evacuation and the formation of a tract. However, before the method is employed care should be taken to be assured that the abscess is not chronic, as other- wise the operation will fail. In several of the vn-iter's cases with an abscess with a capsule which approached the surface it was evacuated in this way, mistaking it for an acute abscess. Post-mortem revealed that, had the abscess been properly eradicated, the patient undoubt- edly would have recovered. " Lemattre, F. : Exclusion of Subarachnoid Space ; Bevue de CMrurgle. 1919, Tome 57, p. 497. (Abstracted In Jour. Am. Med. Boo., June 12, 1920, Vol. 74, No. 24, p. 1680.) Fig. 18.— Part Two. Collapse of abscess, 4, 6, 7, 8. Difficulty in entrance by blunt instrument, 3, 4, 6. Capsule holders in place, 6, 6, 7, 8. ABSCESS OP MIDDLE FOSSA 55 Teohnio of Subgioal Treatment op Cheonio Adjacent Inteacerebbal Abscess WITH Capsule. Complete Evacuation; Difficulties. — The teclmic depends upon -whetlier eradication — complete evacuation, cleansing and oblit- eration of the cavity — or simple drainage is to be attempted. In evacuating a chronic intracerebral abscess vpith a limiting membrane situated fairly near the surface, after the first nish of pus has been removed care should be taken to evacuate only a small quantity of pus through the exploring searcher. Unless this precaution is taken the exploring searcher, having entered a small abscess or perforated a dense capsule, the partial withdrav^al of the pus vpill result in the collapse of the opposing cavity walls from the external pressure of the surrounding brain tissue, thus locking in a quantity of pus and ren- dering difficult the proper placing of the encephaloscope. The more pus evacuated the greater the flaccidity of the portion of the abscess vrall impinged upon by the blunt encephaloscope; consequently, by preserving the distention of the abscess the difficulty of perforating the capsule by the encephaloscope and placing the instrument within the abscess cavity is lessened. The fact that the encephaloscope is correctly placed is shown by the free escape of pus through the lumen. This locking in of pus invariably happens in all intracerebral abscesses, chronic or acute, when evacuation is attempted through the exploring searcher, unless the searcher has entered the abscess cavity at its most dependent portion and has passed well into the cavity itself. If l^e searcher has entered the upper portion of the abscess (especially if the abscess is multilocular in shape), the partial evacuation of the abscess with the collapse of its walls, will leave the remainder of the pus at such an angle from the exploring searcher's tract, that if it is necessary that another instrument, such as an encephaloscope or forceps carrying drainage material be passed along the searcher it may not enter the cavity, this portion of the cavity having now become a mere slit between two opposing walls and away from the remainder of the still pus filled cavity, to which it is united by an obliterated tract at right angles to the exploring searcher. This tract can be followed if the abscess is held by the retaining searcher, by lifting apart its collapsed walls, thus allowing entrance into all parts of the remaining cavity. (Fig. 18.) The writer has frequently failed to find the cavity of the abscess after the evacuation of a quantity of pus through the exploring instrument, although' 56 BEAIK ABSCESS considerable pus was still locked in an extremity, the position of the remaining pus being distant perhaps by several centimeters from that portion of the cavity obliterated by the partial evacuation. An abscess once entered by an exploring instrument shovM never be lost. This is of tlie ixtmost importance. As soon as pus is definitely located ty the searcher its flow should be stopped, because when the abscess becomes flaccid greater difficulty is experienced in finding it with the abscess holder, and in entering it with the in- specting instrument. In the case of a chronic intracerebral abscess with a firm capsule, if the capsule is of delicate structure, on passing the encephaloscope over it pus will appear in the instrument at the recorded depth. If, however, the limiting membrane is of more than three weeks' duration, it may be dense enough to resist the entrance of the encephaloscope, in which case, although the cavity of the encephaloscope remains free from pus, the pressure will appreciably increase the flow of pus through the exploring canula. The abscess is again perforated by the abscess holder and if on withdrawing the stylet pus flows from it the inspecting instrument is passed over it. Although Whiting's encephaloscope'' is invaluable for the complete evacua- tion, cleansing and obliteration of the cavity and for the introduction of drainage material, on many occasions the writer has been unable to place it properly within the abscess cavity because, ( 1 ) it is introduced heside the searcher and, consequently, if the searcher has perforated an extramity of the abscess (Fig. 18, Diagram 3), the encephaloscope may miss it entirely; and, (2) because, being blunt, the instrument may simply indent a, firm abscess capsule (Fig. 18, Dia- gram 4). Both accidents have occurred in the writer's experience. To obviate the former accident the author has devised a modiflcation of Whiting's encephaloscope, which is to be introduced over the exploring searcher, whose track occupies the center of the inspecting instrument. (Figs. 19, 20, 21.) Cleansing and Oblitebation op Cavitt of Abscess with "Staik" ob Near COETICAL STJETACE. A brain abscess with a capsule, if near the cortical surface, should be thoroughly evacuated, its walls inspected and cleansed, and its cavity obliterated, so that on withdrawal of the inspecting encephalo- scope, the surgeon should know that no recess of the abscess has been overlooked. Examination of recorded cases of "second" brain abscess demonstrates that separate and distinct multiple brain abscesses (excepting those of metastatic or traumatic origin) are very rare — "second abscess" simply being a prolongation of the original " Whiting, F. : The Differential Diagnosis of Acute and Chronic Brain Abscess by Means of the Encephaloscope. Traneactions Americcm Otological Society, 1903, Vol. VIII, p. 285, Fig. 19. — Author's modifi- cation of Wliiting's enceplial- oscope. Allows of passage of encephaloscope over searcher ; aimed to prevent the "losing" of the abscess after its partial evacuation — a frequent and disastrous accident. This instrument is adapted only to cases which, from their compara- tively short duration, are believed to be surrounded by a delicate capsule. Fig. 20. — Author's capsule retaining searcher and enceplialo- scope (closed). Fig. 21. — Author's capsule re- taining searclier and enceplialo- scope ( open ) . Adapted only to cases surrounded by a very firm capsule Avhicli will allow of manipulation and traction out- ward from the interior of the capsule. ABSCESS OF MIDDLE EOSSA 67 abscess united to tlie main cavity by a narrow entrance which has been obliterated by the collapse of the surrounding cerebral tissue during evacuation. Technic. — Complete illumination of all hidden recessea is of primary im- portance; a Klaar's headlight worn by the operator has proved moat satisfactory. All instruments used within the brain should be held by the operator himself, whose eyes should never for an instant leave the enoephaloscope, the obturator or a cleansing instrument being placed in his hands by an assistant. The re-intro- duction of an obturator, with the slightest forward or lateral movement of the instrument, will prevent tearing and consequent confusing hemorrhage. In the latter part of the thorough evacuation, cleansing by absorbent cotton on appli- cators and moistened with salt solution, furnishes the greatest assistance. If the abscess is superficial, situated within two centimeters of the surface, the entire cavity may be cleansed by this method. Drainage. — In a chronic abscess, with a firm limiting membrane, some form of drainage is desirable, although in my experience the subsequent discharge in carefully cleansed abscess has been so slight that with our present understanding of tissue disinfection and control of localized infection by the tissues themselves, many cases of chronic brain abscess do not require drainage. Personally, however, the writer never has had the courage to omit drainage. If the evacua- tion has been thorough, the very slight subsequent discharge is sim- ply the product of tissue repair ; "free drainage," in the sense of com- bating infection, plays no further part. Technic. — Before withdrawing the encephaloscope, a wick of rubber tissue should be placed within the cavity. Gauze in any form is very irritating, as is shown by the invariable hemorrhage which accompanies its removal. The irrita- tion of its presence favors the development of hernia cerebri. Technic of Drainage Following Incomplete Evacuation. — If the external wall of the abscess cavity is more than two centimeters from the surface of the cerebral cortex, the abscess is to be as completely evacuated as is possible through the exploring instrument, assisted by gravity. After the stoppage of the flow of pus, turning the patient in different direc- tions, to the right or left, lowering or elevating the head, may liberate addi- tional pus. Because of collapse of the absceas walls and the attending diflBculty of intro- ducing drainage material within the cavity (see p. 55), the exploring instru- ment (graduated soft rubber catheter) should be utilized for subsequent drain- age and the formation of a tract, and firmly anchored to the soft parts. In one instance, in a deeply situated abscess, as it was imposaible to enter the abscess cavity with an investigating instrument, the writer used the metal searcher as a permanent drain by cutting it off a little beyond the cortical sur- face. Rubber drainage tubing is much better, as later, if the abscess is deeply situated, and if its limiting membrane is firm enough to have offered considerable resistance to the passage of the searcher, cleansing by irrigation through the searcher offers the best prospect of cure. The filling of the abscess cavity ia accomplished by the weight of the syringe piston, and it ia emptied by means of suction." "Muck has demonstrated cUnically that during the dressing of a brain abscess the rotation of tlie head in tlie sitting position markedly influences the size of the 68 BKAIN ABSCESS Secondary Compression. — Compression favors suppuratioQ and prevents the protective and nutritive mechanisms of the brain from functioning. With a closed dura, excessive action of any of the processes — infective, traumatic, or reparative — ^may cause in- crease of the intracerebral pressure, the compression being followed by extension of any remaining infection ; consequently, after evacua- tion, the decision must be made whether the dura shall be more or less tightly closed or whether a subsequent enlargement of the brain's bulk demands a large dural opening. In deciding whether the dura is to be closed, the most important consideration is: Has the suppuration been completely controlled, and if so, will the secondary reactive oedema be excessive ? Without complete primary evacuation, there will be extension' of the suppuration from refilling of the abscess or its extension into the already infected adjacent area, thus causing compression. With compression from excessive secondary oedema, especially when associated with injury to normal cerebral tissue such as may accompany attempts at eradication, the remaining slight infec- tion is given a new start. Even with complete evacuation the normal reactive forces of the brain are to be considered, for if excessive they may give rise to compression. In brain abscess, especially acute abscess, the nutritive and pro- tective mechanisms of the brain are greatly disturbed by the infec- tion itself, by limitation, and by operative trauma. Following evacua- tion these mechanisms, in their efforts at re-establishment, may occasion such excessive re-active changes as to give rise to compres- sion. (Fig. 22.) In a review of the author's cases he is convinced that three resulted fatally from subsequent compression — ^probably preventible — ^which caused extension of the suppurative process (Case VIII, A. M. N"., Chapter Four, p. 37, and Case IX, G. W., Chapter Four, p. 38) ; while in at least two others (Case XIII, Mrs. H., Chapter Four, p. 63, and Case XVII, Miss M. D., Chapter Five, p. 11), the large dural opening, one resulting in a large hernia cerebri, probably became the saving factor. (See also Case X, C. H., Chapter Four, p. 43.) Principles in Technic of Decompression. — To leave the dura open is to risk a most distressing hernia cerebri, with its attending abscess cavity and consequently Its drainage. The size of the cavity Is altered, he believes, by the hindering of the escape of the venous blood from the head through pressure Induced by rotation of the head. Muck, V. : Wle soil der Hlrnabszesskranke nach der Operation gelagert werden ? (Position of Patient after Operation for Brain Abscess) ; ZeUschritt fUr OhrenheU- kunde. 1920, Vol. 79, p. 86. Fig. 22. — Original drawing from brain containing a temporo-splienoidal lobe abscess whicli had been almost completely evacuated. Shows obliteration of the posterior horn of ventricle on abscess side and the dilatation of tlie ventricle of the opposite side; shows, also, extension of infiltration and increase in size of hemisphere. ABSCESS OF MIDDLE FOSSA 59 danger of secondary infection, and yet not to provide for compression may be fatal. Decompression, by displacement of the brain sub- stance, is in itself a cause of secondary oedema. If tbe dura is to be left open a wide opening must be provided ; otherwise the hernia- tion through a small opening may cause strangulation of the brain. With a decompression the brain must be entirely covered by soft parts. The sewing in of a large piece of fascia lata furnishes a most efficient protection for the brain in non-suppurative cases. Its similarity to the dura renders it less irritating to the cortex than either muscle or skiu. Immediate After-treatment. — Following operation the patient should remain on the operating table for many hours, preferably until the next morning, or at least until complete consciousness has been regained. To move a patient immediately after a profound operative disturbance of his cerebral tissue adds an unnecessary tax to his en- durance which may result disastrously. Since attention has been called to this important detail by Gushing,^® the writer has been impressed by the frequent collapse of patients after being trans- ported to the ward, not only in cerebral cases but in other types of serious operation. If the hospital routine cannot permit the brain abscess cases to remain in the position operated upon, the institution is not a proper place for the operation. Continued After-treatment. — ^After thorough efvacuation, most delicate cleansing, and complete obliteration of the cavity, the dura and the external wound should be almost entirely closed, and no matter how great the temptation to do so, the brain itself should not again be disturbed for many days; if possible, not for several weeks. In the author's experience further manipulation invariably militates against the patient's recovery. The drain may be allowed to be gradually expelled from the brain itself. In most of the suc- cessful cases re-introduction of drainage has been unnecessary. "Second Absckss," oe Dotjbu! and Secondaky Abscess. In traumatic brain abscess (secondary infection of necrotic cere- bral tissue, blood detritus, etc.), two or more separate abscesses fre- quently occur. In abscess from direct extension from adjacent suppurativa " Gushing, Harvey : Tumors Nervus Acusticus ; 1917, W. B. Saunders Company, Pbiladelpbia and London, 60 BEAIN ABSCESS lesions or from retrograde thrombophlebitis with nutritional death, two or three abscesses must of necessity be of infrequent occurrence. Most of the abscesses recorded as "second," or "double," are in reality secondary, though a few cases of double adjacent abscess are re^ ported.*^ A second abscess, originating from the original brain abscess is, however, of frequent occurrence, but from an etiological standpoint such are rather secondary to the original adjacent abscess and should be so designated. Secondary abscess is due, in order of frequency, to (1) "loss of abscess" before complete evacuation, or by collapse of its walls; (2) encephalitis induced in surrounding tissue by the trauma of exploration or evacuation; (3) encephalitis by direct extension from the primary abscess, the path of infection, though frequently small, being discoverable by careful examination. W. K. : Double Cerebellar Abscess, the second abscess resulting from loss of primary abscess associated imth cerebral trauma; operations; recovery. Boy, aged 14, always in good health, but had poor memory. Six years ago had discharge of pus from right ear for three weeks. Mother said at times a whitish mass protruded from the ear, which was very sensitive to touch. History. — Awakened in the night with severe pain which lasted three days. He was then struck on the head by a ball, knocked down, but not rendered un- conscious. Two days later the ear pain returned, followed in three more days by a flow of foul pus from the ear, which lasted a week. During this week he suffered from pain in the head and ear, occasional vomiting, slight attacks of screaming without apparent cause; probably dizzy, as he would catch at articles in going about the room. Lost flesh rapidly. Indistinct history of a chill. At the end of seven days he became drowsy and in the next three days seemed dazed and yawned frequently. On the eighteenth day he was found lying on his right side on the floor, his eyes wide open and apparently blind, in which condition ha remained all night and was thought to be dying. It was noticed that his arm and leg of the opposite side frequently twitched. The next morning, though still in stupor, he could be aroused. He was emaciated, tongue coated, yawned fre- quently, eyes wide open, temperature 99.3 degrees, pulse 62. There was slight lateral deviation of the eyes to the opposite side. Pupils were equal and re- sponded to light. The pupil on the unaffected side was observed to dilate more widely than on the side of the lesion. There was marked right optic neuritis, with banning left optic neuritis. Absence of both patellar reflexes. Operation. — Half an ounce of pus was found in cerebellar tissue near the posterior surface of the petrous portion of the temporal bone. The finger was introduced. Cavity held open by the forceps, when the latter accidentally slipped, " Coates, G. M. : Temporo-sphenoidal Abscess, Double ; Annals oj Otology, RMn- olotgu and Laryngoloffy, June, 1917, Vol. 26, p. 408. Two cases: CASH I Temporo-sphenoidal ; no symptoms whatever ; discovered by accident by bulgine of dura ; sterile pus ; chronic. CASB III Two abscesses ; no stalk ; 1 em. of cerebral tissue between two cavities • both apparently acute. History not explicit enough to eay whether or not it was 'meta- static ; could not have been caused by trauma as patient died on table. ABSCESS OP MIDDLE FOSSA 61 and the flow of pus stopped. Careful search failed to re-disoover the cavity. A drainage tube was introduced along the tract. During the next week the boy did well, was rational, no deviation of the eyes, co-ordination normal, but at times he would cry out, and there was involuntary defecation and urination. Optic neuritis increased in the left eye, and there was nystagmus when the eyes were moved toward the side of the lesion. Seven days after operation, the pulse and temperature being normal, paresis of the arm of the same side developed; the eyes deviated to the opposite side. On the tenth day the woTind was ex- plored with the finger, but nothing was found. On the fourteenth day after the operation he was in the same condition as primarily; pulse 60, respiration 14, complete paralysis of the arm and hand of the same side. Second Operation. — On. exposing the original sinus tract a large dbsoeaa cavity was found, rimning toward the median line; two ounces of pus were evacuated, after which the hernia, which had developed during the first weeh, disappeared. During the following three weeks the patient was so violent as to require restraint, and screamed frequently. Discharged from hospital; the sinus was healed and remains so though on two occasions a small opening has developed over the site of the wound. His mental condition is very poor, though his mother says he is as bright as he ever was. Present Condition. — Perfectly well; complains of headache. Served with American Expeditionary Forces in France. ACUTE BRAIN ABSCESS, In acute intracerebral abscess the outstanding pathological process is acute cerebral tissue death, with intense oedema, and but slight pro^ tective limitation, the rapid formation of the abscess precluding the formation of a protective capsule. As the technic of the surgical treatment of chronic brain abscess with a capsule utilizes the capsule in the thorough evacuation, cleansing and obliteration of the abscess, the surgical technic of acute brain abscess must be largely modified to adapt itself to differences in the pathological processes. Recovery in acute intracerebral abscess is much rarer than in brain abscess with a capsule, and yet I am persuaded that. with a proper operative regard for the differences in processes, the mor- tality from acute abscess should not be much higher than in chronic cases. Pathology. — The pathological changes in an acute brain abscess are the same as those occurring in an abscess formation in any part of the body, altered only by the special structure involved. Fol- lowing the infection we have the same death of tissue and the same protective processes that occur elsewhere. A microscopic specimen exhibits an inner zone of dead tissue and pus, necrosis from strangulation, and leucooytosis. If the infec- tion is virulent enough to break dovm completely any attempted resistance of the part, there follows an extension of this process — 62 BEAIN ABSCESS an extending death of tissue — and beyond, in tlie still living cerebral tissue, an intense oedema with thrombosis of the vessels, and hemor- rhage. In such a case death of the patient occurs within a few hours of the original infection : fulminating infective encephalitis. When the infection is not so virulent, protective processes are present. In the microbiotic zone, in which the bacteria and their toxins have caused a disappearance of the nerve cells, the glial cells, although altered, are still present, and external to this zone there is an area of round cell infiltration — from which iJie leucocytes have been called from the blood vessels to the brain for its protection — \ associated with vascular thrombosis and with a meshwork of fibrin.^* The microscopical picture of an acute brain abscess gives the gen- eral impression that the chief limiting process is thrombosis of the vessels, and hemorrhages, just as the formation of a new connective tissue is the chief limiting process in chronic brain abscess. In this area of infiltration from the lymphocytes, the nerve cells are also dying or dead, but the neuroglia on the other hand show a certain amount of proliferation. Blood vessels now rapidly bud in this zone, each blood vessel simply being a blind endothelial tube from which fibroblasts spring. Surgical Pathology. — If an acute abscess is now attacked by the surgeon, and during the evacuation and the subsequent intro- ^uption of a drain hemorrhage from the vessels occurs, the delicate protective mechanism is broken down, the oedema of the adjacent cerebral tissue is greatly increased, the inflammatory process acquires a fresh momentum from the trauma of the operation and the irrita- tion of the drain, and death is apt to follow rapidly. (See Figs. 23, 24.) The Surgical Aims should be limited to, (1) the location of the abscess; (2) the relief of compression by as complete evacuation of the abscess as possible without trauma to the cerebral tissue; and, where the suppuration is intracerebral, to (3) the establishment of an area of protective adhesions into the abscess cavity. Methods of Treatment. — A clinical diagnosis of acute abscess without capsule having been made, one of two methods must be adopted. Either, (1) exploration through a large dural opening, followed by complete evacuation if a piarachnoid abscess is located, or, if an intracerebral abscess, by as complete evacuation as is pos^ sible through the searcher, with tight closure of the dura excepting such as is sufiicient to admit of the exit of the searcher ; or, (2) a •• HasBln, G. B. : Hlstopathologlcal Studies In Brain Abscess ; Medical Record, January 19, 1918, Vol. 93, p. 91. %' Fig. 23. — Microjihotograph showing intense oedema, round cell infiltration and multiple hemoirhages in an acute cerebral abscess. Death 24 hours after evacuation, without return of consciousness. Fig. 24. — Microphotograph showing areas of hemorrhagic encephalitis, fol- ABSCESS OF MIDDLE FOSSA 63 hollow needle puncture through the intact dura, the primary aim of the puncture being the location of the abscess and the establishment of a tract of protective adhesions through the piarachnoid into its cavity. Were it possible uniformly to differentiate acute non-capsvlated introrcerehral, from piarachnoid abscess prior to operation, the punc- ture method would be preferable, since in acute intracerebral abscess the puncture, with but slight damage to the cerebral tissue, partially relieves the compression by the partial evacuation. Unfortunately our diagnostic methods do not allow of such accu- rate differentiation, and if the puncture method is uniformly adopted many superficial piarachnoid abscesses will fail of localization, as has been the author's repeated experience. Consequently he has for years advocated and practised a dural opening large enough to admit a thorough inspection of the adjacent piarachnoid; and in case a piarachnoid abscess is not found, exploration into the brain sub- stance without injury to a cortical vessel, with partial evacuation of the abscess and tight closure of the dura around the exploring instru- ments, which may or may not necessitate a second operation for com- plete evacuation, cleansing, and obliteration after the capsule has been found. In 1914, before the New York Academy of Medicine, the author recorded: — "I am persuaded that the operation for acute intracerebral abscess, especially if situated more than two or three centimeters from the surface, should be con- ducted in two stages. My opinion is based upon almost a complete failure to effect a cure by means of exploration and introduction of drainage material into the brain in cases of acute, subcortical, intracerebral abscess. Post-mortem examinations of acute intracerebral abscesses so treated re- vealed intense cedema and multiple punctate hemorrhages, while the drain was invariably found lying in the brain itself, entirely outside the abscess cavity, thus only exaggerating a previously bad condition. In my opinion it is better not to introduce drainage material at all than to damage brain tissue in an un- successful attempt to drain the cavity. When the operation is undertaken in two stages the first procedure should consist simply of the evacuation of the cavity with a minimum of traumatism." CASE xrn. Mrs. H.: — Acute Adjacent Temporo-sphenoidal Lobe Abscess. Eight middle ear disease, without discharge two weeks previously. Present History. — Fourteen days previously suddenly had a severe pain in the right ear, accompanied by a chill. No discharge. Pain lasted twenty-four hours and then stopped. Temperature about 102 degrees. Few days later: — temperature ranged from 102 to 105 degrees; respiration, 32 to 36; pain in back " Lemaltre, P. : "L'Bxclusion des especes sous-arachnoldiens" (Bxcluslon of the Subarachnoid Spaces; application to the treatment of cerebral and cerebellar abscesses of otitic origin, and in a general way to brain surgery) ; Revue de Ohirurgie, 1919. Tome LVII, p. 497. 64 BEAIN ABSCESS of head recurred and persisted. Consolidation of lung was diagnosed, although no cough was present. A few days before examination there were mental symptoms; pulse slow; patient delirious at times, at other times more or less lethargic; temperature normal. No vomiting, hut nauseated once — thought to be due to tobacco smoke in the room. No dizziness. Temperature irregular, ranging from normal to 103 degrees. Examination on fourteenth day of illness: — patient more or less lethargic; can be aroused and answers questions well — it seems as if she answers too well, for although she keeps her eyes closed she is conscious of all that goes on around her. Eight optic disc margin slightly indistinct, veins full; left margin clear, but veins full. Hears well with both ears. Slight weakness of left arm, which appeared for first time at this examina- tion. Has a very bad odor to her breath. The membrane of her mouth is swollen. She has no Kernig; no Babinski. Temperature which had ranged from normal to 101 degrees in last few days, suddenly rose to 103: slight chill. Lumbar puncture gave high cell count; no bacteria. Two Days Later. — ^In deep coma; cannot be aroused; incomplete paralysis of left arm. During last two days several attacks of choking and cessation of respiration. Operation on Sixteenth Day of Illness.— As there was some doubt whether patient was suflfering from encephalitis lethargica or brain abscess, the only ear symptoms recorded having been pain which lasted twenty-four hours and had never been followed by discharge, it was decided to explore the mastoid first, and if evidence of disease was found, then to explore the brain. The mastoid antrum and a few cells were found to contain granulations and a few drops of pus. (Smear and culture from cells and antrum negative.) Through a clean field above the mastoid and ear the bone under the temporal muscle and over the squamous portion of the temporal was removed and the dura exposed for an area about two inches in length by one and one-half inches in breadth. A small opening through the dura failed to reveal pus in or on the surface of the brain. A puncture of the brain through the opening, with hypo- dermic needle at depth of one inch from the cortex revealed thin pus. On account of small size of needle the flow was very slow and soon stopped altogether. Needle left, and held in position by numerous small pledgets of wet cotton pyramided around it. Muscle and skin closed except for pyramided area. At the beginning of the operation the blood pressure was 170, rising to 190 and falling immediately to 155 upon the partial evacuation of the abscess. Cul- ture from pus from brain revealed streptococcus. Two Days after Operation. — Patient has regained consciousness, recognizes objects and talks, but is still very lethargic. Left arm and leg both almost com- pletely paralyzed. Slight papillcedema of both eyes. No drainage through the needle, but considerable over and around it, as if it had discharged for some time and then stopped. On passing wire through needle there was no pus. Patient gradually improved. Moved fingers of left hand and toes of left foot for first time in several days. Subsequent History. — During the subsequent treatment of the abscess it was twice lost, and refound because of filling again with pus. A larger drainage tube was at last properly placed within the abscess cavity. The papillcedema persisted for over six weeks after the operation. The patient ultimately com- pletely recovered. Comments. — In this case we caused (1) slow evacuation, thus relieving the compression; then (2) the establishment of a small tract; later (3) the en- largement of the tract and again evacuating. During this treatment there waS ABSCESS OF MIDDLE FOSSA 65 opportunity for the acute abscess to be converted into (4) a chronic abscess with a capsule. The continuation of the papilloedema may have been due to the lack of a wide decompression, or a displacement of the brain bulk may have been a factor. The abscess was certainly touched at its side and not in the center — the collapse of its walls twice causing the loss of the cavity, which was not found again until it had refilled with pus, thus demonstrating the necessity of as com- plete evacuation as possible in acute as well as in chronic abscesses. The leucocytosis three days after the operation was 24,000, with 83% pqly- morphonuclears. It rapidly fell to normal — 6200 to 8800 — in spite of the abscess refilling twice, showing that routine cell counts are of very limited value after evacuation as to the progress of the case. The object of the operation is the evacuation of the abscess and the collapse of its walls, with the least possible associated trauma to the cerebral tissue. By the evacuation some of the infective material is removed and this, with the associated relief of tension, may allow time for the tissue to develop resistance and the formation of a capsule. Later, should the symptoms recur, the area of suppuration being now limited, the abscess may again be explored, when, as in one of my cases, the meninges will be found walled off — a very important aid. The abscess may now be fully evacuated and drain- age material introduced. Technic. — In exploring for an acute abscess, three inches of the end of a soft rubber catheter containing two holes, with a flexible metal stylet, should be used. The stylet should occupy but a small part of the lumen of the catheter, so as to allow the thin pus to flow through the catheter with the stylet in place. On locating the abscess the greatest care must be taken not to displace the catheter. All pus presenting is collected by a suction apparatus. After pus has ceased flowing the stylet is removed and the catheter cut off flush with the skin, to which it is attached by a silk suture. The patient should then be in- verted. If the abscess is very acute the catheter may be withdrawn; if of longer duration, the dural opening should be entirely closed except for the small open- ing through which the catheter passes and which it should entirely flU. The skin opening should be tightly closed, except for a similar opening. The technic of the second complete evacuation is that adopted in chronic intracerebral abscess. CLOSUKB. In all cases of brain abscess, chronic or acute, the abscess having been entirely evacuated, the brain should be as completely covered as possible. If the technic of evacuation has been perfect, the dura can be almost closed, the small area which carries drainage into the abscess cavity alone being unprotected by the dura. Many otologists and surgeons disregard the fact that all drain- age material within the dura is dangerous, especially if it is absorbent. To place dry gauze over an exposed area of piarachnoid over which 66 BEAIN ABSCESS a dressing is introduced, is simply to invite disaster, As a proof of this, witness the very extensive superficial brain necrosis often found at autopsy after so-called "free" drainage. If a drainage tube or strip of rubber tissue has been introduced into the abscess cavity, a tract for the drainage material should be made to the nearest external surface, through dura, bone, and skin. Over all the remaining area, dura, bone and skin should be covered, unless the soft parts are so wet that it is thought advisable to place a drain between the dura and the bone. It is not an uncommon experience to find, at the end of an intra- dural manipulation, that the protruding brain prevents the complete closure of the dura. When it does occur, the piarachnoid should be covered with a piece of fascia lata stitched firmly to the dural defect, over which as much as is possible of the bone flap should be placed, and the fascia, muscle and skin lightly closed. It is best to leave all drainage undisturbed for several days, dur- ing which an organized wall is being built along the tract, thus plac- ing the tract in reality outside the brain tissue. Further manipula- tions along this tract, such as the re-introduction of drainage or of the encephaloscope, should be conducted, if at all, without the slight- est injury to this wall. During recent years, in my successful cases, the drainage material has been left entirely alone for rather long periods. As it is slowly expelled by the brain, it is carefully cut off, care being taken to anchor the end. After a period of from two to five weeks, depending upon the depth of the abscess, its size, duration and amount of discharge, the last piece of drainage is removed. Additional Referenoes to Double Ahsoess. Miiller, R. : Doppelter otitisoher Schlaf enlappenabszess ; Zeitsehrift filr Ohren- heillcunde, 1910, Bd. LXI, S. 183. Urbantschitsch, E. : Zweifacher rechtsei tiger Schlaf enlappenabszess : Opera- tion: Heilung; (Double Right-sided Temporal Lobe Abscess; Operation; Re- covery) ; Wiener Klimsche Wochensehrift, 1916, Bd. XXIX, No. 47, S. 1507. Additional References to Tem/poro^ Sphenoidal Brain Absoess. Ruttin, E.: Schlafeulappenabszess mit Infektion des rechter Unterhoms, Pyocephalus, Meningitis, Exitua; International OentraXhlatt filr Ohrenheilkunde, 1909-10, Bd. VIII, S. 379. Voss, F.: Encephalitis hemorrhagica und Schlafeulappenabszess nach Otitis media; Zeitsehrift filr Ohrenheilkunde; Bd. LXI, S. 323. Beliuoff, S. ; Ein Beitrag zur Kasuistik des otitischen Hirnabszesses; Klim- ische Beitrage emr Ohrenheilkunde, 1919, p. 89. (Adjacent abscess lighted into activity by trauma.) Urbantsohitsoh, E.: Eitrige Meningitis und Schlafeulappenabszess; (Puru- ABSCESS OP MIDDLE FOSSA 67 lent Meningitis und Temporo-sphenoidal Lobe Abscess) ; Wiener Klmisoher Woohensohrift, 1918, Bd. XXXI, S. 794. Mlygind, S. H. : Haemorrhagia Meningea, resembling cerebral abscess of otitic origin; Ugesk. for Laeger K0henh., 1919, Vol. LXXXI, pp. 1836-38. Bodkin, H. : A Case of Cerebral Abscess of Otitic Origin; British MecUoal Journal, 1917, I, p. 510. Nauwerck: Zur Kenntniss des chronischen, traumatischen Hirnabszesses; Miinohener medisinisoher Wochensohrift, 1917, Bd. LXIV, S. 109. OHAPTEK V. METASTATIC ABSCESS. CLASSIFICATION. The accepted classification of brain abscess of otitic, rhinitic, or metastatic origin calls for modification. Many abscesses orig- inating from the ear and the nasal sinuses are pathologically and clinically metastatic and should be so classified, their symptomology permitting differentiation from the usual adjacent (secondary) abscess of aural or nasal origin. The classification of brain abscess into Adjacent (secondary to aural or nasal suppuration), and Metastatic (from lungs, heart, ear, etc.), as suggested elsewhere in this monograph (Chapter III., p. 17), is based upon two distinct types of pathological process: — the adjacent type, invading the brain by direct extension either through tissue suppuration, or by way of a thrombophlebitis, or perivasculitis, and the metastatic form, which is of hematogenous origin. Erom a pathological standpoint a brain abscess which originates from an infection free in the blood stream is truly metastatic whether the primary focus be situated in the ear or in the lung. The classification into Adjacent, Metastatic and Traumatic will explain many reported cases otherwise enigmatic — such as abscess of otitic origin of the opposite hemisphere^ — ^while clinically it will prove of assistance in diagnosis and surgical treatment. DEVELOPMENT. Adjacent Abscess. — Adjacent brain abscess, as the name im- plies, is anatomically adjacent to the primary focus of infection, viz., mastoid antrum and middle ear, labyrinth, or nose, to which it is directly connected by a pathological process. Its position within the brain, therefore, must be more or less definite, being prescribed by anatomical relationship. The infection from the ear or nasal sinus extends into the cerebral tissue by continuity of tissue sup- puration, or necrosis, or by contiguous extension through a venous 68 METASTATIC ABSCESS 69 wall or a perivascular space — retrograde thrombophlebitis or peri- vasculitis. Eetrograde thrombophlebitis of a cerebral or pial vein follows the course of thrombotic formation in general; it advances in the wall of the vein — a phlebitis — or in a perivascular space. The phlebitis or perivasculitis is followed first by a parietal, and later by an obliterating thrombus. A blood-stream infection, if present at all, is secondary to the thrombus formation. In accordance with thrombotic formation in general, the process is comparatively slow. The chief surgical and diagno&tic difference between the forma- tion of an abscess from retrograde thrombosis and from a metastasis is based on the fact that in the former the protective mechanism of the brain has time to assert itself while the circulation is still ■ active and before the death of cerebral tissue takes place. If the symptoms are present at all at this time, they must of necessity be trivial since they are due to a normal reactive process. Likewise, the clinical symptoms of adjacent abscess develop gradually; they are never apoplectiform. Metastatic Abscess. — ^Metastatic abscess follows the occlusion of a cerebral vessel by an infected nidus circulating freely vnthin the blood stream itself. Bacterial infection of the blood stream alone apparently is not sufficient to produce a brain abscess. In the numerous experiments of Weed and his associates ^ with direct blood- stream infection, only one superficial abscess (from infection of a perivascular space) developed. The blood stream is intolerant of the presence of micro-organisms within itself. EoUowing injections of micro-organisms into the blood stream, the blood soon eliminates them and rapidly becomes sterile again. An additional factor, apparently, is necessary ; this is probably supplied by a minute septio nidus small enough to pass through the capillaries. Toxaemia causes great damage to the intima of the blood vessels because of the slow- ness of the venous circulation, and a toxsemic nidus finds a favorable condition in the intima for the rapid growth of a thrombus which soon may become of embolic nature. Metastatic Vascular Occlusion. — The onset of metastatic brain abscess is sudden, apoplectiform, because the bacteria, sud- denly closing the vessel, cause apoplectiform symptoms — a sudden, violent headache, transient dizziness, projectile vomiting. These symptoms may be slight, and apparently transient, but the sudden J Weed, D. H., Wegeforth, P., Felton, J. B., and L. D. : Meningitis Produced by Intravenous Inoculation ; Monographt Bookefeller Institute for Ue^ical Reieareh, Marcb 25, 1920, No. X2, pp. 57-112. 70 BEAIN ABSCESS vascular occlusion causes immediate nutritional death of the cerebral tissue.^ The focus of original infection is generally distant from the brain — in the lungs, the heart, or the pleura — ^but numerous cases are on record of the infecting nidus originating from blood vessels contiguous to the ear. In a case reported by Berens,* infection originated from thrombus of the internal carotid artery; in one of the writer's from the lateral sinus. Oases resulting from abscess at the surface of the body are not of common occurrence, but Kutzinski and Marx * report one in which abscess of the frontal lobe apparently resulted from a purulent process in the finger. All such cases should be classified as metastatic. The usual explanation that metastatic abscess is always of embolic arterial origin has not been substantiated by the author in an examination of the post-mortem records.^' ® Won-suppurative arterial occlusion is comparatively frequent, but it does not occasion abscess formation although the symptoms may simulate those of abscess when associated with a suppurative process. CASE xrv. A. S.: Thrombosis of Cerebral Vessels. Child, aged seven months. History. — The father died from tuberculosis when the child was only a few months old. The child seemed perfectly well until one day it suddenly cried, had a convulsion, and was brought to hospital with twitching of its right upper lid, corner of mouth, and right arm and leg, with a lateral deviation of its eyes to the left. O. E. negative. On following day spastic paralysis of right arm and leg. Developed otitis media in left ear; right ear began discharging about four days after admission to hospital, with swollen area over mastoid. Nystagmus to left, continued lateral deviation of eyes to left. Continued twitching of right arm and leg; facial paralysis; frequent slight convulsions, followed by profuse perspiration. Increasing coma. Temperature normal until three or four days before death, when it ran to 105 and 108 degrees. Child died three weeks after admission to hospital. Diagnosis. — Inherited tuberculosis from father, . followed by acute tubercu- losis, with thrombosis of cerebral vessels from tuberculous infection. Autopsy Findings. — On opening skull the left frontal lobe was found soft- ened — not an abscess, but nutritional disturbance from vascular occlusion. The softening extended over to right frontal lobe, with portions of infiltration where blood had been effused into the brain. The right hemisphere showed signs of increased intracranial pressure. Embolus in anterior cerebral artery, causing degeneration of the whole frontal lobe. Around the place where the thrombus ' Moore, John T. : Blastomycosis. With Report of Case Dying from Abscess of the Brain ; Sur., Oyn. and Ots., December, 1920, pp. 590-594. " Berena, T. Passmore : Atmale of Otology, RMnology and Laryngology, 1913, Vol. XXII, p. 448. * Kutzinski, A., and Gerlchtsarzt, Marx : Hirnabszess als Polge peripherer KBrperei- terung naeh einem UnfaU ; MonatschHft fUr Paychiatrie und Neurologle, October, 1914, S. 255. ■ Schorsteln : Lancet, 1909, II, p. 843. " Cayley : Abscess of the Brain Associated with Bronchiectasis ; TratuacHons of the Pathological Sooiety of London, 1884, Vol, XXXV, p. 12. METASTATIC ABSCESS 71 occurred there was hemorrhagic infiltration. Examination of right ear showed grumous material in the middle ear and antrum; area of bone around seemed softened. The left ear also contained grumous material. Metastatic Abscess of Venous Origin. — The vast majority of, if not all, metastatic brain abscesses are undoubtedly of venous origin, for bere, as in embolus of thrombotic origin in general, conditions are favorable for its development, while the rapidity of the arterial flow, assisted by the brain's protective mechanism, tends to prevent the lodgment and growth of a small infected nidus in the arterial circula- tion. This view explains and is substantiated by the relative infre- quency of brain abscess in ulcerative endocarditis, in which large numbers of infected nidi are carried to the brain by the arterial cir- culation. Origin of Thrombotic Nidus. — Parietal venous vegetations are more frequently associated with mastoiditis and sinus phlebitis than is generally supposed, the vegetations grossly resembling those of the heart in acute endocarditis. CASE XV, B.; Meningitis from Labyrinthitis; with Beginning Thrombi and Vegetating Thrombus in Ixjngitudinal Sinus ; Male. History.— Always subject to headache. Had had an attack of influenza, fol- lowed by sharp pain in right ear. Spontaneous rupture of drum membrane. Ear continued to discharge for about six weeks; during entire time patient swayed to right and complained of pain on right side of head. Lost considerable flesh. Attended to his business until physician ordered him to country. While away, had a distinct chill and severe headache, and vomited during the night. Lumbar puncture gave an excessive amount of fluid imder pressure, slightly turbid or yellowish, looking like urine and containing a large number of polymorpho- nuclear leucocytes; apparently sterile. Totally deaf in right ear. Examination revealed no discharge from this ear. A teat-like projection was seen in lower quadrant. Marked nystagmus at outer comer. 0. E. gave fulness of the veins; no spontaneous pointing deviations. Operation. — Mastoidectomy. The whole mastoid was sclerosed, being abso- lutely solid. Exploration of the cerebellum negative. Patient was in deep coma the day following operation, and died three days later with marked symptoms of suppurative meningitis. Autopsy Findings. — The bone was hardly cancellous to the naked eye and was sawed with great difficulty. The piarachnoid was infiltrated with pus. The Pacchionian bodies were prominent alongside the longitudinal sinus. On opening the superior longitudinal sinus the cavity was found to contain a cluster of vegetations posteriorly to a plane corresponding to the occiput. These vegeta- tions were not unlike those seen in the valves in bacterial endocarditis. Some were friable and could be torn off easily, the majority were fibrous, were well organized and could not be stripped off. They almost obliterated the lumen of the sinus. The right labyrinth, converted into one large, mouse-eaten cavity, contained a thick film of foul-smelling pus. Smears made from the right middle ear, labyrinth, meninges, and some of the vegetations in the longitudinal sinus, showed streptococci. Sections of the longi- 72 BEAIN ABSCESS tudinal sinus where the vegetations occurred showed the wall to be thickened by fibrosis. The vegetations sprang from the intima and consisted of a stem of connective tissue in which there was a marked infiltration of small and large mononuclears and polyblasts. In some of the more recent ones polynuclears were abundant. Comment. ^Undoubtedly the severe pain in the back was due to lodgment of embolic portions of the sinus in the small vessels of the cord. Without having obliterated the sinus, the vegetations were being given off into the circulation all the time. A venous sinus vegetation, if detached, need not necessarily go through the entire circulation before again entering the cerebral venous circulation. Arnold "^ has demonstrated experimentally that, on injection of bran into the large veins of the neck in case of inter- ference with the normal intrathoracic negative pressure, particles of the bran are found in the opposite venous sinus. According to his experiments the venous circulation from the head toward the heart is reversed when a positive intrathoracic pressure is encountered. Mechanically, then, disturbance of the return venous circulation, such as an occluding thrombus or temporary compression from a tampon, may cause a reversal of the current from one venous sinus to that of the other side, there being no obstructing valves.® These factors, asso- ciated with a disturbance of the protective mechanism of the brain, render possible the lodgment and growth of the embolic thrombus. The protective mechanism of the brain is easily interfered with by circulatory disturbance, as demonstrated by Weed,® by the produc- tion of meningitis from a blood-stream infection by jugular decom- pression. Arnold's ^^ observation provides an explanation of abscess of the brain on the opposite side from the ear lesion, such as that referred to by Japha,^^ Quimby,^'^ Lossen,^^ and Maier,^* or of any of the unusual sites of abscess formation in the frontal or occipital lobe from ear suppuration,^^ or in the parietal from nasal infection. Feequenot. Abscesses of the brain of metastatic origin, while of relatively rare occurrence, are much more frequent than is generally recognized. 'Arnold, J.: tJeber RUckiauflgen Transport; ArcMv. fur Pathol., Anat.. und Physiol., 1891, Ba. 124, S. 385. • EJQOtt, J. F. : The Cerebral Sinuses and their Variations ; Trans. Int. Med. Con- gress, London, 1881, Vol. I, p. 191. • Weed, L. H. : Production of Meningitis by Release of Cerebro-spinal Fluid : Jour. Am. Med. Assoo., 1919, Vol. 72, p. 191. w Arnold, J. : Loo. cit. " Japba, A. : Zur Diagnostil£ der Herderkranlsungen des Gehirns : Zeit. fur Prak. Aerate, 1898, VII, 701. " Qulmby, Wm. O. G. : Personal Communication. "Lossen, W. : BeitrSge zur Diagnose und Therapie der Kleinhirnabszesse (Case I) ; BeitrUge z. KUih Chvrurgie, 1903, Bd. 39, S. 804. "Maier, M. : Erfahrungen iiber den otitischen Hlrnabszess : Arohiv filr Ohren- heiVmnde, 1914, Bd. 95, S. 163. / ' " «">"' "Berens, T. Passmore: Abscess of Frontal Lobe of the Brain, with Exhibition of Specimens; Tr von Hinsberg, V. : Ueber flen Infektionsmechanlsmus bei Meningitis nach Stlrn- Mhleneiterung : Verhandhmgen ier Daiischen Otologischen Oesellsahaft, 1901, Bd. 10, S. 191. " Streit, Herman : Weitere BeitrSge zur Histologie und Pathologle der Meningitis und Sinusthrombose ; ArcMv Jiir Ohrenheilkunde, 1912, Bd. 89, S. 177. FRONTAL LOBE ABSCESS 119 ditions, the subdural space itself being generally skipped in the ex- tensive infective process from the frontal sinus to the subarachnoid. He presumes that a subdural abscess probably is the second stage in the development of leptomeningitis. The value of Streit's and von Hinsberg's microscopical and experimental work lies in its demon- stration that pachymeningitis interna and small foci of subdural pus, which have not given rise to symptoms and whose presence is con- sequently unsuspected, may exist, and, by the trauma of operation on an infected frontal sinus, may give rise to virulent leptomeningitis or brain abscess. Adjacent Piabachnoid Abscess. The reported cases make it appear that this type of meningeal abscess is not as frequent in the frontal as in the temporo-sphenoidal region, nor does it attain as large a size. These characteristics are probably accounted for by the absence of cancellous tissue in the nasal region, an irritating area of bony caries, consequently, being much less frequent in this region than in the temporal. Piarachnoid abscess is originally of toxic origin from the irrita- tion of an adjacent bony inflammation — serous meningitis — ^which later becomes infected by the invasion of micro-organisms into the protective collection of cerebro-spinal fluid. As in the temporo-sphenoidal region, if the irritating cause is re- moved before the infection occurs, the collection of cerebro-spinal fluid will disappear. Cases are recorded of the disappearance of the cerebral symptoms by sinus operation alone, without the opening of the dura. ADJACENT ABSCESS "WITH STALK." This type of abscess is of relatively more frequent occurrence in the frontal lobe than in either the middle or the posterior fossa. As with temporo-sphenoidal abscess, and for the same reason, abscess with a stalk offers the best prospect of recovery. Although only twenty cases of frontal lobe abscess have recovered, three have been spontaneously cured by rupture and evacuation through a stalk. The establishment or utilization of a stalk — ^nature's method of cure — in frontal lobe abscess, as in temporo-sphenoidal abscess, should be the fundamental surgical aim. With a stalk present the operative mor- tality should be low. 120 BEAIN ABSCESS ADJACENT INTRACEREBRAL ABSCESS WITHOUT MACRO- SCOPICAL EVIDENCE OF CORTICAL INVOLVEMENT. This type of abscess is generally situated in the white medullary substance, about one-half inch from the cortex. It is usually of a small size and of very low virulence, remaining latent for long pe- riods of time. The literature records a few cases of the abscess growing backwards, involving the speech area on the left side, and then the face and arms. Metastatic Abscess is relatively more frequently encountered in the frontal lobe than in other portions of the brain, and the left frontal lobe is attacked more frequently than the right. -^^ The special predilection of metastatic foci to find lodgment in the frontal lobes would favor the view that the return circulation through the veins of the frontal lobe furnishes a favorable condition for thrombotic-embolic formation — slowness of current and ebbing with poor resistance.^* This latter condition may be assisted by the anatomical peculiarity of the arterial supply of the frontal lobe, coming as it does from a loop of a loop — the anterior cerebral artery ; and therefore the arterial supply, while ordinarily ample, is easily disturbed by traumatic or inflammatory influence. Among metastatic abscesses should be included all frontal lobe abscesses of otitic origin, as a careful examination of the literature — Lombard,^ ^ Berens,'^* Schwabach,^'' Nonne,^® von Hinsberg^® — will demonstrate that they all possess the diagnostic peculiarities of meta- static abscess, namely, an apoplectiform onset, which although often so mild as to escape notice, still can be elicited by careful examina- tion and location of the abscess at a distance from the primary in- fection, to which site it has been conveyed by an intercurrent osteo- " Couteaud : Metastatic Abscess in the Brain ; Hevue de Chirurgie, Paris, 1913, Vol. XXXIII, No. 7, pp. 1-172. (States that "The left side and the frontal lobe are most frequently involved.") " Browning, In an examination of 200 cases of supracerebral veins, found 59 in the frontal region, jumping over from the piarachnoid to the dura at 3-4 cm. from the longitudinal sinus, and only 9 in the posterior, superior and central; thus, he thinks, favoring infection. Browning, W. : The Veins of the Brain and its Envelopes : their Anatomy and Bearing on the Intracranial Insulation ; Monograph, Brooklyn, 1884. '= Lombard, Bloch A., and Moulouguet, A. : Un cas d'abscfts frontal du c6t6 opposS fi une otite suppurfie chronique (Frontal Lobe Abscess of Otitic Origin) ; Awnalea iet italades de I'Oreille, etc., 1914, Tome 90, p. 749. '» Berens, T. Passmore : Abscess of Frontal Lobe of Otitic Origin ; Armala of Otology, RMnology and Laryngology, June, 1913, Vol. XXII, p. 433. " Schwabach, D. : Beitrag zur pathologlschen Anatomic des inneren Ohres, und zur Frage vom primaren Hirnabszess ; Beltrdge stur Ohrenheilkunde, Lucae Festschrift, 1905, S. 55. '" Nonne, M. : Ueber FBUe von benignen Himhauttumoren ; ueber atyplsch ver- laufene FUlle von Hirnabszess, sowie weitere klinische und anatomisehe Beftrage zur Frage vom "Pseudo-tumor Cerebri" ; Deutsche Zeitachrift fiir Nervenhellkunde, 1907, Bd. 33, S. 316-357. " von Hiusberg, V. : Ueber den Infections-Mechanismus bei Meningitis und Stirn- hShleneiterung ; Terhandlungen der Deutsohen Otologiechen Oeaellachaft, 1901, S. 191. (Gives microscopical findings of path of invasion by blood vessels and lodgment In glib^ural space, with pilcroscoplcal illustrAtions.) FEONTAL LOBE ABSCESS 121 myelitis or the involvement of a large venous cliannel, sucli as the longitudinal sinus. The surgical importance of the relative frequency of metastatic abscess being situated within the frontal lobe, especially on the right side, should be more generally appreciated, as in a case in which a metastatic abscess is suspected (with symptoms of cerebral suppura- tion but without localization), the operative exposure should be large enough to admit of exploration of the frontal lobes, especially of the left. TRAUMATIC FRONTAL LOBE ABSCESS. As would be expected from its exposed position, traumatic abscess is relatively common in the frontal lobe, and for the reason that this area is silent, the encapsulated suppuration is apt to be overlooked until a fatal meningitis has developed. (See Case XXII, p. 125.) Experience has taught the author that, given a history of trauma of the frontal region, especially if a fracture of the frontal bone is known to have occurred, slight but continued symptoms — such as headache, slight changes in disposition, dizziness, etc. — call for an exploration of the frontal region. In the author's experience the results of operative treatment of localized frontal lobe abscess of traumatic origin are most satisfactory, the operative mortality being very low, in contradistinction to the high recorded mortality in adja- cent frontal lobe abscess. Immediate Occasion of Adjacent Abscess. In a large proportion of the reported cases the adjacent frontal abscess has been preceded by operative trauma on an accessory sinus. So uniformly has this occurred that it is necessary to assume either that the operation on the sinus was the immediate occasion of the intradural suppuration, or that the intracranial origin of the symp_- toms was not appreciated by the surgeon at the time of the sinus operation.^" While the latter supposition indubitably explains many of the cases, the writer is of the opinion that undue trauma during a sinus operation is also frequently responsible. The forcible curetting of " Iieegard, Fiithjof : Cerebral Abscess of the Frontal Lobe ; Annals of Otology, Rhinology and Laryngology, March, 1919, p. 115. ("Often the mode of procedure Is to operate for the sinusitis. If the symptoms do not disappear, as had been expected, if they continue and increase, it gradually becomes clear th^t there exists something more than an inflammation in the frontal sinus, and then finally the cerebral abscess is diagnosed. Such a state of affairs is so typical that on reading through the history of cases we find these conditions recurring again and again, almost with the regularity of a law.") 132 BRAIN ABSCESS the firmly adherent membrane from the posterior wall of the frontal simis produces a condition similar to an acute virulent infection hy liberating into the damaged bony tissue micro-organisms which have been attenuated by the protective mechanism of the accessory sinuses; these organisms again become virulent, attack the blood vessels of the denuded bones and produce a thrombophlebitis with extension into the central tissue by their transplantation into new soil, finding here a favorable medium from the damage done to the tissues by the operator. Situation of Adjacent Feontai Lobe Abscess. The situation depends upon the point of infection. As the frontal sinus has great variations in its size, the abscess may be situated in any part of the frontal lobe. It is consequently of great importance that a roentgenogram be taken, depicting at least the limitations of the frontal sinus. Among the recorded cases such a high proportion present necrosis of the posterior wall adjacent to which the abscess was situated, that the writer is led to believe that such an inflam- matory defect is of greater surgical assistance than is the operative finding of a defect of the posterior. Either in itself is more or less a guide to the location of the abscess. Where the abscess is due to com- plicating osteomyelitis, longitudinal, lateral or cavernous sinus throm- bosis, it may be situated at a great distance from the infecting sinus. Presence of Capsule : Adjacent frontal lobe abscesses follow the same rule as regards capsule formation as do abscesses of the middle fossa; although, on account of the low order of the virulence, the limiting membrane is frequently slight in spite of the long duration of the abscess. Opeeative Eesult in Eecoeded Cases op Adjacent Abscess. An exceptionally high mortality — disproportionately much greater than abscess in any other region of the brain — attends frontal lobe abscess. Of the 87 cases collected by Boenninghaus,^^ only 15, or 17 per cent, recovered, a mortality of 83 per cent. Of the 15 that recovered three are reported as having been evacuated spontaneously, leaving but twelve out of the 87, or about 14 per cent, of the total number as successfully operated upon. Boenninghaus's compilation thus demonstrates that the surgical means adopted had been inadequate, " Boennlngliaus : CWrurgle der NebenhBhlen inkl. Chlrurgle der Dndokranlellen Kompllkationen ; Haniiuch aer spex. Ohirurgie dee Ohres und der oteren Luftwege, Bd. Ill, Part II, S. 239. FEONTAL LOBE ABSCESS 123 or had been misdirected, especially as nature, unaided, successfully evacuated 20 per cent, of the total recoveries ; whereby the inference is forced that with proper technic the mortality should not be high. Treatment. — As in a large number of the reported cases of frontal lobe abscess the patient died suddenly before a positive diag- nosis had been made, operation must be performed while the diag- nosis is still largely problematic, and consequently must be more or less exploratory. Principles of Exploratory Intradural Operation. — Surgical pro- cedure must meet two requirements of all intradural explorative operations. It must be through a clean field, so that, with failure to locate the abscess, the dura may be tightly closed; it must be so conducted that direct 6r indirect damage to cerebral tissue is most improbable. Operative Intradural Policy. — ^In proposing a policy of surgical procedure for frontal lobe abscess the surgical observations previously described should receive consideration. As the operative results in adjacent frontal lobe abscess have been much poorer than in adjacent abscess of the middle or posterior fossa, while post-operative papiU- oedema and hernia cerebri are frequent; and as traumatic secondary compression is frequently the cause of the fatal result ; and, moreover, while nature, unaided, has cured one-fifth of all the cases that have recovered by spontaneous evacuation — ^for few deaths result after spontaneous evacuation — ^therefore, any operative procedure should be planned to evacuate the abscess as nearly as possible after the method of nature. Technic of Operations for Suppurative Lesions of the Accessory Nasal Sinuses. — ^All operations on the paranasal sinuses should con- sist of simple drainage through the nose, or of an external operation with delicate but thorough eradication of the diseased mucous mem- brane, simple drainage being insufficient and forcible curetting dan- gerous. Streit,^^ von Hinsberg,^^ and Zemann ^* have demonstrated microscopically that pachymeningitis interna and small subdural foci may be converted into a general septic meningitis. Termination. — Cases of adjacent frontal lobe abscess rarely de- velop compressive symptoms — coma, slow pulse, papilloedema — death generally occurring suddenly while the patient is still active. The 22 Streit, Herman : Weltere Beitrage zur Histologie und Pathologle der Meningitis und Sinusthrombose ; ArcMv. fiir Ohrenheillmnde, 1912, Bd. 89, S. 177. " von Hlnsberg : Ueber den Infektions-Mechanismus bel Meningitis nacb Stern- hohlenelterung ; Verhandlung der D&utscTven Otologischen Oeaellschaft, Bd. 10, S. 191. " Zemann, W. : Beltrag zur Kenntniss der endokranlellen Komplikatlonen nach chronlscber Nebenhiihleneitemng ; Zeitsohrift fiir Laryngol., Bhinol., und ihre Qrern- geblete, 1913-1914, Bd. VI, S. 545. 134 BEAIN ABSCESS absence of compression symptoms until but a few hours or even minutes before death accounts for the large number of unrecognized frontal lobe abscesses, the patients dying without intradural explora- tion. The immediate cause of death is either unknown or is trace- able to rupture of the abscess through the piarachnoid or into the lateral ventricle. With rupture into the piarachnoid space death may be almost instantaneous, convulsions ushering in the demise; or it may be preceded by a virulent meningitis, lasting but a few hours. (See Case, p. 125.) (Fig. 30.) Sudden death frequently occurs without rupture into the ven- tricle or the subarachnoid space. For some reason, brain abscess in any part of the brain frequently terminates suddenly, the post-mor- tem failing to reveal either a leak into the ventricles or any other apparent cause for the sudden termination. It is probably due to an acute toxaemia which paralyzes the vital centers, as death is preceded by a sudden elevation of tanperature, with respiratory failure. According to Gerber's ^^ collection of recorded cases of frontal lobe abscess, 65 in number, eight recovered. Of the remaining 57, in 21 cases, or 37 per cent., the cause of death was unknown. Of the remainder, with known cause of death, 36 in number, the great ma«- jority ruptured into the subarachnoid space. In 13 per cent, of the total number the lateral ventricle was involved. Of the fatal cases in which the cause of death was stated, 88.8 per cent, died of purulent leptomeningitis. In MoUer's case a latent abscess caused death in five hours.^* In Pfingst's case, without symptoms of brain abscess, excepting head pains on the side of an orbital suppuration, the patient died suddenly in convulsion. Autopsy showed a large encapsulated ab- scess, frontal lobe, entirely within the cortical surface.^'' Surgical Aims of Operation for Adjacent A bscess of Frontal Lobe. — The osseous flap should be large enough to permit of inspection of the intradural surface over the posterior wall of the frontal sinus, the roof of the ethmoid, and the orbit, as adhesions between the dura and the brain call for evacuation through the protected area.^' ^* The intracerebral manipulation should be confined to, (a) the 2=Gerber, P. H. : Die Komplikatlonen der Stirnhohleneutziindungen : Monograph, Berlin, S. Karger, 1909. 2" Schausboe : Bin Fall von Empyema Sinus Frontalis mit Stirnlappen-Abszess ; Trang. Danish Otal. Laryngol. Sooiety, March, 1915 : Inter. Oentralhlatt filr Lan/naol.. 1915. Bd. XXXI, No. 12, S. 396. J » 1/ , "Pflngst, A. O. : Brain Abscess (circumscribed purulent encephalitis). Its Course and Pathology; Miss. YaMey Med. Jour., Ijoulsville, 1918, Vol. 25, p. 193. ^Elschnlg: Der orbitogene Hirnabszess ; Prager med. Wochemschritt. 1914 Bd. XXXIX, S. 37. J ' • " Piffl : Zur Kasulstik der rhinogenen Stirnabszesse : Prager med. Wochenachrift. 1914, Bd. XXXIX, S. 39. Fig. 30. — Chronic encapsulated intracerebral frontal lobe abscess with stalk, unrecognized although present for months. Sudden death from acute lepto- meningitis. No rupture into ventricle. The cause of sudden death in cases of brain abscess without rupture into the ventricle has not as yet been fully explained. PEONTAL LOBE ABSCESS 135 thorough evacuation of the abscess; (b) the utilization or the estab- lishment of a tract ; (c) the accomplishment of both without trauma or infection of the normal cerebral tissue; and (d) the avoidance of secondary compression. Technic. — The osteoplastic flap should be as large as possible and low down over the frontal avoiding, if possible, the diseased frontal sinus; its base should be external. Ventricular puncture before opening the dura will allow the dura to be incised without prolapse. After incision of the dura the placing of the head over the edge of the table will permit the brain to fall upward and toward the opposite side sufficiently to allow of elevation and inspection of the under surface of the frontal lobe. If adhesions exist between the brain and the dura, the abscess should now be drained through the area of protective ad-v hesions, into the frontal sinus, as reconuuended in detail in the discussion of temporo-sphenoidal lobe abscess. In intracerebral abscess without macroscopieal evidence of cortical involve- ment the abscess should be thoroughly evacuated and a tract established, as recommended in the location of temporo-sphenoidal lobe abscess. No attempt at eradication should be made, as the frontal lobe does not stand trauma well on account of the poor circulation. At the completion of the operation, if the slightest doubt exists that trauma, has been occasioned, a large dural opening should be left by the sacrifice of the bony flap, the brain being covered by fascia lata. Puncture of Dura and Evacuation of Abscess through Posterior Wall of the Frontal Sinus — This is advisable only when an extradural abscess or a defect in the posterior wall is accidentally found at an operation for frontal sinus disease. It is apt to be associated with cerebral trauma, does not admit of complete evacuation of either subdural or intracerebral abscess, or of decompression for secondary oedema. CASE Chronic Encapsulated Frontal Lobe Intracerebral Abscess with Stalk, follow- ing Trauma and Secondary Infection of Frontal Sinus. Chief Complaint. — ^Headache, dizzy spells and defective vision of right eye. History. — Had skull fractured from explosion of stone three months pre- viously. Speaks but little English. Examination.— Old wounds across forehead: Eyes: right cornea, dense scar across centre; Vision 10/70; left cornea, media and fundus normal; Vision 20/20. Ears: hearing, — right, whisper, 20 feet; left, whisper 10 feet. Bone conduction apparently shortened. Rotation to right; past-pointing, — right arm, no past- pointing; left arm, past-pointing to left. Rotation to left; past-pointing,— right arm, past-pointing to right; left arm, no past-pointing. Rotation to right; nystagmus 24 seconds, falling normal. Rotation to left, nystagmus 20 seconds, falling normal. Examination unsatisfactory. Three months later re-admitted to hospital. Chief Complaint. — ^Hiccough. States that "'nothing bothers him." Head- aches; no dizziness. Has been unable to work well since accident. Examination. — Patient speaks but little English, is very unintelligent, and at times appears drowsy. Hiccough at irregular intervals. Temperature and pulse normal. Reflexes normal; no paralysis or anesthesia; no aphasia. Eyes: 126 BEAIK ABSCESS Papilloedema bilateral; edges of discs indistinct; veins tortuous. No hemor- rhages. X-Ray Examination. — "Old fracture of frontal bone." Following day hiccough disappeared. Following day vomited, seemed brighter. Suddenly chill followed by convulsions. Temperature suddenly ele- vated from normal to 105. In deep coma. Lumbar puncture. Fluid turbid. Cell count 19,000. Streptococci. Death within a few hours. Post-Mortem Examination. — ^Leptomeningitis; abscess of brain of right frontal lobe, with very thin capsule surrounded by several areas of small second- ary pus formation. Both frontal lobes degenerated; tip right frontal lobe forced into defect in posterior wall of right frontal sinus, result of old fracture. Mucous membrane of frontal sinus thickened. Remarks. — From the post-mortem examination it would appear that the fracture extended through the posterior wall of the frontal sinus, and was asso- ciated with injury to the frontal lobe and herniation of the brain into the frontal sinus. An infection of the mucous membrane of the sinus being now in direct contact with the brain, resulted in the formation of the brain abscess and the development of a purulent leptomeningitis. CHAPTEK VIII. HEENIA OEEEBEI. In tlie treatment of all intradural lesions the introduction of any drainage material is dangerous. OusMng's painstaking tight closure, in layers, of the operative wound has contributed largely to his low mortality following operation for brain tumor. He has long taught that "backing out," being a reconstructive process, must of necessity consume at least as much time as the destructive approach. In non- suppurating intradural lesions failure of water-tight closure fre- quently results in hernia cerebri of the fungating variety, which ter- minates in death from meningitis. Since it is but rarely possible in operating for brain abscess com- pletely to eradicate the suppuration, some form of drainage is neces- sary. In a considerable proportion of cases drainage of whatever kind is followed by hernia cerebri. This is particularly apt to occur if the evacuation is not complete,^ if the trauma of the operation ex- cites severe reactive oedema, or if the dural opening is improperly placed. The problems involved in the causation, pathology and treatment of hernia cerebri have recently attracted renewed attention because of the frequency of hernia from shell injuries during the world war. Etiology. In the presence of a dural defect hernia cerebri will follow any increase of the brain's bulk, or increase in the intracranial but ex- tracerebral pressure. Increase in the intracranial pressure per se, although generally followed by hernia, is not necessarily the cause of this condition ; the increased bulk may be outside the brain itself, as in serous meningitis when, if the dural defect is directly over the serous effusion, no herniation results, whereas if away from it, her- niation follows. In abscess of the brain, hernia cerebri may result from: (1) In- » Molllson, W. M. : Case of Cerebral Abscess ; hernia cerebri ; avulsion of abscess wall : complete homolateral ophthalmoplegia ; recovery ; Proceedmgs Boy. Soc. Med., London, 1917-1918, Vol. II, Sec. Otol., p. 61. 127 128 BEAIN ABSCESS crease in the cerebral tissue bulk, viz., tbe abscess and its surround- ing suppuration and reactive changes, — capillary thrombosis, hemor- rhages, perivascular infiltration, round-cell infiltration and associated oedema — to which is added, after operation, cerebral death from trauma, secondary reactive oedema, extension or. re^fiUing of abscess, and encephalitis. (2) Obstruction in the exit of the cerebro-spinal fluid from the ventricles. (3) Increase and alteration in the amount of the fluid produced, the alteration probably seriously interfering with exit (such as occurs in the eye in acute secondary glaucoma), although this has not been demonstrated.^ (4) Strangulation, death, suppuration, and secondary oedema of the hernia itself. By the reaction of these factors, one upon the other, a vicious circle is established. Post-mortem reports show that in a very large proportion of cases brain abscess is associated with internal hydrocephalus. In an examination of 124 post-mortems of cerebellar abscess internal hydrocephalus was recorded as present in 27 cases. The vast ma- jority of the reports, however, contain no mention whatever of its presence or absence, the association between the two apparently not being recognized. (See Appendix II, Cerebellar Abscess.) A certain degree of internal hydrocephalus probably accompanies all brain abscesses. The brain abscess and suppurative meningitis experimentally produced by Weed * in cats were invariably associated with internal hydrocephalus, although no obstruction existed.* The affected hemisphere is frequently displaced beyond the median line, the displacement obstructing one of the main channels of the cerebro- spinal fluid system, thus causing obstructive hydrocephalus. (See p. 129.) In the production of increased intracranial pressure — an over- filling of the dural envelope — the various factors are so dependent the one upon the other that they should not be considered separately. The intradural suppuration by bacterial, chemical and mechanical irritation induces an associated cerebral oedema and is accompanied by an increased production of cerebro-spinal fluid. At the same time its rapid removal from the interior of the brain is prevented by a mechanical obstruction of the large cerebro-spinal fluid circulatory channels from mechanical displacement of the brain substance — ob- ' Rawling, L. B. : Cerebral Edema (Excess Cerebrospinal Fluid) ; Brit. Med. Jour., May 4, 1918, p. 499. ' Weed, L. H., Wegeforth : Meningitis Produced by Intravenous Inoculation ; Monographs of Rockefeller Institute for Medical Besearoh, March 25, 1920, No. 12, pp. 57-112. * Dandy, W. E. : Extirpation of Choroid Plexus of Lateral Ventricles In Com- municating Hydrocephalus; AnnaU of Surgery, December, 1918, 68, p. 569. HEENIA CEREBRI 129 structive hydrocephalus, — or from occlusion of the eliminating chan- nels of the cortex, (the subarachnoid spaces) — from the associated meningitis — communicating hydrocephalus. Argot,^ from observation of forty cases of hernia cerebri follow- ing war injuries, contends that infection is always the cause, and that the infection induces a localized or general meningitis, with or with- out abscess formation, with the production of an excessive amount of cerebro-spinal fluid. He describes a localized meningitis with cyst formation around the dural opening, and contends that if the infec- tion can be combated the hernia will recede. Argot's observations have been substantiated experimentally by the frequency with which traumatic brain abscess is complicated by subdural abscess situated away from the dural defect.* CiRCULATOBY FACTORS. Anything that obstructs the return circulation from the head will cause increased intracranial pressure and herniation, if a dural defect exists. The writer has seen ligation of the jugular vein followed immediately by longitudinal sinus thrombosis and intense optic neu- ritis with total blindness. The blindness, after persisting for several days, was relieved by rupture of the dura and by development of a hernia cerebri. At autopsy the lateral sinus on the opposite side was found to be of very small calibre. The following case illustrates the circulatory disturbances that may follow ligation of the internal jugular vein in sinus thrombosis, with the development of hernia cerebri : "^ CASE XXIII. D. S. : Hernia Cerebri. Boy, 9 years. Previous History. — Scarlet fever five years ago, followed by left otitis media purulenta; this subsided and was followed by fair-sized dry central perforation of membrana tympani, which several times had discharged and subsequently became absolutely dry, remaining so for several months at a time. Present History. — Suddenly slight pain, redness, and tenderness over mastoid, accompanied by very profuse discharge. Temperature 100 degrees. Vessels of left optic disc rather full. Following day all mastoid symptoms had disap- peared, discharge much less, follicular tonsilitis, although no complaint of throat. Perfectly well in three days. Five days later, sudden dizziness and rise of temperature to 104 degrees. Temperature rapidly fell again to normal, and patient appeared to be perfectly well. Same sudden rise of temperature repeated next day. Following day temperature 104 degrees, which fell in five ' Argot, G. : Pathogfinie et Traitement des Hernles Cfir^brales ; Lyon Annates de Chirurgie, 1917, Tome 14, p. 814. • Esslck, C. R. : Pathology of Experimental Traumatic Abscess of the Brain ; AreMoes of Neurology ani Fathologv, 1919, Vol. 26, p. 1083. » From ArohMes of OtologVi 1906, Vol. XXV, No. 2, p. 91. 130 BEAIN ABSCESS Lours to 100.2 degrees, and rose again in five hours to 103.4 degrees, and again fell in six hours below normal, 98.1 degrees. Blood examination showed numerous plasmodia malarias. Quinine given in large doses, but in spite of this there was a further sudden rise on following day. Operation. — ^Mastoid absolutely normal; no bleeding from diploic veins. Sinus exposed at knee; normal appearance, but blackened well down towards bulb, and small opening in wall very low down through which drop of pus oozed. Jugular ligated; immediately followed by a profuse flow of blood from upper wound, both from soft parts and from bone. On passing probe into opening in sinus, profuse hemorrhage, which was controlled by pressure from above. Free bleeding thought to come from below. Firm tamponage necessary to control hemorrhage. Following day general condition good, but mfirked double optic neuritis, although none had heen present one-half hour prior to operation; chilly sensa- tion, rather restless. Two days later: Temperature 100-103.4 degrees; pain in back of neck oij moving eyes; retinal veins enormously dilated and tortuous, arteries smallT Numerous hemorrhages in retina. Ether given; again very profuse hemorrhage, supposed to come from below as well as above. Very firm tamponage necessary to control bleeding. Four days later: Veins over whole of sioalp and upper part of chest very much distended. Eleven days later: General condition very much improved, but can see very little. The enlarged veins in the scalp have felt like irregular cords imder the finger, as if filled with firm thrombi, but now are gradually disappearing. Has had two lumbar punctures during past weelc. Fluid clear, under pressure, microscopical examination negative, first puncture apparently improved vision somewhat. Great difficulty has been experienced in changing dressings because of the hemorrhage which succeeded any disturbance of the firm packing. Nineteen days later: Very free discharge of clear cerebro-spinal fiuid, escap- ing from small opening in inner wall of sinus. Dressings soaked several times daily. Twenty-four days later: Hernia cerebri. During the next month symptoms of cerebellar abscess, irregular projectile vomiting, vertigo, on left side loss of coordination of both arm and leg, but chiefly of arm. Deviation of tongue, but no loss of flesh. During this time the cerebellum was twice explored; nothing found. Thirty-four days later: liapid rise in temperature; delirium; inability to swallow; collapse; death. Report of Autopsy. — "Nothing abnormal noted over the surface of the brain. The optic nerves and vessels cut and the medulla divided and the brain lifted out. It separated easily except at the site of the hernia cerebri, which was the left side of the cerebellum. "On opening the sinuses, the left lateral, the torcular, the inner one-fourth of the right, nearly the whole of the superior longitudinal, were all thrombosed. The cavernous and the petrosals were normal. "The hernia cerebri involved nearly the whole of the left lateral lobe of the cerebellum; extending from it was an area of softening involving the left lateral portion of the pons. "Two specimens were taken for microscopical study; one, the lateral por- tion of the pons and the other the medulla. The specimen taken from the medulla, on cross-section in its upper part, showed in the median line of the floor of the fourth ventricle a hemorrhagic area extending inwards and slightly to the left. The floor of the fourth ventricle showed microscopically extensive round-celled HERNIA CEEBBEI 131 infiltration. Medulla: both specimens show evidences of rather extensive menin- geal inflammation." Examination of the wet specimen of this dura several months later showed the free right lateral sinus to be only about one-half the size of the thrombosed left lateral sinus. Stxegical Pathology and Physiological Factors. Hernia cerebri from a surgical standpoint may be divided into two groups: (1) non-vlcerative, and (2) ulcerwtive or fungating. Non-ulcerative hernia cerebri, even in the presence of infection, may serve a useful purpose, as by its development, compression whicb is favoring an extension of the suppuration may be relieved, the protective forces of the brain being enabled thereby to limit the suppurative process, which otherwise will prove fatal. A non-ulcer- ating hernia cerebri is covered with piarachnoid; it is smooth and glistening, and pial vessels run over it. It occurs with large dural defects. The surgical treatment calls for the preservation of this normal piarachnoid. Unfortunately, in the presence of suppuration, non-ulcerative hernia cerebri generally becomes ulcerative or fungating. Fungat- ing hernia is not covered with piarachnoid, its surface is ulcerative or gangrenous. It occurs in small dural openings, and is partly the result of strangulation of cerebral tissue. Fungating hernia cerebri, examined microscopically, is found to contain little normal cerebral tissue, even when the hernia is of large size. In the presence of suppuration a large part of the cerebral tissue protruding from the dural opening rapidly degenerates and is replaced by vascular inflammatory exudate, with the formation of granulation tissue. The area of oedema and granulation tissue passes imperceptibly into the area of normal cerebral tissue, so that if the hernia is excised, the irritation of the operation is sufficient to start the process afresh.* Several painful experiences have impressed this upon the writer. Moreover, it is impossible to stop the growth of a hernia by pressure, as the irritation of the compression increases its size. Normally, the cerebral tissue is bathed in warm, mildly alkaline cerebro-spinal fluid. If a non-ulcerative cerebral hernia is exposed to the air for but a few minutes, its surface becomes dry from evapora- tion,' the pathological fluid of the cedema coagulating rapidly. Dry- ing of the surface of a cerebral hernia results in local areas of gan- grene, a frequent and to a large extent unavoidable complication of ■ Sargent and Holmes : The Treatment of the Cranial Injuries of Warfare : Brit. Uei. Jour., 1915, I, p. 537. 132 BEAIN ABSCESS cerebral hernia. This superficial gangrene continues uninterruptedly whenever any absorbent material is used on the hernia.® SXJRGICAL TREATMENT. Pehventiok of Hernia ; Site of Dural Defection. Experimental evidence and clinical experience demonstrate that dural defects over the vault of the cerebrum or the lateral lobes of the cerebellum are much more frequently followed by herniation than over the under surface of the temporo-sphenoidal lobe, the inner and lower angle of the forehead, or the anterior surface of the cerebellum, the dura and the brain, at the latter points, being held firmly together by vessels and nerves, and the intracerebral and intracerebellar pres- sure being minimized. Consequently, drainage should be at the site of the dural defect, unless a protective non-ulcerative hernia is de- sired for the control of compression. An effort should be made in every case of hernia cerebri to de- termine the causative factor or factors. As the underlying cause in many cases of hernia cerebri following abscess formation is an incomplete evacuation of the abscess, if a fistulous tract in the abscess cavity can be located without injury to the cerebral tissue its complete evacuation will be followed by a recession of a large part of the hernia. (See Case XII, W. K., Chapter TV, p. 60, of Double Cere- bellar Abscess, in which hernia, probably from "second abscess," was relieved by evacuation.) Likewise, the evacuation of a meningeal abscess or retention cyst, situated near the edge of the dural defect, — ^both frequent complica- tions,- — will promptly relieve the hernia. The treatment of hernia cerebri involves the avoidance of irri- tation from surgical interference or dressings; the protection of the hernia from injury, dryness, cold, or secondary infections ; and pos- sibly the reduction of increased intracranial pressure. It has long been recognized clinically, as previously noted, that excision of the hernia is invariably followed by its reappearance and that, in many cases, it ushers in a fatal meningitis, the rapid increase in the hernia resulting from the mechanical irritation of the opera- tion itself. Surgeons have learned to leave the protruding tissue alone, confining their efforts to attempts at covering the protruding mass. The observation of Essick, Weed and Wegeforth ^" in experi- » steed, KeUogg : Gunshot Fracture of the SkuU ; Jour. A. U. A.. ; May B, 1917, Vol. LXVIII., p. 1299. "ioo. cif. HERNIA CEREBEI 133 mentally produced brain abscess of a fatal meningitis from recrudes- cence of a latent infection, following operation for the closure of cranial defects, in abscesses wMch have been healed for several months, explain the complicating meningitis, and should make most cautious the slightest surgical intervention. Even attempts to probe apparent fistulous tracts in the hernia should be avoided, unless instillation with a bismuth solution, followed by X-ray examinations, shows that the fistula leads to a definite cavity within the dura] opening. ^^ Protection, — During exposure for dressing, the hernia should be continually but gently flooded with warm salt solution containing a small quantity of calcium salts. (Gushing has found that sterile normal salt solution without calcium salts is toxic to normal cerebral tissue.) The hernia should be irrigated but infrequently, to avoid all unnecessary irritation of the cerebral tissue and to facilitate the growth of new connective tissue over the hernia.-^ ^ During the war Dakin's solution was used freely on cerebral tissue; its apparent harmlessness must be because the hernia no longer consisted of cere- bral tissue, although Argot washes out the cerebral wounds with Dakin's solution immediately after the injury. Gushing ^® instills dichloramin-T in the cerebral tract ; its use, however, can be justified only by extensive destruction of cerebral tissue. The writer has seen a hernia become gangrenous with rapidly fatal result, following ap- plication to its surface of a weak formalin solution. After irrigation with normal salt solution, the hernia should be thoroughly covered with sterile wet rubber tissue coated with vase- line, over which a dressing is placed. As the rubber tissue prevents the evaporation of the fiuid, it should be changed only at infrequent intervals — ^not more than once every ten days or two weeks — even though the discharge from contiguous suppuration be irritating to the skin and surrounding parts. In the case reported (page 135) the odor from the eczema induced in the surrounding skin by the non-changing of the dressings permeated the whole floor of the hospital, but the attendants were not permitted to disturb the hernia unnecessarily. The outer dress- ing was changed once or twice weekly, and a non-irritating ointment applied to the surrounding skin, but the dressing on the hernia itself was removed only every fourteen days. At these times the hernia was merely flooded with a warm salt solution. " Tobey, Dr. G. L. : Personal OoinmunieaUon. " Adami and McCrae : Text Book of Pathology, 1914, II Edition, p. 124. " Gushing : Notes on Penetrating Wounds of the Brain : Brit, Jf erf, Jour., Feb. 83, J918, p. 321, 134 BRAIN" ABSCESS Several months later a small piece of rubber tissue, wbicb had been lost under the osteoplastic flap at the time of the operation, came away followed by a piece of the bone of the flap. Slight re- cession of the hernia followed ; from which it would seem that the irritation from the foreign bodies was responsible, in part at least, for the hernia. Under non-operative treatment the granulating mass gradually assumes a very even appearance and begins to shrink; later, islands of epidermization appear in it, gradually covering the hernia. (Figs. 31, 32.) All the cases of hernia cerebri which the writer has known to recover have been treated without operative interference upon the hernia itself. Reduction of Incbeased Intkacranial Pressube. Smith,^* and Sargent and Holmes ^^ advise frequent lumbar punctures, using a saline solution manometer to measure the degree of pressure of the cerebro-spinal fluid. Technic. — "Normally we have found that the column of saline thus sup- ported varies from 15 to 25 cm. The amount of fluid to be withdrawn will roughly depend upon this reading and varies from four to eight fluid drachms, according to the initial pressure recorded. Even where the initial pressure is very high — in one of our cases it amounted to 108.5 cm. — it is not necessary to remove more than from 4 to 8 fluid drachms, as the pressure recorded after the removal of this quantity will rarely register much above the normal. It is important, too, that the fluid be withdrawn slowly, almost drop by drop, as otherwise the hernia, with too much sudden relief of pressure, may sink back through the bony opening into the brain, leaving a deep cavity where before there was a large hernia. This is dangerous, for adhesions may be broken down and a septic meningitis lighted up." " Although the writer has no personal experience with lumbar puncture in cerebral hernia, such a procedure is based upon sound mechanical and clinical grounds provided the hernia is of cerebro^ spinal fluid origin. The author has seen a marked papilloedema, the result of traumatism, quickly disappear under one lumbar puncture. In another cage, following an operation for compound depressed frac- ture without injury to the dura, the patient, through failure on the part of the medical attendant to appreciate the condition, continued " Smith. S. : Notes on the Treatment of Hernia Cerebri ; British Medical Jmimal, July 22, 1916, p. 103. >= Sargent and Holmes ; Treatment of Penetrating Wounds of the Skull ; British Journal of SurgetV, 1916, Vol. Ill, No. 11, p. 475. '" Cassidy and Page : A Method of Determining the Absolute Pressure of the Cerebro-spinal Fluid ; Proo. Boy. Med. Soc, 1910-1911, Vol. 4, pt. 1, Clinical Section, p. S6. Fig. 31. — Cerebral hernia following evacuation of temporo-sphenoidal lobe abscess. Note outline of osteoplastic flap, all of which is slightly elevated and the lower part of which had been sacrificed. The wide decompression thus furnished was the deciding factor in the recovery. Some months later a small bony sequestrum was spontaneously expelled, but in spite of this loss the patient has a good bony covering over the whole region except just above the ear. Fio. .32. — The same case as Fig. 31, three years after the evacuation of the abscess, showing recession of hernia and its complete covering by skin without operative intervention or the application of pressure. HEE"NIA CEEEBEI 135 in a state of active delirium for three weeks and when seen was ap- parently dying from exhaustion. One lumbar puncture, however, was followed by almost immediate return to consciousness and rapid recovery. The writer also has seen several cases of fracture with intradural hemorrhage in which each lumbar puncture was followed by marked and immediate improvement of the patient's mental con- dition. In fact the results of repeated lumbar puncture in traumatic cases have been so satisfactory that witb the author it is a routine practice if the operation on the skull is not followed by immediate and continued improvement.^'' Argot, ^* as the result of his large experience in cerebral hernia, condemns lumbar puncture as being apt to cause a dissemination of the localized infection, meningitis, or rupture of a localized abscess internally. CASE XXIV. J. G. : Bernia Oerebri Following Operation for Temporo-splienoidal Aiscess. Woman. Admitted to hospital December 23, with history of chronic relapsing otitis media for many years. Of nervous disposition; subject to night terror. Operation on mastoid showed acute exacerbation of chronic process. Dis- charged January 1, doing well. Hearing: voice, 7 inches; whisper, 3 inches; watch, 2 minutes. Weber referred to left. Three days later, January 4, became delirious at night, singing, more or less irrational. Ee-admitted to hospital the next day. Examination: no nystagmus, could hear with left ear, no spontaneous pointing deviation. January 6, patient able to walk and execute all movements; irregular con- tractions over body; active abdominal reflex; no neck stiffness; mastoid wound re-opened; dura over middle fossa found covered with granulations. Sinus accidentally opened; profuse bleeding. The following day there was spontaneous nystagmus on looking towards right side, and aphasia, — ^naming centre was slightly involved, but the aphasia seemed to he rather a carrying over of a previous impression. Shown a pencil, named it and said it was something to write with; shown a knife, called it a knife; shown a bunch of keys, called it a knife and said it was something to whistle with. Shown a match, she said it was something to light a fire with; shown a pad called it a piece of paper; shown a hospital card, said it was a piece of paper to put your name on. Convulsive seizures, in which both hands rotated on themselves inward. Lateral deviation of the head and of eyes to the left. The left pupil gradually became much larger than the right, the right apparently becoming much smaller. On coming out of the convulsion undoubtedly had a Bahinski, especially on left. The face was drawn to the left as if there were paresis of the right side. As patient became further conscious the left pupil became widely dilated; the right pupil becoming small. At this time there was marked rotary nystagmus to the right. Between convulsive seizures left patellar reflex absent, no hemianopsia. Named objects well for a few minutes and then gradually relapsed into a drowsy condition, repeating one word to everything, although she undoubtedly named the use of things better than the name itself. " lioblnger, A. S. : Cerebral CEdema in Intracranial Trauma ; Calif ortda State Journal of Medicine, June, 1918, Vol. 16, p. 303, u Argot : Loc. at. 136 BEAIH ABSCESS Caloric producing nystagmus not associated with any dizziness or vomiting and apparently no pointing deviation, although of this cannot be sure, because of stuporous condition of patient. January 9. Several convulsive seizures. Eight hand cold, left warm; slight double papilloedema, especially on left disc. Toxic delirium. Internal squint, left eye. Diagnosis. — Temporo-sphenoidal lobe abacess, without capsule as length of time since initial cerebral symptoms is too short to allow of formation of capsule. Operation. — Large osteoplastic flap turned upwards. Incision of dura showed cortex to be normal. There was marked prolapse of brain through dural opening. Lumbar puncture was done but resulted in a few drops only of cerebro- spinal fluid; canula left in position. Exploration of temporo-sphenoidal lobe was followed by a gush of pus and the immediate free discharge of cerebro- spinal fluid from trocar in lumbar region. The greatest delicacy in cleansing abscess. No hemorrhage. Rubber drain. Replacement of flap. Almost tight closure. February 11. Large hernia about half the size of a tangerine orange directly above ear. Under slight pressure, small amount of pus observed at upper edge. Hernia not gangrenous, kept covered by rubber tissue. Pus seen in two or three places along edge of hernia. Patient apparently perfectly well; able to name objects correctly. Hernia could be reduced by one-third by pressure; it was soft, perfectly smooth, and cystlike in appearance, not like brain; probably com- posed of granulated or (Edematous tissue. Some weeks later. Hernia, which had been carefully protected, was very much smaller. A piece of rubber tissue was discovered which had been lost during drainage. Loose sequestra of bone removed and hernia gradually reduced. Patient made a complete recovery. Comment. — It was undoubtedly the irritation from the lost drain that caused the hernia. CHAPTER IX. PROTECTIVE MECHAmSM OE THE BRAIN. The protective mecliaiiism of the brain is one of the functions of the delicate, anatomical and physiological relationship which exists between the cerehro-spinal fluid circulatory system and the circula- tory system of the blood, by means of which bacterial invasion is prevented, or, having occurred, the invading toxins are eliminated. The brain is unable to function properly when it is the seat of suppu- ration ; it is also profoundly influenced by toxemia ; consequently na- ture has furnished especial protection both from external infection and from the blood which circulates through it. In addition to the bony cranium an external protection — the dura — is essential, not only because the cranium is liable to injury, but because it contains an organ,- the nose, which is the natural habitat of many forms of bac- terial life, while another organ, the ear, is the frequent site of infec- tion, both of these being contiguous to the cranial cavity itself. Eur- thermore, as the blood stream, which circulates through and nourishes the brain, is constantly invaded by micro-organisms (one of its func- tions being to devour them) there must be a special mechanism whose purpose it is to guard the brain, not only from the organisms them- selves, but as far as possible from the influence of the toxins which may be contained within the blood. Prevention of Infection. — Consequently the brain normally is protected from infection from without by (1) the dura; and from within by (2) the normal Encephalo-Chorio-Meningeal Mechanism, consisting of an intimate anatomical and delicately adjusted physi- ological relationship between the blood circulatory system and the cerebro-spinal fluid circulatory system within the dura, the chief function of which is the nutrition of the brain from the circulating blood (the same as all other tissues of the body) . At the same time it affords protection from any mechanical or bacterial irritant that may be circulating within the blood, and from the toxins in waste products discharged into the blood stream again. In this mechanism the chief protective elements are furnished by (a) the blood in the blood vessels, (b) the blood vessels them- 137 138 BEAIN ABSCESS selves, (c) the pia and the external layer of the subarachnoid space, (d) the eerebro-spinal fluid, and (e) the glial tissue of the brain. Surgical Application: It is the presence of a special internal protective mechanism which explains the fact that although abscess of the kidneys, skin, etc., is frequent in suppurative endocarditis, abscess of the brain is of very rare occurrence, and then generally as a terminal manifestation, in spite of the fact that the blood infecting micro-organisms have a straight-away course from the heart to the brain. In the presence of infection the brain repels the invasion (1) by the incorporation of bacteria and deleterious products within the sub- stance of the phagocytic cells, which in the brain substance come from two sources, (a) the leucocytes and (b) the polynuclears from the blood vessels (as in other tissues) and (c) the macrophages from the cerebral tissue itself. These macrophages — a cell peculiar to the nervous system and produced from the external layers of the piarach- noid, the pia and the glia — play a most important part in combating suppuration and in repair. Their chief function, apparently, is (2) the transference and removal of dead and deleterious matter from the central nervous system by incorporating it within their sub- stance and discharging it (a) into the blood vessels and (b) into the perivascular spaces of the eerebro-spinal fluid circulatory system, by which all waste or deleterious material is conveyed into the sub- arachnoid space, and thence discharged into the venous sinuses or the extracranial lymphatics. During this process there occurs (3) an immunization of the eerebro-spinal fluid in the subarachnoid and perivascular spaces, while at the same time elements are produced from the blood vessels and the brain tissue which (4) limit the sup- puration by (a) the production of polymorphonuclear cells (b) the proliferation of glial tissue, and (c) the formation of new connective tissue. Pathological Peocesses in Infection. Infection enters the brain by four methods : (1) By the extension of contiguous tissue suppuration, causing a necrosis of the dura, an intrapiarachnoid abscess, a superficial brain necrosis, or a suppurative meningitis ; (2) From the blood vessels, (a) through retrograde thrombo- phlebitis of the veins of the ear or nasal sinus which perforate the dura and enter the brain, thus causing adjacent (secondary) brain abscess ; or retrograde thrombophlebitis of the veins which enter the large venous sinuses from the brain substance, thus causing inter- current (tertiary) brain abscess ; (b) by invasion of the perivascular PEOTECTIVE MECHANISM OP THE BEAIN 139 channels surrounding tlie blood vessels — perivasculitis ; (c) through bacterial embolus within the vessels — the method of cerebral invasions of all infections that primarily are of blood-stream origin (cerebro- spinal meningitis, streptococcsemia with secondary meningitis, pneumococcus meningitis, metastatic abscess from the lungs, etc.) ; (3) By invasion of the prolongations of the subarachnoid spaces which surround certain nerves — chiefly the olfactory, the optic, and the auditory nerves — ^by means of which the subarachnoid spaces be- come extracerebral. (The filtrable virus of poliomyelitis probably enters the nervous system from the nasal mucosa by way of the perivascular prolongations which surround the olfactory nerves) ; (4) By interference with the normal operation of the meningeal protective mechanism, which, in the presence of blood-stream infec- tion, may allow entrance into the meninges, the perivascular spaces, or the cerebral substance itself, of micro-organisms from the blood stream. This latter method probably is a frequent factor in the pro- duction of streptococcus meningitis and pneumococcus meningitis of aural and nasal accessory sinus origin. PROTECTIVE MEOHA:sriSM OF THE BRAIN. I.— By the Dura. Surgically the chief function of the dura is to prevent the en- trance of micro-organisms into the brain. On the approach of an adjacent infection the dura fortifies itself and combats the poison by the formation of granulation and subsequently of new connective tissue, both on its external and internal surface — a pachymenin- gitis externa and interna. In the development of the latter process the central protective mechanism, especially the arachnoid cella, takes an active part. Points of Vulnerability of the Dv/ra: Although the enclosing dura is the chief protection of the brain against direct invasion by micro-organisms, it con- tains areas of vulnerability, especially where it is perforated by certain nerves and blood vessels. The subarachnoid space prolongations surrounding these blood vesels extend well into the foramina through which the nerves and blood vessels enter and leave the cranium. At these sites the subarachnoid space ac- tually becomes intracranial; The subarachnoid prolongation around the nerves causes a perineural space in three places ; ( 1 ) along the nerve of the special sense of hearing and orientation, where the intralabyrinthine fluid is part of the eerebro-spinal fluid; (2) along the nerve of the special sense of smell — the olfac- tory nerve — ^where the perineural sheaths descend into the nasal mucous mem- brane, and (3) along the nerves of the special sense of sight, where the subarach- noid space is continued for a certain distance along the optic nerve as the inter- vaginal space. It is more than a coincidence that all these prolongations of the subarachnoid space are directly connected with three of the organs of special sense. There is 140 BEAIN ABSCESS experimental evidence tliat it is through the extradural or extracranial prolonga- tion of the perivascular spaces of the vessels and of the perineural spaces of the nerves that infection frequently enters the brain, and that within these recesses micro-organisms long continue to persist after their elimination from the general subarachnoid space. II — By the Subdural Space. — The subdural space apparently is very immune to infection, as it offers especial resistance to the growth of bacteria. In meningitis or brain abscess it generally is unaffected, altiiough as a brain abscess approaches the cortex the subdural space may become com- pletely obliterated; but in cases of pachymeningitis interna the in- fecting micro-organisms may project well into the subdural space without involving it, as demonstrated by Streit.^ In this situation they may remain more or less dormant for long periods of time. If trauma is now added, breaking down the adhesions, a general fulminating meningitis may follow, as has occurred in many cases following an operation for a chronic aural or nasal sinus suppura- tion. Surgical Application: Although meningitis or abscess primarily confined to the subdural space is a very rare occurrence from aural infection,* it apparently is more common in nasal sinus suppuration, probably because of the communica- tion of the subdural space with the mucosa of the frontal sinus by way of the perimeningeal spaces." However, in experimentally produced traumatic abscess,' large subdural abscesses were frequent, and microscopic examination found the adjacent subarachnoid space to be free from micro-organisms, demonstrating the extreme degree of resistance of the external layer of the arachnoid and explain- ing the clinical experience that a subdural abscess is a frequent complication of hernia cerebri following evacuation of an intracerebral abscess. The occurrence of a hernia should always awaken suspicion of its origin in a localized collection of pus in the subdural space, and should cause the surgeon carefully to expose the regions adjacent to the hernia before again entering the brain surgically. Ill — By the Subarachnoid Spaces. — In the normal state the subarachnoid spaces, in which the cere- bro-spinal fluid circulates, are kept free. On the approach of bac- teria to the dura the subarachnoid space fortifies itself by an over- production of cerebro-spinal fluid containing a large number of phagocytic cells — ^polymorphonuclears. Swrgical Application: Serous meningitis is a protective process. In aseptic meningitis the perivascular spaces apparently are not involved, but the velum 1 Streit, Hermann : Weitere Beltrage zur Hlstologie und Pathologie der Menln^tia und Slnusthrombose ; Archvo fUr Ohrenheilkunde, 1912, Bd. 89, S. 177. ' Case VIII, Chapter Four, p. 37. " ZwilUnger, H. : Experimentelle Untersuchungen zur Mechanlk der Intrakranlellen und cerebralen Komplikationen der Stirnhohlenentzundungen. (From the Anatomical Institute of the University of Budapest.) ArcMv fur Laryngologie und RMnologie, 1914, Bd. XXVIII, S. 271. * Bssick, Charles B. : Loc. cit. PEOTECTIVB MECHANISM OF THE BRAIN 141 interpositum and choroidal stroma are infiltrated with polymorphonuclears. The high polymorphonuclear count without organisms in lumbar puncture is simply a sign of a protective meningitis. Later, as the process becomes quiet, mononuclear cells and lymphocytes predominate.' On the entrance of bacteria into the subarachnoid spaces of the cerebro-spinal fluid circulatory system, the meningeal protective mechanism combats infection chiefly by the action of macrophages coming from the glial tissue and from the piarachnoid cells. ANATOMY OF THE CEREBRO-SPHSTAL FLUID SYSTEM.' Tlie cerebrospinal fluid circulates within closed cavities and tubes — the ventricles, the cisterna and the subarachnoid spaces con- stituting the cerebro-spinal circulatory system — ^just as the blood circulates in the blood vascular system; and like the vpaUs of the venous system, the walls of the cerebro-spinal circulatory system are normally impermeable to the contained fluid. The cerebro-spinal fluid finally empties into the blood stream after performing its functions in the brain, passing by osmosis into the venous sinuses of the head, and at certain points where the sys- tem has passed outside of the cranium, communicating again by osmosis, with the extracranial lymphatic system. This communica- tion occurs along the arachnoid prolongations around the sheaths of certain nerves, especially the olfactory and the auditory. Thus, while the cerebro-spinal fluid circulatory system is a closed system without an apparatus for the puriflcation and return of its fluid such as the vascular system has in the heart and lungs, it utilizes both the vascular and the lymphatic system for its dis- carded material much in the same way as the blood vascular system utilizes the kidneys; with this difference, however, that while the blood discharges through the kidneys only its deleterious material the entire cerebro-spinal fluid constantly is being discharged into the blood or the lymphatic system. Viewed then in a large way, both anatomically and physiolog- ically, the cerebro-spinal fluid circulatory system must be of impor- tance to the cerebral functions.'' *° ^' ' Ayer, J. B. : Loo. eit. ' Bagleton, W. P. : Operative Treatment of Suppurative Meningitis wltli special reference to Irrigation of the Cranial and Spinal Subarachnoid Spaces, and the Impor- tance of Protective Meningitis from a Prognostic and Therapeutic Standpoint ; Trans- actions American Otological Society, 1921. ' Weed, Lewis H. : Studies on Cerebro-Spinal Fluid ; Journal of Medical Beaecurch, September, 1914, Vol. XXXI, pp. 21-117. 8 Wegcforth, Paul, and Weed, Lewis H. : Studies on Cerebro-Spinal Fluid ; Jotimal of Medieal Research, September, 1914, Vol. XXXI, pp. 167-176. • Weed, Lewis H., and Gushing, Harvey : Studies on Cerebro-Spinal Fluid ; Amerioan Jmirnal of Pht/aiology, January, 1915, Vol. XXXVI, No. 2. "• Cushing, Harvey, and Weed, Lewis H. : Studies on the Cerebro-Spinal Fluid and its Pathways; Johns Hopkins Hospital Bulletin, November, 1915, Vol. XXVI, No. 297. 143 BRAIN ABSCESS The circulatiiig cerebro-spinal fluid is produced chiefly from the choroid plexus within the ventricles, the walls of which are lined by cells, the endyma, which are impervious to the fluid. From the ventricles the fluid passes by a process of overflow through the aqueduct of Sylvius into the fourth ventricle and leaves it by the medial foramen of Magendie and the lateral foramen of Luschka; from these it spreads over the base of the brain, accumulating in the large basal cistema, whence it is distributed by way of the sponge-like, communicating meshes of the subarachnoid spaces over the cortex, through the vessels and convolutions, and empties at last by osmosis into the venous sinuses. In its passage over the cortex there is contributed from the cere- bral substance — through the prolongations of the subarachnoid spaces along the vessels entering or leaving the cerebral tissue, called the perivascular spaces — a small amount of cerebrospinal fluid which has a somewhat different composition from the cerebro-spinal fluid formed in the ventricles. These perivascular channels opening di- rectly into the subarachnoid spaces of the cortex, are undoubtedly the means of direct communication between the intracellular juices of the brain cells — the perineural system, and the general cerebro- spinal circulatory system. The cerebro-spinal fluid acts to remove the waste products of the brain, but whether it supplies any nutritive ingredient neces- sary to the continued functioning of the brain is not known. It is inconceivable that it does not possess some such quality, especially since its normal content is a sugar-reacting subs.tance. IMPBEGN ABILITY TO INFECTION OF CEREBEO-SPINAI. FLUID SYSTEM. The cerebro-spinal fluid system, while anatomically composed of very delicate cells, is very resistant to infection when attacked either upon its external surface, or internally from the cerebral tissue; and while in close anatomical proximity to the blood circu- latory system — ^being separated from the pial vessels by only one layer of cells and actually surrounding the vessels as perivascular " Weed, Lewis H. : The Formation of the Cranial Subarachnoid Spaces ; The Anatomical Record, May, 1916, Vol. X, No. 7. " Weed, Lewis H. : An Anatomical Consideration of the Cerebro-Splnal Fluid ; The Anatomical Record, May, 1917, Vol. XII, No. 4. " Weed, Lewis H., and McKibben, Paul S. : Pressure Changes In the Cerebro- spinal Fluid Following Intra-Venous Injection of Solutions of Various Concentra- tions; Americwn Journal of Plvyaiology, May, 1919. Vol. XLVIII, No. 4. " Weed, Lewis H., and McKibben, Paul S. : Sxperimental Alterations of Brain Bulk ; Amerieam, Journal of Physiology, May, 1919, Vol. XLVIII, No. 4. " Weed, Lewis H. : The Cells of the Arachnoid ; Johns Hopkins Hospital Bulletin, October, 1920, Vol. XXXI, No. 356. i» Maeklin, Charles Clifford, and Macklin, Madge Thurlow : A Study of Brain Repair In the Eat by the Use of Trypan Blue ; ArchAmes oj Neurologjf and Psyohiatry, April, 1920, Vol. Ill, pp. 353-394. PROTECTIVE MECHANISM OF THE BEAIN 143 spaces — ^the cerebro-spinal fluid system, when uninjured, does not allow of invasion of the subarachnoid spaces by bacteria circulating free in the blood stream. However, a very small disturbance of the meningeal protective mechanism in the presence of a blood- stream infection may allow the invasion of the meninges from the blood stream. The subarachnoid space bacteriologically resembles the perito- neum, each being a mesothelial-lined cavity which, on account of its blood supply and its contained fluid, furnishes a favorable soil for the development of micro-organisms. The cells of the subarachnoid space, however, both of the external layer toward the subdural space and of the pial layer, are very resistant to infection; but the cells lining the cavity itself possess much less resistance if once infected. Likewise there is experimental evidence that the cerebro-spinal fluid normally possesses to a high degree immunizing bodies which under favorable circumstances may considerably increase. On the other hand, anything which alters the integrity of the meningeal choroid protection, or upsets the operation of the meningeal mechanism, di- minishes or removes its protective function. In suppurative processes the arachnoid membrane thus serves to limit the spread of infection from the outside into the subarachnoid space, or, when the subarachnoid space itself is infected, it prevents infection from spreading inward into the deeper layers of the pia and the substance of the brain. In abscess of the brain, although the perivascular spaces may be flUed with exudate, no micro-organisms and but few cells may be found in the subarachnoid space at a dis- tance from the infection. Surgical AppUoation: It is the resistance of the piaraohnoid to invasion from the subarachnoid space that explains the clinical fact that while suppurative men- ingitis both local and general, frequently follows intracerebral abscess, localized meningitis never is followed by the latter, although frequently accompanied by a superficial brain necrosis. Note: The cerebro-spinal circulatory system seems to have resisting power to infection in itself, as the infiltrable virus of poliomyelitis — ^which apparently finds its path into the venous system by the nasal mucous membrane — ^probably in a normal state is prevented from entering the brain by the meningeal mechanism; but microscopical changes of the meningeal mechanism, such as the production of an aseptic meningitis by the injection of a normal horse serum or a normal salt solution — -Ringer's or Locke's solution — or slight hemorrhages which have a demonstrable effect upon the meningeal mechanism, "sufSce to remove the power of the intact organism to exclude the virus of poliomyelitis from the interstices of the central nervous tissues." " " Flexner, S., and Amoss, Harold L. : Relation of the Meninges and Choroid Plexus to Poliomyelitie Infection ; Jmimal Experimental Medicine, 1917, Vol. 25, p. 525. 144 BRAIN ABSCESS iNTECTIOISr OF ClaiKBEO- SPINAL FLtTID SYSTEM FBOM BlOOD StEEAM. Normally infection is prevented from reaching the brain through the blood vessels by two factors: (1) the intima of the blood vessels of the brain, and (2) the encephalo-meningeal protective mechanism, virhich includes the choroid plexus. Given an injury to the intima — a toxemia causing degeneration, or a traumatic injury — a thrombus develops which interferes with the nutrition of the cerebral tissue and, being septic, implants micro- organisms in the already damaged cerebral tissues. Again, without thrombosis, if the meningeal protective mechanism itself is upset — as by lumbar puncture, compression of the jugular, cessation of the heart, — in the presence of pathognomic micro-organisms free in the blood stream at the time of the disturbance, certain micro-organisms may enter the leptomeningeal spaces in sufficient numbers to occasion a fatal leptomeningitis.^* Brain Abscess from Meningitis. In all the experimentally produced meningitis, only one brain abscess occurred — this a superficial one — showing that it is not the micro-organisms in the blood stream that causes a brain abscess^ — there must be another factor added to this. This factor is undoubtedly thrombosis of a vessel, and the affinity of certain micro- organisms for cerebral tissues. CASE XXV. F. v.: Case of Streptococcus Meningitis from Disturbance of the Meningeal Protective Meohojnism of the Brain hy Liirnbar Puncture in the Presenos of a> Blood-sttream Infection from a Suppurative Thromhophlebitis of the Leg. Male. Entered hospital October 3, with chief complaint of pain in left leg and groin, which caused inability to walk, sleeplessness and slight headache. History. — Present illness dates from a week before admission to hospital, when he received a blow on the head — in left parietal region. He was not un- conscious and worked next day. The following day felt better. Three days be- fore admission he began to have severe pain in left thigh and groin. Past history negative. Physical Examination. — Patient did not look ill; head showed no evidence of injury; eyes, nose and ears, negative; slight tenderness over left hip; knee jerks diminished; no paralysis or sensory changes. There were two eye-ground reports, one that the discs were indistinct, the other that they were clear. X-ray for fracture of skull and enlargement of sella turcica both negative; for left hip injury, negative. Cell count, 18,000; polynuclears, 76%; lymphocytes, 24%. Temperature, 102°. October 4 — (Next day) — ^Lumbar puncture; spinal fluid clear, transparent, no nebula; globulin, negative; cell count, 3 per cnam. That evening temperature began to rise, thereafter running a typically septic course, ranging between 100° and 105°. The after-history of the case is typically a septicemia. Another lumbar punc- » Weed, Lewie H. : Meningitis Produced by Intra- Venous Inoculation ; Mono- . graph! of Rooheteller Institute ]or Medical Research, No. 12, March 25, 1920, pp. 57-112. PEOTECTIVB MECHANISM OP THE BEAIN 145 ture was performed October 14, which showed markedly bloody fluid, containing pus cells and numerous chains of streptococci. October 15 — Patient became delirious and remained so to the end. Octoler 24— Death. Autopsy : Head. — Brain covered by plastic, purulent meningitis, having greenish-yellow look; also a slight encephalitis; sinus free and clear; no fracture to be seen. Abdomen.— X/iver slightly enlarged; all organs in abdomen show acute cloudy swelling; inferior vena cava from level of fourth lumbar vertebra down, and extending' into iliacs and femorals on both sides, was the seat of a purulent, septic thrombosis; at most central part of involvement was an organizing clot; there was an involvement of the tissues surrounding the vessels. Chest. — ^Acute, cloudy swelling of heart, and oedema of lungs, with congestion of bases. Probable Cause of Death. — Suppurative meningitis (streptococcus), with original focus a suppurative thrombophlebitis. Secondary, or Terminal Lesions.^-Acute, cloudy swelling of heart muscle, liver and spleen; pulmonary parenchymatous nephritis. Elimination of Baotebia fbom the Subarachnoid Space. While the protective mechanism of the brain prevents the en- trance of bacteria into it from the blood stream, when the subarach- noid space has actually been invaded by them the protective mech- anism avails itself of the blood stream for their elimination. Experimental injections of bacteria into the subarachnoid space invariably are followed by finding the micro-organisms in the blood stream.^® Experimental injection into the subdural spaces of large amounts of normal solution, on the other hand, shows no changes in the brain, but a severe hyperemia of both lungs, with hemorrhages. Surgical Application : Patients in coma or convulsions frequently have a com- plicating pneumonia, due to a lowering of the resisting power. Immunization. — Immunization in general is so imperfectly un- derstood — especially as comparatively few experiments in this field have been made — that little real knowledge is to be expected regard- ing its application to the brain and subarachnoid spaces. It is known, however, that full blood contains components which retard the growth of bacteria and in the majority of cases kill them. By this means the blood stream constantly purifies itself. It is also known that the removal of immunized blood from the body allows a continuation of these components for varying times for different micro-organisms. After the third day, however, these component elements of the blood rapidly disappear. " Felton, L. D., and Wegeforth, Paul : The Production of Experimental Menin- gitis by Direct Inoculation into the Subarachnoid Space; Monographs of Bockefeller Institute for Medioal Research, March 25, 1920, No. 12, p. 7. 146 BEAIN ABSCESS It has been proved experimentally that immunization of the cerebro-spinal fluid is much more difiicult than immunization of the blood, because the cerebro-spinal fluid, being constantly emptied into the venous circulation, cannot very long contain the immunizing sub- stances. Sera injected into the cerebro-spinal fluid are passed into the blood in about twenty minutes. Surgical Application: It is an established surgical fact that the dura can be incised with greater immunity through the area of a neighboring infection — over the tegmen, for instance — ^than over an area which is not the seat of an infection. Immunization probably exists in the cerebro-spinal fluid and in the brain area, but the immunization does not extend far nor does it last long. Under such circumstances, the surgeon cannot with impunity enter the dura and explore the brain for any great distance. By so doing he carries infection into an area that is not immunized, while the trauma of the exploration kills cerebral tissues which furnished a most favorable soil for the development of cerebral suppuration. Susceptibility of Cerebkal Tissue to Bacterial Virulence. The ordinary pathogenic micro-organisms are from forty to two hundred times more virulent in the subarachnoid space than in any other part of the body structure. The toxins of tubercle bacillus, for instance, apparently have a specific affinity for meningeal tissue. Extracts of cholera bacillus are about forty times more toxic in the subarachnoid space than when injected into the blood. Anthrax extract produces hemorrhage into the pia, while many other forms of infection — such as streptococcus capsulatus, or pneumococcus type three — ^have a distinct action on the blood, causing hemorrhage into the brain. Newborn infants are subject to certain infections to which adults are less liable, or not at all susceptible. During infancy the colon bacillus is a frequent cause of infection of the brain tissue and of the meninges as well as of the kid- neys. Artificially fed infants are much more liable to infection by the colon bacillus than are breast-fed infants. In adults the colon bacillus is only feebly virulent. It would seem that infants during the nursing periods acquire an immunity from the mother. When deprived of this immunity they must build up immunity for themselves. Bull's™ experiments on dogs and rabbits demonstrated the pathological effect on the nervous system of streptococci from the blood stream. In dogs sections of the central nervous organs showed multiple abscesses in the cerebrum, the pons, medulla and the white matter of the spinal cord. In some of the rabbits obvious clinical symptoms were wanting, but a purulent meningitis was found at autopsy. The sections showed at times focal lesions associated with the meningitis, usually affecting the cerebrum, the cerebellum, and medulla and the pons. 2° Bull, Carroll G. : Pathologic Effects of Streptococci from Cases of Poliomyelltla and Other Sources; Journal of Experimental Meixoine, 1917, Vol. XXV, p. 657. PEOTECTIVB MECHANISM OF THE BRAIN 147 Sensitiveness of Beain to Toxic Influences. To function properly tlie brain must be bathed in its own normal fluid and at a normal temperature. It is not only bigbly sensitive to toxio influences, but it is profoundly influenced by any change in the composition of the cerebro-spinal fluid wbich surrounds it; even sterile normal salt solution (if it does not contain a small amount of calcium salts) is highly toxic to the brain, causing irritation if in- jected into the subaraclmoid space, and respiratory embarrassment and death if irrigated through the cerebro-spinal fluid system. ^^ Note: "Changes in the structure or function of the meningeal-choroid plexus complex too slight to be detected by cellular or chemical changes in the cerebro- spinal fluid, or by morphological alterations, are sufl[icient to diminish in an essential manner its protective powers. An immune serum injected intra-spinally is protective, but the degree of its efficiency is more or less proportional to the freedom from injury to the meningeal structure by the irritating substances em- ployed. The slighter the inflammation the more readily and quickly the injury is repaired," and consequently, "Aseptic fluids which irritate, inflame, or even slightly alter the int^rity of the meninges and choroid plexus, diminish or remove their protective function." "Injury to the blood vessels of the meninges also promotes an infection. This may be due either to the escape of the inoculated virus from the blood through the injured vessels into the meninges, or, what is more probable, to the entrance of the blood into the subarachnoid space, thereby setting up a mild inflammatory reaction which suffices to promote the infec- tion." ^ PROTECTIVE MECHANISM IN THE BRAIN ITSELF. The protective mechanism in the brain itself is made up of two parts — (1) those structures which prevent the entrance of micro- organisms into the cerebral tissue and (2) those forces which com- bat, destroy, or limit infection which has gained entrance. They frequently act in both capacities. The chief protective agent in the brain in combating infection is the blood, the blood vessels furnishing the elements which defend the cerebral substance from infection. Consequently, the cortex, which is well supplied with blood, is in- frequently infected, while the deep substance of the brain, relatively poorly supplied with terminal blood, may easily become the seat of an abscess. In the presence of infection, infiltration of blood into the substance of the cerebral tissue undoubtedly favors the extension of the infection, probably by causing death of the cerebral tissue by pressure. =1 Weed, Lewis H., and Wegeforth ; ioc. oi*. ^ „ „ ■ ^ ,^ „ '^ Flexner S and Amoss, Harold L. : Relation of the Meninges ana Cnorold Plexus to Poilomyelitic Infection ; Jmimal of Experimental Medicine, 1917, Vol. 25, p. 525. 148 BEAIN ABSCESS Note: There is experimental eTidenc© that the red corpuscles themselves help to limit the extension of infection in certain parts of the brain and under certain conditions, probably by some form of mechanical protection. "A large intra- arachnoid space hemorrhage completely protected the subarachnoid space from infection, although the brain substance was one large abscess." Free red blood cells are also found in considerable numbers in the neerobiotio zone of intracere- bral abscess.^ Varying Degrees of Sensitiveness to Infection. The different elements of the brain possess relatively different degrees of resistance to infection. The gray matter of both the cortex and the central ganglia is very resistant. In traumatic abscess the different zones of this gray matter also differ in their susceptibility. An intracerebral abscess in its growth usually does not affect the ganglionic tract, but follows the white fiber tracts. Limitation of Suppuration within the Brain. The blood vessels furnish the elements which encapsulate a sup- puration, while by the blood are contributed the phagocytes which help to remove the products of tissue disorganization. The cerebral tissues — ^the arachnoid, the pia and glia — furnish the macrophages which by a process of digestion assimilate into themselves the dead tissue and carry it to the blood vessels and cerebro-spinal fluid system, that remove it from the brain. In this process the perivascular spaces of the blood vessels play a large part; consequently, in all* suppurative lesions of the brain the adjacent perivascular spaces are found crowded with round cells and with micro-organisms. Note: For a detailed description of how a suppurative process into the brain is limited, reference is made to Part II, page 47. Extension of Infeotion. The three great factors in the death of cerebral tissue, and conse- quently, in the development of a cerebral abscess are (1) thrombosis, (2) compression, and (3) operative trauma. After encapsulation, a brain abscess extends by two processes, (1) a seeping of infected material through the capsule and (2) an extension through pressure erosion. Extension of infection within the cerebral tissue is favored by death of cerebral tissue largely because the myelin discharged from its sheath furnishes a favorable soil for the growth of bacteria. The blood vessels play such an important part in the proper "Essick, Charles B.: Loo. dt. PEOTECTIVE MECHANISM OF THE BEAIN 149 function of tlie brain that any disturbance of the circulation in the presence of infection, favors extension. Thrombosis of the blood vessels furnishes a large part of the pathological picture in the early stages of brain abscess. In acute abscess the first extension of the abscess is entirely through thrombosis ; consequently, anything which causes dislocation of the brain mass, favors thrombosis and prevents the reactive forces of the brain from operating properly. Compres- sion by favoring thrombosis has a similar action: thus, vdth an intact dura, dilatation of the ventricles by increase of the intracranial pressure is an aid to extension of the infection. Surgical AppUoation: In the early stages of brain abscess relief of intra- cranial pressure by lumbar puncture undoubtedly assists in the limiting of the process, as the brain's bulk is primarily not seriously increased, the abscess being due to nutritional death. It is the reactive forces of the brain itself that occasion a part of the increase of the intracranial pressure. Eemoval of Dead Tissue. Dead tissue v^ithin the brain is taken care of by two processes: (1) removal, chiefly by the phagocyte cells of the brain itself — ^the macrophages — and (2) encapsulation of the dead area. In the for- mer process the same exhaustion of reaction happens in the brain that happens with other tissues ; namely, if suppuration is long continued a limited area of suppuration is allowed to exist indefinitely. Experi- ments with vital dyes show that the macrophages are able to remove a certain amount of dead tissue, but, after a time they lose their activity. Surgical Application,: The surgeon must guard, therefore, against allowing the activity of the protective elements to become exhausted. Aseptic meningitis is dangerous, although it contains no septic factors, because it exhausts the pro- tective elements in their effort to remove the cause of irritation. Repair. — ^Repair of cerebral substance is accomplished by one of two processes: (1) by cyst formation, if the lost tissue is adjacent to the meninges, the pia filling the gap. This accounts for the fre- quency of meningeal cysts in areas injured. The cysts are filled with cerebro-spinal fluid and the degenerated elements of the blood cells; and (2) by proliferation of glial tissue — a gliosis. Recrudescence of Latent Infection. — Recrudescence of latent infection is a very frequent occurrence in the nervous system. This is of the greatest surgical importance because, a brain abscess having been cured, there undoubtedly lurk in parts bacterial elements which await opportunity again to become active ; ^* consequently, no further " EagletOD, W. P. : Meningitis, Case 3, Tr. Am. Otological Soe., 1921, p. 919. 150 BEAIN ABSCESS surgical interference should he undertaken at least for a consider- able period of time. Weed and Wegeforth,'* after curing experimental brain abscess, found that meningitis resulted on further manipulation in trying to close the dural defect. Conclusions. — It would seem then, that it is the close and delicate relationship between the cerebro-spinal fluid circulatory sys- tem and the blood circulatory system, which furnishes the chief mechanism in the protection of the brain substance. Both are necessary for the prevention, combating, limiting, and removal of deleterious matter from the brain into the subarachnoid spaces and so out into the circulation. Anything, therefore, which in the pres- ence of micro-organisms interferes with the capillary blood stream within the brain, renders an infection of the brain liable, while any- thing, operative or therapeutic, which upsets the cerebro-spinal fluid circulatory system increases the likelihood of cerebral abscess or meningitis. In abscess of the brain the chief causative influence in infection is thrombosis of the small vessels ; for in consequence of the presence of small thrombi an area of cerebral substance not only undergoes nutritional death but, because of the accompanying peri- vasculitis, it has eliminated from it the avenue whereby infective material is removed from the brain. Thus, both the blood stream and the cerebro-spinal fluid circulatory system are thrown out of action in this area, while the dead cerebral tissue becomes a favorable ^ soil for the growth of micro-organisms. RELATIONSHIP BETWEEN SUPPURATIVE MENINGITIS WITH BRAIN ABSCESS AND PROTECTIVE MENINGITIS. Although suppurative meningitis is usually the terminal process of brain abscess, it is an important fact that with micro-organisms free in the spinal fluid (as shown by lumbar puncture) an existing brain abscess is the only type which offers a probable chance of re- covery, because the protective character of the process which origi- nated from the abscess was already active at the time of the invasion of the cerebro-spinal fluid by the bacteria. Of all the cures of true suppurative meningitis, (not of blood stream origin, reported in the literature) — 27 in number, over two-thirds had a protective menin- gitis at the time of the invasion of the subarachnoid space by the bacteria; of these, five were secondary to a brain abscess and were cured by evacuation of the abscess, together with lumbar puncture or the injection of serum into the spinal cavity. '■ Weed and Wegeforth : Loo. cU. PEOTECTIVE MECHANISM OP THE BEAIN 151 "Two were preceded by brain abscess — Day : One was associated with intrapiaracbnoid abscess — Held & Kopetsky; and two were associated with or preceded by subdural abscess (traumatic), Kost- livy & Poirier." ^e It should be recognized that the protective meningitis which de- velops to ward off the brain abscess from the subarachnoid space may be the deciding factor in controlling the infection when the micro- organisms actually invaded the cerebro-spinal fluid system itself. Consequently, in suppurative meningitis, complicating a brain ab- scess, in spite of the presence of the invading micro-organisms in the cerebro-spinal fluid, evacuation of the abscess should be undertaken with a fair prospect of recovery from the meningitis. CASE XXVI. T. p.: General Suppurative Meningitis (Streptococcic, Hemolytic) originated from a latent and unsuspected cerebral abscess of eighteen rmmths' dwration treated by cerebral and cerebro-spinal subarachnoid irrigation. Resume of Case : About one and a half years previously the pati«nt attempted suicide by shooting himself in the right temple with a revolver. He was brought to the hospital and operated upon by the author who removed a pistol bullet from the left parietal region, the ball having passed through both frontal lobes. The X-ray after the operation showed small fragments of bone or bullet near the wound of entrance, but the patient made a very good recovery and apparently has been quite well since. It is interesting to note, however, that after this time his history states that he has become a drug addict. A few days before his death, the patient waj found by the police in a more or less dazed condition and brought to the City Hospital, where he was placed in the observation ward for psychopathies, little attention being paid to his former cerebral injury. It was noticed that he had a stiff neck, the patient walk- ing around the ward in this condition. The interne performed a lumbar puncture which showed a cloudy fluid under pressure; with numerous pus cells and many Gram positive cocci, many arranged in chains. A diagnosis of streptococcic sup- purative meningitis was made. Two attempts were made to wash out the subarachnoid cerebral space, and anti-meningococcic serum was given intraspinously. The patient grew worse after the second operation, but had appeared in much better condition after the first. Post-mortem disclosed three latent abscesses, the oldest of which doubtless was present from the time of the original injury eighteen months previous. One abscess had perforated the lateral ventricle and slowly discharged its contents into it. From this the infection had passed to the basal cisterna and the cere- bellar surface, the subarachnoid spaces of the cortex remaining unaffected. History: June 7, admitted to City Hospital. Temperature 100.2 degrees and pulse 100. Psychiatric Examination, Wednesday, June 8: "I've been here three or four weeks." (Was admitted yesterday.) Does not know day, month or year. Says "1821." At 10 a. m. says it is about 3 o'clock. "I don't know why I =* Eagleton, W. P. : Operative Treatment of Suppurative Meningitis wltli special Reference to Irrigation of the Cranial and Spinal Subarachnoid Spaces, and the Importance of Protective Meningitis from a Prognostic and Therapeutic Standpoint ; Transactions American Otological Society, 1921. 152 BKAIN ABSCESS am here. I don't know who brought me here, either. I wasn't drunk. I don't know what was the matter with me." Why do you stay here? "I don't know that, either." Using drugs? "No." Anything hurt you? "No." Were you here before? "I imagine so." Have any trouble? "We had quite an argument — ^my brother — a little family affair." Did the police bring you in? "I don't know." Did you try to kill yourself? "No." "Harding is President; Wilson before him." "4 X 4 = 16 4- 10 c= 26 — 8 = — ^well — " (Then no answer). "9X9 — 814-9^81 — oh, well — " (Then no answer). "6 X 6 = 36 -|- 8 = — well — " (Then no answer). "20 — 1 = 19." (Correct, but slow). "Before July comes August; before December, November; before October, September — " (after some thought). Name the months of the year. "This month — " (Then no answer). Memory for numbers poor — "3, 4, 8, 7." No dysarthria. Both pupils very sluggish to light — both irregular. Suspicion of Romberg. Knee jerks exaggerated. Urine dribbled during examination. Executes commands sluggishly. Gait somewhat spastic. Marked tremor of fingers. June 9: Incontinent; neck stiff. Lumbar Puncture. — Fluid cloudy under slight pressure; Wassermann nega- tive; direct smears show streptococci. Operation. — Cerebral and spinal subarachnoid irrigation. Three trephine openings made in right fronto-parietal region; in the first it was found impos- sible to enter fluid because of apparent adhesion of dura to brain, although the opening was away from the skull opening through which the ball had been extracted, by at least one and one-half inches. Two other openings were then made: opened into the subarachnoid space, and tap made into cisterna magna. Needle inserted underneath dura and arachnoid and surface of brain flushed out with Einger's solution and drained through needle in cisterna. Process repeated twice through trephine one inch posterior to first opening on the same side. Later the excess fluids were drained through a lumbar puncture. Flaps closed with black silk. June 11: Temperature 99 degrees; pulse 96. Nurse's Note: "Patient ap- pears to be much better. Answers intelligently to questions. Neck still very rigid and head thrown back." Lumbar puncture; 28 c.e. withdrawn, fluid cloudy, slightly yellow, under slight pressure. Anti-meningococoic serum 20 cubic centimeters injected. At this time the author examined the patient; the man was in excellent condition. He recalled all about the previous experiences in the hospital eighteen months ago. 6 p. m. : Second subarachnoid irrigation. Anterior flap opened; stitches removed; needle inserted into arachnoid and irrigation carried on as on the previous day. Drained through cisterna and lumbar puncture. Fluid yellow and somewhat turbid. 8 a. m. : Answered when spoken to. Pulse fair. 8:30 a. m. : Patient suddenly became cyanosed and pulseless and ceased to breathe. Autopsy and Report by Db. Habbison S. Maitland. Head. — In the cortex of the middle of the right frontal lobe is a small, cortical and sub-cortical abscess, measuring about 1.5 cm. in size and filled with thick, creamy pus containing a few small fragments of bone; the wall of the pavity is about 2 mm. in thickness. PEOTECTIVE MECHAmSM OP THE BEAIN 153 Situated deeper in the brain substance, its outer edge encroaching on the small abscess already described, is another more recent and larger abscess, measuring about 2.5 cm. in diameter, and containing a slightly greenish pus; its walls are about 1 mm. in thickness. The lower and inner portion of this abscess cavity, about 1.5 cm. in size, leads directly into the anterior horn of the right lateral ventricle, the opening being soft and necrotic brain tissue. The right ventricle is distended with greenish-yellowish pus, and there is an extensive exudate clinging to the choroid plexus; the ependyma lining the cavity contains numerous punctate hemorrhages, and the surrounding brain tissue is soft, cedematous, and in places distinctly necrotic. This same condition is found in the left lateral ventricle, although not to so marked an extent. The third ventricle contains purulent exudate and fluid pus, and the inter- peduncular cisterna is distended with purulent exudate. The fourth ventricle is dilated, as is also the iter, and contains a purulent exudate and free pus. This has leaked out through the foramina of Magendie and Luschka and infected the cisterna magna, which is filled with a plastic, purulent, yellowish exudate, which extends up over the inferior and lateral surfaces of the cerebellum and stops. The cisterna basilis and chiasmatis contain considerable plastic exu- date, which apparently comes from extension from the cisterna magna, and pos- sibly also from the close proximity of the infected third ventricle. The outer surfaces of the brain and the spinal cord and its meninges are practically free from exudate. Extending from the wound of entrance in the middle of the frontal lobe passing across the frontal lobe on its superior surface, to the left and slightly backward, through the left frontal lobe on its superior surface, and stopping at the bone opening in the left parietal region, is a somewhat collapsed brain tract of the old bullet wound. The brain tissue is stained a gamboge yellow around this old tract and there are numerous piarachnoid adhesions over this area. Comments. — Of course, a brain abscess should have been suspected, and an attempt made to drain it, possibly associated with subarachnoid irrigation. Subarachnoid irrigation, however, would of course have been useless without the removal of the cause. In view of the excellent condition of the patient just prior to the second irrigation — with the rapid rise of blood pressure and the sudden termination, one is forced to the conclusion that death resulted from cerebral compression, probably induced by the irrigation. In addition to the over-looked abscess, the patient probably was over-treated both as to lumbar puncture and serum injections, and subarachnoid irrigation. ADDITIONiAL REFERENCES FOR PROTECTIVE MECHANISM. Weed, Lewis H., Wegeforth, Paul, Ayer, James B., and Felton, Lloyd D.: A Study of Experimental Meningitis. A Series of Papers from the Army Neuro- surgical Laboratory; Monographs of the Bochefeller Institute for Medical Re- search, No. 12, March 25, 1920. Weed, Wegeforth, Ayer and Felton: The Production of Meningitis by the Release of Cerebro-Spinal Fluid; Jowmal A. M. A., Jan. 18, 1919, Vol. 72, pp. 190-193. Wegeforth, Paul, and Essick, Charles R.; The Effect of Sub- Arachnoid In- jections of Antiseptics upon the Central Nervous System; Journal of Pharma- cology arul Experimwntal Therapeutics, July, 1919, Vol. XIII, No. 4. Weed, Lewis H., and Wegeforth, Paul: Experimental Therapeutics. July, 1919, Vol. XIII, No. 4. Felton, L. D. : The Intra-Meningeal Virulence of Micro-organisms; Mono- 154 BRAIN ABSCESS graphs of the Bockefeller Institute for Medical Research, March 25, 1920, No. 12, p. 45. Weed, Lewis H., and Wegeforth, Paul: Experimental Irrigation of the Sub- Arachnoid Space; Journal of Pharmacology and Eooperimental Therapeutiosi, July, 1919, Vol. XIII, No. 4. Ayer, J. B. : Experimental Acute Hematogenous Meningitis; Monographs of Rockefeller Institute for Medical Research, March 25, 1920, No. 12, p. 119. Fig. 3.3 (a). — Cross section of left optic nerve — showing perineural infiltra- tion with thrombosis of small vessels and degeneration of the nerve fibers in a case of frontal lobe abscess which, after evacuation of the abscess, perforated tlie lateral ventricle and was followed by a closed empyema of the ventricle, causing blindness. Tlie O.E. picture was tliat of strangulatioii of the vessels — "Stupeur Arterielle." (The shrinkage of the sections due to the hardening process in foi'malin is proportional in both right and left optic nerves; the atropliy due to pathological conditions was much greater in riglit optic nerve than in left.) Fig. 33 (b). — Cross seelion riglit optic nerve — near chiasm — showing peri- neural infiltration with thrombosis of small vessels and degeneration of the nerve fibers in frontal lobe abscess which, after evacuation of the abscess, per- forated the lateral ventricle and was followed by a closed empj'ema of the ven- tricle, causing blindness. The O.E. picture was tliat of strangulation of the vessels — "Stupeur Artiirielle." (Tlie shrinkage of the sections due to the hardening process in formalin is proportional in both right and left optic nerves; the atrophy due to pathological conditions Avas much greater in right optic nerve than in left.) PART III. SURGICAL DIAGNOSIS. CHAPTEK X. DIAGNOSIS OF BEAIN ABSCESS IN GENEEAL. In the presence of a known focus of inf ection^ either from tiie ear, nose, lungs, or other organ, with cerebral symptoms, brain abscess is to be differentiated from (1) blood-stream infection, (2) meningitis, (3) vascular lesions, (4) brain tumors. The symptomology peculiar to brain abscess should be divided into I— EVIDENCES OF CEREBRAL SUPPURATION. II— SYMPTOMS OF CEREBRAL COMPRESSION. Ill— LOCALIZING SYMPTOMS. In the usual descriptions aU the symptoms are intermingled more or less indiscriminately. This not only causes confusion, but often actually hinders an early diagnosis, for if the graver symptoms of . cerebral compression — ^papilloedema, slow pulse, coma, etc. — are absent in the early stages of the abscess, to include them in tiie de- scription minimizes the importance of the signs of cerebral suppura- tion which are always present and, while never so outspoken as those of cerebral compression, are capable of yielding a diagnosis at an early period if properly interpreted. The literature is filled with records of cases where a diagnosis was not made "because of the absence of the, so-called, symptoms of brain abscess." Review of these cases will show that what in reality prevented the surgeon from making a diagnosis was not the absence of the symptoms of cerebral suppuration — ^for they were present — but the absence of those symptoms which point to an increase in the intracranial contents, the signs of cerebral compression. Few cases of brain abscess present evidences of cerebral compres- sion in the early stages ; the majority of them not for some time, as the bulk of the brain is not increased; while a considerable number, 155 156 BEAIN ABSCESS especially those in which the frontal lobe is the site of the abscess, never cause compression. The importance of this fact is not gen- erally appreciated. In a doubtful case — and most cases are doubtful in the early stages — ^the surgeon should approach the subject with a broad view- point. In attempting a diagnosis he should adopt a definite mental policy. He should endeavor to distinguish between the manifesta- tions of cerebral suppuration on the one hand and those of compres- sion and localization on the other — ^though both of the' latter may be absent. In the course of his experience the author has adopted the fol- lowing policy: (1) he asks himseK (a) is cerebral suppuration pos- sible? and (&) if possible, is it probable? Should these questions be answered in the affirmative, he then tries to decide (2) is cerebral compression present? Then, and not until then, is (3) the localization of the suppuration, to be con- sidered, when in, the majority of cases the solution of the three for- mer questions will have made apparent the probable site of the (1-a) Is Cerebral Suppuration Possible? In a case that pre- sents cerebral symptoms the absence of evidences of suppurative dis- ease of the ear, nose, lungs, or heart at the time of examination re- moves the probability of a brain abscess. Although cases of otitic brain abscess are on record in which the abscess has remained quiescent for a long period of time during which the ear ceased to discharge, the author believes that a careful examination of the history of such cases would reveal that marked cerebral symptoms accompanied or immediately followed the aural suppuration. On the other hand an accompanying focus of suppuration in the ear, nose, or lungs (bronchiectasis), renders possible a localized in- tradural suppuration. In such a case, although the cranial symptoms may be indefinite, the patient should immediately be admitted to a hospital for observation and routine examination. (1-&) Is Cerebral Suppuration Probable? In the presence of cerebral symptoms with a known focus of suppuration of the ear or nose, intradural suppuration becomes not only possible, but probable. In such cases an early positive diagnosis is rendered possible by at- tention to a multitude of details to each of which the surgeon must give careful consideration. During this stage there generally is no one symptom which is pathognomonic. Too much significance should not be attached to the presence or — ^more especially — ^the absence of any one symptom. The surgeon must construct the picture by atten- DIAGNOSIS OF BEAIN ABSCESS IN GENERAL 167 tion to minor evidences and after its construction he must consider it as a whole. I— EVIDENCES OF CEREBRAL SUPPURATION. (a.) Initial Vague Chill. — The "initial vague chill" indicates the beginning of an intradural suppurative process. It occurs when the infection invades the brain tissue. This initial vague chill gen- erally is described by the patient as "not a chill, but a chilly feeling," and consequently the account of it is obtained only by a systematic inquiry into the patient's history. Careful questioning will establish not only the occurrence of the chill, but also the fact that from the time of its occurrence the health of the patient was not so good as previously to it. The eliciting of the exact date of the "initial vague chill" is of the greatest clinical importance, since from that can be computed the probable duration of the abscess, the degree of viru- lence of the suppuration, and the possible presence or absence of an encapsulating membrane, all of which will greatly influence the surgical procedure to be adopted. (&) Headache. — This, in the author's opinion, is always pres- ent. It will vary, from a dull headache to severe attacks in which the patient may become almost maniacal from pain. No other one symptom is of such uniform occurrence, or of greater assistance to a positive diagnosis. Its importance frequently is minimized by the patient; he "always has had headaches." Psychologically, there ex- ists a disposition on the part of both patient and physician to disre- gard the headache because of this previous disposition. Questioning, however, will demonstrate that the headache is of somewhat different type from that previously complained of. Usually it is necessary for the surgeon to point out the difference to the patient. In the presence of a known focus of suppuration in the ear or nose, very severe headaches preceded by a vague chill render an in- tradural suppuration extremely probable. In one of the writer's cases these were the only evidences demonstrable at the time of operation ; and in numerous instances no other symptoms appeared for a long time, although the patients all along were suffering from encapsulated brain abscesses. It is to be understood, however, that encapsulated, aseptic serous meningitis may cause this syndrome; but a localized meningitis fre- quently is the initial stage of an intrapiarachnoid abscess. (c) Vomiting. — As with headache, the importance of vomiting 'as a symptom of brain abscess frequently is not appreciated, espe- cially if the patient heretofore has had "vomiting spells" associated 158 BRAIN" ABSCESS with headaclie. True projectile vomiting rarely occurs in the earlier stages of intracranial suppuration prior to the appearance of com- pression; but irregular vomiting without a definite cause is a fre- quent occurrence and should always be regarded as presumptive evi- dence of meningeal or cerebral suppuration. In one of the author's cases a boy, nine years of age, had for several weeks following a mastoid operation no symptoms of cerebral suppuration other than irregular headaches, two or three intermittent attacks of vomiting, and a slight peevishness of disposition, yet during this time there was a large collection of pus in the temporo-sphenoidal lobe. Examina- tion of the recorded cases of frontal lobe abscess shows that in a large proportion of them headache and vomiting were the only symptoms present until shortly prior to death. (d) General Malaise. — Loss of appetite, coated tongue, and dry skin always are present to a greater or less degree with cerebral suppuration. In cerebellar abscess the loss of flesh is one of the most characteristic symptoms. The combination of headache, vomiting, and general malaise, each or all out of proper proportion to the mani- fest local condition, preceded by a vague chill and a known focus of suppuration, associated with a high cell count in the cerebro-spinal fluid, calls for an exploration within the skull. (e) Disproportion. — (Value of, in diagnosis of cerebral sup- puration) : A certain disproportion always exists between the com- monly recognized symptoms of cerebral suppuration. This has its value in diagnosing between the symptoms that arise from the caus- ative lesion — mastoiditis, or frontal sinusitis — and the symptoms of cerebral suppuration. The causative agents of a brain abscess — mas- toiditis or a frontal sinusitis, themselves suppurative processes — produce the same general symptoms as intracranial suppuration, (chills, pain, headache, vomiting, temperature, general malaise and high cell count), and this complicates the problem. The symptoms originating from each, however, frequently can be distinguished by a study of the proportional relationship between the lesion and the severity of the symptoms. In a determination of whether the symptoms presented arise from intracranial suppuration or from the mastoiditis, the surgeon must visualize the possible course of the different Jjathological processes. In the case of the boy referred to, he had a mastoid; an extradural abscess had been found at operation, but after its evacua- tion he became peevish and had irregular vomiting and headache. A child of nine years, recovering from a mastoid operation, might have attacks of vomiting from overeating. The disproportion was evident DIAGNOSIS OF BEAIN ABSCESS IN GBNEEAL 159 in tliis case, therefore, because children of that age rarely have asso- ciated vomiting and headache without an intracranial involvement. An adult, on the other hand, might be liable both to vomiting and to headache, but in the boy's case the repetition of such an association would signify a complication of the mastoiditis, or at least a pachy- meningitis interna — itself a stage of intracranial suppuration — or a serous meningitis. But, it may be asked, is not a pachymeningitis interna gener- ally harmless? And are not pachymeningitis interna and serous meningitis protective processes, both self -limited ? True. And do they not frequently disappear upon removal of the cause? True, also. Then why not reopen the mastoid and thoroughly clean it out ? The answer lies in whether, in an individual case, a pachymeningitis interna or a serous meningitis could exist alone. In the case cited the diseased mastoid had been thoroughly exenterated, but in spite of this the peevishness, headache and vomiting subsequently ap- peared. Consequently, it could not be a pachymeningitis interna, because if that had been present at the time of the operation it would have been cured, and it had no reason to develop subsequently as the diseased bone had been thoroughly removed. The disease could not have followed this sequence. If the operation had been incom- plete, or if a sinus thrombosis had existed, then a pachymeningitis might have been present. A visualization of the possible intracranial course of the indi- vidual lesion will reveal any disproportion between the symptoms due to mastoiditis or to sinusitis alone. The following chart is offered as an aid to such visualization : Sequences in Adjacent Pathological Processes Entering the Brain. In the case of Mastoiditis, acute; there may be an associated Extradural Abscess; Pachymeningitis Interna ; Toxic localized leptomeningeal effusion — Serous Meningitis. Mastoiditis, acute or chronic; may be followed by (Extradural Abscess) ; Brain Abscess from direct extension of suppurative tissue or retrograde thrombophlebitis. Mastoiditis, acute or chronic; may have caused a Labyrinthine or Perilabyrinthine involvement; from which may originate Cerebellar Abscess from direct extension or retrograde thrombosis. Mastoiditis, acute or chronic ; may be followed by Labyrinthine or Perilabyrinthine involvement; and at the same time cause a Sinus Thrombosis; from which may originate Brain Abscess secondary to sinus thrombosis. 160 BEAIN ABSCESS Mastoiditis; Sinus Thrombosis; Brain Abscess. Frontal Sinusitis; Pachymeningitis Externa (extradural abscess) ; Meningeal Abscess. Frontal Sinusitis; Brain Abscess from direct extension of suppurative tissue. Frontal Sinusitis; Brain Abscess from retrograde thrombosis. POSITIVE EVIDENCES OF CEREBRAL SUPPURATION. (a) Protective Meningitis. — During the past few years, wiien- ever infection of the ear or nose is present with cerebral symptoms, the demonstration of a protective meningitis by lumbar puncture has become one of the cornerstones of the author's diagnosis. A high cell count in the cerebro-spinal fluid from lumbar puncture is clinical evidence of intracranial involvement sufficient to warrant an intra- cranial exploration. The protective meningitis may be the evidence of a serous meningitis from the irritation of a neighboring infected focus, but if the adjacent suppuration in the ear or nose has been fully removed, the persistence of a protective meningitis is absolute evidence of intracranial suppuration. In a high cell count the character of the cells is of the utmost importance. A high per cent, of polynuclears in the early stages of the disease indicates that the process is an active one, such as a serous meningitis from extradural irritation or from an irritation caused by an intracerebral abscess which approaches the surface. The cells, if largely mononuclear, show a subsiding process, for the function of mononuclear cells is to remove the debris from the intra- leptomeningeal spaces. In meningococcus meningitis Neal ^ has shown that as the infection subsides the pus cells disappear and the percentage of mononuclears increases. In Case XVII ^ the following report of the cerebro-spinal fluid examination was of material assistance in differentiating between a possible brain abscess and a cerebral vascular lesion: "Pressure slightly increased; transparency — clear, watery; no sediment after centrifugalization ; globulin — ^moderate increase; cells — 21 to the cmm., mostly polynuclears; Fehling's reduced. Bacteriological ex- ' Neal, Josephine B. : Meningeal Conditions Noted During the Epidemic of Influenza ; Department 0} Bealth of City of New York, Reprmt, Series 77, February, 1919, p. 4. "The mononuclear cells and the normal reduction of Fehling's solution are practically never present in a pyogenic meningitis." ^ Case XVII, Miss M. D. ; Chapter Five, Metastatic Abscess, p. 77. DIAGNOSIS OF BEAIN" ABSCESS IN GENEEAL 161 animation — sterile. Conclusion — secondary protective meningitis, probably from brain abscess." The cell count may not be increased although an intracerebral abscess may be present at the time. In fact, the cell count is in- creased only when the meninges themselyes are irritated, or during the stage of localization of the suppurative process. In intracerebral abscess from retrograde thrombophlebitis the cell count is not in- creased as long as the abscess does not approach the meninges. The writer's conception is that a high cell count in the cerebro-spinal fluid, with increase of globulin, occurs at an early stage in nearly all cases of brain abscess which originate by direct extension from the ear or nose. For an understanding of the absence of a high cell count the course of the pathological process must be considered. During the course of localization of a meningeal process or a cerebral suppura- tion, the evidences of the protective meningeal reactions are exhibited in the general cerebro-spinal fluid for a few days only, as experi- mental evidence shows that after the production of an aseptic menin- gitis the cell count for the lumbar fluid is high only during the active stage, while the process in the cerebral meninges, although limited, may still be present. After the abscess is walled off from the meninges and the surrounding cerebral substance, the cerebro-spinal fluid obtained by lumbar puncture is nearly normal in constitution and the cell count, also, becomes normal. Later, when the abscess approaches the meninges, the cell count will again increase. A high cell count, then, is important in diagnosis, but its absence should not militate against the probability of an intracerebral sup- puration. In its absence the possible duration of the suppuration should be considered. In one of the author's cases, ^ on the eighteenth day of the disease, although an abscess was present in the cerebellum, the lumbar puncture fluid was clear and escaped rapidly by drops (consequently it was not under much pressure) ; reduced Fehling's, and contained only flve leucocytes to the cubic centimetre. In blood- stream infections there is no protective meningitis and the cell count in the cerebro-spinal fluid remains normal. (6) Convulsion. — In the author's experience a convulsion oc- curring in the presence of suppuration in the ear or nose is a posi- tive sign of intracranial involvement. Although a few cases are recorded in which the removal of the focus of primary infection with- out the opening of the dura was followed by the disappearance of all symptoms, he is of the opinion that a localized serous meningitis " Case No. XXXI, W. J. : Chapter Twelve, p. 203. 162 BRAIN ABSCESS • — the first stage of an intrapiarachnoid abscess — existed at the time. In four instances in which the conservative course of removing only the adjacent foci of infection vi^as adopted, all subsequently were found to be suffering from brain abscess, although the primary opera- tion on the mastoid or nasal sinuses was followed by a period of im- provement, an improvement which in one case lasted for several weeks. In the light of these experiences the author regards convul- sions as positive indication of an intracranial involvement and their subsidence on the removal of the infected foci should not blind us to the fact that the intradural contents were affected. Association of convulsions with a known focus of infection calls for exploration within the dura. In frontal lobe abscess, especially in children, convulsions are frequent. In one case to which the writer was called in, consultation a child had two convulsions following orbital abscess. When first seen the child appeared perfectly normal. An intradural operation was refused. A surgeon subsequently operated on the ethmoid alone, disregarding the earlier convulsions; death followed in two days, with indications of a ruptured abscess. Convulsions are of relatively infrequent occurrence in adjacent brain abscess except as a terminal manifestation of meningeal or ventricular rupture. It is to be remembered, however, that irritation of the temporo-sphenoidal lobe from brain tumors is much more apt to be associated with convulsions than is an irritation in any other portion of the brain. Especially with children it has been the author's experience that the first symptom of brain abscess was a sudden convulsion- — in two cases occurring while the child was at play apparently in perfect health, although suffering from a chronic running ear. In an examination of the recorded cases the author has been im- pressed with the comparatively frequent occurrence of convulsion in metastatic abscess. The explanation probably is that in metastatic abscess the cortex often is suddenly involved before a protective process has had time to guard the brain from the septic invasion. In adjacent intrapiarachnoid abscess such protection takes place before the cerebro-spinal fluid accumulation becomes purulent. From observation the author is inclined to regard the occurrence of convulsions in brain abscess as suggestive either of (1) cortical involvement by an intracerebral abscess — convulsion being the ex- pression of a more or less generalized cortical instability; * (2) ab- « MacRobert, KiisseU G., and Feinler, Laurent : Cause of Epileptic Seizures !n Tumors of the Temporo-sphenoidal Lobe; Journal Amerioan Uedioat Attodation, Feb- ruary 19th, 1921, p. 500. DIAGNOSIS OF BEAIN ABSCESS IN GENEEAL 163 scess of metastatic origin and consequently not apt to be situated adjacent to tlie site of suppuration; ^ or (3) abscess of the temporo- sphenoidal lobe. (c) Subnormal Temperature. — During brain abscess the body temperature remains irregularly subnormal — a fact which is of the greatest diagnostic importance. No satisfactory explanation has been offered to account for the failure of a localized suppuration within the cerebral tissue to give the usual body reaction to a bacterial irri- tant — i. e., rise of temperature. The theory that failure to maintain the normal body temperature is due to interference with the heat-regulating mechanism of the brain by cerebral suppuration — on the supposition that the brain and spinal cord possess two sets of cells which cause an increase or a loss of heat according as one or the other is stimulated,* should be abandoned, although importance still is to be attached to the effect of stimulation of the vaso-motor center. There is experimental evidence that the heat^regulating centers are situated in the basal segment of the mesencephalon. It has been found that removal of the cerebral hemispheres and the thalamus destroys the mechanism for regulating the body temperature.'^' ^' * The daily normal temperature curve is due to fluctuation in tonus of the vegetative system, the center for the regulation of the tonus being situated, it is believed, in the hypothalamus. The secretions from the endocrine organs — the thyroid, pancreas, and adrenals — influence the tonus by stimulating the tonus center. Over-stimula- tion from over-action of the thyroid and other glands causes a mod- erate rise in the temperature curve, while diminished tonus — a fatigue phenomenon — is followed by a lowering of the normal daily tempera- ture curve; both actions, stimulation and depression of the tonus, occur irrespective of the metabolic — digestive — processes.^" It has been established that the secretions of the brain contribute ' Sautter, C. M. : Journal American Medical Association, February 5, 1921, Vol. 76, No. 6, p. 378. Also, Laryngoscope, December, 1920, p. 823. Reports a case of a boy of thirteen witb a temporo-spbenoidal lobe abscess of otitic origin. Ten days after a simple mastoid operation convulsions intervened and the patient sank into deep coma. A decompressive operation was followed by improvement. Six days later convulsions returned. Evacuation of pus from area of frontal convolutions. Recovery. "Adami and McCrae: Textbook of Pathology, 1914, p. 146. » Rogers, Fred T. : Relation of the Cerebral Hemispheres to Arterial Blood Pres- sure and Body Temperature Regulation ; Am&rican Journal oj Phvaiology, 1919, Vol. 49, p. 271. • Rogers, Fred T. : Studies on the Brain Stem — IV : On the Relation of the Cere- bral Hemispheres and Thalamus to Arterial Blood Pressure ; Am&ricwn, Journal of PhysioloffV, December, 1920, Vol. 54, No. 2. • Rogers, Fred T., and Wheat, D. S. : Studies on the Brain Stem — V : Carbon Dioxide Excretions after the Destruction of the Optic Thalamus and the Reflex Functions of the Thalamus in Body Temperature Regulation ; American Journal of Pht/Biologv, September, 1921, Vol. 57, No. 2. "> Mayer, A. : Pathologic Physiology of Human Body Temperature ; Deutsche Uediginisohe Wochenaehrift, 1919, Bd. 452, S. 138S. 164 BEAIN ABSCESS somewliat to tlie maintenance of a normal body temperature. Crile's ^^ conception is that there is a normal secretion from the brain tissue itself, as well as from the pituitary and other glandular bodies, which contributes to the maintenance of the body tempera- ture. The easily induced subnormal temperature of old age is a cere- bral tissue manifestation associated with degenerative cerebral changes as shown by the cholin in the cerebro-spinal fluid. The sub- normal temperature of hibernating animals is associated with an under-secretion of known glandular cells during hibernation. In a general way hibernation resembles brain abscess in its symp- toms. Hibernating animals have "subnormal temperature, tachy- cardia, slowed respiration, with diminished output of carbon dioxide, lowered blood pressure, relative peristaltic activity and marked in- sensibility to painful and emotional stimulus" — symptoms closely simulating cerebral suppuration. Additional Factors in Subnormal Temperature — Absence of Lymphatics; Autolysis. Cerebral suppuration being associated with an irregular sub- normal temperature, the intermittent rises probably are due to a slight leptomeningeal space involvement. The author suggests that a factor is the absence in the brain of lymphatic channels which in the body tissues in general play such a large part in the conveyance and control of infection. The delicate perivascular spaces surrounding the blood vessels empty into the subarachnoid spaces and are the channels whereby the dead tissue or other deleterious substances are removed from the brain. The phagocyte cells either absorb them or they are emptied into the blood vessels of the cerebral tissue, or are carried from the leptomeningeal spaces by the arachnoid villi. The high temperature in meningitis is due to the micro-organisms or toxins passing into the general blood stream, probably through the subarachnoid villi. Drainage into the large venous sinuses carries off the blood-stream infection in a considerable proportion of the cases of meningitis. Thrombosis of the blood vessels in the area of the cerebral sup- puration not only obliterates the vessels, but causes the perivascular spaces to become so filled with cells that they are no longer capable of functioning, and thus the remaining connection with the general circulation is removed ; for as long as they remain within the cerebral substance they may remain inactive. " Crlle, George W. : Origin and Nature of the Emotions ; W. B. Sounder* Company, Philadelphia, 1916, p. 138. DIAGNOSIS OF BEAIIT ABSCESS IN GBNBEAL 165 It is a clinical fact of diagnostic importance that suppuration within the cerebral tissue, at a distance from the meninges, not only fails to produce the well-recognized reaction of suppuration — an ele- vated temperature — but, on the contrary, frequently is accompanied by an irregularly subnormal temperature. The author suggests that possibly the absence of fever in brain abscess is due to the fact that a brain abscess has little or no commu- nication with the general circulation, being cut off from the vascular circulation by thrombosis of the vessels, and from the cerebro-spinal fluid circulation by obliteration of the perivascular spaces by exu- dates; while the irregular subnormal temperature in brain abscess may result from a disturbance of the heat-regulating mechanism of the brain. The toxins or micro-organisms which cannot reach the general circulation may depress the normal temperature either by depression of the tonus center or by direct action of the heat-regulat- ing center, or possibly by interference with the normal secretions of the brain, as occurs in hibernation. The resistance of the brain substance to autolysis may also play a part, for of aU the soft tissues, the brain and the skin are the least affected by autolysis. Cholin, which is not highly toxic, is liberated by the autolysis of nerve tissues. 11— SYMPTOMS OF CEREBRAL COMPRESSION. Nothing has done more to delay diagnosis than the habit of re- garding the manifestations of compression as direct symptoms of brain abscess. In many cases there is no increase in the brain bulk in the earlier stages, the pathological process being largely necrotic, the result of nutritional death from a retrograde thrombo-phlebitis. Later there may or may not be an increase of the intradural contents from the growth of the abscess, with an associated or reactive cedema and obstruction to the cerebro-spinal system circulation. It will be of assistance if we do not regard the symptoms of com- pression as distinctly those of cerebral suppuration, but as the result of increase in the brain bulk which may or may not be present at the time of examination. Only a limited degree of compression is possible in a brain ab- scess. The extreme cerebral compression so frequently associated with cerebral tumors never is present in suppurative intracranial lesions. Emphasis is laid upon the distinction. A neoplasm in- creases the brain bulk either by displacement of the cerebral tissue or by infiltration into it ; an abscess grows by the destruction of cerebral 166 BEAIK ABSCESS tissue. The reactive forces of nature are paralyzed in the priesence of suppuration by a very limited degree of the suppuration, and the nutrition of still unaffected parts is so interfered with that the sup- puration rapidly extends and death soon follows. Therefore, the manifestations of extreme cerebral compression seen in cerebral tumors are never witnessed in brain abscess. SPECIFIC SYMPTOMS OF COMPRESSION. In the presence of cerebral compression, all the cerebral functions are lowered. We have low temperature, slow pulse, and stupor, in contradistinction to the excitation of meningeal stimulation from suppuration, when there is high temperature, a rapid pulse, and cerebral excitement. (a.) Slow Pulse. — A continuous slow pulse is a distinct symp- tom of cerebral compression, but when present it generally is asso- ciated with other signs — such as papilloedema or coma — which enable a diagnosis. Of greater importance, however, in the early diagnosis of brain abscess is the appearance of periods of slow pulse followed by a rapid return to normal. In abscess of the brain a slow pulse may be recorded for a few hours — probably due to an acute oedema — only to disappear as the oedema subsides or, what is more important, as compensation is established. (&) Blood Pressure. — The blood pressure uniformly should be taken at frequent intervals during the time the patient is under ob- servation, chiefly because of its later value when surgical assistance will be necessary. With acute cerebral compression the blood pres- sure will rise, but in brain abscess, as a rule, compression develops slowly, in which case no variation in the systolic pressure will be recorded. It has taken the author many years to realize that hourly blood pressure readings, although of the greatest diagnostic assistance in acute compression with involvement of the medullary centers, are of little or no value in subacute or chronic compression, the mech- anism of the two conditions being unlike. Cerebral pressure is synchronous with the pressure of the veins within the skull. If the intracranial contents are suddenly increased the splanchnic system is suddenly called upon to re-establish the equilibrium between it and the increased intracranial contents. Con- sequently, the blood pressure rises to prevent the threatened medul- lary anemia and immediate death. In chronic compression com- pensation is established by factors within the cranium itself, and con- sequently, although the intracranial tension may be high, the blood DIAGNOSIS OF BEAIN ABSCESS IN GENEEAL 167 pressure is not greatly, if at all, elevated. In one of the author's cases of acute temporo-sphenoidal lobe ahscess in which signs of com- pression developed early and rapidly, the blood pressure rose from 130 to 170, while under ether 190 was recorded. Immediately upon evacuation of the abscess the blood pressure fell to 155, and on com- plete evacuation to 130. (c) Pulse Pressure. — In acute cerebral compression not in^ volving the medullary centers a rising pulse pressure is of diagnostic importance, as normally there is a close connection between the sys- tolic, the diastolic, and the pulse pressures. A rising pulse pressure means acute cerebral compression away from the medullary center. Whether it is of any diagnostic assistance in acute abscess cases the author is unable to say ; but in traumatic cerebral cases it has been of the greatest assistance to him. (d) Projectile Vomiting. — This is of very infrequent occur- rence in cerebral compression. It is, however, of frequent occurrence in cerebellar abscess, even without marked cerebral compression. (0) Ocular Paralysis. — Ocular paralysis is of no localizing value whatever, the external rectus being the most frequently in- volved in any suppurative lesion. Its value as a sign of intradural suppuration is also greatly mitigated by the fact of its frequent oc- currence in suppurative processes of the mastoid cells or of the apex of the petrous portion of the temporal, perhaps from an exudate at the base of the brain. The sixth nerve as it passes over the apex of the bone may be very susceptible at this point to involvement from an inflammatory exudate. Third nerve paralysis, also, is of no localizing value — as demon- strated by Gushing. It is apt to be compressed between the area of transmitted intracranial pressure and the internal carotid artery. It is of much more value, however, than a sixth nerve paralysis as a sign of cerebral suppuration ; but both are of great value as symptoms of transmitted intracranial pressure. In one of the author's cases there was an external paralysis of the opposite side from a temporo- sphenoidal lesion. ^^ (/) Coma. — This generally is the terminal stage of compres- sion. If we await the development of coma before exploration, the mortality will be high, as cerebral compression favors the extension of cerebral suppuration. If we would have a lessened mortality from brain abscess, the abscess must be evacuated before compression has damaged the cerebral tissues, paralyzed the reactive mechanism of « Case IX, G. W. > Chapter Four, p. 38. 168 BRAIN ABSCESS the brain, and so damaged the surrounding tissues as to make them a favorable soil for an extension of the abscess. (g) Papilloedema. — Clinically it is seldom possible to differen- tiate between an optic neuritis and a papilloedema. The nerve-head manifestations of brain abscess usually are a combination of both. The causes giving rise to them are not thoroughly understood. The generally accepted view of cerebral compression as the sole factor in their production is not consistent with clinical and experi- mental evidence. While general cerebral compression plays a part, other causes undoubtedly are operative. A better understanding of the exact pathological conditions producing papilloedema becomes necessary because of the widely accepted belief that it is solely of mechanical cerebral compressive origin — a view which frequently has occasioned the fallacious inference that an absence of papilloe- dema is clinical evidence of lack of increase in the intracranial pressure and has led to unnecessary delay in diagnosis. In consid- ering the significance of the presence or absence of papilloedema the following factors must be recognized : (1) The Presence of Increased Intracranial Pressure; (2) Interference with the Venous Return Circulation from the Cranial Cavity (sufficient to cause nerve-head changes) ; (3) Location of the Lesion (whether or not it interferes with the cerebro-spinal fluid circulatory system) ; (4) Alteration in the Composition of the Fluid (contained with- in the piarachnoid prolongations of the cerebro-spinal fluid system around the optic nerve, into which the parenchyma- tous fluids of the optic papilla and nerve are discharged) ; (5) Induced "Stupeur Arterielle" (due to an involvement of the periarterial sympathetic from the action of toxemia or trauma upon the central sympathetic system.) (1) The Intluencb of Increased Intbaoeanial Peessuee in the PBODtrcnow OF Papilloddema. Cerebral compression is not always manifested by papilloedema. The intense form of papilloedema — choked disc — is, of course a symptom of greatly increased pressure, but a mild or even a severe form of compression may entail no papilloedema. Choked disc oc- curs when the extracranial portion of the optic apparatus suddenly is filled with fluid or distended with exudates and inflammatory products, as in obliteration of the iter from pressure by a cerebellar tumor. ^* " WVirrlngton, W. B. : Serous Meningitis ; Quarterly Journal of Medicine. 1914, p. 105. DIAGNOSIS OP BEAIN ABSCESS IN GENERAL 169 The etiological features of choked disc are (a) distension of the intravaginal sheath, (b) infiltration into the substance of the optic nerve, and (c) venous stasis from interference with the return venous circulation from the eyeball or from the cranium itself, such as fol- lows from the ligation of an enlarged jugular, with extensive throm- bosis of the intracranial sinuses — ^the cavernous and the superior longitudinal. Distension of the intravaginal space is not always accompanied by choked disc. In several cases of fracture of the base of the skull involving the apex of the orbit, the author has observed an immediate blanching of the nerve head, and on subsequent post-mortem the optic sheath was found to be filled with blood. This explains the clinical observation that hemorrhage into the sheath from fracture may not occasion a papilloedema, but a primary optic nerve atrophy may follow within a few weeks. A high degree of increase of the brain bulk may be tolerated without papilloedema when the position of the lesion causes no ob- struction of the intracerebral portion of the cerebro-spinal fluid cir- culation. If papilloedema were occasioned by increase in the intra- cranial pressure alone, or even by direct pressure upon the optic sheath, nerve-head changes would be an early manifestation of abscess of the frontal lobe, because of the location of the abscess almost directly above the optic nerve and chiasm. In frontal lobe abscess, however, papilloedema rarely occurs, al- though an abscess of large size may be present. It is this almost uni- form absence of papilloedema in frontal lobe abscesses that has been one of the causes of failure to diagnose them. Examination of the recorded cases of frontal lobe abscess reveals the fact that although papilloedema is very infrequent before operation, it frequently de- velops after evacuation of the abscess, demonstrating that an increase in the intracranial pressure from abscess in front of the central por- tion of the cerebro-spinal fluid system is not associated with papilloe- dema and that the addition of another factor is necessary. The author has observed niimerous cases of cerebral injuries which during life gave distinct evidences of increase of intracranial pressure — confirmed at autopsy — but showed no nerve-head changes whatever." (2) Inteefesiencb with Venotts Retuen Cikculation from Ckanial Cavitt in THE PBODUOTION OF PAPILLCEDEMA. Intense choked disc may develop from an acute obstruction of the return circulation from the cranial cavity and retina, but the " Eagleton, W. P. : Fracture of the Skull ; Archi/ves of Surgery, July, 1921, Vol. Ill, pp. 140-153. 170 BEAIN ABSCESS papilloedema of brain abscess never is due to an obstruction of the vascular supply to tbe nerve bead alone. A moderate increase of tbe intracranial contents sucb as occurs in brain abscess can not give rise to sufficient pressure to occasion papillcedema by strangulation of tbe vessels of tbe optic nerve and papilla, but wben pressure is applied to an area vpbere it obstructs tbe cerebro-spinal fluid system or interferes witb tbe discbarge of tbe intracellular juices of tbe nerve bead into tbe subaracbnoid pro- longations of tbe nerve it will occasion a moderate papilloedema. Increase in intracranial pressure, by a temporary obstruction of tbe circulation, may occasion tbe tortuous and dilated veins and red- ness of tbe disc so frequently seen in septic processes, but from tbis temporary congestion tbe vessels quickly recover.^® Congestion of tbe disc from increased intracranial pressure does not lead to papilloedema. Altbougb frequently described as tbe first stage, it probably bas but little to do witb tbe development of a true papilloedema.^' For tbe development of a true nerve-bead swelling it is necessary tbat to a venous obstruction tbere be added an increase in tbe cerebro- spinal fluid system circulation. Tbe increase in tbe amount of cere- bro-spinal fluid from tbe irritation of an inflamed sinus wall, and dis- turbance in tbe outflow from alteration in its composition, undoubt- edly is tbe origin of tbe mild papilloedema often seen in sinus tbrombosis. Tbe writer bas seen a cboked disc witb bemorrbages and blind- ness immediately follow a ligation of tbe jugular for jugular bulb tbrombosis and occasion an immediate complete venous stasis. The venous stasis occurred because tbe ligated jugular was tbe main vessel for tbe return of blood from tbe cranial cavity — tbe opposite jugular foramen being very small — or because a tbrombosis occluded tbe superior longitudinal sinus.^'^ Tbe intense papilloedema probably originated in part from an associated acute internal bydrocepbalus due to increase of tbe cerebro-spinal fluid from irritation and from interference witb tbe discbarge of venous blood from tbe cerebral veins tbrougb tbe veins of Galen, its discbarge tbrougb tbe arach- noid villi being at tbe same time prevented by tbe tbrombosis of tbe longitudinal sinus. Tbe increased amount of cerebro-spinal fluid '"Martin and Crowe state that pressure on the internal Jugular vein may cause increase In the venous dilatation at the fundus. This observation, if verified, should be of some diagnostic value. (Martin, H. H., and Crowe, S. J. : Lateral Sinus Disease — Case Keport; Laryngoscope, December, 1920.) '» Pick, L. : Pseudo Neuritis Optica — Oedem der Papilla Nervi Optici — Neuritis Optica ; Zettechrift fUr Augenheilkunde, 1904, Bd. XI, S. 221. " Bagleton, W. P. : Circulatory Disturbances Following Ligation of the Internal Jugular Vein in Sinus Thrombosis — with Report of Case ; Arohwes of Otologv, 1906, Vol. XXXV, No. 2, p. 91. Case XXIII, chap. VIII, p. 129. DIAGNOSIS OF BEAIN ABSCESS m GENEEAL 171, with diminislied outflow resulted in an acute distension of the ven- tricles in addition to the venous stasis/®' ^® In another case a mild papilloedema on the homolateral side fol- lowed an operation for a cervical adenitis. The papilloedema origi- nated when an ascending retrograde thromhus, which developed in the jugular vein in the neck, entered the cranial cavity. (3) Influence of Location of Lesion in the Peoduotion of PApuxcedema. Papilloedema appears at once when the central portion of the cerebro-spinal fluid circulation is suddenly interfered with, causing an obstructive internal hydrocephalus. Abscess of the cerebellum, also frequently occasions a mild papilloedema, chiefly because the pressure upon the iter between the third and fourth ventricles dis- places the median line of the cerebellum and thus interferes with the cerebro-spinal fluid circulatory system. The intense choking of the disc so frequently seen in brain tumor, however, never occurs in cerebellar abscess. Obstruction of the central cerebro-spinal fluid system is the cause of the mild papilloedema in many cases of temporo-sphenoidal lobe abscess,^" while the almost uniform absence of papilloedema in fron- tal lobe abscess is, primarily, due to the fact that the central cerebro- spinal fluid system is not involved, papilloedema developing only when the abscess attains a large size or another factor is added.^^ Very large lesions involving the cortex alone, large hemorrhages, or growths, frequently cause but little change discoverable by the ophthalmoscope. Direct pressure on the optic chiasm exerted from below, (as in hypophyseal tumors conflned to the sella), and conse- quently not interfering with the central cerebro-spinal fluid circula- tory system, do not cause papilloedema. When situated above the chiasm, however, as in suprasellar growths involving the floor of the third ventricle, bilateral papilloedema usually is present although without great venous stasis. The author's experience with tumors of the hypophysis causes him to regard the absence of papilloedema as an indication either that the growth is suprasellar or that, having been primarily sellar in location, it has broken through the dural envelope and invaded the general cerebral cavity. " Stolz : XTeber die Unterbindung der Vena jugularls interna ; Correspondenzblatt filr Schioeixer Aerzte, 1918, Bd. XLVIII, No. 13, p. 415. '° Ruttin, B. : Venenektasie in retra auriculSren Operatlonafeld und Stauungs- paplUe naeh Jugularis Unterbindung ; International Centralblatt fik- Ohrenheilkunde, 1919-llj Bd. IX, S. 301. ^ Case X, Chapter Pour, p. 43 ; in which lumbar puncture performed during operation liberated but little fluid prior to evacuation, but the tapping of the abscess immediately was followed by free flow from the needle — an evidence of obstruction. " Bollack, J. : Stase Papillaire et Dilation des Ventrieules au Cours des Tumeurs C€r€brales; Annates d'OcuUstique, 1919, Tome 156, pp. 538-571. 172 BEAIF ABSCESS (4) Influence of Alterations in Composition of Pabenohymatous Fluid {of the nerve head and the optio nerve, which is discharged into the prolongations of the cereiro-spinal fluid system surroimd- vng the optio nerve). Papilloedema in brain abscess frequently originates from a block- ing of the pathways by which the parenchymatous fluids from the nerve head and the optic nerve are discharged into the subarachnoid prolongations of the optic nerve, the blocking being caused by changes in the parenchymatous fluid itself, or in the cerebro-spinal fluid. Intbacbllulab Pathways of Optic Neeve and Retina. "The optic nerve is not an outgrowth from the brain to the ter- minus as are the other cranial nerves, but a growth from the nervous elements of the retina into the brain." ^^ "Histogenetically it is merely an association path of the central nervous system correspond- ing to the other association paths." Primitively, the retina is a part of the cerebral cortex. If at an early stage the "eyeball is removed and the optic nerve cut, the gen- iculate, the pulvinar, and the anterior quadrigeminal bodies do not undergo complete development." ^^ The trophic center, therefore, which controls the development of these deep-lying ganglionic parts is in the retina. The intracellular fluids of the anterior part of the eye are dis- charged through the ligamentum pectinatum, the canal of Schlemm, and Montana's spaces ; those from the posterior part of the eye, how- ever, the retina and the optic nerve — the cerebral portion of the eye — discharge into the optic prolongations of the leptomeningeal channels of the cerebro-spinal fluid circulatory system.^*' ^^ Verhoeff's cases apparently would furnish evidence that if an optic nerve tumor involves the subarachnoid space a papillodoema develops, while atrophy alone appears when the space is not attacked. (Verhoeflf, F. H. : Primary Intra- neural Tumors (Gliomas) of the Optic Nerve; Transactions American Medical Association/ — Section on Ophthalmology, Boston, June 8-10, 1921, pp. 87-127. This system of intraneural, pericapillary, and perivascular path- ways of the retina and optic nerve frequently but erroneously is " Gradle, H. S. : Development of Human Eye — Ocular Embryology ; American Enovclopedia Ophthalmology, Vol. V, pp. 3862-3920. " Ryder : Development of the Bye ; Norris and Oliver Syatem oS Disease of the Eye, Vol. I, p. 60. « Weed, Lewis H. : Dual Source of Cerebro-spinal Fluid — Studies on Cerebro- spinal Fluid; Journal Medical Research, September, 1914, Vol. XXXI, No. 1 (New Series, Vol. XXVI, No. 1), pp. 21-117. " Wegeforth, Paul, and Weed, Lewis H. : Analogous Processes of Cerebral and Ocular B^uids — Studies on Cerebro-spinal Fluid : Journal Medical Research, September, 1914, Vol. XXXI, No. 1 (New Series, VoL XXVI, No. 1), pp. 167-170. DIAGNOSIS OF BEAIN ABSCESS IN GENEEAL 173 spoken of as lympliatic,^* although there probably does exist a com- munication at the apex of the orbit of this system with the true lymphatic system. Normal cerebro-spinal fluid does not coagulate, but alterations in its chemical properties — ^from irritation or inflammation — causes it to become coagulable to a greater or less degree. The author suggests that it is the filling of the intravaginal space with a pathological coag- ulable fluid,^'' or alteration of the perineural, pericapillary, or peri- vascular fluids — ^thus causing obstruction in the pathways — ^which is the additional factor generally operative in the production of papil- loedema in abscess of the brain ; much in the same way that interfer- ence — by inflammatory or hemorrhagic exudates — with the filtration of fluids from the anterior portion of the eyeball by blockage of the canal of Schlemm will precipitate an attack of acute glaucoma. ^^ The most intense choked disc with hemorrhage and venous tortuosities that the author has observed, having its origin from a brain abspess occurred in a very small temporo-sphenoidal lobe abscess, situated adjacent to the posterior horn of the lateral ventricle, and in which the ventricle fluid itself at operation coagulated. Prior to the operation the intensity of the choked disc occasioned doubt whether it could possibly be due to an abscess. It is probably the cellular reaction to the toxic influence of an altered cerebro-spinal fluid which is the cause of the mild papillce- dema seen in many localized suppurative processes — such as that associated with an involvement of the cells at the base of the petrous pyramid which is accompanied by "Gradenigo's syndrome," all of which symptoms disappear on evacuation of the adjacent mastoid area. The toxic reaction from the altered cerebro-spinal fluid has here a direct pathway into an optic nerve prolongation from the interpeduncular and chiasmal cistema. This is also the explanation of the frequently seen unilateral mild papilloedema associated with otitic sinus thrombosis — ^thrombophlebitis.^^ "' Behr, C. : Zur Entstehung der Stauungspapille ; v. Graefa ArcMv fUr Ophthal- mologie, 1920, Bd. 101, S. 165. =" Weed, Lewis H. : Dual Source of Cerebro-spinal Fluid ; Journal Medical Re- search, September, 1914, Vol. XXXI, p. 103. (States "Intra-leptomeningeal cbannela of pathological coagulable fluid probably cause obstruction of tbe perineural, pericapil- lary, and perivascular system of the optic nerve.") ^' Schiek believes from his histological examination of six cases that papilloedema arises from an obstruction to the "axial output from the eye" — a lymph stasis at the papillar end of the optic nerve, especially from over-filling of the intravaginal sbeath with cerebro-spinal fluid. Schiek, F. : Die Genese der StauungspapiUe ; Centralblatt fii/r Innere Medizm, 1910, Bd. XXXI, S. 484. ™ Rados produced papilloedema experimentally by the cerebral inoculation of extracts from virulent tumors. Rados, A. : Histologische Veranderungen an der experimentalen StauungspapiUe ; Archiv filr Augenheillcunde, 1915, Bd. LXXIX, S. 199. Lewlneohn demonstrated by animal experiments that the injection of glycerine, oil, or liquid paraffine into the subdural space caused a delayed change in the papilla, which must have originated from obstruction by the altered fluid and not simply from 174 BEAIN ABSCESS (5) Induced "Stupetjb AKTERisaxE" in the PEODUcraoisr of Papillcedema.*' Arterial contraction from disturbance of the central sympathetic nervous system in the brain — as the result of trauma or toxemia — undoubtedly is a factor in the production of nerve-head changes in certain cases. The author has seen a mild papillcedema from an enormous frontal lobe abscess foUovs^ed, after evacuation, by oblitera- tion of the arteries and veins, vs^ith blindness due to an accumulation of pus in the lateral ventricle of the affected side, as shov^n at post- mortem. The basal eistema was also enormously distended. (Figs. 33 a and b.) Contraction of the vessels of the nerve head frequently is an early manifestation of fracture of the skull from — the author sug- gests — a disturbance of the fibres of the sympathetic nerves surround- ing the arteries and veins. On the following day the nerve head appears normal 'unless a hemorrhage of the optic nerve sheath has occurred. In these cases the fracture generally passes through the apex of both orbits. In one case, following a fracture which went through both orbital roofs, both discs were white, the arteries being obliterated. On the following day after the removal of bone the discs were normal. In spite of the normal discs, however, greatly increased intracranial pressure was present, as was shown during life by the large amount of fluid under great pressure in the lumbar punctures, and later at autopsy by whiteness of the cortex and obliteration of the sulci. Both optic nerves were tightly held and indented where they passed through the orbital foramina, as if they were compressed. Microscopical ex- amination of the nerve, however, failed to reveal any pathological change. In another case a white nerve head accompanied an extensive hemorrhage of the head of a new-bom infant. The white disc per- sisted after the removal of the clot. At post-mortem a large intra- piarachnoid abscess was found, with an obstructive hydrocephalus from closure of the iter. increase of Intra-eranial pressure, as this would immediately have been manifest. Lewinsohn, G. : Expcrimenteller Beitrag zur Patlaogenese der Stauungspapille ; ArcMv fur OphthalmoToffie, 1912, Vol. 81, p, 15. Klauber, from clinical and histological examinations of wounds of the head, found papillcedema to be more frequent in the 'presence of infectious complications, due to an endocranial lymph stasis from the toxic irritation caused by necrotic brain tissue and extrayasated blood. Klauber, E. : Klinische und histologische Betrachtungen iiber das Oedem des Schnorenkopfes bei Gehirnverletzten ; Klmische MonatsWatter fur Augenheakunde, 1918, Bd. LX, S. 504. »»Leriche, Rcii(? : Some Kesearches on the Peri-arterial Sympathetica: Annala of Surgery, October, 1921, Vol. LXXVI, No. 4, p. 387. DIAGNOSIS OF BEAIN" ABSCESS IN GENBEAL 175 DIAGNOSTIC DEDUCTIONS FROM PEESENCE OR ABSENCE OF NERVE- HEAD CHANGES IN BRAIN ABSCESS. (1) A moderate grade of papilloedema is a frequent manifesta- tion of cerebellar abscess. It originates from an obstruction in tbe central cerebro-spinal fluid circulatory system (a) by cerebral dis- placement at the iter, or (b) by the accumulation of a pathological fluid from an associated arachnoiditis in the basal cistema ; (2) The same explanation of displacement accounts for the papilloedema frequently seen in occipital lobe abscess, the pressure being applied from above, consequently necessitating the suppurative process being well forward in the occipital lobe ; (3) The presence of a papilloedema in a temporo-sphenoidal lobe abscess depends (a) upon whether the abscess sufficiently dislo- cates the brain to cause obstruction in the cerebro-spinal fluid system by pressure, or (b) upon the toxic action of an altered cerebro-spinal fluid in the nerve head. (In the latter case it primarily should be regarded as a manifestation, not of compression, but of cerebral sup- puration.) (4) The usual absence of papilloedema in frontal lobe abscess is due to the fact that — in spite of the greatly increased intracranial pressure — ^none of the above factors are present; (5) Although when present papilloedema is of great diagnostic assistance in a case of brain abscess, its absence in the presence of other signs of intracerebral suppuration should not occasion delay in intradural exploration ; (6) Intense choked disc with swelling of several dioptres of the papilla and multiple hemorrhages never occurs from brain abscess alone. Its presence, when brain abscess is present, signifies that another factor also must be active— such as an acute, sudden obstruc- tion to the venous return from the eye from thrombosis of, or pres- sure upon, the cavernous sinuses; (Y) Obliteration of the arteries of the nerve head, with blind- ness out of proportion to the visible ophthalmic changes, when asso- ciated with brain abscess is suggestive of involvement of the central portion of the sympathetic system such as would occur from empy- ema of the lateral ventricles. CHAPTEK XI. DIAGNOSIS OF ADJACENT TEMPOKO-SPHENOIDAL LOBE ABSCESS. LOCAI-IZING SYMPTOMS. If, from a study of a case from tlie point of view of the symp- tomology of intradural suppuration in general, it is decided tliat a brain abscess exists, tbe next step in the diagnosis involves the locali- zation of tbe patbological process. Localizing Value of Primary Focus of Infection. — The im- portant thing to be determined in the localization of a brain ab- scess in the early stages is the original point of entrance of the infection, since the abscess will be found adjacent to this except in the case of abscesses of metastatic character. The chief point in localization, therefore, is to determine whether the infection has entered the brain from the ear; whether it involves the labyrinth; whether it has entered from the nose or accessory sinuses. If the labyrinth is involved the abscess is apt to be situated in the cerebellum; if there are no labyrinthine symptoms the abscess probably is temporo-sphenoidal ; if the suppuration exists in the frontal nasal sinus, the abscess is apt to be adjacent to the posterior wall of the frontal sinus. In the latter case the X-ray is an important aid in localization. In a brain abscess following aural suppuration the elimination of the cerebellum as the site of infection is of the greatest importance in localization; for, in adjacent abscess from the ear the abscess, if not metastatic, will be situated either in the temporo-sphenoidal lobe or in the cerebellum. If, in the absence of a spontaneous nystagmus, cold caloric in either ear in the upright position gives a normal nystagmus and normal vertigo, the cerebellum can probably be ex- cluded. The pointing deviations are so uncertain that induced point- ing variations may be largely disregarded.^ ' Barany, Eobert : Temporary Depression of the Function of the Cerebellar Cortex after the Method of Trendelenburg, evidenced by the pointing test; Journal of Lanyn- gology, Rhimoloay ami Otologv, August, 1911, Vol. 26, p. 444. 176 ADJACENT TBMPOEO-SPHBNOIDAL LOBE ABSCESS 177 Pathognomonic Symptoms in Temporo-sphenoidal Lohe Abscess. — The temporo-sphenoidal lobe is a silent area of the brain. Even when it is the seat of a large collection of pus no localizing symptoms may be present. Two pathognomonic symptoms, however, frequently are present and outspoken — i.e., aphasia (naming), and (an easily overlooked symptom) hemianopsia. (a) Aphasia. — One of the author's cases suddenly manifested a sensory (naming) aphasia which lasted for a few hours and then entirely disappeared. In reviewing this case he is inclined to be- lieve that in many of the adjacent temporo-sphenoidal abscesses which later develop aphasia, an incomplete aphasia is present off and on for several days prior to its becoming sufficiently outspoken to com- mand the attention of the patient or the physician. In a right-handed man with an abscess in the left hemisphere the presence of a naming aphasia is pathognomonic. The aphasia in the early stages is apt to be transient, appearing suddenly and as sud- denly disappearing. At the time of the examination the patient may talk very well, but his family will state that on a certain date he was "out of his head." In one of the cases, careful questioning showed that the patient was unable to name an object which he wanted; after repeated attempts to name it, he got out of bed and got it for himself; but in a few hours the aphasia had disappeared entirely. Personal experience has taught the writer not to be deceived by an apparent improvement. In one case a young man, following two operations on the jugular bulb, suddenly became aphasic. When seen on the following evening his speech was perfect, but from the de- scription of his aphasia by his physician, the author felt warranted in advocating a temporo-sphenoidal exploration. On account of the previous operation and the — at the time — excellent physical condi- tion of the patient, his family refused. A few weeks later he pre- sented himself to all appearances in perfect health. Ophthalmoscopic examination revealed a slight papilloedema, however. The following summer he suddenly became comatose and died within a few hours from rupture of the abscess. The reports of frontal lobe abscess contain several cases with a similar history. The transient nature of the aphasia undoubtedly comes from involvement by oedema of the associated tract ; later the oedema is sufficiently abated to allow of complete restoration of function. A "naming aphasia" is seldom complete until signs of compres- sion develop. In the presence of suppuration within the ear, pre- 178 BEAIlSr ABSCESS ceded by a vague chill, and associated with headache, exploration of the temporo-sphenoidal lobe is demanded. Even when complete, the aphasia disappears entirely after operation, so that the tract can not have been destroyed. The "naming" character of the aphasia, how- ever, although incomplete, usually can be demonstrated if properly investigated. Frequently it can be elicited only by careful ques- tioning. When incomplete this type is rather definite. The patient, when he names an object correctly, realizing its correctness, will repeat the same name for the next object; but while he may or may not know that this is the wrong name, he invariably can use or properly describe the use of the object.^ (6) Word Deafness. — The labyrinth contains, developmen- tally, the end organ of one of the most primitive of the special senses and one of the latest of all — the vestibular, and hearing apparatus. If we except speech, audition is the most highly specialized of all our special senses. In spite of the general conception that the eye is the most highly specialized sense, hearing as we understand it, undoubt- edly is. It is the only one of the special senses below speech which has even a tendency to be localized in one cerebral hemisphere. Hearing is a specialization of a special sense — that of sensation, touch — and it is out of the specialization of hearing that speech has been acquired by man. While experimental and histological evidence would place the cortical center for hearing bilaterally in the transverse temporal gyri of Heschl and in two-fifths of the temporal convolutions,^ a total deafness of the central organ is of rare occurrence for the reason that the hearing centers are bilateral — situated in both temporo- sphenoidal lobes — and consequently total central deafness follows only upon the destruction of both lobes. The transverse temporal gyri, probably of both sides but certainly of the left side, contain the primary centers for the reception and analysis of auditory stimuli ; they represent the uppermost link in the chain of auditory neurons.* Interference with the functioning of the cortical center for hearing such as would be caused by the pres- sure of a temporo-sphenoidal lobe abscess may give rise to a complex of symptoms which are of great diagnostic value. Of these, word deafness — a form of aphasia — is the most important. In general, » Gordon, Alfred : A Contribution to tlie Study of Apliasia ; New York Medical Journal, January 4, 1913. • Kennedy, Foster : Symptomology of Temporo-splieiioidal Tumors ; Archives of Internal Medicine, September, 1911, Vol. 8, pp. 317-350. ' Campbell : Histological Studies on the Localization of Cerebral Functions : 1905. ADJACENT TEMPOEO-SPHENOIDAL LOBE ABSCESS 179 aphasia is the inability to call a word, or the use of inappropriate words. Word deafness, as defined by Laiguel-Levastine,^ is rather a "syndrome characterized by the absence of adaptation of the words to the ideas and of the ideas to the words." In one of the author's cases *' "^ word deafness was a manifestation of a large, left-side, intrapiarachnoid temporo-sphenoidal lobe abscess. The patient, although possessing hearing in both ears, and affected by a Wernicke "naming aphasia" which allowed him to use numbers but not proper names, had a complete word deafness. He was un- able to call, repeat, or understand any proper names, but recognized and appreciated objects by sight alone. When he desired anything — ^lemonade, for instance — ^he uniformly would say, "Help me — ^help me ;" then, realizing his inability to make his want known by words, would add, "Show me." When shown the right object — ^the lemon, perhaps — ^he instantly would recognize it as the thing de- sired and assent by saying "Yes." He recognized his physician and friends but could not call their names nor even understand the names when they were spoken. Com- mands given him with nouns in the sentences he did not understand, but commands without nouns were understood, although imperfectly. When told to lie down he did so, asking, "Is this what you mean ?" He was conscious of and annoyed by a paresis of his right arm and described it by saying, "All in." Following the evacuation of his abscess the word deafness imme- diately disappeared, but the "naming aphasia" continued. He then could understand a name and could repeat it. When shown a knife, for instance, he could not say what it was, but when asked if it was a knife he not only recognized it but understood the name of it. He was imperfectly able to read printed numbers and letters, but appar- ently did not completely comprehend the command to read, as he generally tried to copy them instead of reading. He often inverted the letters and figures in writing them, but as he was writing with his left hand, the right still being paralyzed, this may account for it. In the writing teats he made the figures 2 and 6 upside down; a 7 he wrote 9; and 8 he also wrote 9, and a 9 was written 10. For 24 he drew an indeter- minate scrawl. The figure 2 he read two, but the 10 he called five. The letter W he read aright, but the letter P he was unable to read. ' Laiguel-Levastine : Aphasie et Apraxie ; Le Bulletin KMical, 1920, Vol. XXXIV, D 277 » Case VII, J. C. C. : Chapter Four, p. 35. ' Not© : Cases of brain abscess with word deafness have been reported by Brown, W. G. Mastoid Disease with Cholesteatoma Complicated by a Cerebral Abscess ; Medioal JaamM of Australia, 1920, I, p. 212 ; and Wiener, Alfred : A Case of Brain Abscess Following Traumatism and Acute Mastoiditis — Operation — Recovery ; Archives of Otology, 1906, Vol. XXXV, No. 4. 180 BEAIN" ABSCESS (c) Hemianopsia — Transient or Fixed. — ^Hemianopsia is one of the most important localizing signs of temporo-splienoidal lobe abscess. It is due to an involvement of tbe association fibers running from the cortical optical center in the cuneus to the geniculate bodies — the cuneo-pulvinar tract (Meyer's Tract) — which passed through the temporo-sphenoidal lobe. Gushing* has demonstrated that in temporo-sphenoidal lobe tumors this tract is caught between the tumor and the distended ventricle. This undoubtedly also is the explanation in temporo-sphenoidal lobe abscess cases. In a brain abscess as well as in a brain tumor case the author has seen a complete hemianopsia for colors which disappeared entirely on the following day. In his experience the hemianopsia has been latent in all abscess cases and he believes that a transient hemian- opsia is of much more frequent occurrence in temporo-sphenoidal lobe abscess than generally is appreciated, since it is not an outspoken symptom and not recognized by the patient himself, even when com- plete for form as well as for color. Consequently, if the surgeon is to avail himself of a localizing hemianopsia in making a diagnosis, it is necessary to examine the visual fields repeatedly both for form and for colors. (Fig. 34.) Hemianopsia persists long after the subsidence of suppurative symptoms, and in some cases even after the abscess has been cured. In a re-examination of two of the author's healed cases of temporo- sphenoidal lobe abscess * hemianopsic sections of the field were still found wanting after an interval of three and five years. (Figs. 35 and 36.) CASE NO. XXVII. E. L. : Hemianopsia a Deciding Factor in Exploring Temporo-sphenoidal Lobe. Boy. In the case referred to on page 177 the abscess was of many weeks' duration, during which time the mastoid wound and drum membrane had entirely healed, the hearing returned to normal, and no nerve-head changes were present. The only suspicious symptoms during these weeks were irregular vomiting and a mild form of headache — the former having been attributed to errors in diet and the latter to eye-strain from a refractive error. Five weeks after the prescribing of the glasses the headache became suddenly severe, the vomiting frequent, an intense choked disc developed and the vision was reduced. On examination a diagnosis of a probable brain abscess was made, based upon (1) the presence of a previous aural suppuration; (2) irregular vomiting and headache; localization of the pus in the temporo-sphenoidal lobe was sus- pected because repeated examinations of the field for form and colors had on one occasion — two days previously — shown a distinct tendency to ( 3 ) a hemianop- ' Gushing, Harvey : American Neurological Association, Atlantic City June 1921. » Case X, C, H,, Chapter Four, p. 43 ; and Case XVII, M. D., Chapter Five 270' Left Eye Right Eye (Solid line shows form field, dotted line color field.) Fig. 34. — Bilateral suggestive hemianoptie indentation of color fields in a case of left adjacent temporo-sphenoidal lobe abscess. (Case XXVII, E. L., Chapter Eleven, p. 180.) (Solid line ■ shows form field, dotted line color field.) Pig. 35. — Persistent hemianoptie indentation of field of right eye of patient three years after operation for a left-sided adjacent temporo-sphenoidal lobe ab- scess. (Case X, C. H., Chapter Four, p. 43.) Left Eye Eight Bye (Solid line shows form field, dotted line color field.) Fig. 36. — Unappreciated hemianoptio indentations of fields in a cured case of metastatic abscess of right internal capsule five years after operation. (Case XVII, M. D., Chapter Five, p. 77.) Left Eye Eight Bye (Solid line shows form field, dotted line color field.) Left Bye Eight Eye (Solid line shows form field, dotted line • - color field.) Fig. 37, Upper Figure. — Transient suggestive hemianoptic 'field in case of left adjacent temporo-sphenoidal lobe abscess. Lower Figure — Two days later; disappearance of hemianopsia for form, but indentation for colors. ADJACEISTT TEMPOEO-SPHENOIDAL LOBE ABSCESS 181 tie contraction in the eye of the affected side and a corresponding indentation in the opposite eye (Fig. 37) ; while the patient gave (4) a history of having a few days hefore had difficulty in recalling several names, among them the word "scapular" — a familiar word for a Roman Catholic who had worn one for several years. The abscess, which was of very small size with a very firm capsule, was located near the posterior horn of the lateral ventricle. After the evacuation of about two drachms of thick pus in a misguided effort at complete evacuation, the searcher was forced into the adjacent lateral ventricle. The cerebro-spinal fluid discharged was so viscid that it formed a cast within the searcher. As the ventricle was not dilated — as shown by both ventricular and lumbar puncture — it undoubtedly was the change in the character of the fluid itself which occa- sioned the intense choked disc. (d) Facial Paralysis of Opposite Side. — Generally the first manifestation of involvement of the motor area of the brain by an adjacent temporo-sphenoidal lobe abscess is a paresis of certain of the muscles of the opposite side of the face. This facial paresis is of the cortical, not of the peripheral type. It involves the lower portion of the face and is elicited only by spontaneous emotional movements, such as laughing, when the lower portion of the face appears flat- tened, while the eye, which the patient can close on command, does not close reflexly by volition so frequently nor so completely as the other. Facial paresis is of the greatest importance in diagnosis. It long precedes weakness of the arm and the leg. In the presence of sup- puration in the ear, with a history of vague chill and headache, a cortical paralysis of the face of the opposite side to the aural suppura- tion makes a diagnosis positive. (e) Paralysis of Contralateral Arm. — A weakness — paresis or paralysis — of the arm, which comes and goes, is a frequent localizing manifestation of brain abscess. (/) Contralateral Hemiplegia. — Complete hemiplegia in tem- poro-sphenoidal lobe abscess is a very rare condition. When it occurs it can be differentiated from a vascular lesion by the progressive na- ture of the paralysis, the face first becoming involved, then the arm, and last of all the leg, the involvement of the groups being separated by appreciable intervals. This is in contradistinction to vascular disease in which the onset is sudden and involves face, arm and leg simultaneously.^ " In the presence of a complete contralateral hemiplegia which has appeared suddenly, the probability is that the surgeon is not deal- ing with an adjacent temporo-sphenoidal lobe abscess, since an adjacent abscess by reason of its location away from the internal M Case XVII, M. D., Chapter Five, p. 77. 182 BRAIN ABSCESS capsule cannot cause a complete hemiplegia unless it is of enormous size, but with a vascular lesion or an abscess of metastatic origin. A metastatic abscess may cause a complete hemiplegia either (1) of internal capsular origin — its causative retrograde thrombophlebitis involving the vascular supply of the internal capsule — or (2) of. cortical origin, the infecting nidus having been confined to the motor area by way of a secondary thrombosis of a dural or pial vessel, the intercurrent intradural or extradural abscess being situated over the motor area at least three inches above the ear. CASH NO. xxvm. P. Q. : Case of Intercurrent Superficial Brain Necrosis\, Situated Three Inches Aiove the Ear, Over the Motor Area of the Gereiral Cortex (with Necrosis of Dura and Extradural Abscess) to which Point the Infection Was Carried from the Original Focus in the Middle Ear by an Intercurrent Thrombosis of a Dural Vein. History: The man was brought to the hospital complaining of intense pain in his left ear; dizziness, vertigo, noises in his ear. He had had bilateral run- ning ear in both ears for many years, but during the past year the discharge had stopped in his right ear; it had not stopped in his left. An examination revealed a dead labyrinth. The headaches and dizziness gradually disappeared and he was discharged from hospital. He was admitted the same day, with high temperature. It was now found he had a high cell count of his cerebro- spinal fluid; it was under great pressure, and cloudy. He had a leucocytosis of 13,000. He was rigid and had the symptoms of meningitis. However, to the surprise of everybody, this cleared up and the patient was again discharged. Four months later he was again admitted to the hospital. He now had a paralysis of the right arm. He had a slight facial paralysis of the right side. He had no "naming aphasia," but apparently had some difficulty in talking. He had two convulsions the night of admission and had had two or three the day before. He was apparently deaf in the left ear. He was able to walk and did not have a Romberg. From the history of the case it seemed certain that the man had an encapsu- lated brain abscess of the temporo-sphenoidal lobe, though it was hard to account for the lack of "naming aphasia," and "how a right-handed man could have a right-handed paralysis of the arm and face without a 'naming aphasia,' if the abscess had extended upward from the tegmen in the ordinary way." It was also certain that the abscess was near the surface, because of the convulsions. For the same reason — because of the convulsions — it was judged to be a metastatic abscess, the author not having seen convulsions in an adult except in a metastatic abscess. Operation. — A. large osteoplastic flap was turned up in the usual way, over the middle fossa. On drilling the last hole — ^that is, the anterior hole, well up toward the vertex— very profuse bleeding occurred. On passing the searcher from this to the next hole there was a free discharge of pus. Another hole was drilled between number one and two — on a straight line — ^because of the adherence of the dura. About two drachms or half an ounce of pus was dis- charged from the two holes. The abscess was found to be extradural with necrosis of dura and superficial brain necrosis. A large dura vein, which was thrombosed, ran directly upward in the anterior portion of the exposed area. At the upper end of it, it formed the extra-dural abscess, which had been com- pletely evacuated. An incision was made in the dura. Along its whole course ADJACENT TEMPOEO-SPHENOIDAL LOBE ABSCESS 183 the large thrombosed vein was firmly adhereut to the brain underneath as well as to the dura. The brain was searched in the upper portion to a depth of about six centimeters, but nothing was found. The entire bone flap was sacrificed; tight closure and drainage from the exposed dura — ^the area of exposed brain — and another drain above. Comment. — ^The case is remarkable being a metastatic abscess secondary to a thrombosis of a dural vein that originated over the whole of the arm area of the same side. A lumbar puncture done at the time of the operation revealed very little fluid. After the operation the paralysis of the arm gradually disap- peared; temperature fell to normal; and the patient recovered. SYMPTOMS OF ASSISTANCE IN DIAGNOSING TEMPOKO-SPHENOIDAL LOBE ABSCESS. (a) Pain in Teeth on the side of tlie affected hemisphere, together with symptom of pain behind the eye must he due to in- volvement of the Gasserian ganglion at the apex of the petrous pyra- mid. In one of the author's cases of temporo-sphenoidal lohe abscess which followed a chronic suppuration of the petrous pyramid,-^ ^ the pain in the teeth had been so severe that a dentist repeatedly had been consulted. On the development of the brain abscess the cerebral symptoms were so outstanding as to overshadow the pain in the teeth, although for several weeks that had been the most prominent syna.p- tom. As the post-mortem showed a very extensive involvement of the cellular structure of the petrous labyrinth, without destruction of the auditory apparatus, the author is of the opinion that the pain in the teeth was due to the bone lesion and not directly to the abscess. ^^ (6) Pain behind the Eye. — In two cases of temporo- sphenoidal lobe abscess in which drainage tubes had been inserted, irrigation occasioned pain behind the eye in the affected hemisphere whenever the cavity was distended by the fluid, the pain disappearing ■ immediately upon the release of the fluid. The pain behind the eye was produced by each distension and could be uniformly produced as long as the drainage tube remained in place.^^ The author has no evidence to warrant including it among the symptoms of temporo-sphenoidal abscess, but he is persuaded that pain behind the eye of the affected side should be considered as a localizing symptom of more or less value, depending upon the indi- vidual case. The pain behind the eye probably is due to irritation of the ophthalmic branch of the trifacial in the middle fossa, and not to irritation of the Gasserian ganglion. " Case VIII, A. M. M., Chapter Four, p. 37. " Cadwalader, Williams B. : Significance of Facial Pam in Determining the Location of Intracranial Tumor; Aro7i4/oes of Neurology and Peychiatrv, August, 1920, Vol. IV, pp. 182-184. »» Case XIII, Mrs. H., Chapter Four, p. 63. 184' BRAIN ABSCESS Pain behind the eye of the homolateral side should not he con- fused with the pain behind the eyes of both sides which, the author has come to believe, is of considerable diagnostic significance; the bi-lateral, post-ocular pain being caused by a distension of the lateral ventricle from an obstructive internal hydrocephalus such as is seen in cerebellar tumors with obstruction of the iter. The distended ventricles cause irritation of the nervous distribution of the fifth to the dura, and a general headache follows ; or, pressure downwards on the sensory root of the fifth as it enters the middle fossa from the posterior, irritates the first branch of the fifth. (c) Convulsions — Localizing Value.^* — ^While epileptic seiz- ures are of much more frequent occurrence in tumors of the temporo- sphenoidal lobe than in tumors in any other location in the brain — ;-noted in about fifty per cent, of all the recorded cases — they are very infrequent in abscess of the temporo-sphenoidal lobe. McEobert and Feinier ^^ have shown that the cause of convulsions in temporo- sphenoidal lobe tumors probably is pressure involvement of the vas- cular system of the middle central area. This probably also explains the convulsions in Case XIV, Chapter Five, p. 70, in which con- vulsion was due to something other than pressure, as the patient had two convulsions after the evacuation of the abscess at operation. (d) Dreamy State. — This occurs in a small proportion of cases and often is overlooked entirely or mistaken for the semi-somnolent condition which is common in cerebral compression. There is, how- ever, a distinct difference between the two conditions. In one of the author's cases there were dreamy state attacks from temporo- sphenoidal lobe tumor. The patient was admitted to the hospital in a semi-stup- orouB condition, accompanied by the statement that: "About three or four weeks previously he complained of severe headache and told his friends he was losing his mind. This was followed hy a con- vulsion, since which time he has been unable to do any work. During the past week he has been in a more or less semi-conscious condition but could be aroused." The patient being unable to make a connected statement, the following account was obtained: "Had not noticed anything wrong until one month previous, when the patient's tone of voice changed and he 'said some things which seemed unnatural.' Later he would stop in the midst of a task and stare into space. About three weeks before his admission to hospital he had a fit. After that he stated frequently that he was losing his mind. For the past two weeks had been ill, sometimes complaining of pain in left side of head, frontal and parietal regions. Had several attacks of vomiting, not projectile. " See p. 161, Convulsion, a Positive Evidence of Cerebral Suppuration. " McEobert, Eussell G., and Feinier, Laurent : The Cause of Epileptic Seizures in Tumors of the Temporo-splienoidal Lobe; Journal American Medical Association Feb- ruary 19, 1921, Vol. 76, No. 8, p. 500. (In forty-one recorded cases bad arani mal attacks, and In five minor cases lesser types of convulsions.) ADJACENT TEMPOEO-SPHENOIDAL LOBE ABSCESS 185 Lately refused to have anything to do with his friends— said he thought they had something against him." Post-Mortem. — Cortex normal; in left temporo-sphenoidal lobe two large areas about two inches long and one inch wide, of gliomatous infiltration, in the upper one of which were a large number of hemorrhages with secondary degeneration. (e) Psychic Manifestations of Toxic Delirium.^" — In one of the author's cases ^'^ a toxic delirium was the most outspoken symp- tom. The patient, a single woman past the menopause, having just previous to her attack been impressed by accounts of the white slave trade, was obsessed by this during the whole of her illness until after the evacuation of the abscess. The author has knowledge of another case in which the toxic in- sanity caused the commitment of the patient to an insane asylum where she remained for several months. Although the attendant physicians were aware of her suffering from a discharging ear, no importance was attached to it until the post-mortem revealed a tem- poro-sphenoidal lobe abscess. (/) Uncinate Symptoms. — There are no cases on record of uncinate symptoms in temporo-sphenoidal lobe, but the author be- lieves this is due to a combination of vague mentality on the part of the patient and carelessness in the investigation of the history. The anatomical site of the temporo-sphenoidal lobe must so frequently involve the anterior poles of the lobe as to produce illusions of the sense of taste and of smell. CASE NO. XXIX. M. C. : Case of Brain Abscess Illustrating Transient Nature of Aphasia and Paralysis, with Apparent Complete Recovery without Operation; Sudden Exten- sion of Metastatic Abscess Five Months Later; Death. Male, 18 years of age. History.^April. Had had discharging right ear for 17 years, which caused no other symptoms until one month previous, when he complained of consider- able headache and had fever and several chills. He was seen by an ear specialist, who advised mastoid operation. Parents refused operation and family physician treated patient for a month for malaria because of chills and fever, although three blood examinations were negative for plasmodia. Operation; diseased mastoid, pre-sinus abscess, and apparently thrombosed sinus. The following day internal jugular resected and removed broken down clot from the sinus. After operation patient had two chills and persistent headache. Two days after operation complained that he saw double — -had to close his eyes in order to see well. (Undoubtedly had paralysis of internal rectus of left eye at this time.) This gradually disappeared. Temperature returned nearly to " Henderson, D. E., Mulrhead, W., and Fraser, J. S. : A Case of Toxic Exhaustive Insanity Associated with Chronic Suppurative Otitis Media, Labyrinthitis, and Extra- dural Abscess ; Review of Nearologv and PsyCMatry, Edinburgh, 1913, Vol. 17, pp. 565-576. " Case XVII, Miss M. D., Chapter Five, p. 77. 186 BEAIF ABSCESS normal; boy was thought to be recovering and was allowed to leave hospital, although complaining of headache. Suddenly developed pain in left ear; mastoid was opened; some creamy mate- rial found in cells. Some time later, in May, it was noticed that patient had weakness of lower portion of face on right side and that he talked with left side of face; but mother said he always had done so. A few days later patient suddenly became completely paralyzed on right side, both arm and leg being involved. When seen a few minutes after attack, hemiplegia was complete, and patient was aphasic. He knew what he wanted but was unable to name the object. When he wanted anything he would say, "I don't — I ," but when the name was suggested to him he recognized it. The paralysis lasted about an hour and then disappeared. When seen by the author within a few hours all signs of paralysis and aphasia had disappeared. Examination showed an intense papilloedema, with a swelling of 7 dioptres with hemorrhages and multiple spots of degeneration, "showing it to be an old papillitis." His palate went up toward the left side as if he had a, paralysis of the right palate. Diagnosis. — Abscess of the left temporo-sphenoidal lobe. Comment at Time of Examination. — "The patient immediately following his sinus thrombosis had an extension of the infection to the opposite side, and interference with the return circulation, or a free nidus was deposited in the vein of Galen. This caused the intense papilloedema and also the paralysis of the left rectus, from which !he then suffered,. I have never seen a papilloedema of 7 dioptres from an abscess alone. The present abscess must be an old one and have a capsule." Operation refused. July H; Patient presented himself at the office of the author, apparently in perfect health. For five weeks had had no symptoms whatsoever; no headache; had gained flesh and looked well. Examination. — Eyes. — Still has marked papilloedema of 4 dioptres — more marked in left — with multiple small hemorrhages and streaked spots in the retina such as seen in degeneration following a retinitis. y 200 y 40 Talks with left side of face, but mother says patient has always done so. Palate goes up to right side; tongue in median line; B patella reflex increased. Comment. — "The fact that the boy is now perfectly well would look as if he had an encapsulated abscess, or that the whole trouble had been vascular, from a plugging at the time of the original sinus thrombosis." Subsequent History. — Early in September patient returned from a pro- tracted stay in the country. He had now developed a paralysis of the left side. As the author had entered the Service the patient was taken to a hospital in New York City. Hospital Record. — Septemher 12; Physical Examination. Well nourished white man, age 18 years. Head; old scar over mastoids; swelling on top of skull. Neclc; old scar over right jugular vein. Face; paralysis on left side of face. Eyes; pupils equal and normal in size, react to light and accommodation. Nose; negative. Arms; paralysis of left arm and hand. Lrnigs; no dulness, breath sounds clear. Eewrt; no murmurs. AMomen; no tenderness. Blood ooimt; E.B. C, 4,800,000; H., 85; W. B. C, 25,000; P., 91; L., 9. ADJACENT TBMPOEO-SPHENOIDAL LOBE ABSCESS 187 Spinal Fluid Culture. — Cell count, 100; polynuclears, 75 per cent.; lymph- ocytes, 26 per cent.; Buty., 1+; Culture, Negative. Diagnosis.^AbseesB pocket on top of head; acute mastoiditis; meningitis. Operation. — Secondary radical mastoid; drainage of pus pocket. "There was a scar over old mastoid with small wound, unhealed. Posterior wall of middle ear found partially down from previous operation; many granu- lations in this region and also in the middle ear, and some free pus. Sinus was not pulsating; no definite avenue of access to the brain by infection found or determined; dura looked healthy. A transverse incision made into pus pocket on top of head at the junction of the coronal and parietal sutures; contained about four ounces thick, white pus; abscess and necrotic tissue cleaned out. September 13; Diagnosis, Brain Abscess. 0. D. Typical: Papillitis with change in retina suggestive of fatty change, especially around the region of macula, where they assume shape of a ring with the macula, the center also along the arteries. O. S. Typical: Papillitis with similar changes in the retina, only fatty degenerations are more disseminated. Changes along arteries. Pathological Findings. — Bone over centers of arm and leg on right side was softened; dura looked unhealthy and on incision much pus was evacuated. Spinal Fluid Cell count, 250. Butyric, positive. Scalp abscess culture negative. September H; Brain abscess culture, staphylococcus albus. 8eptem,ber 15; Spinal fluid, cc. 56; butyric, positive; polynuclears, 75 per cent.; lymphocytes, 25 per cent.; culture, negative. September 17; Spinal fluid cell count, 60; butyric, positive; culture, nega- tive. September 19; W. B. C, 20,000; polynuclears, 90 per cent. September 22; Death. Comment. — ^This case probably had an encapsulated left temporo-sphenoidal abscess and a thrombophlebitis which extended to the opposite side. Later the thrombus caused a separate intercurrent cortical abscess of the opposite side, which was drained, and which originated the meningitis from which he died. (g) Past Pointing. — There is some evidence to warrant the be- lief that the intracranial portion of the vestibular apparatus also may have one of its cortical centers in the temporo-sphenoidal lobe, al- though the evidence is so contradictory that it is possible the cortical center or centers for pointing deviations is situated in the frontal lobe. Temporo-sphenoidal lobe lesions give clinical manifestations only by an involvement of association tracts vphich pass through it in their course from the frontal lobe to the cerebellum, much in the same way that hemianopsia is produced. EoENTGEN Rat Diagnosis." Although many cases of brain abscess have been subjected to an X-ray examination, the following case is the only one recorded in which the findings were definitely diagnostic prior to evacuation. " Glegg, W., and Blacfe, H. : A Case of Roentgen Ray Diagnosis of a Chronic Cerebral Abscess Secondary to Frontal Sinus Suppuration; The Lanoet, 1915, No. 1, p. 124. 188 BRAIlSr ABSCESS The X-ray showed an area, semi-spherical in shape, of a shadow in the temporo-sphenoidal lobe. The shadow was due to the presence of gas in the upper part of the abscess, the result of micro-organic growth. (See Fig. No. 38.) ■ The X-ray was made when the patient was in a recumbent posi- tion. Post-mortem revealed the presence of anaerobic micro-organ- isms which produced bubbles of air and fluid, changing its shape with the change in position of the patient, the straight posterior line show- ing the level of the fluid. In such a condition a positive diagnosis of brain abscess was possible from an X-ray alone. This one expe- rience should encourage a routine X-ray examination of all cases of suspected brain abscess. Together with the experimental work of Dandy,^' moreover, in the injection of air into the ventricles, it should, in the author's opinion, encourage after evacuation the injection of air in different positions of the head through the drainage tube, followed by a routine X-ray examination in different positions of the head, to ascertain whether complete evacuation of the abscess has or has not occurred. as Muck ^° has demonstrated, the size of the abscess changes with alteration in the position of the head while in the sitting position. J. B. : Roentgen Ray Diagnosia. Male, 42 years of age. Patient admitted to hospital in stuporous condition; had had ©araehe for several days; no history of discharging ear. When brought to hospital was suffering with pain in left ear. No temperature; slow pulse. Lumbar puncture showed almost clear fluid; globulin, -| — |-, and high cell count — over 200 per field; many polynuclears ; direct smears showed no organisms. Slight double Kemig; no marked neck rigidity. Cleared mentally after puncture, but unable to talk. When seen two days later was in deep coma; Cheyne-Stokes respira- tion. Temperature, 99-100; pulse, which had been 60, had risen to 160. O. B., negative. Profuse discharge from left ear. X-ray showed shadowy area, semi-spheroidal in shape, directly above external auditory canal, the straight line of its base being nearly vertical to the external canal although slightly in front of it. The anterior portion was oval. Autopsy and Rbpoet by De. Haebison S. Maetland. On removing calvarium bone quite normal; the course of middle meningeal arteries had produced deep grooves in calvarium and there were a few small, rarefied areas in the bone. Dura normal over the top of cerebral hemispheres. On deflecting dura, which was tense, brain showed very marked picture of com- pression. Convolutions markedly flattened and sulci thin. The whole brain appeared dry. Small amount of subarachnoid yellowish exudate over superior surface of both cerebral hemispheres, mainly confined to regions near the longi- tudinal sinus and over the course of the middle cerebral arteries. " Dandy, W. B. : Localization or Elimination of Cerebral Tumors by Ventriculo- graphy; Surgery, Qynecalogy and Oiatetrice, April 20, 1920. =»See Note 35, Chapter IV, p. 57. Fig. 38. — X-ray photograph showing gas of anisrobic origin in cavity of temporo-sphenoidal lobe abscess. X-ray taken witjh patient in recumbent position. Straight line at base in "shadow" shows level of pus in abscess cavity — the gas tilling the upper (anterior) portion of cavity. Note typical location of cavity of adjacent temporo-sphenoidal lobe abscess as shown by the air filling its anterior one-third. Fig. 39. — Encapsulated adjacent temporo-splienoidal lobe abscess. Lower surface of brain removed, exjiosing abscess cavity, the anterior tliird of wliicli was filled with gas of bacterial formation, and produced a distinct shadow in the X-ray picture. (See Fig. 38.) ADJACENT TEMPOEO-SPHBNOIDAL LOBE ABSCESS 189 On removing brain left temporo-sphenoidal lobe was tightly compressed into left middle fossa and there were present recent fibrinous adhesions between inferior surface of lobe and posterior surface of left petrous portion of tem- poral bone. On breaking up these adhesions in removing brain, about 40 cc. of creamy, greenish-yellow pus escaped, and several large bubbles of gas. The large abscess cavity occupied two-thirds of left temporo-sphenoidal lobe; anterior end rounded, situated 3 cm. distant from anterior tip of lobe, opening 1 cm. in size on inferior surface of lobe. Total antero-posterior diameter of cavity 6 cm.; lateral width, 4 cm., and height, 2.5 cm. Inferior wall of abscess in thinnest place about 4 mm. thick, and in thickest areas about 1 cm., this being the distance separating the abscess cavity from the cortex of the brain. (Fig. 39.) Abscess cavity showed wall or capsule entirely surrounding it which had internal grayish-white layer uniformly about 1 mm. in thickness; clinging to its inner surface were purulent shreds which gave it a shaggy appearance; outer part of wall reddish in color, about 2 mm. thick, making a total thickness of 3 mm. Surrounding brain substance was slightly (edematous. Dura imme- diately over attic showed a small perforation, circular in shape, about 0.5 cm. in size, with necrotic and blackened edges; roof of attic, necrotic; attic, middle ear, and mastoids filled with fluid pus. Cultures from abscess showed rapid formation of gas. Type of anserobe not determined. Pus had distinctive odor, similar to that found in gangrene of the lung, which is characteristic of anaerobic infection. CHAPTEE XII. DIAGNOSIS OF CEKEBELLAK ABSCESS. Surgically considered, the cerebellar hemisplieres are largely "silent areas," as they can be extensively destroyed without produc- ing outspoken clinical manifestations. Cerebellar abscess, therefore, usually is much more difficult to localize than temporo-sphenoidal lobe abscess, because in the majority of cases there is an absence of the symptoms which justly may be regarded as pathognomonic, espe- cially during the early stages. Even when the abscess has attained considerable size, if its growth is slow it frequently is not associated with any symptoms that properly may be regarded as pathognomonic. This absence of localizing manifestation is due largely to the com- pensation in function which is established in the cerebellum more completely and with greater rapidity than in any other portion of the central nervous system. However, at any time during the growth of the abscess, symptoms may develop which may be sufficient to localize the suppuration in the cerebellum ; of these, spontaneous vertical nystagmus, spontaneous pointing deviation, falling, commanding vertigo, lateral deviation of the eyes, cerebellar attitude, and paresis of the arm and leg of the homolateral side are the most common. Unfortunately, none of these symptoms generally are present until symptoms of compression also have appeared. Consequently, during the early stages,, when surgi- cal interference is most promising, the diagnosis in the majority of cases must rest, not on the pathognomonic symptoms, but on the ability of the surgeon to combine (a) the manifestations of cerebral suppuration with (&) the probability of the suppuration being in the cerebellum (because of the existence of a suppurative disease of a structure by way of which the cerebellum usually is invaded), with (c) the exclusion of other possible sites of cerebral abscess, and (d) slight symptoms of impaired cerebellar function, into enough of a localizing cerebellar picture to warrant exploration. LOCAllZINQ VALTTE OF A KNOWN LABYRINTHITIS OB LATERAL SllTOS Thkombosis. Post-mortem examinations show that the path through which the cerebellum is invaded is by the labyrinth in 44 per cent, of the 190 DIAGNOSIS OF CEEEBELLAK ABSCESS 191 recorded cases, and by tlie perilabyrintih — caries of tlie petrous bone — in 18 per cent, more, making a total of 62 per cent, of all tbe recorded cases. Consequently, in tbe presence of a suspected localized cerebral suppuration, a non-reactable labyrinth is pre- sumptive evidence tbat the abscess is situated in tbe cerebellum. This is a clinical fact of the highest cerebellar localizing value. In several instances the author has made a diagnosis of cerebellar abscess — the patient being in deep coma — from the presence of chronic running ear, a mild associated papilloedema and inability to induce a nystagmus by the injection of cold water into the affected ear, the absence of reaction shovring a dead labyrinth. Again, post-mortem evidence and clinical experience both dem- onstrate that another large proportion of all the cases of cerebellar abscess — 33 per cent. — is secondary to a lateral sinus thrombosis.-^ While a lateral sinus thrombosis may cause an abscess in the cere- brum, .the proportion of such cases is very small. Consequently, with a suspected brain abscess the presence of a known lateral sinus thrombosis is at least suggestive that the abscess is in the cerebellum. Symptoms Moeb oe Less Chaeacteeistic ov Cekebeixae Abscess. Unlike temporo-sphenoidal lobe abscess, cerebellar abscess rarely presents in the early stages any symptoms which are absolutely pathognomonic; but careful and repeated examinations usually will elicit one or more symptoms which are of more than merely suggestive value. These may continue throughout the disease, or, what is more frequent, they may rapidly disappear. This is especially true of vertical nystagmus and lateral deviation of the eyes, both of which, when present, are definite indications of cerebellar involvement; al- though the former — ^vertical nystagmus — ^may occur from irritation of the cerebellum from a protective meningitis, the irritating cerebro- spinal fluid in the basal cisterna originating from a distant abscess situated in the cerebrum. Classificwtion: Cerebellar symptoms may be divided into I — ^Manifestations oe Impaieed Ceeebbllae Functions; (a) asynergia, or inco-ordmwtion of homolateral side — adiadoJcohine- sis; (b) homolateral "cerebellar paresis"; (c) forced cerehella/r attitude; (d) cerebellwr ataxia; (e) hypermetria. » See Appendix II, Cerebellar Abscess. 193 BEAIN ABSCESS II — ^Manifestations of Involvement of Ceeebbixab Poetions of thk Ves- TiBtTLAK Apparatus; (a) spontaneous or (b) induced abnormalities of (1) nystagmus, (2) vertigo, (3) past- pointing, and (4) falling. Ill — Manifestations fbom Direct Pressure; (a) cranial nerve symptoms — 9th, 10th, 11th, and 12th; (b) motor pyramidal tract sym,ptoms; (c) sensory tract symptoms; (d) sympathetic nerve symptoms — pupillary. IV — ^Manifestations of Transmitted Pressure from Induced Internai, Hydrocephalus. I— MANIFESTATIONS OF IMPAIRED CEREBELLAR FUNCTION EXCLU- SIVE OF THE VESTIBULAR TRACT. A better understanding of the clinical manifestations of cere- bellar abscess may be obtained by recalling a few physiological facts about the cerebellum : (A) The cerebellum is neither a motor nor a sensory, but may be regarded in a broad sense as a reflex organ, as it is by way of the cerebellum that certain sensory — peripheral — impulses influence muscular movement. The cerebellum is "related through its va- rious lobules to the various centers in the cerebrum and the tonus centers in the medulla, in the same way that a posterior root ganglion — sensory — is related (in a motor sense) through its motor cells in the anterior horn of the cord to a certain muscle complex." ^ While it does not in any way originate motion, the cerebellum exercises a synchronizing influence on muscular movements of the same side, largely by reacting to centripetal impulses; consequently, it acts as (a) a co-ordinator, (b) a regulator, and (c) an inhibitor. In experimental ablation of the cerebellum the primary oub standing symptoms are: (1) interference with the proper perform- ance of certain voluntary muscular movements of the trunk or extremities, depending upon the particular part of the cerebellum attacked, this interference affecting chiefly the same side as the experimental removal; and (2) an associated alteration in the muscles in a state of rest, especially during the early stages after the ablation. Experimental ablation of the cerebellum thus causes: (a) homolateral muscular asthenia or lack of strength; (b) homo- lateral muscular atonia or loss of tone; (c) homolateral muscular astasia or muscular unsteadiness — this being a combination of tremor, titubation (tottering) and rhythmical oscillatory movementa ' Myers, I. L. : Cerebellar Localization ; Transactions of the Section on Nervmis and Mentai Diseases, A. M. A.j 1916, p. 92. DIAGNOSIS OF CEEEBELLAE ABSCESS 193^ — and (d) hypermetria, or lack of proper muscular inhibition. Whether the hypermetria is part of the general muscular disturb- ance, or exists as an independent disturbance is not at yet fully established. All these cerebellar functions are intimately interwoven and probably all are parts of the disturbance of one function, muscular synergia — active sympathy or co-ordination.^ Consequently, a study of the clinical manifestations of cerebellar abscess results in all the symptoms being divided into : (a) disturbance of co-ordination, viz., asynergia, or inco-ordination, of which adiodokokinesis and ataxia are the best known; (b) disturbances of muscular tone, or atonia-^ rhythmic oscillations, tremors, or forced positions; (c) disturbances of inhibition of voluntary muscular movements — ^hypermetria. (B) In all cerebellar destructive lesions there are two stages; (1) the stage of exaltation of function, in contradistinction to the effect of invasion of the cerebrum, in which a suppurative process always is accompanied by a period of inhibition of function — such as the transient aphasia and hemianopsia of temporo-sphenoidal lobe abscess. On the other hand an invasion of any area of the cerebellum is associated with exaltation of function — such as cerebellar convul- sion or a sudden lateral deviation of the eyes.*' ' As the cerebellum is of low genetic origin, compensation from injury is easily established; consequently, following the stage of ex- altation, there is (2) the stage of compensation by the restoration of the functions in those muscular movements and position ordinarily employed, whatever impairment of function that may remain being manifest only on attempting little-used movements — such as balan- cing on one foot — or on the induction of a reflex (as an induced nystagmus). As cerebellar abscess usually develops slowly, these two stages frequently are present at the same time and it is impossible to dis- tinguish one from another. Although at a given moment there may be outspoken symptoms of cerebellar deficiency, the establishment of compensation may cause them rapidly to disappear, with the result that at the time of examination, the composite of the two stages may give little or no clinical manifestation of impaired cerebellar func- tion. It is the early establishment of compensation which makes the • Mills, Charles K., and Weisenburg, Theodore H. : Cerebellar symptoms and CerebeUar Localiisation ; Transactions of the Section on 'Nervous and Mental Disease; American Medical Assooiation, Atlantic City, June 23-26, 1914, p. 107. •Case XXXI, W. J., Chapter Twelve, p. 203. "Meyers, I. L. : Loo. oit. ("The phenomena of cerebellar deficiency are accord- ingly to be interpreted as phenomena of hyperfunctional and not hypofunctlonal activity,") 194 BEAIN ABSCESS diagnosis of cerebellar abscess so difficult and at the same time makes an altered or transient impairment of cerebellar function of diag- nostic importance. Paetiai. OB Complete Obliteea.tion' of a Symptom the Result of Ceeebedlae Compensation.' While it may be impossible to distinguish any one symptom as the direct result of compensation, the obliteration of the symptom by compensation should be regarded as the important thing in an attempt to interpret a vague cerebellar manifestation in the case of a suspected cerebellar abscess. Cerebellar Paralysis. — The cerebellum undoubtedly has control of the co-ordination of the muscular movements of the body as well as of the tonicity of the individual muscular group. It thus acts as a "reinforcing" station. For this reason the presence of a lesion within the cerebellum may produce an apparent muscular paralysis. Unless the pyramidal tract is invaded the paralysis is never complete and affects only the side of the body on which the lesion is located. Homolateral, incomplete paralysis, therefore, is an aid to the locali- zation of an abscess. When a true motor paralysis occurs in a cere- bellar lesion, it is due to the effect of transmitted pressure in the pyramidal tracts and not to involvement of the cerebellum itself. Cerebellar Ataxia. — Cerebellar ataxia is made up of three parts: muscular asthenia — ^loss of strength, or debility; muscular atonia — a lack of tone ; and muscular astasia, the latter being a com- bination of titubation, or tremor, with rhythmical oscillatory move- ments, and hypermetria, a lack of inhibition. Ataxia is but infrequently seen in cerebellar abscess because long before it has become of sufficient severity to be of diagnostic assist- ance, marked symptoms of compression have developed. The author is of the opinion, however, that a careful study of the "vertigo" so frequently classed as labyrinthine, chiefly because of the presence of a non-reactable labyrinth, would disclose evidences of cerebellar ataxia enough to warrant at least a suspicion of cerebellar involve- ment. Hypermetria — "Failure of Inhibition." — One of the functions of the cerebellum is inhibition of muscular movement. Whether this •Lndonl, Lul^: Htimcm Phyaiologji, 1915, Vol. Ill, Muscular and Nervous Sys- temEl, p. 481. ("Functional compensation Is tlie purposive and voluntary acts by whicn the effects of deficient or lost cerebellar Innervation Is abrogated.") Rossi, GUberto: AroMmio di flMologla, 1912, Vol. X, p. 251. (Tbe cerebrum also assists in the establishment of compensation, as "The immediate effect of heml- extlrpatlon of a dog's cerebellum Is diminution of excitability in the motor cortical area of the opposite hemisphere.") Quoted by Luciaul in Human Phyaiologu, 1915, Vol. Ill, p. 483. DIAGITOSIS OF CEEEBELLAE ABSCESS 195 is intimately related to, or really is a part of the other functions of this part of the brain — synergia, tonia, co-ordination, and so on — has not been definitely established. In one of the author's cases a test of the past-pointing of the homolateral side revealed the inability of the patient to control the backward movements of his arm. He invariably brought the arm so far back that it struck the bar at the top of the bed with sufficient force to cause pain — an evidence of hypermetria. There was also a lack of co-ordination laterally, yet he could touch the fingers together fairly well. On operation it was found that the abscess was 3 cm. inward and upward, probably involving the arm center; there^ fore, the asynergia, or inability to synchronize the movements of the joints and muscles, was in the arm or shoulder (probably in the latter). Cerebellar Convulsions. — ^Experimentally, on the removal of certain parts of the cerebellum there follow oscillatory or contractile movements of the homolateral side, resulting in a to and fro move- ment of the head or a forced position of the trunk. On superficial cauterization of the same cerebellar region, however, a similar condi- tion occurs on the opposite side of the animal.'' Whether this phe- nomenon is due to irritation or to the removal of inhibitions is still in dispute. While convulsions are of but infrequent occurrence in tumors of the posterior fossa,^ they are frequently associated with cerebellar abscess. Forced Cerebellar Attitude. — Lying on one side in a semi- flexed attitude is frequent in cerebellar abscess during the stage of compression. Its presence prior to this stage is of the first diagnostic importance even though it be imperfectly developed. Likewise, a lateral deviation of the eyes occurring prior to compression should be regarded as a forced cerebellar position. The lateral deviation of the eyes observed in Case No. XXXI, W. J., Chapter Twelve, p. 203, following a convulsion was a manifestation of the "sustained tonicity" which is characteristic of cerebellar convulsive movements. In sev- eral other of the author's cases a forced position on one side — has been the guiding diagnostic manifestation. Speech Defects. — A dysarthria — a scanning or ataxic speech — is a frequent manifestation of cerebellar abscess. It is one of the many manifestations of muscular inco-ordination. ' Ferrier : See Luelani, Human Phygioloffv, Vol. Ill, Muscular and Nervous Sys- tems, p. 434, • McKobert, R. G., and Feinier, Laurent : Cerebellar Fits ; Archwee of Neurology and Psychiatry, March, 1921, Vol. V, p. 304. 196 BEAIK ABSCESS II_VESTIBULAR MANIFESTATIONS. Unfortunately, the same vestibular syndrome — spontaneous nystagmus, past-pointing, and falling — ^wMch always accompanies acute labyrinthitis, is also produced by an acute, destructive lesion of the cerebellum, and as cerebellar abscess in a large proportion of the cases is a complication of a suppurative labyrinthitis, differentiation is thereby rendered difficult. To be fully successful the attempt to differentiate must be made immediately upon the appearance of any one of the symptoms common to both, for while theoretically there are many points of difference between the vestibular manifestations of a suppurative labyrinthitis and an intracranial involvement ^ (the falling, for instance, in a labyrinthine involvement being in- fluenced by a change of position of the head while in a cerebellar lesion it is not), in actual practice such is the case only when the cerebellar lesion is acute, limited and destructive. In cerebellar abscess, however, the slow growth may allow ample time for the re- establishment of compensation, with the result that at the time of examination either no vestibular symptoms may be present at all or they will be so modified as to have lost their distinctive cerebellar characteristics. If assistance in the early diagnosis of cerebellar abscess is to be obtained from the vestibular manifestations it can be accomplished only by repeated observations, and recording at the time of observation, all data as well as all vestibular manifestations normal and abnormal, for in this way alone a changing character will be appreciated. If to-day no nystagmus is present in the recum- bent or in the erect position, and to-morrow there is a slight nystagmus to the right in the same position, and on the following day it is again absent or has changed to a slight nystagmus to the left, the record of the three days may make an early diagnosis possible, while failure to record one or the other manifestation at the moment of observation may result in doubt. DiFFEBENTIAl, VALUE OF MODB OF OnSBI. In acute labyrinthitis the onset of the suppuration is sudden and complete, the limited area of the bony capsule causing a complete inhibition of function. The spontaneous nystagmus, past-pointing, and falling, all appear at the same time; and as compensation is established the symptoms individually and gradually disappear, first the nystagmus, then the falling, and last of all the past-pointing. In cerebellar abscess, on the other hand, there is a disproportion in the complete onset and the progressive disappearance of the • Moulouquet, A. : Cerebellar Abscess of Aural Origin ; The Lancet, 1921, I, p. 283. (States "In cerebeUar abscess the disturbances are more equilibrating than vertiginous, Willie in labyrinth disease It Is the vertiginous character which predominates.") DIAGNOSIS OF CBREBELLAE ABSCESS 197 symptoms. Consequently, an incomplete onset is of especial im- portance in diagnosing a cerebellar lesion. Spontaiteous Ntstagmus. The spontaneous nystagmus of cerebellar abscess is apt to be tran- sient and of changing character during the early stages. It is also of a somewhat different type from that of involvement of the labyrinth. The nystagmus of cerebellar abscess, being due to asynergia of the ocular muscles, is in consequence more or less oscillatory in nature, while the nystagmus of vestibular origin is rhythmic.^** Cerebellar nystagmus usually is toward the side of the lesion, with a vertical tendency. Too much attention should not be paid to this, however, as the ease with which the cerebellum establishes compensation not only may alter the character of the nystagmus but may eliminate it alto- gether. Lateeal Deviation of the Eyes. Lateral deviation — the cerebellar component of a nystagmus — generally occurs when compression or destruction is sufficient to cause an abolition of the cerebral control. The author is of the opinion that compression sufficient to cause coma and lateral devia- tion is much more easily induced in cerebellar than in cerebral abscess. When an otitis media is the primary focus of a brain abscess the appearance of a lateral deviation of the eyes should be regarded as evidence that the posterior fossa is the site of the infec- tion since an adjacent temporo-sphenoidal lobe abscess can not cause a spontaneous lateral deviation of the eyes. Vertigo, Spontai^eous Faixinq and Spontaneous Past-Pointing. The combination of vertigo and falling with marked nystagmus so frequently seen in cerebellar pontine angle tumors is rarely pres- ent in the early stages of cerebellar abscess, or if present is so com- plicated by disease of the labyrinth as to make interpretation difficult. (a) Vertigo: While a symptom of disease of the labyrinth with- out intracranial involvement, vertigo frequently is the only outstand- ing indication of cerebellar abscess as it occurs as a marked symptom in about one-third of the cases. ^^ Contrary to the generally accepted '° Wilson, J. Gordon, and Pike, F. H. : Mechanism of Labyrinthine Nystagmus and its Modification by Lesions in the Cerebellum and Cerebrum. An Experimental Investigation ; Oxford Univeraity Presg, Henry B^owde, 1914. Also Journal American Medical Aaaodatum, December 18, 1915, Vol. 65, p. 2156. M Dench, Edward Bradford : Otitic Brain Abscess ; Reprint from, Amerioan Journal of Medical ScAeneeg, November, 1907, p. 3. 198 BEAIN ABSCESS view vertigo may be entirely absent in tlie early stages of the dis- ease.^^ Spontaneous vertigo may be of localizing value, as inability to alter tbe vertigo by the application of caloric and rotating tests is presumptive evidence that the lesion is in the cerebellum. (b) Falling: Physiologically, it would be expected that in abscess of a cerebellar hemisphere falling when present would be toward the side of the lesion and would not be influenced by changing the position of the head. Due to the establishment of compensation by the cerebellum, however, the direction and the type, and even the presence of falling may promptly be altered or abolished. In one of the author's cases of adjacent cerebellar abscess the falling was backward and away from the lesion; but so many cases are recorded in which the falling is similarly paradoxical and even in- fluenced by a change in the position of the head,^^ that, like nystag- mus, it must lose its clinical localizing signiflcance. When the vermis primarily is involved — a rare situation in cerebellar abscess except in metastatic cases — the falling probably would be backward. (c) Spontaneous Past-Pointing Deviations: Spontaneous point- ing deviations occur in the early stages of brain abscess, but abnor- malities are so frequent that they cannot be considered as symptoms of great localizing value. Induced Abnormal Vestibitlab Reactions. Too much reliance has been placed upon the value of one com- plete examination of induced vestibular reactions in locating the presence of, or eliminating the cerebellum as the site of an abscess, as clinical experience has demonstrated that only by repeated tests can the functioning of the cerebellum be shown to be in perfect order. ^* The tests must be made before the patient becomes dulled. The author's experience has been that all patients — even small children — can be subjected to the tests provided the examiner will devote sufficient time and patience to making them. " Case XII, W. K., Chapter Four, p. 60. " Rohardt, W. : Ueber Zeige und Fallreaktionen bel Kleinhirnkranken ; Zeitachrift fUr die ffes. aeuralogie und, Fsydhiatrie, 1919, VoL 49-50, p. 167. ^* Reported Oases o/ Cerehellar Abscess &imng Spontanemis and Induced Vestibular Reaction and Demonstrating their Changing and Bizarre Character. Hohngren, G. : Opererad oeh lakt liUhjarnabseess med skada a ett ave Barany'a centra ; SiiensMi LUkaresiillskapets Handlingas, 1916, Vol. XLII, p. 516. Jones, I.: Equilibrium and Vertigo; 1918, p. 369 (Case by Pislier). Hill, Frederick Thayer: Report of a Case of Cerebellar Abscess Following Shell Wound of Skull and Showing No Symptoms for Period of Five Months; Military Surgeon, September, 1919. Rohardt, TO. : Ueber Zelge and Fallreaktionen bel Kleinhirnkranken ; Zeitachrift filr die ges. Neurolagie und Psychiatrie, 1919, Vol. 49-50, p. 167. Jessaman, L. W. : Brain Abscess as a Complication of Acute Infection of Nasal Accessory Sinus; La/ryngoscope, March, 1920,' Vol. XXX, No. 3, pp. 147-149. Martin, H. H., and Crowe, S. J. : Lateral Sinus Disease — Case Report ; Lan/nao- scope, December, 1920. \ DIAGNOSIS OF CEREBELLAE ABSCESS 199 Cri^QiNG Characteb of Abnoemal Spontaneous ob Induced Veshbulab \ Manifestations. The author's experience leads him to believe that there is no set formula for the diagnosis of cerebellar abscess by abnormalities of the vestibular reactions alone, but that the induced reactions, like the spontaneous manifestations, are apt to be of a very changing nature, especially during the early stages of the disease. This changing character he has come to regard as highly suggestive of cerebellar involvement. In one of his cases ^' the only symptom present at the time of examination was an abnormal falling; there was no spontaneous nystagmus, and aside from the falling, the vestibular reactions apparently were normal; but suddenly the patient had a convulsion, followed by a lateral deviation of the eyes. Small, acute, and destructive lesions, such as hemorrhages in- volving the so-called "vestibular pathways," will produce symptoms or give localizing manifestations; but cerebellar abscess is a gross lesion which at the time of examination generally has progressed slowly to the point of giving rise to an increased intracranial pres- sure, not only of the posterior fossa but also of the whole intra- cranial contents. During the slow, progressive growth of a cere- bellar abscess the cranial contents have had ample time for read- justment — ^the establishment of compensation. This compensation the vestibular apparatus — one of the most primitive of the special senses — is especially able readily and easily to accomplish; with the result that at the time of examination no diagnostic abnor- malities of induced vestibular reactions may be present, while the vestibular manifestcdions of the increased intracranial pressure over- shadow and obscure all others. For several reasons not yet fully explained an increase of intracranial pressure interferes with the reactability of the intracranial portion of the fibres of the vertical canals of both ears long before the fibers to the horizontal canals are affected. Whether this affection occurs on the auditory canal itself, or in the intracranial portion, is not definitely established, but it is probably in the latter. Diagnosis of Increased Inteackanial Peessube, Especially of the Postebiob Fossa, by Induced Vestibulae Eeactions. The outspoken vestibular manifestation of increased intracranial pressure — absence of reactability of the vertical canals of both ears to " Case XXXI, W. J., Cliapter Twelve, p. 203. SOO BEAIN" ABSCESS the cold caloric — ^first described and properly interpreted by tbe author,^' while an early manifestation of increased intracranial pres- sure prevents an accurate localization by the vestibular reactions alone. It is of the greatest value, however, in the early diagnosis of increased intracranial pressure as it appears long before and inde- pendently of papilloedema. Its assistance in the diagnosis of cerebellar abscess by demon- strating an increased intracranial pressure cannot be over-emphasized. As the result of many vestibular examinations and subsequent lumbar punctures for diagnosing obscure nervous diseases, the author testi- fies that the vestibular manifestations of increased intracranial pres- sure are uniformly the earliest symptom present and consequently the most valuable as yet known. CESEBEILLAB COBTICAl liOOAlIZATIOIT IN RELATION TO VESTIBTILAB EEACHON. Horsley and Clark ^"^ demonstrated that the cerebellar cortex con- tains no areas which are irritable by the faradic current, such as exist in the motor areas of the cerebrum. When muscular contrac- tion occurs from such irritation it is due to involvement of the deep ganglia. There is, however, considerable experimental and clinical evidence to substantiate Barany's contention ^* that the cortex of the cerebellum contains areas the destruction of which — or pressure upon them — causes alteration in the ability to execute certain voluntary movements properly. IXDUOED VESTIBXTLAB MANIFESTATION EEOM PeESSUBE UPON THE CEEEBELLAB COETEX. The author has observed that pressure from a protective exudate over the anterior surface of the cerebellum opposite the internal auditory meatus uniformly results in (a) an immediate reduction of the duration of the obtainable nystagmus from the horizontal canals by turning, and (b) a great reduction, or complete absence, of irritability of the superior vertical canals of both sides on the ap- >• Bagleton, W. P. : Decompression for Kelief of Disturbances of the Auditory Apparatus of Intracranial Origin — Report of Three Cases with a Previously Unde- scrlbed Aural Condition ; Tramactlons American Otological Society, June 10, 1912, Part III, p. 564. Also Laryngoscope, 1913, Vol. XXII, p. 592. " Horsley and Clark : On the Intrinsic Fibers of the Cerebellum, its Nuclei and its Different Tracts; Braiki, 1908, Vol. XXXI, p. 138. (Quoted by Lucianl, in Human physiology, 1915, Vol. Ill, Muscular and Nervous Systems, p. 484.) " Barany, R. : The Vestibular Apparatus and the Central Nervous System ; Laryngoscope, 1912, Vol. XXII, p. 81, demonstrated that the cooling of "small areas of the cerebellar cortex situated directly behind the attachment of the external ear," results In a spontaneous past-pointing of the arm outward, from, he believes, a paralysis of the inward pointing centre, while cooling an adjacent area causes a spon- taneous past-pointing imeard. DIAGNOSIS OF CEREBELLAE ABSCESS 201 plication of the cold caloric/® the latter from increase of the intra- cranial pressure. If this interpretation of the clinical observation is correct, the vestibular symptom complex — viz., reduction by about 50 per cent, of the normally obtainable nystagmus from pressure on the cerebellar cortex opposite the internal auditory — should render pos- sible an early diagnosis of intrapiarachnoid abscess of the anterior surface of the cerebellum (the most frequent site of intrapiarachnoid abscess from labyrinth suppuration). Ill— LOCAL SYMPTOMS FROM DIRECT PRESSURE PRESUMPTIVE OF CEREBELLAR ORIGIN. (a) Hyperesthesia, of the face and diminution of the corneal re- flex on homolateral side — fifth nerve involvement; (b) Deviation of tongue — twelfth nerve involvem^ent. Deviation of the tongue may be due to direct pressure or it may be due to involvement of the nucleus of the twelfth in the medulla or of the supra-nuclear pathway. In the former case the tongue will deviate away from the side of the lesion and in the latter toward it. Absence of corneal reflex probably is due to direct pressure as it occurs on the side of the lesion. It probably is caused by pressure of the upper fibres of the sensory root against the firm dural opening where the root passes out of the posterior fossa into the Meckel's space. On the involvement of the ninth — the glosso-pharyngeal — the author's only experience was in one case, in which the patient com- plained of difficulty in swallowing. The respiratory and circulatory disturbances of the tenth hardly can be expected to be elicited in cerebellar abscess. PUKLLAEY DiSTUBBANCES. The dilatation of the pupil so frequently seen in cerebellar abscess is due more to action of the toxemia upon the sympathetic centers than to any direct effect of the abscess. Geneeal Symptoms Suggestive of Cebebellab Involvement. (a) Suboccipital tenderness and rigidity of neck; (b) Yawning; "(a) Eagleton, W. P.: Aural Manifestations in Surreal Intracranial Lesions; Address before OlinAcal Congress oj Surgeons, Fhiladelpliia, Oct. 25, 1921. (b) Eagle- ton, W. P. : Value of Vestibular Manifestations In Surgical Intracranial Conditions — with Report of Four Cases; Address Annual American Laryngological, Rhinologicai and OMogical Soeiety, Atlantic City, June, 1921. 203 BRAIN ABSCESS (c) Rapid loss of flesh; (d) Alteration in Icnee jerks; (e) Projectile vomiting; (f ) Psychic disturbances and cerebellar fits. Suboccipital Tenderness. — Gushing and Grey ^° have called attention to the greater frequency of suboccipital tenderness in cere- bellar than in cerebral tumors. The author's experience would lead him to believe that this is also the case in cerebellar abscess. Yawning. — Although yawning frequently is present in suppura- tive disease of any part of the brain, in the author's experience it is more marked in cerebellar abscess than in abscess in other regions. Rapid Loss of Flesh. — Emaciation in cerebellar abscess is much more rapid than in suppuration in other parts of the brain.^^ It is partially due to the effect of the cerebral suppuration in disturbing the general metabolism. In cerebellar cases, however, there is added more or less of a specific action from the disturbance of the trophic reactions presided over or reinforced by the cerebellum, which results in a rapid emaciation. When the abscess becomes completely encap- sulated and quiescent, the emaciation stops. In the presence of a probable cerebral suppuration the author has come to regard rapid emaciation as suggestive of cerebellar abscess. Experimentally, in- jury to the cerebellum results in "retarded growth of the cutaneous elements, particularly of the skin, and the lowering of resistance to the injurious action of external agents." ^^ Knee Jerks, — Alteration in the patella reflexes depends upon the involvement of the pyramidal tracts; it generally occurs on the homolateral side, but it may be bilateral. Vomiting. — Vomiting is much more sudden and severe in cere- bellar abscess than in abscess in other locations. In the author's experience in the presence of a suspected localized cerebral suppura- tion, continuous projectile vomiting is suggestive of cerebellar abscess. Psychic Disturbances. — In the presence of compression there always occurs a cloudiness of the sensorium — ^poor perception and at- tention — and possibly disorientation for time and place.^^ In intra- cerebellar abscess the author has found a certain degree of optimism in the patient which is not warranted by his physical condition. In " Grey, Ernest G. : Studies on the Localization of Cerebellar Tumors ; BepHnted from Annals oj Surgery, February, 1916. "Luclanl, Lulgl: Humcm Physiology, 1915, Vol. Ill, Muscular and Nervous Systems, p. 472. =' Lucianl, Lulgl : Loo. dt. " Mlngazzim, G. : Abscess e Tumori del Encefalo ; Elv. di Patol., Nov., 1919, Part 3-4 and 5-8. Abstracted In Arohimea of Neurology and PaycMatry, 1919, Vol. 2. DIAGNOSIS OF CEREBBLLAE ABSCESS 203 one of his cases the patient, throughout his illness aud even when dying, continued to insist that he felt fairly well. IV— SYMPTOMS DUE TO AN ACCOMPANYING INTERNAL HYDEOCEPHALUS. On account of its position in the posterior fossa, cerebellar abscess is much more frequently associated with an internal hydro- cephalus from obstruction by pressure and displacement of the iter, than is an abscess in any other portion of the brain. Stupor, altera- tions in the reflexes, epileptiform seizures, intense and paroxysmal headaches, sub-occipital tenderness, opisthotonos, sugar in the urine, vomiting — all are frequent and all, partially at least, originate from the internal hydrocephalus; while the marked papillcedema of cere- bellar abscess is, in the author's opinion, entirely of this origin, the distance of the site of the suppuration away from the optic nerve being best explainable by the induced internal hydrocephalus. To this group belong also the sixth nerve paralysis, from pressure, as the nerve passes over the apex of the petrous base in its separate dural compartment. Third nerve paralysis probably is from pres- sure exerted between the internal carotid and the distended floor of the third ventricle and the intra-chiasmal cisterna. The slight exophthalmos very rarely seen in cerebellar abscess probably originates from the pressure of the internal hydrocephalus, and the hyperesthesia of the fifth probably has a similar origin. CASH NO. XXXI. W. J.: Case of cerebellar abscess, Illustrating vagueness of early symptoms, followed by remission of all symptoms ; then sixth nerve paralysis. No localizing symptoms whatsoever until nineteenth day, when suffered from dizziness for first time. Tempero-sphenoidal lohe exploration from, erroneous diagnosis. Sudden onset of marked cerebellar manifestations; several incomplete cerebellar evacuations. Changing character of vestibular manifestations. Extension of abscess. Autopsy. — ^Multilocular abscesses of cerebellum. History. — Boy. March 1 : Cold, accompanied by pain in right ear, followed by discharge. March 12: Mastoid operation. March 23: Severe headache through forehead and back of head, thought to be due from chilling from sudden change in weather. Invasion of cerebellum undoubtedly occurred at this time. Ma/rch 24-29: Perfectly well. March 30: General malaise and "some fever." March Sl-April 3: Again perfectly well. April 4: Nauseated; from this date was never entirely well. April 5: Sudden double vision; which caused slight feeling of unsteadiness which disappeared upon closing one eye. Nosebleed. 204 BRAIN ABSCESS April 6: Vomited; nose bleed; felt well enough to go to physician's office for dressing. April 8: Vomited; tongue coated; severe parieto-oecipital headache; con- fined to bed. For first time looks ill. April 11: Lumbar puncture; fluid clear, not under pressure; Fehling's reduced; low cell count, 5; vomited after lumbar puncture. April 12: Admitted to hospital, complaining of headache, vomiting, double vision. To-day has had first attack of real dizziness (nineteen days after cere- bellar involvement). "When he turns in bed feels sick at stomach." Slight aching in right shoulder and right hip. Patient thinks there is a slight weak- ness in right leg, "especially since having needle inserted into him" — the lumbar puncture. Examination. — Memory good; has rather "dopey'' manner; answers ques- tions intelligently but in a low voice. Brightens up on being questioned; speech rather thick as though tongue were thick; patient says he has noticed change himself — that he cannot pronounce words as rapidly as he should. Thinks it is due to the thick coating on his tongue. April 13: Pulse 84-90; complained of severe pain in head. Examination to-day shows slight nystagmus on looking toward extreme right (this is the first suspicion of any nystagmus since the beginning of his illness). Hears with his right ear. April IJf: Lumbar puncture, fluid clear. Fehling's reduced normally, cell count 57 per cm.; no organisms. Diagnosis, probable abscess of the temporo- sphenoidal lobe with capsule, because vestibular reactions apparently demon- strated increased intracranial pressure with an intact cerebellum. Resume: An absence of vestibular reaction of his vertical canal and a normal reaction to the horizontal. Operation. — Temporo-sphenoidal lobe exploration; no pus but accidental tapping of the lateral ventricle. On account of the puncture going into the ven- tricle at a very short distance, decided that patient either had a serous meningitis, or that he had a cerebellar abscess. Condition at the completion of the operation very bad; pulse very fast; decided not to explore the cerebellum until he had time to recover. April 16: Pulse 80; has vomited several times. April 17: Restless; complains of severe pains in temples. Lumbar punc- ture 15 cc. fluid clear, cell count 118; Fehling's reduced normally. April 18: Had a convulsion. Became unconscious, following which had lateral deviation of eyes to left ( away from the site of the lesion ) . Left eye now looks down and out. Co-ordination, right hand not so good as left, tongue apparently protrudes to the right. A Romberg; Operation. Cerebellar Exploration. — April '18: Ligation of lateral sinus. Area of caries in the posterior portion of the petrous pyramid exposed, from which infection had entered the cerebellum. Encapsulated abscess, located at distance of 3 cm. from cortex. Slow evacuation through small exploring canula. Smear from abscess showed streptococcus and Gram positive, bacillus and sarcinse. Operative comments: "The abscess is probably much larger than evacuated; a larger exploring canula should have been used. The abscess was apparently 'lost' before complete evacuation. Patient stood the ether very well, which is remarkable, as at the previous operation he nearly died on the table, and to-day he is in very much worse physical condition. This may be explained by the accidental tapping of the ventricle and the relief of pressure at the previous operation.'' April 21: Evacuation; marked nystagmus on looking toward the right — toward the lesion, while previous to the evacuation he had a lateral deviation of both eyes to the left. Patient now in excellent mental condition. DIAGNOSIS OF CEEBBELLAR ABSCESS 205 April ZS: Abscess apparently not evacuated completely. Patient in rery good condition but sweats too much. Still has a marked spontaneous nystagmus, which has a tendency to be vertical in character. April 26: Patient has become more and more drowsy; has nystagmus; can- not tell whether it is to the right or to the left, but it certainly has a vertical tendency up and down. No choked disc, undoubtedly because he has such a large decompression. Marked hypermetria of the right arm. Operation. — Evacuation of abscess well up toward the tentorium and in the anterior portion of the cerebellum. May 1 : Patient vomited for first time since April 24th ; recurrence of head- ache. No rise in temperature; pulse 82; culture from abscess streptococcus proteus. May 2: Mild papilloedema of right eye; left n^ative. Head back, slight nystagmus to left in outer corner. Spontaneous past pointing both hands ele- vated slightly to left spontaneously. Head erect, no perceptible spontaneous nystagmus; spontaneous past pointing; tendency of right hand to deviate to right; left deviates to left. May 6: Still indistinctness of upper margin of right disc, but much less than three days ago. Still incoordination of right arm, fingers to nose test. Rotates right hand much slower. Spontameoiis nystagmus becomes marked on changing position. During the whole of this time patient remained in a rather apathetic con- dition, saying he felt pretty well, but having a tendency to sleep, the sleep not being of a natural type. May 13: Erect position; spontaneous nystagmus on looking up, but not so marked on looking to right — side of lesion, but marked on looking to left — away froon lesion. Legs: touches hand with left toe, but right leg shows incoordination. Astereognosis. O. E. : right eye, indistinctness toward nasal side. Left eye may be slightly hazy above. Pupils large in proportion to amount of light in room,, but react promptly. No Babinski, no Oppenheim. Speech slow and rather cut off — ^talking somewhat like a Chinaman, without proper modula- tions, in a monotonous tone. Repeats and fumbles over parts of words — then repeats the word and goes on again. Tongue protrudes slightly to the right side — side of lesion; when sits up sways (trunk muscles involved); slight dizziness. All signs of extension of cerebellar suppuration. May H to July 3: Abscess evacuated on several occasions. Increasing stupor. Death. Post-Mortem Notes. — ^Autopsy and report by Dr. F. A. Sutton. Dura over right cerebellar area adherent. Considerable pus. The right cerebellar lobe little more than a shell. The abscess cavity extending over beyond the median line into, the left lobe and almost through the cortex on the superior surface. On dissecting cerebellum there were several cavities containing from one-half to a dram and one-half of pus. The abscesses resulted in almost complete destruction of the right cerebellar lobe and practically one-half left lobe of cerebellum. The drainage was not complete because the abscess was multi- locular. Several small harder areas near the surface of the cerebellum, consisted of normal brain tissue surrounded by blood vessels. Lateral ventricles free. The third ventricle slightly distended with fiuid. OHAPTEE XIII. DIAGNOSIS OF FKONTAL LOBE ABSCESS. Frontal lobe abscess is the most difficult of all types of abscess to diagnose, (1) because the symptoms usually present in acute and chronic frontal sinus or ethmoid disease closely simulate those of frontal lobe abscess; (2) because the region of the frontal lobes in- volved in adjacent abscess is a "silent area" and consequently there are but seldom any definite manifestations of cerebral involvement; (3) because of the small space occupied by the frontal lobe, the abscess does not attain to any considerable size before it ruptures into the ventricles or the subarachnoid space. An examination of the recorded cases of frontal lobe abscess (see Appendix III, Frontal Lobe), reveals that a large proportion were not diagnosed during life, a sudden and fatal termination having occurred as the result of rupture of the abscess. Therefore, if the diagnosis is to be surgically useful, it must be made before the signs of compression have appeared, since a frontal lobe abscess usually does not give signs of compression, at least not until immediately before the fatal termination. An early diagnosis of frontal lobe abscess is made possible only by a systematic method of reasoning, together with repeated and thorough examinations, with minute attention to certain small details This is especially true if the abscess is latent and of small size. The diagnosis must depend largely upon: (1) the presence of a known point of infection which is apt to cause an abscess of the frontal lobe — in the frontal sinus, the ethmoids or the orbit; (2) the history of an acute invasion or an acute exacerbation of a chronic suppuration— tenderness, redness of the external frontal wall, orbital phlegmon, or trauma, accidental or operative — since such irregtdari- ties are more or less constantly present; and (3) the general symp- toms of cerebral suppuration. Orbital Abscess, Osteomyelitis and Extradural Abscess — Dispro- portion; value of. — The presence of any one of these conditions pre- supposes a possibility of a frontal lobe abscess. When associated with symptoms disproportionate to the known lesion, or with symp- toms of cerebral suppuration, they call for exploration within the 206 DIAGNOSIS OP FRONTAL LOBE ABSCESS 207 dura. The scar of a traumatic woiiiid of the frontal sinus, followed by headache, should presuppose frontal lobe suppuration. Many cases of frontal lobe abscess subsequent to an injury, are on record, in which careful examinations have failed to reveal any mental dis- turbance or psychic effect, the only symptoms present being head- ache, insomnia and anorexia — ^general symptoms of cerebral sup- puration. Symptoms of Cerebral Suppuration. — There is a certain look about the patient which, to the trained eye, is very significant; the tongue is coated, the skin dry, there is loss of flesh, and the leucocyte count is high. Headache is uniformly present and in many cases is the only symptom. It frequently dates from an acute exacerbation of a chronic frontal sinusitis, and if so should be always regarded with suspicion. The headache may be continuous or intermittent, but it is of a more severe type than that which occurs with frontal sinus suppuration alone. If, to the above, is added vomiting, and if the cerebro-spinal fluid frona a lumbar puncture gives a high cell count, exploration of the frontal lobe is indicated. The cerebral explora- tion should precede, not follow, an operation upon the accessory sinuses. On the other hand if an extradural abscess is accidentally located at the time of a sinus operation, the existence of an associated intra- dural abscess would be suggested. Convulsions.— In the author's opinion convulsions are positive evidence of intracranial involvement. While it is possible that a convulsion may occur from a protective piarachnoid accumulation, when the sinus has been opened or free nasal drainage has been estab- lished, the occurrence of convulsions should be regarded as distinct evidence that the disease has extended beyond the accessory sinuses themselves. The oases of cerebral symptoms which have been cleared up by operations on the frontal sinus are due to "serous meningitis" of toxic origin. Diabetes Insipidus. — Foerster ^ calls attention to the appearance and development of diabetes insipidus in serous meningitis. As it cannot occur from an acute sinus disease alone, it should be classi- fied among the symptoms of cerebral origin. Symptoms of CEasEBEAL Compeession. Coma. — The coma of frontal lobe abscess is somewhat different from the coma seen in general cerebral compression. It simulates '■ Foerster : Munich, med. Wochenschrift, 1918. 208 BEAIN ABSCESS normal sleep more than the coma of suppuration in other parts of the brain. ^ In one of the author's cases this so-called "frontal-lobe coma" was present for several weeks. At the autopsy one of the ventricles was found to be distended with pus. Papilloedema. — If papillcedema were caused by direct pressure it would be of frequent occurrence in frontal lobe abscess. Such is not the case, however. In frontal lobe abscess papillcedema is rarely present.*' *• ° An examination of the records of over one hundred cases of frontal lobe abscess shows only three to have exhibited definite nerve head changes, all associated with symptoms of compression. The almost uniform absence of papil- lcedema in frontal lobe abscess is due to the fact papillcedema is largely dependent upon an obstruction of the central cerebro-spinal fluid circulatory system. The situation of a frontal lobe abscess causes no such obstruction. It is not unusual, however, to have papillcedema appear immediately upon the evacuation of the abscess, which demonstrates that the trauma of the operation furnishes a factor necessary to the produc- tion of papillcedema, although the increased intracranial pressure had been relieved. Post-Neubitic Retrobulbar NEURrris. The author has seen one case of the retrobulbar neuritis described by Ken- nedy" in a frontal lobe tumor; it is not recorded in any case of abscess of the frontal lobe. Localizing Symptoms. (a) Loss of Smell. — Loss of the sense of smell on the affected side probably occurs very frequently. If present it is of distinct diagnostic value. (b) Aphasia. — In frontal lobe abscess aphasia occurs only when the abscess has attained considerable size. At first it is apt to be transient, due probably to an extension of oedema to the Island of Eeil. In many of the recorded cases of frontal lobe abscess of the left side, associated with paresis or paralysis of the arm of the op- posite side, motor aphasia has been the first symptom. ' Milian, G. : Le Coma Frontal ; PaHa Medical, 1920, Vol. X, No. 40, page 256. ' Denker, A. : Ehinogener Frontallappenabszess : ArcMv fur iMryngol, und Bhinol., 1900, X, S. 411. Blurring of the left disc; pulse 55-60. ' Faunz, M. : Khlnogener Hirnabszess ; Archii,< fUr Laryngol. und Bhinal., 1902-03, XIII, S. 427. (Venous hyperBemia of the outer fundus ; had compression, pulse being 60-66.) ' Jessamon, L. W. : Brain Abscess as a Complication of Acute Infection of Nasal Accessory Sinuses ; Laryngoscope, 1920, Vol. 30, p. 147. •Kennedy, Foster: American Journal of Medical Science$, September, 1919. V.,- pus. Improvement, but almost constant headache and intermittent discharge of pus. Swelling left forehead and epidural abscess found on incision. Head- ache, drowsiness, nausea, vomiting. Osteomyelitis. Ethmoid labyrinth thor- oughly removed. Convulsions. Wound re-opened and multiple abscesses found. Hernia cerebri. Gradual recovery. HUED, L. M.: (1) Chr. pansinusitis. Epidural abscess; frontal lobe abscess. Meningitis. Death. GoxTLTEB, B. J.: (1) Trauma to left orbit (piece of wood) through upper eyelid. 248 BRAIlSr ABSCESS Convergent squint and diplopia. Swelling on orbit incised. Three months later apathy. Loss of memory; subnormal temperature. Both eyes proptosed. Paralysis left external rectus. Choked disc. Skull trephined. Frontal lobe abscess. Month later twitching right arm and leg. Second abscess tapped. Keoovery. Fagge, C. E.: (1) Empyema frontal sinus. Badical operation. Headache; apathy. Subnormal temperature. Abscess left frontal lobe. Death. Post- mortem showed abscess nearly to anterior horn of lateral ventricle. ElEIMEB: (1) Acute right frontal sinus Inflammation. Three operations. In third large abscess extending close to lateral ventricle evacuated. Death five days later. Laubxtb, M. p. ; (1) Chr. frontal sinusitis. Operation. Posterior bony wall intact. Abscess frontal lobe. Infection of brain through venous or lymphatic channels. Recovery. Fbeudewthai., W. ; (1) Acute frontal sinusitis. Headache, nasal discharge. CEdema right eye. Posterior wall of sinus eroded. Convulsions left side. Death several days later. Rawling, L. B. : (1) Frontal headache. (Edema, right upper eyelid. Coma. Paralysis left side of body and face. Vomiting. Optic neuritis. Operation; abscess found. Recovery. Two later operations for return of symptoms. Headache. Left hemiplegia; marked hernia. Frontal sinus contained carious bone. Recovery. Mayeb, H.: (1) Radical sinus operation for left-sided frontal sinus empyema. Death. Frontal abscess; purulent meningitis. Thrombosis of sagittal and cavernous sinus. Bone intact. Infection occurred by way of blood vessels. Veins of roof of frontal sinus filled with pus and coagulated blood. Hammesfahb: (1) Left-sided frontal sinus empyema and frontal lobe abscess. Symptoms of brain pressure eight weeks later. Operation. Abscess found in posterior pole of lower frontal convolution. Recovery. Infection occurred by way of venous channel. RoEPKB: (1) Left frontal sinus and maxillary suppuration. Subperiosteal and extradural abscess. Second operation frontal lobe abscess. Death. Probable rupture into lateral ventricles. RoEPKB (second case) : (1) Bilateral frontal sinus suppuration. Osteomyelitis. Frontal lobe abscess. Meningitis. Three operations. Abscess had ruptured into meninges and into the lateral ventricle. Death. Gosis: (1) Chr. frontal sinusitis. Fever, vomiting, convulsions. Operation; evacuation extradural abscess. Death. Post-mortem showed frontal lobe abscess. GoBis (second case) (1): Frontal sinusitis. Meningitis. Death, three days after operation for extradural abscess. Post-mortem showed frontal lobe ab- scess. ClBNEBOS: (1) Frontal sinusitis. Evacuation of ethmoid. Operation for brain abscess. Disintegration large portion right frontal lobe. Death from menin- gitis. Settebt: (1) Bilateral empyema frontal sinus. Removal nasal polyps. Death five days later. Post-mortem showed abscess right frontal lobe. Continuity infection posterior wall through lymphatics or blood vessels. MnJJOAN, W.: (1) Left frontal and ethmoidal sinus disease. Supra-orbital incisions. Nasal drainage. Abscess left frontal lobe. Extensive basal menin- gitis. Death. MmiGAN, W. (second case): (1) Left frontal and maxillary sinus disease. Supra-orbital incision. Alveolar drainage. Abscess left frontal lobe. Exten- sive basal meningitis. Death. GAjnPTJT: (1) Acute frontal sinusitis. Orbital phlegmon. Two operations. Death. Post-mortem showed abscess frontal lobe at level of meningeal and APPENDIX III 249 bone lesions. Microscopical abscess on cortical surface of brain. Incipient osteitis orbital roof. Eeinhabd: (1) Left-sided frontal sinus suppuration, and frontal lobe abscess. Extradural abscess. Meningitis and brain pressure after operation. Loss of consciousness. Death. Post-mortem showed behind extradural abscess, abscess on floor of second left frontal convolution. Layer of healthy brain tissue between. HuBBABD: (1) Ozena. Acute mastoiditis. No operation. Two months later mental dullness and headache. Mastoid tenderness: death. Post-mortem showed abscess centre frontal lobe. Dura adherent to under surface right frontal lobe. Linden: (1) Empyema left frontal sinus. Brain abscess. Death. Post-mortem showed dura and pia adherent. Thick-walled abscess. No direct communica- tion between abscess and sinus. Path of infection — sequestration of posterior wall. PAtWZ, M.: (1) Acute left frontal sinusitis. Headache and vomiting. Dilated sluggish pupils. Venous hyperemia of eyegrounds. Operation — bulging dura. Incision of dura and brain substance; pus aspirated. Death. Heezfeld: (1) Coryza. Left-sided frontal headaches. External operation. Posterior wall frontal sinus carious and removed. Epidural abscess found. Dura incised. Subdural abscess evacuated. Fistula in frontal lobe of brain. Recovery. Denkeb: (1) Pain left temple and eye. Intranasal operation for left frontal sinusitis and ethmoiditis. One month later external operation. Headaches, somnolence, blurring left optic disc. Posterior wall frontal sinus removed. Epidural abscess exposed. Dura incised. Brain incised and abscess evacuated. Recovery. Tratjtmann: (1) Empyema left frontal sinus. Perforation into orbit and anterior cranial fossa. Abscess left middle frontal lobe. Caries orbital roof. Death two weeks later. Post-mortem showed dura adherent to left frontal lobe and brain. Perforation of posterior wall. Circular orifice in bone com- municating with frontal sinus. Wilson : ( 1 ) Abscess frontal sinus and frontal lobe. Perforation external and internal wall. Death. PEINGST, A. 0.: (1) Ethmoidal involvement. Head pains on side of orbit. Convulsions. Sudden death. Post-mortem showed large encapsulated abscess in frontal lobe. Path of infection through blood vessels. Jessamon, L. W. : ( 1 ) Tenderness over left frontal sinus and ethmoids. Nasal operation. Temperature. Thick speech. Aphasia. Paresis right arm. Com- plete paralysis right hand. Posterior wall frontal sinus removed. Congestion optic disc. Aphasia increased. Third operation subdural abscess. Death. Post-mortem showed dura thickened especially over ethmoid, and discolora- tion over ethmoid bone. Adjacent Feontal Lobe Abscess feom Ethmoid Disease. Vangehitchten : (1) Anomaly of ethmoid sinus cause of infection. SiLEX: (1) Empyema of ethmoid cells and frontal sinus, previous to two abscesses of frontal lobes. Williamson: (1) Large frontal (right) abscess after influenza, with profuse nasal discharge and frontal and occipital headache. Small amount of pus in right ethmoid cells. Knapp : ( 1 ) Abscess left frontal lobe after orbital phlegmon evacuated from pus. Anterior ethmoid cells filled with offensive pus. Symonds: (1) Chronic suppuration of ethmoid sinus. Death from diffuse meningitis. Post-mortem showed two abscesses under surface left frontal lobe. 350 BRAIN" ABSCESS Dura mater beneath frontal lobe adherent to brain. Neither abscess opened lateral ventricle. Extension to orbit. Stmonds (second case) : (1) Chronic suppuration ethmoidal and frontal sinuses with abscess left frontal lobe. Influenza. Nasal discharge. Operation for suspected subdural or cerebral collection. Death. Cerebral infection from ethmoid. Extension to orbit. ScHAEFEB, H. : (1) Orbital phlegmon with death from meningitis. Post-mortem showed abscess. Destruction right ethmoid labyrinth rupturing through lamina papyracea, resulting in osteitis and periostitis of orbit. Later pachymeningitis and purulent leptomeningitis and death. STRtrTCKEN, H. J. L. ( 1 ) Eight-sided headache with rapidly developing oedema of surroundings of right eye and protrusion of eyeball. Ethmoid cells opened and most of them removed. Large abscess behind eyeball opened. Later another abscess. Operation. Eecovery with partial amnesia and persistent loss of smell on right side. Manasse : ( 1 ) Acute accessory sinus suppuration which led to enormous orbital phlegmon. Frontal sinus revealed pus during after-treatment. Cerebral symptoms in form of vomiting, headaches, fever. Frontal sinus diseased, and closed ethmoid cell found attached to its posterior wall. Three operations, and at last frontal lobe brain abscess found imder this frontal ethmoid cell. Suppurative process passed from frontal ethmoid cell to bone and then to cranial contents, through preformed vascular channels. Recovery. Uffenokde, W. : (1) Ozena and left-sided frontal sinus and ethmoid suppura- tion leading to orbital phlegmon through iistula. Operations (2) revealed extradural abscess and frontal sinus abscess. Two months later frontal abscess and meningitis. After rupture of frontal lobe abscess into ventricle. Death. HoscH, P. H. : ( 1 ) Bilateral maxillary sinusitis and right-sided frontal and ethmoidal sinusitis. Extradural perisinus abscess; frontal lobe abscess found at base of right frontal brain after death. Purulent meningitis. Hmmajst, Th.: (1) Bilateral empyema antrum of Highmore and left-sided frontal sinusitis. Bilateral earache. Severe headache and vomiting. Sudden death. Autopsy showed extradural abscess. Right lobe and both frontal sinuses, ethmoid and maxillary sinus filled with pus. Abscess with stalk. Diffuse meningitis. Bkeens, T. p. : ( 1 ) Pansinusitis right side. Radical external frontal, ethmoidal, and sphenoidal operations performed. Gradual recovery. Three years later frontal headache. Swelling of cicatrix right frontal region. Incision through old frontal wound revealed frontal lobe abscess. Author convinced patient carried large collection of pus for months in frontal lobe and that this was source of nasal trouble. ZBatANN, W. : (1) Chr. bilateral frontal sinusitis; fistula through left eyebrow. Left-sided ethmoid cell suppuration. Radical operation left side. Subperi- osteal abscess cavity. Two weeks later operation right frontal sinus. Death in three days. Autopsy showed adhesion right frontal lobe to posterior sur- face of frontal sinus. Two deeper abscesses in frontal lobe behind superficial cortical abscess in white brain-substance frontal pole, and separated from cor- tical abscess by layer of brain tissue. McCoT, J.: (1) Pneumonia; swelling of eyelids, one week later incised. Fistu- lous opening showed eroded bone. Double ethmoiditis perforating both orbital plates. Extension necrosis frontal and forehead regions. Osteomyelitis. Epidural abscess left upper forehead. Nausea, vomiting. Cerebral symptoms; paralysis right side. Coma. Disintegration entire frontal lobe. Death. McCoT, J. (second case) : (1) Pain left eye; frontal sinus relieved considerable pus. Improvement, but almost constant headache and intermittent discharge of pus. Swelling left forehead and epidural abscess found on incision. Head- ache, drowsiness, nausea, vomiting. Osteomyelitis. Ethmoid labyrinth thor- APPENDIX III 251 oughly removed. Convulsions. Wound re-opened and multiple abscesses found. Section of bone removed from temporal region. Hernia cerebri. Gradual recovery. HcED, L. M. : (1) Chr. pansinusitis. Epidural abscess. Frontal lobe abscess. Meningitis. Death. Stuckt: (1) Traumatic ethmoiditis. Meningitis. Abscess frontal lobe. No localizing symptoms. Death. Post-mortem showed necrotic cribriform plate. Fracture through table left frontal sinus. Cerebral convolutions softened. CiSNEBOS ; ( 1 ) Frontal sinusitis. Evacuation of ethmoid operation for brain abscess. Disintegration large portion right frontal lobe. Death from menin- gitis. MiLUGAN, W. (1) Left frontal and ethmoidal sinus disease. Supraorbital in- cision. Nasal drainage. Abscess left frontal lobe. Extensive basal menin- gitis. Death. Denkeb: (1) Pain left temple and eye. Intranasal operation for left frontal sinusitis and ethmoiditis. One month later external operation. Headaches. Somnolence. Blurring left optic disc. Posterior wall frontal sinus removed. Epidural mass exposed. Dura incised. Brain incised and abscess evacuated. Recovery. Ppingst, a. O. : (1) Ethmoidal involvement. Head pains on side of orbit. Convulsion. Sudden death. Post-mortem showed large encapsulated abscess in frontal lobe. Path of infection through blood vessels. Jessamon, L. W. : (1) Tenderness over left frontal sinus and ethmoids. Nasal operation. Temperature. Thick speech. Aphasia. Paresis right arm. Com- plete paralysis right hand. Posterior wall frontal sinus removed. Congestion optic disc. Aphasia increased. Third operation. Subdural abscess. Death. Autopsy showed dura thickened especially over ethmoid and discoloration over ethmoid bone. Adjacent Fbontal Lobe Abscess feom Fbontal Sirrns. CiSNEEOS: (I) Latent sinusitis (acute) with complete obstruction of frontal canal. SoLOWCEJOZTK and Kabbowski: (1) Chr. latent frontal sinus suppuration with intracranial complications in the form of epidural abscess. SoHOTJSBOE: (1) Empyema frontal sinus and anterior ethmoid cells compli- cated by orbital abscess and frontal lobe abscess. Improvement after opera- tion. Later dull and indifferent, loss of appetite,, vomiting, retarded pulse. Craniotomy. Recovery. MOEULEE (Quoted by Schousboe) : (1) Left maxillary sinus empyema, orbital abscess; ethmoid cells and sphenoid cavity evacuated. During convalescence from operation sudden nausea and death. Frontal sinus empyema and frontal sinus abscess quoted as cause of death. Manasse: (1) Acute frontal sinusitis followed by left frontal, left temporal and left occipital abscess. Eckstein: (1) Subperiosteal abscess at lateral end of left supraorbital mar- gin. Grubning: (1) Chr. suppuration of ethmoid cells and frontal sinus after nasal pneumococcus invasion which resulted in brain abscess. Pbetsinq: (1) Left-sided frontal lobe abscess following empyema left maxillary sinus, frontal sinus and ethmoid cells from gangrenous purulent process of left nose. Stbibse: (1) Post-mortem showed abscess in left frontal lobe and perforation in posterior wall of frontal sinus. KoEBBX: (1) Right frontal abscess after combination of mastoid, antrum, and frontal sinus suppuration. 353 BEAIN ABSCESS Luc: (1) Eight frontal abscess following bilateral chronic frontal sinus sup- puration. RafiN: (1) Eight frontal abscess and right-sided frontal sinusitis. TBeitel: (1) Purulent discharge left side of nose, pain in forehead and cheek. Polyps left side of nose, and middle turbinate removed. Operation frontal sinus. Post-mortem showed large abscess frontal lobe; dura adherent to brain; meningitis ; hemiparesis. SiLEX: (1) Empyema ethmoid cells and frontal sinus, followed by abscesses (2) both frontal lobes. Dmochowsky: (1) Right frontal abscess in case of antrum inflammation. Kbeckl: (1) Left frontal abscess after discharge of pus from nose and nasal polyps. Operation for swelling above left eye. Weeping fistula; frontal sinus found to be filled with pus. ZiEM : ( 1 ) Frontal lobe abscess arising laterally from optic nerve. Post-mortem also showed mucosa of left frontal sinus discolored grayish black. KOBHLER: (1) Abscess behind dura. No communication between frontal sinus and nose. Forehead tender on pressure. No history obtainable. Fluctuating swelling on left frontal tuberosity. ScHiNDLEB : ( 1 ) Left-sided frontal lobe abscess following inflammation of frontal sinus. Post-mortem showed abscess in second and third frontal convolutions. Williamson: (1) Influenza and profuse nasal discharge and frontal and occipital headache. Progressive increasing mental dullness. Right optic neu- ritis. Large abscess anteriorly right frontal lobe on autopsy. Weichselbaum : ( 1 ) Abscess right upper eyelid and pus in right maxillary and frontal sinus and between wall, right frontal sinus and dura mater. Purulent pachymeningitis and leptomeningitis and brain abscess. SiLLAE: (1) Abscess frontal lobe with empyema frontal sinus (left) after long standing sinusitis. Death. Reimek : ( 1 ) Abscess left frontal lobe with cerebral symptoms and bone disease. Extensive caries frontal bone. Meningitis? Diminished hearing. Paralysis left sixth nerve. BOTJSQTJET: (1) Acute empyema right frontal sinus. Subperiosteal orbital abscess and necrosis of frontal bone. Puncture of orbit. Later trephining frontal bone, not sinus. Death. Symonds ( Case 2 ) : ( 1 ) Chronic suppuration ethmoidal and frontal sinus with abscess left frontal lobe. Influenza. Nasal discharge. Operation for suspected subdural or cerebral collection. Death. Cerebral infection from ethmoid sinus. Extension to orbit. Strltyoken, H. J. L.: (1) Severe headache; pus from right nostril. Frontal sinus opened; cerebral symptoms. Puncture cranial cavity. Drainage. Re- currence brain symptoms. Later a second abscess opened. Incomplete recov- ery with persistent amnesia. Manasse: (1) Acute accessory sinus suppuration which led to enormous orbital phlegmon. Frontal sinus revealed pus during after treatment. Cerebral symptoms in form of vomiting, headache, fever. Frontal sinus diseased and closed ethmoid cell found attached to its posterior wall. Three operations, and at last, frontal lobe brain abscess found under this frontal ethmoid cell. Suppurative process passed from this frontal ethmoid cell to bone and through to cranial contents, through preformed vascular channels. Recovery. Uffenoede, W. : ( 1 ) Ozena and left-sided frontal sinus and ethmoid suppuration, leading to orbital phlegmon, through fistula. Operations (2) revealed extra- dural abscess and frontal sinus abscess. Two months later frontal abscess, meningitis after rupture of frontal lobe abscess into ventricle. Death. WiENBE, A.: (1) Persistent headache; empyema of frontal sinus right side, with two operations. Later frontal lobe abscess. Operated. Recovery. APPENDIX III 253 HoscH, P. H.; (1) Bilateral maxillary sinusitis and right-sided ethmoidal and frontal sinusitis. Extradural perisinus abscess. Also frontal lobe abscess found at base of right frontal brain after death. Purulent meningitis. Meuregss: (1) Bilateral frontal sinusitis with abscess right frontal lobe. Sud- den pain left eye. Operation left frontal sinus. Recurrence severe headache and sudden death in collapse. Post-mortem showed abscess right frontal lobe, with delicate membrane cranial sinuses free from pathological changes. Feeitdenthal, W.: (1) Acute empyema frontal sinus. Diffuse suppuration frontal lobe. Two operations. Death after second. Catheter then introduced struck only a fluid mass so that more than the frontal lobe seemed to be bathed in pus. Feeudenthai, W. (second case) : (1) Influenza; frontal sinusitis. Extradural collection of pus. Abscess of frontal lobe. Two operations. Headaches. Dis- colored bone. Abscess between it and intact dura. Eecovery. Feettdenthal, W. (third case): (1) Acute empyema sphenoid sinus. Infection extended to other accessory sinuses with abscess in temporal lobe. Heiman, Th. : (1) Bilateral empyema. Antrum of Highmore and left-sided frontal sinusitis. Bilateral earache. Severe headache and vomiting. Sudden death. Autopsy showed extradural abscess. Right lobe and both frontal sinuses, ethmoid and maxillary sinus filled with pus. Abscess with stalk. Diffuse meningitis. Gbunwald, L. : (1) Ozena; empyema both frontal sinuses. Carious destruction posterior sinus wall. Right-sided pachymeningitis. Abscess frontal lobe discovered eight days after primary operation. Recovery. MuiiiN, W. v.: (1) Pain over frontal sinuses and pus from nasofrontal ducts. Later pus from frontal sinuses and pain across forehead more severe left side. Sudden death. . Autopsy showed abscess left frontal lobe. Necrosis extended from surface all the way through frontal lobe and perforated into left lateral ventricle. Beeens, T. p. : ( 1 ) Pansinusitis right side. Radical external, frontal, ethmoidal and sphenoidal operation performed. Gradual recovery. Three years later frontal headache. Swelling of cicatrix right frontal region. Incision through old frontal wound revealed frontal lobe abscess. Author is convinced patient carried large collection of pus for months in frontal lobe, and that this was source of nasal trouble. PiFFL, O. : (1) Chr. left-sided frontal sinusitis and exophthalmos. Radical operation. Removal orbital roof and incision of exposed dura. Frontal lobe adherent to orbital roof and frontal abscess found at autopsy. Elschnig, a. (third case) : (1) Chr. frontal sinusitis. Incipient orbital phleg- mon. Radical operation after incision at upper inner orbital margin. Abscess found in frontal brain. Death. Autopsy showed abscess reaching to area of second frontal convolution. Incipient encephalitis remainder frontal lobe and adjacent temporal lobe. Purulent meningitis entire right cerebral hemisphere. Zhmann, W. : (1) Chr. bilateral frontal sinusitis; fistula through left eye- brow. Left-sided ethmoid cell suppuration. Radical operation left side. Sub- periosteal abscess cavity. Two weeks later operation right frontal sinus. Death in three days. Autopsy showed adhesion right frontal lobe to pos- terior surface of frontal sinus. Two deeper abscesses in frontal lobe behind superficial cortical abscess in white brain-substance frontal pole and separated from cortical abscess by layer of brain tissue. Lttbbbes, K. : (1) Chr. frontal sinusitis and fistula right eyebrow followed by osteomyelitis frontal bone and frontal sinus empyema. Abscess right frontal lobe which author believed had existed for eighteen months. Recovery. EiscHE, H. i (1) Headache; swelling above left eye. Incised. Pus evacuated. Stupor, vomiting. External frontal sinus operation. Dura incised. Abscess found in frontal lobe. Recovery. 254 BRAIN ABSCESS BtnzENGEiGEE, 0.: (1) Infection nasopharynx and frontal sinua, pus rupturing to outside causing external abscess right side of forehead. Simultaneously inward progression of infection. Operation. Eight frontal sinus exposed. Frontal abscess found. Eight days later headache, vomiting. Wound re- opened for reiilling of abscess. Hernia cerebri. Ablation. Recovery. White, J. A.: (1) Chr. frontal sinusitis. Dullness of intellect. Operation disclosed frontal lobe abscess. Unconsciousness. Lost use right arm and muscles of face. Second abscess found in Eolandic fissure. Death. McCoy, J.: (1) Pneumonia; swelling of eyelids one week later; incised. Fis- tulous opening showed eroded bone. Double ethmoiditis perforating both or- bital plates. Extension necrosis frontal and forehead regions. Osteomyelitis. Epidural abscess left upper forehead. Nausea and Vomiting. Cerebral symp- toms; paralysis right side. Coma. Disintegration entire frontal lobe. Death. MoCoT, J. (second case) : (1) Pain left eye. Frontal sinus operation; consider- able pus. Improvement, but almost constant headache and intermittent dis- charge of pus. Swelling left forehead and epidural abscess found on incision. Headache, drowsiness, nausea, vomiting. Osteomyelitis. Ethmoid labyrinth thoroughly removed. Convulsions. Wound re-opened and multiple abscesses found. Section of bone removed from temporal region. Hernia cerebri. Gradual recovery. HuED, L. M.: (1) Chr. pansinusitis; epidural abscess; frontal lobe abscess; meningitis; death. Fagge, C. H.: (1) Empyema frontal sinus. Radical operation. Headache; apathy. Subnormal temperature; abscess left frontal lobe. Death. Post-mor- tem showed abscess nearly to anterior horn of lateral ventricle. Keimer : ( 1 ) Acute right-sided frontal sinus inflammation. Three operations. In third large abscess extending close to lateral ventricle evacuated. Death five days later. LAMBtra, M. P.: (1) Chr. frontal sinusitis. Operation. Posterior bony wall intact. Infection of brain through venous or lymphatic chaiinels. Abscess frontal lobe. Recovery. Cabgill, Tubnek, and Thomas: (1) Orbital cellulitis incised. Later irritability and optic neuritis. Frontal sinus opened. Posterior wall necrotic. Brain covered with granulations. Abscess frontal lobe evacuated. Recovery. FEEaDENTHAL, W. : (1) Acute frontal sinusitis. Headache. Nasal discharge. Oildema right eye. Posterior wall of sinus eroded. Convulsions left side. Death several days later. Rawling, L. B. : (1) Frontal headache. (Edema right upper eyelid. Coma. Paralysis left side of body and face. Vomiting. Optic neuritis. Operation. Abscess found. Recovery. Two later operations for return of symptoms. Headache. Left hemiplegia. Marked hernia. Frontal sinus contained carious bone. Recovery. Mayer, H. : (1) Radical sinus operation for left-sided frontal sinus empyema. Death. Frontal abscess. Purulent meningitis. Thrombosis of sagittal and cavernous sinus. Bone intact. Infection occurred by way of blood vessels. Veins of roof of frontal sinus filled with pus and coagulated blood. Hammesfahe: (1) Left-sided frontal sinus empyema and frontal lobe abscess. Symptoms of brain pressure eight weeks later. Operation. Abscess found in posterior pole of lower frontal convolution. Recovery. Infection occurred by way of venous channel. ROEPKB: (1) Left frontal sinus and maxillary suppuration. Subperiosteal and extradural abscess. Second operation frontal lobe abscess. Death. Probable rupture into lateral ventricles. RoEPKB (second case): (1) Bilateral frontal sinus suppuration. OsteomyelitiB. APPENDIX III 255 Frontal lobe abscess. Meningitis. Three operations. Abscess had ruptured into meninges and into the lateral ventricle. Death. HoFFMAifN, R. : (1) Bilateral chr. sinus suppuration. Multiple brain abscess. Left-sided traumatism. Two operations. Recovery. Recurrence five months later. Death. Post-mortem showed infection by lymphatics. GoRiS: (1) Chr. frontal sinusitis; fever, vomiting, convulsions. Operation. Evacuation extradural abscess. Death. Post-mortem showed frontal lobe abscess. GoEis (second case) : (1) Chr. frontal sinusitis. Meningitis. Death three days after operation for extradural abscess. Post-mortem showed frontal lobe abscess (subdural). ClSNEEOS: (1) Frontal sinusitis. Evacuation of ethmoid. Operation for brain abscess. Disintegration large portion right frontal lobe. Death from menin- gitis. Seifeet: (1) Bilateral empyema frontal sinus. Removal nasal polyps. Death five days later. Post-mortem showed abscess right frontal lobe. Continuity infection posterior wall through lymphatics or blood vessels. MiLLiGAN, W.: (1) Left frontal and ethmoidal sinus disease. Supra-orbital incisions. Nasal drainage. Abscess left frontal lobe. Extensive basal men- ingitis. Death. MiLLiGAN, W. (second case): (1) Left frontal and maxillary sinus disease. Supra-orbital incision. Alveolar drainage. Abscess left frontal lobe. Exten- sive basal meningitis. Death. Gariput: (1) Acute frontal sinusitis; orbital phlegmon. Two operations. Death. Post-mortem showed abscess frontal lobe at level of meningeal and bone lesions. Microscopical abscess on cortical surface of brain. Incipient osteitis orbital roof. Rbinhaed : ( 1 ) Left-sided frontal sinus suppuration and frontal lobe abscess. Extradural abscess. Meningitis and brain pressure after operation. Loss of consciousness. Death. Post-mortem showed behind extradural abscess one on floor of second left frontal convolution. Layer of healthy brain tissue between. Linden : ( 1 ) Empyema left frontal sinus. Brain abscess. Death. Post-mortem showed dura and pia adherent. Thick-walled abscess. No direct communica- tion between abscess and sinus. Path of infection — sequestration of posterior wall. Patjnz, M. : (1) Acute left frontal sinusitis. Headache and vomiting. Dilated sluggish pupils. Venous hyperemia of eyegrounds. Operation. Bulging dura; incision of dura and brain substance. Pus aspirated. Death. Hebzfeld, J.: (1) Coryza. Left-sided frontal headaches. External operation. Posterior wall frontal sinus carious and removed. Epidural abscess found. Dura incised. Subdural abscess evacuated. Fistula in frontal lobe of brain. Recovery. Denkee : ( 1 ) Pain left temple and eye. Intranasal operation for left frontal sinusitis and ethmoiditis. One month later external operation. Headache, somnolence, blurring left optic disc. Posterior wall frontal sinus removed. Epidural abscess exposed. Dura incised. Brain incised and abscess evacuated. Recovery. Tbatjtmann: (1) Empyema left frontal sinus. Perforation into orbit and anterior cranial fossa. Abscess left middle frontal lobe. Caries orbital roof. Death two weeks later. Post-mortem showed dura adherent to left frontal lobe and brain. Perforation of posterior wall. Circular orifice in bone communicat- ing with frontal sinus. Wilson: (1) Abscess frontal sinus and frontal lobe. Perforation external and internal wall. Death. 256 BEAIN ABSCESS Jessamoit, L. W.: (1) Tenderness over left frontal sinus and ethmoids. Nasal operation. Temperature; thick speech. Aphasia. Paresis right arm. Com- plete paralysis right hand. Posterior wall frontal sinus removed. Congestion optic disc. Aphasia increased. Third operation. Subdural abscess. Death. Post-mortem showed dura thickened, especially over ethmoid, and discolora- tion over ethmoid bone. Frontal Lobe Abscess with Oebitai. Complications. NoNNE: (1) Choked disc from neuritis optica. SCHOUSBOB : ( 1 ) Empyema frontal sinus and anterior ethmoid cells compli- cated by orbital abscess and frontal lobe abscess. MoELLEE: (1) Left maxillary sinus empyema and orbital abscess; ethmoid cells and sphenoid. Eagleton: (1) Case XXI, D. McS., Chapter Seven, p. 111. Eckstein : ( 1 ) Subperiosteal abscess at lateral end of left supra-orbital margin. Getjening : ( 1 ) Chr. suppuration of ethmoid cells, pneumococcic, involving nasal, ethmoid, orbit, and brain. Steese: (1) Pain in both eyes; dimness of vision and vomiting; abscess left frontal lobe. Steese (second case) : (1) Abscess at upper end of fissure of Rolando and another in occipital lobe. Le!E, J. M. : (1) Traumatic. Penetrating foreign body above eyelid (right upper) and passed through sphenoidal fissure into frontal lobe. VON Schroder: (1) Right frontal abscess after right retrobulbar phlegmon. Incision orbital margin; voided much thick pus. EIbeckl : ( 1 ) Left frontal abscess after nasal discharge of pus and polyps. Operation for swelling above left eye and weeping fistula. Frontal sinus filled with pus. Pain in occipital region. Zdekaur: (1) Left-sided ptosis after traumatic penetrating wound of left side of head from which pus discharged. Redtejtbachek : (1) Abscess apex frontal lobe after abscess left upper eyelid. ZiRM: (1) Frontal lobe abscess coming laterally from optic nerve and showing cellular tissue of orbit congested. (Cavernous Sinus.) BoRELius: (1) Traumatic puncture upper eyelid. Epileptiform seizures and other cerebral symptoms. Twitching more marked left arm and leg. Incision in upper eyelid. Drainage tube; recovery. Williamson: (1) Abscess right frontal lobe after influenza with profuse nasal discharge and frontal and occipital headache. Optic neuritis right eye. Weichselbaum : (1) Abscess right upper eyelid. Eyeball intact. Pus in right maxillary and frontal sinus and between posterior wall of right frontal sinus and dura mater. Pachymeningitis and leptomeningitis and brain abscess. Renton, J. C. : ( 1 ) Abscess right frontal lobe after incision with evacuation of pus along upper eyelid for right orbital cellulitis. Right orbital plate necrosed. No direct conjmunication between pus from orbit and cerebral abscess. Knapp: (1) Abscess left frontal lobe after orbital phlegmon which was incised and pus evacuated. Base of frontal lobe over orbital margin yellowish in color and adherent to dura mater. Some pus flakes on dura. Orbit free from pus. BousQTJET: (1) Acute empyema right frontal sinus. Subperiosteal orbital abscess and necrosis frontal bone. Puncture of orbit. Bone eroded. Sinus flUed with cheesy pus. Stmonds, C. J.: (1) Chr. suppuration ethmoid sinus. Death from diffuse meningitis. Post-mortem showed two abscesses under surface left frontal lobe. Dura mater beneath frontal lobe adherent to brain. Neither abscess opened lateral ventricle. Extension to orbit. APPENDIX III 257 Stmonds, C. J. (second case): (1) Chr. suppuration ethmoidal and frontal sinuses with abscess left frontal lobe. Influenza. Nasal discharge. Operation for suspected subdural or cerebral collection. Death cerebral infection frbm ethmoid sinus. Extension to orbit. ScHAB3T», H. : { 1 ) Orbital phlegmon with death from meningitis. Post-mortem showed abscess. Destruction right ethmoid labyrinth rupturing through lamina papyracea, resulting in osteitis and periostitis of orbit. Later pachymeningitis and purulent leptomeningitis. Death. •' Stbuycken, H. J. L. (second case): (1) Right-sided headache with rapiSly developing oedema of surroundings right eye and protrusion of eyeball. Ethmoid cells opened and most of them removed. Large abscess behind eyeball opened. Later rigidity nape of neck; vomiting. Another operation and another abscess found. Recovery with partial amnesia and persistent loss of smell on right side. Manasse: (1) Acute accessory sinus suppuration which led to enormous orbital phlegmon. Frontal sinus revealed pus during after treatment. Cerebral symptoms in form of vomiting, headaches, fever. Frontal sinus diseased and closed ethmoid cell found attached to its posterior wall. Three operations and at last frontal lobe brain abscess found under this frontal ethmoid cell. Suppurative process passed from this frontal ethmoid cell to bone and then to cranial contents, through preformed vascular channels. Recovery. Uffenoede, W. : (1) Ozena and left-sided frontal sinus and ethmoid suppuration leading to orbital phlegmon through fistula. Operations (2) revealed extra- dural abscess and frontal sinus abscess. Two months later frontal abscess and meningitis after rupture of frontal lobe abscess into ventricle. Death. Maffei: (1) Partial loss of vision followed by vomiting and severe headache. Incipient neuroretinitis. Later pains in nape of neck and rise in temperature. Death from asphyxia. Spontaneous discharge of pus from left nostril and filling throat. No operation. No autopsy, but author believed disease to be in frontal lobe. Mbiueebs : ( 1 ) Bilateral frontal sinusitis with abscess right frontal lobe. Sud- den pain left eye. Operation left frontal sinus. Recurrence severe headache and sudden death in collapse. Post-mortem showed abscess right frontal lobe with delicate membrane. Cranial sinuses free from pathological changes. PirpL, 0.: (1) Chr. left-sided frontal sinusitis and exophthalmos. Radical operation. Removal orbital roof and incision of exposed dura. Frontal lobe adherent to orbital roof and frontal abscess found at autopsy. Elschnig, a.; (1) Chr. tuberculous tumor, lachrymal gland right eye. Opera- tion, extirpation of tumor with temporary resection of lateral orbital wall. Death four weeks after. Abscess found in right frontal lobe directly above base with circumscribed adhesion of meninges. Elschnig, a. (second case): (1) Phlegmon left upper eyelid incised. Paresis right side and mental apathy. Operation left frontal abscess. Removal orbital roof and dura. Recovery. Elsohnig, a. (third case) : (1) Chr. frontal sinusitis. Incipient orbital phleg- mon. Radical operation after incision at upper inner orbital margin. Abscess found in frontal brain. Death. Autopsy showed abscess reaching to area of second frontal convolution. Incipient encephalitis remainder frontal lobe and adjacent temporal lobe. Purulent meningitis entire right cerebral hemisphere. Zemankt, W.: (1) Chr. bilateral frontal sinusitis. Fistula through left eye- brow. Left-sided ethmoid cell suppuration. Radical operation left side. Sub- periosteal abscess cavity. Two weeks later operation rt. frontal sinus. Death in three days. Autopsy showed adhesion rt. frontal lobe to posterior surface of frontal sinus. Two deeper abscesses in frontal lobe behind superficial corti- cal abscess in white brain-substance frontal pole, and separated from corticaj abscess by layer of brain tissue. 258 BRAIN ABSCESS McCoy, J. (second case): (1) Pain left eye. Frontal sinus operation; consid- erable pus. Improvement but almost constant headache, and intermittent discharge of pus. Swelling left forehead and epidural abscess found on in- cision. Headache, drowsiness, nausea and vomiting. Osteomyelitis. Ethmoid labyrinth thoroughly removed. Convulsions. Wound re-opened and multiple abscesses found. Section of bone removed from temporal region. Hernia cerebri. Gradual recovery. CoTTLTEB, E. J.: (1) Trauma to left orbit (piece of wood) through upper eyelid. Convergent squint and diplopia. Swelling in orbit incised. Three months later apathy; loss of memory; subnormal temperature. Both eyes proptosed. Paralysis left external rectus. Choked disc. Skull trephined. Frontal lobe abscess. Month later twitching rt. arm and leg. Second abscess tapped. Recovery. Tatlob, F. L. ; (1) Trauma to rt. eye. Superficial abscess opened one month later. Headache, apathy, emaciation, optic neuritis. Paresis left side of face. Stiffness back of neck. Vomiting. Incontinence of urine and feces. Operation. Et. frontal abscess. Recovery with poor vision. Following year unconscious, convulsions, death. Caequl, Tubnee, and Thomas : ( 1 ) Orbital cellulitis incised. Later irritability and optic neuritis. Frontal sinus opened. Posterior wall necrotic. Brain cov- ered with granulations. Abscess frontal lobe evacuated. Eecovery. Eeis, W. : (1) Traumatic panophthalmitis. Brain abscess. Incision of eyeball. Evacuation of pus. Headache, fever, coma; death from diffuse meningitis. Gamput: (1) Acute frontal sinusitis. Orbital phlegmon. Two operations. Death. Post-mortem showed abscess frontal lobe at level of meningeal and bone lesions. Microscopical abscess on cortical surface of brain. Incipient osteitis orbital roof. Patwz, M.: (1) Acute left frontal sinusitis. Headache and vomiting. Dilated sluggish pupils. Venous hyperemia of eyegrounds. Operation. Bulging dura. Incision of dura and brain substance. Pus aspirated. Death. Deneeb: (1) Pain left temple and eye. Intranasal operation for left frontal sinusitis and ethmoiditis. One month later external operation. Headache, somnolence. Blurring left optic disc. Posterior wall frontal sinus removed. Epidural abscess exposed. Dura incised. Brain incised and abscess evacuated. Recovery. FeoittaIi Lobe Abscess Assooiated with Osteomyelitis. BcHWABACH: (1) Osteitis and osteomyelitis in petrous portion of temporal bone. BOLOWCEJOZYK, A., and Kaebowski, B.: (1) Osteomyelitis of entire cranial vault. Metjbebs: (1) Osteomyelitis of diploe. Reimee: (1) Caries of frontal bone; dura adherent and greatly thickened in neighborhood of abscess left frontal lobe. BotrsQTJBT: (1) Necrosis frontal bone and subperiosteal orbital abscess. Post- mortem showed right frontal abscess. Sinus filled with cheesy pus. Ldbbers, K,: (1) Chr. frontal sinusitis and fistula right eyebrow, followed by osteomyelitis frontal bone and frontal sinus empyema. Abscess right frontal lobe which author believes had existed for eighteen months. McCoy, J.; (1) Pneumonia; swelling of eyelids one week later; incised. Fistu- lous opening showed eroded bone. Double ethmoiditis perforating both orbital plates. Extension necrosis frontal and forehead regions. Osteomyelitis. Epi- dural abscess left upper forehead. Nausea, vomiting. Cerebral symptoms. Paralysis right side. Coma. Disintegration entire frontal lobe. Death. McCoy, J. (second case). (1) Pain left eye; frontal sinus operation; considerable pua. Improvement, but almost constant headache and intermittent discharge APPENDIX III 359 of pus. Swelling left forehead and epidural abscess found on incision. Head- ache, drowsiness, nausea and vomiting. Osteomyelitis. Ethmoid labyrinth thoroughly removed. Convulsions. Wound re-opened and multiple abscesses found. Section of bone removed from temporal region. Hernia cerebri. Grad- ual recovery. BoEPKB (second case): (1) Bilateral frontal sinus suppuration. Osteomyelitis. Frontal lobe abscess. Meningitis. Three operations. Abscess had ruptured into meninges and into lateral ventricle. Death. Metastatic Frontal Lobe Abscess. Casamajoe: (1) Idiopathic double abscess frontal lobe; no history of opera- tion. Death seven days after admission. Autopsy showed double frontal abscess primary on right side, extending through corpus callosum into left frontal lobe. Meninges showed no evidence of involvement. No diagnosis until autopsy. Schwabach: (1) Left-sided otitis media followed by headache and vertigo. Abscess in right frontal lobe found at autopsy with "granulating congested capsule several mm. thick. Extensive purulent disintegration left petrous bone; labyrinth extensively diseased; complete rupture labyrinth capsule. Osteitis and osteomyelitis in petrous portion temporal bone. First symptom hardness of hearing left ear; five weeks later headache with disturbance of equilibrium in form of vertigo and tottering gait. Onset is not fully reported. Lombard, Bloch, and Moulonguet: (1) Operation for left-sided chronic ear sup- puration. Epilepsy with symptoms of intracranial hypertension suddenly five years later. Squama trephined and temporo-sphenoidal lobe punctured. Next day left-sided hemiparesis with hypesthesia and disappearance of cutaneous and tendon reflexes same side. Five days later second intervention with tre- phining of occipital bone and puncture of cerebellum. Death following day. Autopsy showed abscess rt. frontal lobe. PicQTrfi: (1) Influenza without pulmonary complications, but with severe pain in right ear and profuse suppuration. Three months later pain returned with great severity. Violent hemicrania, progressive loss of strength, rise of tem- perature. Mastoid process slightly tender on pressure, and it was decided to perform exploratory trephining operation on mastoid process. Next day rise of temperature, delirium, blunted intelligence and complete left-sided hemi- plegia. Mastoid process trephined; no pus. Hernia cerebri. Intracerebral abscess in front of Eolandic fissure. Autopsy showed generalized encephalitis and second smaller focus of pus behind first. Stebsb: (1) Metastatic from lung. Abscess at upper end of fissure of Rolando; another in occipital lobe. Eeimeb (second case) : (1) Kickets, headache, rigidity nape of neck, contracture right arm, left-sided facial paralysis, convulsions, convergent strabismus, nys- tagmus, fever; idiocy. Autopsy showed frontal convolutions right anterior lobe entirely flattened and almost completely transformed into abscess which had already ruptured into right lateral ventricle. Left anterior lobe con- tained central abscess size of walnut. Bebens, T. p.: (1) Deafness rt. ear. Intermittent purulent discharge. Tender mastoid. Radical operation. Sixteen days later profuse hemorrhage from middle ear cavity. After convulsions headache, stupor, coma. Later, attack of typical Jacksonian epilepsy. Incision through dura revealed pus. Hernia of brain filling bone wound. Death some days later. Autopsy showed subdural abscess over rt. hemisphere. Large abscess also occupying most of rt. frontal lobe with spontaneous discharge into subdural space. Author believes case to be of otitic origin. HiESCHBEEG, O.: (1) Metastatic brain abscess following abscess bronchial 260 BEAIN ABSCESS glands. Fistula from broken down glands to esophagus. Death from purulent meningitis. Autopsy showed abscess rt. frontal lobe and several smaller abscesses. Stdckt : ( 1 ) Acute otitis right ear. Syphilis. Metastatic abscess left frontal lobe. Very chronic as shown by firm capsule. Death from meningitis. Johnston: (1) Left-sided frontal sinusitis. Operation showed healthy bone. Sudden death four weeks later. Large abscess left frontal lobe, evidently present previous to operation. Membranous capsule. ScHOKSTBiN : ( 1 ) Tuberculosis. Bronchiectatic cavities. Facial paralysis left side. Muscular spasm and later hemiplegia rt. side. Death three days later. Autopsy showed two abscesses frontal lobe. ScHORSTEiN (second case): (1) Tuberculosis. Bronchiectatic cavities. Dull- ness and apathy. Death. Post-mortem showed abscess rt. frontal lobe. Lambuk, M. p. : ( 1 ) Chr. frontal sinusitis. Operation. Posterior bony wall intact. Infection of brain through venous or lymphatic channels. Abscess frontal lobe. Eecovcry. Wertheim : ( 1 ) Fever ; headache ; discharge from nose. Tumor over right eye. Incision voided pus. Sinus wall roughened. Death. Post-mortem showed abscess right frontal lobe. Necrosis posterior wall. Circumscribed pachy- meningitis. Frontal Abscess in Opposite Lobe (Metastatic). Casamajob: (1) Idiopathic. Primary in right frontal lobe and extending through corpus callosum to left frontal lobe. ScHWABACH: (1) Left otitis media previous to abscess in right frontal lobe. Lombard, Bloch, and MouLOtrGUET : ( 1 ) Left chr. ear suppuration previous to right frontal abscess. NoNNE: (1) Left tympanic suppuration previous to right frontal abscess. Meurers: (1) Left-sided frontal sinusitis previous to right-sided frontal lobe abscess. Heiman, Th. : (1) Bilateral empyema, antrum of Highmore, and left-sided frontal sinusitis. Bilateral earache. Severe headache and vomiting. Sudden death. Autopsy showed extradural abscess. Eight lobe and both frontal sinuses, ethmoid and maxillary sinus, filled with pus. Abscess with stalk. Diffuse meningitis. Sttjcky, A. : ( 1 ) Acute otitis right ear. Syphilis. Metastatic abscess left frontal lobe. Very chronic as shown by firm capsule. Frontal Lobe Abscess of Aurai, Origin (Metastatic). ScHWABACH: (1) Left otitis media previously to right frontal lobe abscess. Extensive disease in labyrinth. Lombard, Bloch, and Moulouguet: (1) Left chronic ear suppuration previous to right frontal abscess. NoNNE : ( 1 ) Contraction of left tympanic membrane. PiCQufi: (1) Intracerebral abscess after right mastoid symptoms and submenin- geal collections, supervening on influenza. Berens: (1) Subdural abscess in right hemisphere and second in larger portion of frontal lobe. KoEBEL : ( 1 ) Mastoid, antrum, and frontal sinus suppuration of right side previous to abscess of right frontal lobe. Abscess referred to ear disease. Bebens (second case): (1) Deafness right ear. Intermittent purulent dis- charge. Tender mastoid. Radical operation. Sixteen days later profuse hemor- rhage from middle ear cavity. Convulsions, headache, stupor and coma. Then, attack of typical Jacksonian epilepsy. Incision through dura revealed pus. APPENDIX III 261 Hernia of brain filling bone wound. Death some days later. Autopsy showed subdural abscess over right hemisphere. Large abscess also occupying most of right frontal lobe with spontaneous discharge into subdural space. Author 1 believes case to be of otitic origin. Sttjcky, a. : ( 1 ) Acute otitis right ear. Syphilis. Metastatic abscess left frontal lobe. Very chronic as shown by firm capsule. Death from meningitis. Htibbabd: (1) Ozena. Acute mastoiditis. No operation. Two months later mental dullness and headache. Mastoid tenderness. Death. Post-mortem showed abscess centre frontal lobe. Dura adherent to under surface right frontal lobe. Traumatic Frontal Lobe Abscess. Hoffmann: (1) Multiple brain abscesses (4) following bilateral traumatic frontal sinus suppuration. Non-penetrating. Steese (fourth case) : (1) Fracture base of skull. Six months later pain over right eye. Apathy and left hemiplegia. Autopsy showed large abscess right frontal lobe. Steese (sixth case) : (1) Two abscesses frontal lobe. Laceration of cerebellum. Fracture of skull. Steese (seventh case): (1) Bullet removed from head. Entire frontal (rt.), lobe honeycombed with abscess cavities. KoEHLER: (1) Struck forehead against file which penetrated frontal bone. Ab- scess left hemisphere. Cavity communicated with opening in frontal bone and with left ventricle. Third and fourth ventricles also contained pus. Lee, J. M. : ( 1 ) Fell on stub of weed which penetrated upper eyelid, and passed through sphenoidal fissure into frontal lobe of brain. Zdekatjee: (1) Nail penetrated left side of head resulting in right hemiplegia, left ptosis; pus wound over left temporal bone. Puncture of dura. Drainage. Recovery with paresis left hand. BOKELius, J.: (1) Traumatic puncture upper eyelid; epilepsy; twitching more marked left arm and leg; other cerebral symptoms. Drainage tube inserted after deep incision in upper eyelid. Recovery. Wtss, O.i (1) Traumatic abscess involving entire frontal lobe. Sudden onset. Severe pain followed by twitching right arm and leg. Later paralysis right arm and 1^. Fever. Enlargement of head. Coma; convulsions during which child died. YOQL: (1) Traumatic abscess after temporal wound with later cerebral symp- toms. "Vomiting, convulsions and death. Brain tissue found to be disorgan- ized. Abscess communicated with lateral ventricle. Apeblo: (1) Traumatic penetrating abscess left frontal lobe; craniectomy with recovery. Second operation which revealed solution of continuity. Drainage with gauze and glass tube. Later cerebral hernia. Recovery. Complete cica- trization. MaoEwen, Wm.: (1) Trauma to forehead. Unconscious. Headache, somno- lence, vomiting, profuse perspiration. Patellar reflexes diminished. Pupils unequal. Paresis left internal rectus. Bilateral optic neuritis. Convulsions both arms. Operation without narcosis. Abscess frontal lobe. Gradual im- provement all symptoms. MacEwen, WiM. (second case): (1) Trauma of forehead. Headache; wound; roughened bone. Somnolence, vomiting, temperature, chills, convulsions. Aphasia for an hour. Paralysis rt. side improved after several hours. Diag- nosis, abscess in third convolution. Operation refused. Death. Autopsy showed extradural exudate. Hyperemia of dura. Abscess frontal lobe one inch from surface. Kennedy, Fosteb: (1) Traumatic, non-penetrating, right fronto-parietal region. 263 BRAIN ABSCESS Headache and irritability. Optic neuritis left side. Slight left facial weakness. Loss of smell, right side. Gradual increasing left hemiplegia. Operation showed large abscess in frontal lobe. Recovery. Sachs, E.: (1) Trauma to forehead. Dull and irritable. Paralysis right arm and leg. Lumbar puncture yielded clear fluid. Unconsciousness. Convulsions. Vessels left retina tortuous. Operation. Frontal lobe abscess found and drained. Recovery. Damaye, H. : (1) Frontal abscess following fatigue and bombardment. Patient soldier under observation for asthenia and headache, with symptoms of shell- shock. Death. Autopsy showed interlobar abscess right frontal lobe. Dura adherent to pia at level of right frontal lobe. Coulter, E. J. : (1) Trauma to left orbit through upper eyelid. (Piece of wood.) Convergent squint and diplopia. Swelling in orbit incised. Three months later apathy. Loss of memory, subnormal temperature. Both eyes proptosed. Paralysis left external rectus. Choked disc. Skull trephined. Frontal lobe abscess. Month later twitching right arm and leg. Second abscess tapped; recovery. Feeeeei: (1) Trauma left side of head. Operation showed periostitis posterior wall. Sudden death four weeks later. Post-mortem showed left frontal ab- scess. No symptoms during life. Taylob, F. L.: (1) Trauma to right eye. Superficial abscess opened one month later. Headache, apathy, emaciation. Optic neuritis. Paresis left side of face. Stiffness back of neck. Vomiting. Incontinence, urine and feces. Opera- tion right frontal abscess. Recovery with poor vision. Following year, un- conscious. Convulsions. Death. Stuckt: (1) Traumatic ethmoiditis. Meningitis. Abscess frontal lobe. No localizing symptoms. Death. Post-mortem showed necrotic cribriform plate. Fracture through table left frontal sinus. Cerebral convolutions softened. HorrMANN, R. i ( 1 ) Bilateral chr. sinus suppuration. Multiple brain abscesses. Left-sided traumatism. Two operations. Recovery. Recurrence five months later. Death. Post-mortem showed infection by lymphatics. Reis, W. : (1) Traumatic panophthalmitis; brain abscess. Incision of eyeball. Evacuation of pus. Headache, fever, coma; death from diffuse meningitis. Path: op Ijntection of Feontal Lobe Abscess. Casamajor: (1) Extending through corpus callosum to left frontal lobe from right. Lombard, Bloch, and Motjlgugxjet: (1) Left otitis developing right frontal abscess. Thrombophlebitis from sinus, extending along course of a cerebral vein, or arterial or venous embolus from primary infectious focus. Pbeysing: (1) Gangrenous suppurative process in left nose and cavities, caus- ing a circumscribed necrosis of dura over lamina cribrosa. Pia vein passing along lower side of frontal lobe became involved and probably further on thrombotic. Entrance of infective process through this vein and the lymph tracts into frontal lobe. Nonne: (1) Syphilis, alcoholism, albuminuria, and left tympanic contraction previous to rt. frontal abscess. Two months before admission to hospital head- ache, apathy, stupor, gradual right-sided hemiparesis. Complete paralysis rt. side after 3 months and death. Autopsy showed orchitis fibrosa left side. CiSNEKOS: (1) Through lymphatic and blood route. Hoffmann: (1) Multiple traumatic (4). Three abscesses on left side of dura in brain substance — "possibly caused by way of blood vessels or lymphatics." One of four frontal lobe abscesses communicated with left ventricle. Meubees (second case): (1) Second case. Left-sided frontal sinus empyema ruptured through septum and gave rise to similar empyema on rt. side. Longi- APPENDIX III 263 tudinal sinus and later parietal emissary vein were infected by way of veins and frontal diploe and closed by thrombosis. Zemaun: (1) By continuity. Case of meningitis. Three abscesses, one of right lobe, superficial cortical, and two communicating deep-seated abscesses. Vangehuchten : (1) Anomaly of ethmoid sinus through which infection oc- curred. Large abscess left frontal lobe. Gbdeninq: (1). Nasal, ethmoid cells, orbit and brain. Pebysing: (1) Gangrenous purulent process in left nose, and cavities gave rise to circumscribed necrosis of dura and pia over lamina cribrosa; pial veins be- came involved in disease, and thrombosed, and infective process entered through the vein, and the concomitant lymph tracts into the frontal lobe. KoEHLEE: (1) Traumatic abscess left hemisphere. Cavity communicated with opening in frontal lobe and with left ventricle. Third and fourth ventricles also contained pus. Pus had penetrated through foramen of Monro into right ventricle. Leb, J. M. : ( 1 ) Traumatic penetrating foreign body, passed through upper eye- lid and sphenoidal fissure into frontal lobe of brain. SiLEX : ( 1 ) Empyema ethmoid cells and frontal sinus, followed by two abscesses both frontal lobes. Perforation of posterior and lower wall. VON ScHKOEDEB: (1) Caries of orbit or ethmoid cells. Rt. frontal abscess after right retrobulbar phlegmon. ZiBM: (1) Frontal lobe abscess. Post-mortem showed cellular tissue of orbit congested and abscess laterally from optic nerve. ScHiNDLEE: (1) Left frontal abscess following inflammation of frontal sinus. Perforation of posterior upper wall. Post-mortem showed large abscess in second and third left frontal convolution. BoEELins, J.: (1) Traumatic puncture of upper eyelid. Epileptiform seizures and other cerebral symptoms. No paralysis, but twitching more marked left arm and leg. Incision upper eyelid and probe passed through roof of orbit and frontal lobe. Drainage. Recovery. Weichselbatjm : (1) Influenza. Swelling right upper eyelid; eyeball intact. Abscess rt. upper eyelid. Pus right maxillary and frontal sinus and between posterior wall of frontal sinus and dura mater. Process originated from max- illary and frontal sinus where purulent pachymeningitis and leptomeningitis developed with brain abscess. Renton, J. C. : ( 1 ) Abscess rt. frontal lobe after incision with evacuation of pus along upper eyelid for right orbital cellulitis. Right orbital plate necrosed. Dura inflamed over this area. Abscess cavity lined with distinct membrane, and there was no direct communication between the pus from orbit and the cerebral abscess. KiTApp: (1) Abscess left frontal lobe after orbital phlegmon which was incised. Base of frontal lobe was adherent to dura mater; dura was bluish covered with pus flakes. Orbit free from pus. Communication existed between orbit and dilated frontal sinus. Reienee: (1) Abscess left frontal lobe with cerebral symptoms, and bone dis- ease. Extensive caries frontal bone. Reieneb (second case) : (1) Abscess left anterior lobe and also abscess right lobe which was flattened, and abscess had ruptured into right lateral ventricle. BouSQTJET: (1) Acute empyema right frontal sinus and subperiosteal orbital abscess and necrosis frontal bone. Perforation in cranial cavity (posterior and inferior wall). Maas, H.; (1) Nasal polypi and nasophar3mgeal polyp removed. Apathy, ver- tigo. Exophthalmos, delirium, death. Post-mortem showed dura at base of skull covered with pus. Abscess in frontal lobe of brain above ethmoidal region. Lamina cribrosa and upper surface of sphenoid destroyed. YouL; (1) Traumatic abscess at point opposite wound in temporal region. Sur- 264 BRAIN ABSCESS rounding brain tissue much disorganized. Abscess communicated with lateral ventricle. Stmonds, C. J. : (1) Chr. suppuration of ethmoid sinus. Death from diffuse meningitis. Post-mortem showed two abscesses under surface left frontal lobe. Dura mater beneath frontal lobe adherent to brain. Neither abscess opened lateral ventricle. Extension to orbit. Symonds, C. J. (second case): (1) Chr. suppuration ethmoidal and frontal sinuses with abscess left frontal lobe. Influenza, nasal discharge. Operation for suspected subdural or cerebral collection. Death. Cerebral infection from , ethmoid. Extension to orbit. ScHAEFBJB, H. : (1) Orbital phlegmon with death from meningitis. Post-mortem showed abscess. Destruction rt. ethmoid labyrinth rupturing through lamina papyracea, resulting in osteitis and periostitis of orbit. STBtTTCKEN, H. J. L. : (1) Severe headache; pus from right nostril. Frontal sinus opened. Cerebral symptoms. Puncture cranial cavity. Drainage. Re- currence. Incomplete recovery with persistent amnesia. STEUTOKErr, H. J. L. (second case) : (1) Right-sided headache with rapidly de- veloping oedema of surroundings of right eye and protrusion of eyeball. Eth- moid cells opened — most of them removed. Large abscess behind eyeball . opened; later rigidity nape of neck, vomiting. Another operation and another abscess found. Recovery with partial amnesia and persistent loss of smell right side. Aperlo, Gr.: (1) Traumatic penetrating abscess left frontal lobe. Craniectomy with recovery. Second operation which revealed solution of continuity. Drain- age with gauze and glass tube. Later cerebral hernia. Recovery; complete cicatrization. Manasse: (1) Acute accessory sinus suppuration which led to enormous orbital phlegmon. Frontal sinus revealed pus during after-treatment. Cerebral symp- toms in form of vomiting, headache and fever. Frontal sinus diseased and closed ethmoid cell found attached to its posterior wall. At third operation frontal lobe brain abscess found under this fronto-ethmoid cell. Suppurative . process passed from frontal ethmoid cell to bone and then to cranial contents through preformed vascular channels. Recovery. Uffbnorde, W. : (1) Ozena and left-sided frontal sinus and ethmoid suppura- tion leading to orbital phlegmon, through fistula. Operations (2) revealed , extradural abscess and frontal sinus abscess. Two months later frontal ab- scess, meningitis, after rupture of frontal abscess into ventricle. Death. MEtTEEES : ( 1 ) Bilateral frontal sinusitis with abscess rt. frontal lobe. Sudden pain left eye. Operation left frontal sinus. Recurrence severe headache and sudden death, in collapse. Post-mortem showed abscess right frontal lobe, with delicate membrane. Cranial sinuses free from pathological changes. Fbeudenthal, W. : (1) Acute empyema frontal sinus. Diffuse suppuration frontal lobe. Two operations. Died after /second. No autopsy. In second operation catheter was introduced and struck only a fluid mass, so that more than frontal lobe seemed bathed in pus. Fbeiidenthal, W. (second case) : (1) Influenza frontal sinusitis. Extradural collection of pus. Abscess of frontal lobe. Two operations. Headache. Dis- colored bone. Abscess between it and intact dura. Recovery. Fbeudenthai., W. (third case) : (1) Acute empyema sphenoid sinus. Infection extended to other accessory sinuses with abscess in temporal lobe. Meetins, P.: (1) Headache; incision for swelling of glabella. Operation subse- quently showed extradural abscess. Some broken down brain tissue evacuated. Anterior wall of sinus necrosed and fistulous tract from sinus to extradural abscess. GeiiNWAU), L.: (1) Ozena, empyema both frontal sinuses. Carious destruction APPENDIX III 265 posterior sinus wall. Right-sided pachymeningitis. Abscess frontal lobe dis- covered eight days after primary operation. Kecovery. MnLLi]5r, W. V. : (1) Pain over frontal sinus and pus from nasofrontal ducts. Later pus from frontal sinuses and pain across forehead — more severe left side. Sudden death. Autopsy showed abscess left frontal lobe. Necrosis extended from surface all the way through frontal lobe and perforated into left lateral ventricle. Bekens, T. p.: (1) Pansinusitis rt. side. Kadical external, frontal, ethmoidal and sphenoidal operation performed. Gradual recovery. Three years later frontal headache. Swelling of cicatrix rt. frontal region. Incision through old frontal wound revealed frontal lobe abscess. Author is convinced patient carried large collection of pus for months in frontal lobe, and that this was source of nasal trouble. Elschnig, a.: (1) Chr. tuberculous tumor lachrymal gland right eye. Opera- tion. Extirpation of tumor with temporary resection of lateral orbital wall. Death four weeks after. Abscess found in rt. frontal lobe directly above base with circumscribed adhesion of meninges. Elschnio, A. (third case) : (1) Chr. frontal sinusitis. Incipient orbital phleg- mon. Radical operation after incision at upper inner orbital margin. Abscess found in frontal brain; death. Autopsy showed abscess reaching to area of second frontal convolution. Incipient encephalitis remainder frontal lobe and adjacent temporal lobe. Purulent meningitis entire right cerebral hemisphere. Zbmann, W. : (1) Chr. bilateral frontal sinusitis; fistula through left eyebrow; left-sided ethmoid cell suppuration. Radical operation left side. Subperiosteal abscess cavity. Two weeks later operation rt. frontal sinus. Death in three days. Autopsy showed adhesion rt. frontal lobe to posterior surface frontal sinus. Two deeper abscesses in frontal lobe behind superficial cortical abscess in white brain-substance frontal pole and separated from cortical abscess by layer of brain tissue. Bebens, T. p. : (1) Deafness rt. ear; intermittent purulent discharge. Tender mastoid. Radical operation. Sixteen days later profuse hemorrhage from middle ear cavity. Convulsions, headache, stupor, coma. Then attack typical Jacksonian epilepsy. Incision through dura revealed pus. Hernia of brain fill- ing bone wound. Death some days later. Autopsy showed subdural abscess over right hemisphere. Large abscess also occupying most of right frontal lobe with spontaneous discharge into subdural space. Case believed to be of otitic origin. LuBBBMS, K. : ( 1 ) Chr. frontal sinusitis and fistula rt. eyebrow followed by osteomyelitis frontal bone and frontal sinus empyema. Abscess rt. frontal lobe which author believed had existed for eighteen months. Recovery. Dura was reached following fistulous tract. HiBSCHBERG, O. : ( 1 ) Metastatic brain abscess following abscess bronchial glands. Fistula from broken down glands to esophagus. Death from purulent menin- gitis. Autopsy showed abscess rt. frontal lobe and several smaller abscesses. MoCoY, J.: (1) Pneumonia, swelling of eyelids one week later, incised. Fistu- lous openings showed eroded bone. Double ethmoiditis perforating both orbital plates. Extension necrosis frontal and forehead regions. Osteomyelitis. Epi- dural abscess left upper forehead. Nausea, vomiting, cerebral symptoms, paraly- sis rt. side, coma, disintegration entire frontal lobe. Necrosis and destruction of inner plate leading to epidural abscess, thence to frontal lobe by way of blood vessels. Abscess enlarged insidiously invading lateral ventricle. Death. McCoT, J. (second case) : (1) Pain left eye; frontal sinus relieved considerable pus. Improvement, but almost constant headache and intermittent discharge of pus. Swelling left forehead and epidural abscess found on incision. Head- ache, drowsiness, nausea, vomiting, osteomyelitis. Ethmoid labyrinth thor- 366 BRAIF ABSCESS oughly removed. Convulsions. Wound re-opened and multiple abscesses found. Section of bone removed from temporal region. Hernia cerebri, marked choked disc. Gradual recovery. Necrosis and destruction of inner plate leading to epi- dural abscess and thence to frontal lobe by way of blood vessels. Fagge, C. H. : ( 1 ) Empyema frontal sinus. Radical operation ; headache, apathy. Subnormal temperature; abscess left frontal lobe. Death. Post-mortem showed abscess nearly to anterior horn of lateral ventricle. Keimee : ( 1 ) Acute right frontal sinus inflammation. Three operations. In third large abscess extending close to lateral ventricle evacuated. Death five days later. Lambue, M. p. : (1) Chr. frontal sinusitis. Operation. Posterior bony wall intact. Infection of brain through venous or lymphatic channels. Abscess frontal lobe. Recovery. Cakgill, Tdbnek, and Thomas: (1) Orbital cellulitis incised. Later irritability and optic neuritis. Frontal sinus opened. Posterior wall necrotic. Brain covered with granulations. Abscess frontal lobe evacuated. Recovery. Feeudenthal, W.: (1) Acute frontal sinusitis. Headache, nasal discharge, ffidema rt. eye. Posterior wall of sinus eroded. Convulsions left side. Death several days later. Rawling, L. B.: (1) Frontal headache; oedema rt. upper eyelid. Coma; paraly- sis left side of body and face. Vomiting; optic neuritis. Operation; abscess found; recovery. Two later operations for return of symptoms. Headache, left hemiplegia. Marked hernia. Frontal sinus contained carious bone. Re- covery. Stuokt: (1) Traumatic ethmoiditis, meningitis, abscess frontal lobe. No local- izing symptoms. Death. Post-mortem showed necrotic cribriform plate. Frac- ture through table left frontal sinus. Cerebral convolutions softened. Mayub, H. : (1) Radical sinus operation for left-sided frontal sinus empyema. Death. Frontal abscess. Purulent meningitis. Thrombosis of sagittal and cavernous sinus. Bone intact. Infection occurred by way of blood vessels. Veins of roof of frontal sinus filled with pus and coagulated blood. Hammesfahe: (1) Left-sided frontal sinus empyema and frontal lobe abscess. Symptoms of brain pressure eight weeks later. Abscess found in posterior pole of lower frontal convolution. Recovery. Infection occurred by way of venous channel. EoEPKE : ( 1 ) Left frontal sinus and maxillary suppuration. Subperiosteal and extradural abscess. Second operation frontal lobe abscess. Death. Probable rupture into lateral ventricle. EoEPKE (second case): (1) Bilateral frontal sinus suppuration. Osteomyelitis. Frontal lobe abscess. Meningitis. Three operations. Abscess had ruptured into meninges and into the lateral ventricle. Death. Hoffmann, R. ^ ( 1 ) Bilateral chronic sinus suppuration. Multiple brain abscess. Left-sided traumatism. Two operations. Recovery. Recurrence five months later. Death. Post-mortem showed infection by lymphatics. Seifeet: (1) Bilateral empyema frontal sinus. Removal nasal polyps. Death five days later. Post-mortem showed abscess rt. frontal lobe. Continuity Infec- tion posterior wall through lymphatics or blood vessels. GaeipdY: (1) Acute frontal sinusitis. Orbital phlegmon. Two operations. Death. Post-mortem showed abscess frontal lobe at level of meningeal and bone lesions. Microscopical abscess on cortical surface of brain. Incipient osteitis orbital roof. Eeinhaed: (1) Left-sided frontal sinus suppuration and frontal lobe abscess. Extradural abscess, meningitis, and brain pressure after operation. Loss of consciousness. Death. Post-mortem showed behind extradural abscess one on floor of second left frontal convolution. Layer of healthy brain tissue between. Appendix ill ger Linden: (1) Empyema left frontal sinus. Brain abscess. Death. Post-mortem showed dura and pia adherent. Thick-walled abscess. No direct communica- tion between abscess and sinus. Path of infection sequestration of posterior wall. Heezpeld, J.; (1) Coryza. I^eft-sided frontal headache. External operation. Posterior wall frontal sinus carious and removed. Epidural abscess found. Dura incised. Subdural abscess evacuated. Fistula in frontal lobe of brain. Eecovery. WERraEiM: (1) Fever, headache, discharge from nose. Tumor over rt. eye. Incision voided pus. Sinus wall roughened. Death. Post-mortem showed ab- scess rt. frontal lobe, necrosis posterior wall. Circumscribed pachymeningitis. Denker: (1) Pain left temple and eye. Intranasal operation for left frontal sinusitis and ethmoiditis. One month later external operation. Headaches, somnolence, blurring left optic disc. Posterior wall frontal sinus removed. Epidural abscess exposed. Dura incised. Brain incised and abscess evacuated. Eecovery. Tbaittmann: (1) Empyema left frontal sinus. Perforation into orbit and an- terior cranial fossa. Abscess left middle frontal lobe. Caries orbital roof. Death two weeks later. Post-mortem showed dura adherent to left frontal lobe and brain. Perforation of posterior wall. Circular orifice in bone communi- cating with frontal sinus. Wilson: (1) Abscess frontal sinus and frontal lobe. Perforation external and internal wall. Death. Pfingst: (1) Ethmoidal involvement, head pains on side of orbit; convulsion, suddm death. Post-mortem showed large encapsulated abscess in frontal lobe. Path of infection through blood vessels. Fkontal Lobe Abscess Associated with Complications. Lombard, Blooh, and Moulouguet: (1) Operation right frontal lobe which yielded no pus. Day after left-sided hemiparesis with hypesthesia and disap- pearance of cutaneous and tendon reflexes same side. Second operation no abscess found, but autopsy showed right frontal abscess. Nonnb: (1) Eight-sided hemiparesis of character of organic paralysis. Patellar reflex and Achilles jerk absent on both sides. Choked disc from neuritis optica. Disturbances in co-ordination, in standing and walking; ataxia of trunk muscles; absence sense of smell. Complete paralysis of right side before death. SoLOWCYCZYK, A., and Kabbowski, B.: (1) Intracranial. Legaaed: (4) Intracranial. Schousboe: (1) Empyema of frontal sinus and anterior ethmoidal cells. Patient became dull and indifferent. Loss of appetite; vomiting; retarded pulue. MoEiXBat: (1) Left maxillary sinus empyema and orbital abscess. Nauseated after operation. Ethmoid cells and sphenoid. Manasse: (1) Frontal sinusitis. Intracranial complications short time after acute influenza; sinusitis. Left frontal abscess, then left temporal; then intra- meningeal abscess in left occipital lobe. Eckstein : ( 1 ) Somnolence. Suppurative thrombosis of longitudinal sinus with extradural abscess. PlCQirfe: (1) Severe pains right ear. Mastoid tender on pressure. Intelligence blunted. Complete left-sided hemiplegia. Cerebral hernia. Generalized en- cephalitis at autopsy. Smaller focus in addition to first also foimd. Steese: (1) Pain both eyes; dimness of vision. Mental dullness; delirium, stupor. Difiiculty in swallowing and breathing. Frontal sinus disease shown by post-mortem. Vomiting; urinary incontinence; constipation. Death. Steese (second case): (1) Phthisis several months. Paralytic stroke. Left »68 BRAIN ABSCESS hemiplegia. Occasional chronic spasm left side with spasmodic conjugate deviation. Ankle clonus. Steese (third case): (1) Fracture of skull; vomiting; shallow respiration. Abscess right frontal lobe. Steese (fourth case): (1) Abscess in left frontal lobe. Entire lobe softened. Headache; malaise; and chills. Steese (fifth case) : (1) Fracture of skull. Spasms left side of face and ex- tending to leg and arm. Abscess frontal lobe. Laceration of cerebellum. Pneumonia. Steese (sixth case): (1) Bullet removed from head. Headache; stupor; twitching right hand and leg. Slight paralysis left side. DiflSculty in swal- lowing. Right pupil dilated and left contracted. Rigor. Koehleb: (1) Traumatic (penetrating) abscess left hemisphere. Vomiting. Coma. Swelling. Tremor left half of body. Koebel: (1) Post-mortem showed right cerebral hemisphere distinctly en- larged, as compared to left. Cavity at apex and base of medulla right frontal lobe. Lee, J. M. ; (1) Traumatic (penetrating) — foreign body. Convulsions. Spasms. Bulging dura. Rajtin: (1) Right frontal sinusitis and brain abscess. Congestion of brain. Teatel: (1) Abscess frontal lobe after purulent discharge left nose and pain in forehead and cheek. Removal of polyps left nose. Hemiparesis right side. Brain hernia. Convulsions. Removal of ethmoids. Death. VON ScHKOEDEE : ( 1 ) Rt. frontal abscess after right retrobulbar phlegmon. Serous meningitis right hemisphere. Necrosis , orbital roof. Dura under ab- scess inflamed. Kbecki : ( 1 ) Left frontal abscess after discharge of pus and polyps of nose. Operation for swelling above left eye and frontal sinus found filled with pus. Chills, fever, left-sided headache. Pain in occipital region. Apathy. Thicken- ing of dura mater. Soft meninges at base covered with pus. Zdekauee : ( 1 ) Puncture of dura after penetrating traumatic abscess left side of head. Dura found to be fluctuating. Recovery with paresis left hand. Redtenbachee : ( 1 ) Abscess apex frontal lobe after abscess left upper eyelid succeeding influenza. Chronic spasms. Headache; weakness right half of body. Apathy; rigidity of neck. Pus in frontal sinus and necrosis of its posterior wall. Dura adherent to this wall. BOEELIUS, J.: (1) Traumatic puncture upper eyelid resulting in epileptiform and cerebral symptoms. Twitching more marked left arm and leg. Deep incision in eyelid. Drainage tube. Recovery. Williamson : ( 1 ) Abscess frontal lobe after influenza. Nasal discharge. Frontal and occipital headache. Mentality dull which became progressively more marked. Optic neuritis right eye. Weichselbaum : (1) Influenza; swelling rt. upper eyelid; eyeball intact. Head- ache, vomiting, delirium. Abscess right upper eyelid. Pus right maxillary and frontal sinus and dura mater. Pachymeningitis and leptomeningitis. SiLLAK: (1) Empyema frontal sinus. Long standing sinusitis. Abscess in frontal sinus operated. Abscess frontal lobe. Renton, J. C. : ( 1 ) Right frontal abscess after incision with evacuation of pus over inner side of upper eyelid for right orbital cellulitis. Later severe head- ache, vomiting. Spasms left side. Post-mortem convolutions over right lobe slightly flattened. Right orbital plate necrosed and dura inflamed over this area. No direct communication between pus from orbit and cerebral abscess. Knapp: (1) Abscess left frontal lobe after orbital phlegmon, which was incised and pus found. Headache and vomiting. Orbit found free from pus and com- munication existed between orbit and dilated frontal sinus. Reineb: (1) Abscess left frontal lobe with rickets and cerebral symptoms. APPENDIX ill 369 Headache and anesthesia left face. Diminished hearing left side and paralysis left sixth nerve. Reineb (second case): (1) Abscess both anterior lobes. Eight was flattened and abscess was ruptured into right lateral ventricle. Left contained a cen- tral abscess. Headache, rigidity of neck. Contracture right arm. Left-sided facial paralysis. Convulsions. Nystagmus. Dilated pupils. Idiocy. BousQUET: (1) Acute empyema right frontal sinus. Subperiosteal orbital ab- scess and necrosis frontal bone. Puncture of orbit. Bone eroded. Two weeks later contractures, severe oedema, loss of consciousness. Trephining frontal lobe before death. Jactjbasch: (1) Abscess right frontal lobe. Sore in nose; dull headache; ver- tigo, vomiting. Speech slow and difBcult. Apathy. Pain back of head. Left- sided hemiparesis. Wyss, 0. i ( 1 ) Traumatic abscess of entire frontal lobe. Sudden onset of severe pain and twitching right arm and leg. Later paralysis right arm and leg. Fever. Enlargement of head. Coma; dilated pupils. Convulsions during one of which child died. Maas, H. i ( 1 ) Removal of polypi and nasopharyngeal polyp followed by apathy, vertigo, exophthalmos, delirium, death. Post-mortem showed abscess in frontal lobe of brain above ethmoidal region. YouL : ( 1 ) Traumatic abscess in region opposite temporal wound. Cerebral symptoms two weeks after injury; Vomiting. Convulsions; death. Post-mor- tem showed surrounding brain tissue disorganized. Symonds, C. J. : (1) Chr. suppuration ethmoid sinus. Death from diffuse men- ingitis. Post-mortem showed two abscesses under surface left frontal lobe. Dura mater beneath frontal lobe adherent to brain. Neither abscesses opened lateral ventricle. Extension to orbit. Symonds, C. J. (second case) : (1) Chr. suppuration ethmoidal and frontal sinuses with abscess left frontal lobe. Influenza. Nasal discharge. Operation for suspected subdural or cerebral collection. Death. Cerebral infection from ethmoid sinus. Extension to orbit. ScHAEFEE, H. : ( 1 ) Orbital phlegmon with death from meningitis. Post-mortem showed abscess. Destruction right ethmoid labyrinth rupturing through lamina papyracea, resulting in osteitis and periostitis of orbit. Later pachy- meningitis and purulent leptomeningitis. Death. Struycken, H. J. L. : (1) Severe headache. Pus from right nostril frontal sinus opened. Cerebral symptoms. Puncture cranial cavity. Drainage. Re- currence brain symptoms. Later a second abscess opened. Incomplete recov- ery with persistent amnesia. Steuycken, H. J. L. (second case): (1) Right-sided headache with rapidly de- veloping oedema of surroundings of right eye and protrusion of eyeball. Eth- moid cells opened and most of them removed. Large abscess behind eyeball opened. Later rigidity nape of neck. Vomiting. Another operation and an- other abscess found. Recovery with partial amnesia and persistent loss of smell right side. Apeeulo, C: (1) Traumatic penetrating abscess left frontal lobe. Craniectomy with recovery. Second operation which revealed solution of continuity. Drain- age with gauze and glass tube. Later cerebral hernia. Recovery. Complete cicatrization. Manasse : ( 1 ) Acute accessory sinus suppuration which led to enormous orbital phlegmon. Frontal sinus revealed pus during after-treatment. Cerebral symptoms; vomiting, headache, fever. Frontal sinus diseased and closed eth- moid cell found attached to its posterior wall. Three operations and at last frontal lobe brain abscess found imder the fronto-ethmoid cell. Suppurative process passed from ethmoid cell to bone and then to cranial contents through preformed vascular channels. Recovery. 270 BRAIN ABSCESS UrFENOBDE, W.: (1) Ozena and left-sided frontal sinus and ethmoid suppura- tion leading to orbital phlegmon through fistula. Two operations revealed ex- tradural abscess and frontal sinus abscess. Two months later frontal abscess, meningitis, after rupture frontal abscess into ventricle. Death. WiENEB, A. : ( 1 ) Persistent headache. Empyema frontal sinus, right side, with two operations. Later frontal lobe abscess. Operated. Recovery. HoscH, P. H.: (1) Bilateral maxillary sinusitis and right-sided ethmoidal and frontal sinusitis. Extradural perisinus abscess. Frontal lobe abscess found at base of right frontal brain only after death, because of unusual location. Purulent meningitis. Maffei: (1) Partial loss of vision followed by vomiting and severe headache. Incipient neuroretinitis. Later pain in nape of neck and rise of temperature. Death from asphyxia. Spontaneous discharge from left nostril and filling throat. No operation; no autopsy, but author believed disease to be in frontal lobe. Metjbees : ( 1 ) Bilateral frontal sinusitis with abscess right frontal lobe. Sudden pain left eye. Operation left frontal sinus. Recurrence severe headache and sudden death in collapse. Post-mortem showed abscess right frontal lobe. Abscess with delicate membrane. Cranial sinuses free from pathological changes. FEBtTDENTHAL, W. : (1) Acute empyema frontal sinus. Diffuse suppuration frontal lobe. Two operations. Died after second. No autopsy. In second operation catheter was introduced and struck only a fiuid mass so that more than the frontal lobe semed to be bathed in pus. Fbeudenthai,, W. (second case): (1) Influenza, frontal sinusitis. Extradural collection of pus. Abscess frontal lobe. Two operations. Headaches. Dis- colored bone. Abscess between it and intact dura. Recovery. Fkettdenthal, W. (third case) : (1) Acute empyema sphenoid sinus. Infection extended to other accessory sinuses with abscess in temporal lobe. MBatTiNS, P. S. : (1) Headaches. Incision for swelling of glabella. Necrosed bone. Operation subsequently showed extradural abscess. Some broken down brain tissue. Fistula. Death two weeks after operation from pulmonary com- plications. Heiman, Th. : (1) Bilateral empyema antrum of Highmore and left-sided frontal sinusitis. Bilateral earache. Severe headache and vomiting. Sudden death. Autopsy showed extradural abscess, right lobe and both frontal sinuses, ethmoid and maxillary sinus filled with pus. Abscess with stalk. Diffuse meningitis. MuLLiN, W. V. ! (1) Pain over frontal sinuses and pus from nasofrontal ducts. Later pus from frontal sinuses and pain across forehead, more severe left side. Sudden death. Autopsy showed abscess left frontal lobe. Necrosis ex- tended from surface all way through frontal lobe, perforating left lateral ventricle. Bebens, T. p. : (1) Pansinusitis rt. side. Radical external frontal ethmoidal and sphenoidal operation performed. Gradual recovery. Three years later frontal headache. Swelling of cicatrix right frontal region. Incision through old frontal wound revealed frontal lobe abscess. Author is convinced patient carried large collection of pus for months in frontal lobe and that this was source of nasal trouble. PiFFL, 0. ; ( 1 ) Chr. left-sided frontal sinusitis and exophthalmos. Radical oper- ation. Removal orbital roof. Incision exposed dura. Frontal lobe adherent to orbital roof and frontal abscess found at autopsy. Elschotg, a. : ( 1 ) Chr. tuberculous tumor, lachrymal gland, rt. eye. Operation, extirpation of tumor with temporary resection of lateral orbital wall. Death four weeks after. Abscess found in right frontal lobe directly above base with circumscribed adhesions of meninges. APPENDIX III 271 Blschnig, a. (second case): (1) Phlegmon, left upper eyelid incised. Paresis rt. side and mental apathy. Operation left frontal abscess. Removal orbital roof and dura. Eecovery. Elschniq, a. (third case) : (1) Chr. frontal sinusitis. Incipient orbital phleg- mon. Radical operation after incision at upper inner orbital margin. Abscess found in frontal brain. Death. Autopsy showed abscess reaching to area of second frontal convolution. Incipient encephalitis remainder frontal lobe and adjacent temporal lobe. Purulent meningitis entire rt. cerebral hemisphere. Gkunwald, L. : (1) Ozena; empyema both frontal sinuses. Carious destruction posterior sinus wall. Right-sided pachymeningitis. Abscess frontal lobe dis- covered eight days after primary operation. Recovery. Zemann, W. : (1) Chr. bilateral frontal sinusitis; fistula through left eyebrow. Left-sided ethmoid cell suppuration. Radical operation left side. Subperiosteal abscess cavity. Two weeks later operation rt. frontal sinus. Death in three days. Autopsy showed adhesions rt. frontal lobe to posterior surface of frontal sinus. Two deeper abscesses in frontal lobe behind superficial cortical abscess in white brain-substance frontal pole and separated from cortical abscess by layer of brain tissue. Bekens, T. p. : (1) Deafness rt. ear. Intermittent purulent discharge. Tender mastoid. Radical operation. Sixteen days later profuse hemorrhage from middle ear cavity. Convulsions, headache, stupor, coma. Then attack typical Jaeksonian epilepsy. Incision through dura revealed pus. Hernia of brain filling bone wound. Death some days later. Autopsy showed subdural abscess over right hemisphere. Large abscess also occupying most of rt. frontal lobe, with spontaneous discharge into subdural space. Author believes case of otitic origin. MacBwbn, Wm.: (1) Trauma to forehead; unconscious; headaches; somnolence, vomiting, profuse perspiration. Patellar reflexes diminished. Pupils unequal. Paresis left internal rectus. Bilateral optic neuritis. Convulsions both arms. Operation without narcosis. Abscess frontal lobe. Gradual improvement all symptoms. MacEwen, Wm. (second case) : (1) Trauma of forehead; headache; wound; roughened bone. Somnolence. "Vomiting, temperature, chills, convulsions. Aphasia for an hour. Paralysis rt. side improved after several hours. Diag- nosis — abscess in third convolution. Operation refused. Death. Autopsy showed extradural exudate; hyperemia of dura. Abscess frontal lobe one inch from surface. LuBBEBS, K.: (1) Chr. frontal sinusitis and fistula rt. eyebrow followed by osteomyelitis frontal bone and frontal sinus empyema. Abscess rt. frontal lobe which author believed had existed for 18 months. Recovery. HiESCHBEEG, 0. : ( 1 ) Metastatic brain abscess following abscess bronchial glands. Fistula from broken down glands to esophagus. Death from purulent menin- gitis. Autopsy showed abscess rt. frontal lobe and several smaller abscesses. Kennkdy, Fosteb: (1) Traumatic non-penetrating right fronto-parietal region. Headache and irritability. Optic neuritis left side. Slight left facial weakness. Loss of smell right side. Gradually increasing left hemiplegia. Operation showed large abscess in frontal lobe; recovery. Sachs, E. : ( 1 ) Trauma to forehead. Dull and irritable. Paralysis rt. arm and leg. Lumbar puncture yielded clear fluid. Unconsciousness; convulsions. Vessels left retina tortuous. Operation. Frontal lobe abscess found and drained. Recovery. EiscHE, H.: (1) Headache. Swelling above left eye. Incised. Pus evacuated. Stupor, vomiting, external frontal sinus operation. Dura incised. Abscess found in frontal lobe; recovery. BuTZENGEiGEE, 0.: (1) Infection nasopharynx and frontal sinus; pus ruptur- ing to outside causing external abscess right side of forehead. Simultaneously 273 BEAIN ABSCESS inward progression of infection. Operation. Eight frontal sinus exposed. Frontal abscess found. Eight days later headache and vomiting; wound re- opened twice for refilling of abscess. Hernia cerebri. Ablation. Recovery. White, J. A. : ( 1 ) Chr. frontal sinusitis. Dullness of intellect. Operation dis-i closed frontal lobe abscess. Unconsciousness. Loss use rt. arm and muscles of face. Second abscess found in Rolandic fissure. Death. Damate, H. : (1) Frontal abscess following fatigue and bombardment. Patient soldier under observation for asthenia and headache with symptoms of shell shock. Death. Autopsy showed interlobar abscess rt. frontal lobe. Dura ad- herent to pia at level of rt. frontal lobe. SttjckY, a. : ( 1 ) Acute otitis rt. ear. Syphilis. Metastatic abscess left frontal lobe. Very chronic as shown by firm capsule. Death from meningitis. McCoy, J.: (1) Pneumonia. Swelling of eyelids one week later, incised. Fistulous openings showed eroded bone. Ethmoiditis perforating orbital plate, similar condition rt. and left. Extensive necrosis frontal and forehead re- gions. Osteomyelitis. Epidural abscess left upper forehead. Nausea and vomiting. Cerebral symptoms; paralysis rt. side. Coma. Encephaloscope showed entire frontal lobe had disintegrated. Death. McCoy, J. (second case) : (1) Pain left eye. Frontal sinus relieved considerable pus. Improvement, but almost constant headache and intermittent discharge of pus. Swelling left forehead and epidural abscess found on incision. Head- ache. Drowsiness. Nausea and vomiting. Ethmoid labyrinth thoroughly re- moved. Convulsions. Wound re-opened and multiple abscesses found. Section of bone removed from temporal region. Hernia cerebri. Marked choked disc. Gradual recovery. HuED, L. M. : (1) Chr. pansinusitis; epidural abscess; frontal lobe abscess. Meningitis. Death. Coulter, R. J. : (1) Trauma to left orbit (piece of wood) through upper eye- lid. Convergent squint and diplopia. Swelling in orbit incised. Three monthi later apathy. Loss of memory. Subnormal temperature. Both eyes proptosed. Paralysis left external rectus. Choked disc. Skull trephined. Frontal lobe abscess. Month later twitching right arm and leg. Second abscess tapped. Recovery. Fagge, C. H. : (1) Empyema frontal sinus. Radical operation. Headache. Apathy. Subnormal temperature. Abscess left frontal lobe. Death. Post- mortem showed abscess nearly to anterior horn of lateral ventricle. Feereri: (1) Trauma left side of head. Operation showed periostitis posterior wall. Sudden death four weeks later. Post-mortem showed left frontal ab- scess. No symptoms during life. Johnston: (1) Left-sided frontal sinusitis. Operation showed healthy bone. Sudden death four weeks later. Large abscess left frontal lobe, evidently present previous to operation. Membranous capsule. Keimee: (1) Acute rt. frontal sinus inflammation. Three operations. In third large abscess extending close to lateral ventricle evacuated. Death five days later. ScHOESTEiN: (1) Tuberculosis. Bronchiectatic cavities. Facial paralysis left side. Muscular spasm and later hemiplegia rt. side. Death three days later. Autopsy showed two abscesses frontal lobe. ScHORSTBiN (second case): (1) Tuberculosis; bronchiectatic cavities. Dullness and apathy. Death. Post-mortem showed abscess rt. frontal lobe. Lambur, M. P. : (1) Chr. frontal sinusitis. Operation. Posterior bony wall intact. Infection of brain through venous or lymphatic channels. Abscess frontal lobe. Recovery. Taylor, F. L. : ( 1 ) Trauma to rt. eye. Superficial abscess opened one month later. Headache, apathy, emaciation. Optic neuritis. Paresis left side of face. Stiflfness back of neck^ Vomiting; incontinence urine and feces. Operation. APPENDIX III 273 Et. frontal abscess. Eecovery with poor vision. Following year unconscious, convulsions. Death. Cakgill, TuBNESt, and Thomas : ( 1 ) Orbital cellulitis incised. Later irritability and optic neuritis. Frontal sinus opened. Posterior wall necrotic. Brain covered with granulations. Abscess frontal lobe evacuated. Recovery. Feetjdenthal, W. : (1) Acute frontal sinusitis. Headache; nasal discharge. (Edema right eye. Posterior wall of sinus eroded. Convulsions left side. Death several days later. Eawling, L. B. : ( 1 ) Frontal headache. CEdema rt. upper eyelid. Coma. Paraly- sis left side of body and face. Vomiting. Optic neuritis. Operation. Abscess found. Eecovery. Two later operations for return of symptoms. Headache, left hemiplegia; marked hernia. Frontal sinus contained carious bone. Ee- covery. StuokT: (1) Traumatic ethmoiditis; meningitis. Abscess frontal lobe. No localizing symptoms. Death. Post-mortem showed necrotic cribriform plate. Fracture through table left frontal sinus. Cerebral convolutions softened. Mayek, H. : ( 1 ) Eadical sinus operation for left-sided frontal sinus empyema. Death. Frontal abscess. Purulent meningitis. Thrombosis of sagittal and cavernous sinus. Bone intact. Infection occurred by way of blood vessels. Veins of roof of frontal sinus filled with pus and coagulated blood. Hammespahe: (1) Left-sided frontal sinus empyema and frontal lobe abscess. Symptoms of brain pressure eight weeks later. Operation. Abscess found in posterior pole of lower frontal convolution. Eecovery. Infection occurred by way of venous channel. EoEPKE: (1) Left frontal sinus and maxillary suppuration. Sub-periosteal and extradural abscess. Second operation. Frontal lobe abscess. Death. Prob- able rupture into lateral ventricles. EOEPKB (second case): (1) Bilateral frontal sinus suppuration. Osteomyelitis. Frontal lobe abscess. Meningitis. Three operations. Abscess had ruptured into meninges and into the lateral ventricle. Death. Hoffmann, E.: (1) Bilateral chr. sinus suppuration. Multiple brain abscess. Left-sided traumatism. Two operations. Eecovery. Eecurrence five months later. Death. Post-mortem showed infection by lymphatics. GoBiS: (1) Chr. frontal sinusitis. Fever, vomiting, convulsions. Operation — evacuation extradural abscess. Death. Post-mortem showed frontal lobe abscess. GoBlS (second case) : (1) Frontal sinusitis; meningitis. Death three days after operation for extradural abscess. Post-mortem showed frontal lobe abscess. CiSNBaios: (1) Frontal sinusitis. Evacuation of ethmoid. Operation for brain abscess. Disintegration large portion rt. frontal lobe. Death from meningitis. SlEFEBT: (1) Bilateral empyema frontal sinus. Eemoval nasal polyps. Death five days later. Post-mortem showed abscess rt. frontal lobe. Continuity in- fection posterior wall through lymphatics or blood vessels. Reis, W.: (1) Traumatic panophthalmitis. Brain abscess. Incision eyeball. Evacuation of pus. Headache, fever, coma, death from diffuse meningitis. _ MlLUGAN, W.: (1) Left frontal and ethmoidal sinus disease. Supraorbital in- cisions. Nasal drainage. Abscess left frontal lobe. Extensive basal menin- gitis. Death. MiLLlGAN, W. (second case): (1) Left frontal and maxillary sinus disease. Supraorbital incision. Alveolar drainage. Abscess left frontal lobe. Exten- sive basal meningitis. Death. Gabiput: (1) Acute frontal sinusitis. Orbital phlegmon. Two operations. Death. Post-mortem showed abscess frontal lobe at level of meningeal and bone lesions. Microscopical abscess on cortical surface of brain. Incipient osteitis orbital roof. Eeinhaed: (1) Left-sided frontal sinus suppuration and frontal lobe abscess. 274 BEAIK ABSCESS Extradural abscess. Meningitis and brain pressure after operation. Loss of consciousness. Death. Post-mortem showed behind extradural abscess one on floor of second left frontal convolution. Layer of healthy brain tissue between. Hubbabd: (1) Ozena; acute mastoiditis. No operation. Two months later mental dullness and headache. Mastoid tenderness. Death. Post-mortem showed abscess centre frontal lobe. Dura adherent to under surface right frontal lobe. LiKDEN: (1) Empyema left frontal sinus. Brain abscess. Death. Post-mor- tem showed dura and pia adherent. Thick-walled abscess. No direct com- munication between abscess and sinus. Path of infection — sequestration of posterior wall. Paunz: (1) Acute left frontal sinusitis. Headache and vomiting. Dilated sluggish pupils. Venous hyperemia of eyegrounds. Operation — ^bulging dura. Incision of dura and brain substance. Pus aspirated. Death. Heezfbld, J.: (1) Coryza. Left-sided frontal headache. External operation. Posterior wall frontal sinus carious and removed. Epidural abscess found. Dura incised. Subdural abscess evacuated. Fistula in frontal lobe of brain. Recovery. Weethehi; (1) Eever, headache, discharge from nose. Tumor over rt. eye. Incision voided pus. Sinus wall roughened. Death. Post-mortem showed abscess rt. frontal lobe. Necrosis posterior wall. Circumscribed pachymenin- gitis. Denkee: (1) Pain left temple and eye. Intranasal operation for left frontal sinusitis and ethmoiditis. On« month later external operation. Headaches, somnolence, blurring left optic disc. Posterior wall frontal sinus removed. Epidural abscess exposed. Dura incised. Brain incised and abscess evacuated. Eecovery. Tratjtmann: (1) Empyema left frontal sinus. Perforation into orbit and anterior cranial fossa. Abscess left middle frontal lobe. Caries orbital roof. Death two weeks later. Post-mortem showed dura adherent to left frontal lobe and brain. Perforation of posterior wall. Circular orifice in bone com- municating with frontal sinus. Wilson: (1) Abscess frontal sinus and frontal lobe. Perforation external and internal wall. Death. Pfingst, a. O. ; ( 1 ) Ethmoidal involyement. Head pains on side of orbit. Con- vulsions. Sudden death. Post-mortem showed large encapsulated abscess in frontal lobe. Path of infection through blood vessels. Jessamon, L. W.; (1) Tenderness over left frontal sinus and ethmoids. Nasal operation. Temperature. Thick speech. Aphasia. Paresis rt. arm. Complete paralysis rt. hand. Posterior wall frontal sinus removed. Congestion optic disc. Aphasia increased. Third operation, subdural abscess. Death. Post- mortem showed dura thickened especially over ethmoid and discoloration over ethmoid bone. Fbontal Lobe Abscess Associated with EPidtjbal Abscess. EiTBD, L. M.; (1) Chronic pansinusitis; epidural abscess; frontal lobe abscess; meningitis; death. Heezteld, J.: (1) Coryza. Left-sided frontal headache. External operation. Posterior wall frontal sinus carious and removed. Epidural abscess found. Dura incised. Subdural abscess evacuated. Fistula in frontal lobe of brain. Eecovery. Denkeb: (1) Pain left temple and eye. Intranasal operation for left frontal sinusitis and ethmoiditis. One month later external operation. Headaches. Somnolence; blurring left optic disc. Posterior wall frontal sinus removed; epidural abscess exposed. Dura incised. Brain incised and abscess evacuated. Recovery, APPENDIX III 275 Frontal Lobe Abscess AssooiATia) with Exteadueai, Abscess. Eeinhabd: (1) Extradural abscesses discovered at time of operation associated with one on floor of second left frontal convolution. Eagleton: (1) Case XXI — -D. McS., Chapter Seven, page 111. Eckstein : ( 1 ) Subperiosteal abscess at lateral end of left supraorbital margin with suppurative thrombosis of longitudinal sinus, and extradural abscess over upper half left frontal lobe. Uffenoede: (1) Ozena and left-sided frontal sinus and ethmoid suppuration, leading to orbital phlegmon, through fistula. Operations (2) revealed extra- dural abscess and frontal sinus abscess. Two months later frontal abscess, meningitis, after rupture of frontal lobe abscess into ventricle. Death. 'HoscH, P. H. : (1) Bilateral maxillary sinusitis and right-sided frontal and ethmoidal sinusitis. Extradural perisinus abscess, frontal lobe abscess found at base of right frontal brain after death. Purulent meningitis. FeeudbnthAL, W. (second case): (1) Influenza; frontal sinusitis. Extradural collection of pus. Abscess frontal lobe. Two operations. Headaches. Dis- colored bone. Abscess between it and intact dura. Recovery. Meetins, p. : ( 1 ) Headaches. Incision for swelling of glabella. Necrosed bone. Subsequent operation showed extradural abscess. Some broken down brain tissue evacuated. Fistula. Death two weeks after operation from pulmonary complications. Heiman', Th. : (1) Bilateral empyema antrum of Highmore and left-sided frontal sinusitis. Bilateral earache. Severe headache and vomiting. Sudden death. Autopsy showed extradural abscess. Eight lobe and both frontal sinuses, ethmoid and maxillary sinus, fllled with pus. Abscess with stalk. Diffuse meningitis. .MacEwen, Wm. (second case): (1) Trauma of forehead; headache; wound, roughened bone. Somnolence, vomiting, temperature, chills. Convulsions. Paralysis right side. Aphasia for an hour. Paralysis improved after several hours. Diagnosis — abscess in third convolution. Operation refused. Death. Autopsy showed extradural exudate. Hyperemia of dura. Abscess frontal lobe one inch from surface. EOEFKE: (1) Left frontal sinus and maxillary suppuration. Subperiosteal and extradural abscess. Second operation frontal lobe abscess. Death. Probable rupture into lateral ventricle. GoEis: (1) Chr. frontal sinusitis. Fever, vomiting, convulsions. Operation. Evacuation extradural abscess. Death. Post-mortem showed frontal lobe abscess. GoEis (second case) : (1) Frontal sinusitis; meningitis. Death three days after operation for extradural abscess. Post mortem showed frontal lobe abscess. EeinhAED: (1) Left-sided frontal sinus suppuration and frontal lobe abscess. Extradural abscess. Meningitis and brain pressure after operation. Loss of consciousness. Death. Post-mortem showed behind extradural abscess one on floor of second left frontal convolution. Layer of healthy brain tissue between. Hekzfeld, J.: (1) Coryza. Left-sided frontal headaches. External operation. Posterior wall frontal sinus carious and removed. Epidural abscess found. Dura incised. Subdural abscess evacuated. Fistula in frontal lobe of brain. Eecovery. Feontal Lobe Abscess Associated with Subdtteal. Bebens, T. p. : ( 1 ) Deafness right ear. Intermittent purulent discharge. Tender mastoid. Eadical operation. Sixteen days later profuse hemorrhage from middle ear cavity. Convulsions, headache, stupor, coma. Then, attack of typical Jacksonian epilepsy. Incision through dura revealed pus. Hernia of brain flUing bone wound. Death some days later. Autopsy showed subdural abscess over right hemisphere. Large abscess also occupying most of right 276 BEAIN ABSCESS frontal lobe, with spontaneous discharge into subdural space. Author believes case to be of otitic origin. GrOMS (second case): (1) Frontal sinusitis. Meningitis. Death three days after operation for extradural abscess. Post-mortem showed frontal lobe ab- scess (subdural). Heezfeld, J.: (1) Coryza. Left-sided frontal headache. External operation. Posterior wall frontal sinus carious and removed. Epidural abscess found. Dura incised. Subdural abscess evacuated. Fistula in frontal lobe of brain. Recovery. Jessamon, L. W. : (1) Tenderness over left frontal sinus and ethmoids. Nasal operation. Temperature. Thick speech. Aphasia. Paresis right arm. Com- plete paralysis right hand. Posterior wall frontal sinus removed. Congestion optic disc. Aphasia increased. Third operation subdural abscess. Death. Post-mortem showed dura thickened, especially over ethmoid and discoloration over ethmoid bone. Fbontal Lore Abscess Associated with Meningitis. Reinhabd: (1) Purulent leptomeningitis and frontal lobe abscess. Manasse: (1) Death from meningitis after abscess left frontal lobe, left tem- poral lobe and intrameningeal abscess in left occipital lobe. Zemann: (1) Eight frontal lobe abscess in form of superficial cortical abscess. Meningitis. Prbtsing: (1) Left frontal lobe abscess following empyema of left maxillary sinus, frontal sinus, and ethmoid cells. Meningitis. Death. Teeitbl : ( 1 ) Abscess frontal lobe. Basal surface frontal lobe hemorrhagic. Dura adherent over frontal lobe. Purulent basilar meningitis. VON ScHROEDEE: (1) Right-sided retrobulbar phlegmon producing right frontal abscess. Serous meningitis right hemisphere. Kbeckl: (1) Left frontal abscess after frontal sinus operation, for swelling above left eye. Sinus filled with pus. Previously discharge of pus from nose and nasal polyps. Autopsy — soft meninges at base covered with thick greenish pus. Kohler: (1) Abscess behind dura found after fluctuating painful swelling on left frontal tuberosity. Incised. Operation failed to, arrest further extension of meningitis. Hanot : ( 1 ) Abscess frontal lobe giving picture during life of tubercular menin- gitis. Weichselbaxtm : (1) Abscess right upper eyelid. Eyeball intact. Pus right maxillary and frontal sinus and between right frontal sinus and dura mater. Abscess opposite in frontal lobe. Purulent pachymeningitis and leptomenin- gitis. Reiner: (1) Abscess left frontal lobe with cerebral symptoms. Rickets and extensive caries frontal bone. Purulent meningitis at left side of base. Stmonds, C. J. : ( 1 ) Chr. suppuration of ethmoid sinus. Death from diffuse meningitis. Autopsy showed two abscesses under surface left frontal lobe. Dura mater beneath frontal lobe adherent to brain. Neither abscess opened lateral ventricle. Extension to orbit. ScHABPER, H. : ( 1 ) Orbital phlegmon with death from meningitis. Post-mortem showed abscess, destruction right ethmoid labyrinth rupturing through lamina papyracea. resulting in osteitis and periostitis of orbit. Later pachymenin- gitis and purulent leptomeningitis. Death. UrrENORDE, W. : (1) Ozena and left-sided frontal sinus and ethmoid suppuration leading to orbital phlegmon through fistula. Operations (2) revealed extra- dural abscess and frontal sinus abscess. Two months later frontal abscess and meningitis, after rupture of frontal lobe abscess into ventricle. Death. APPENDIX III 277 HosoH, p. H.: (1) Bilateral maxillary sinusitis and right-sided frontal and ethmoidal sinusitis. Extradural perisinus abscess and frontal lobe abscess foimd at base of right frontal brain after death. Purulent meningitis. HeimaM', Th. : ( 1 ) Bilateral empyema antrum of Highmore and left-sided frontal sinusitis. Bilateral earache. Severe headache and vomiting. Sudden death. Autopsy showed extradural abscess. Right lobe and both frontal sinuses, eth- moid and maxillary sinus, filled with pus. Abscess with stalk. Diffuse meningitis. Gbunwald, I.: (1) Ozena. Empyema both frontal sinuses. Carious destruc- tion posterior sinus wall. Right-sided pachymeningitis. Abscess frontal lobe discovered eight days after primary operation. Recovery. Elschnig, a. (third case): (1) Chr. frontal sinusitis. Incipient orbital phleg- mon. Radical operation after incision at upper inner orbital margin. Abscess found in frontal brain. Death. Autopsy showed abscess reaching to area of second frontal convolution. Incipient encephalitis remainder frontal lobe and adjacent temporal lobe. Purulent meningitis entire right cerebral hemi- sphere. HlESCHBEBG, 0. ; ( 1 ) Metastatic brain abscess following abscess bronchial glands. Fistula from broken down glands to esophagus. Death from purulent menin- gitis. Autopsy showed abscess right frontal lobe and several smaller abscesses. Stuckt, J. a.: (1) Acute otitis right ear. Syphilis. Metastatic abscess left frontal lobe. Very chronic as shown by firm capsule. Death from meningitis. Htjbd, L. M. : (1) Chr. pansinusitis. Epidural abscess; frontal lobe abscess. Meningitis. Death. Stucky, J. A. (second case): (1) Traumatic ethmoiditis. Meningitis. Abscess frontal lobe. No localizing symptoms. Death. Post-mortem showed necrotic cribriform plate. Fracture through table left frontal sinus. Cerebral con- volutions softened. Mayee, H. : (1) Radical sinus operation for left-sided frontal sinus empyema. Death. Frontal abscess. Purulent meningitis. Thrombosis of sagittal and cavernous sinus. Bon© intact. ROEPKE (second case): (1) Bilateral frontal sinus suppuration. Osteomyelitis. Frontal lobe abscess. Meningitis. Three operations. Abscess had ruptured into meninges and into the lateral ventricle. Death. GoBis (second case): (1) Frontal sinusitis. Meningitis. Death three days after operation for extradural abscess. Post-mortem showed frontal lobe abscess (subdural). CiSNEBOS: (1) Frontal sinusitis. Evacuation of ethmoid. Operation for brain abscess. Disintegration large portion right frontal lobe. Death from menin- gitis. Reis, W.: (1) Traumatic panophthalmitis. Brain abscess. Incision of eyeball; evacuation of pus. Headache, fever, coma. Death from diffuse meningitis. MiLLiGAN, W.: (1) Left frontal and ethmoidal sinus disease. Supraorbital incisions. Nasal drainage. Abscess left frontal lobe; extensive basal menin- gitis. Death. MiixiGAN, W. (second case): (1) Left frontal and maxillary sinus disease; supraorbital incision; alveolar drainage. Abscess left frontal lobe. Extensive basal meningitis. Death. Reinhaed: (1) Left-sided frontal sinus suppuration and frontal lobe abscess. Extradural abscess. Meningitis and brain pressure after operation. Loss of consciousness. Death. Post-mortem showed behind extradural abscess one on fioor of second left frontal convolution. Layer of healthy brain tissue between. Weetheim: (1) Fever, headache, discharge from nose. Tumor over right eye. Incision voided pus. Sinus wall roughened. Death. Post-mortem showed abscess right frontal lobe. Necrosis posterior wall. Circumscribed pachy- meningitis. 378 BRAIN ABSCESS I^ONTAL Lobe Abscess. BIBLIOGRAPHY. Apeblo: Abscesso del lobo frontale sinistro; Gazzetta degli OspedaU, 1917, XXXVIII, p. 337. Beeens, T. Passmoee: Brain Abscess from Chronic Suppuration in the Frontal Sinus; The La/ryngoscope, 1916, Vol. XXVI, p. 1083. Bekens, T. Passmoee: Abscess of Frontal Lobe of the Brain of Otitic Origin; Transactions of American Otological Society, 1913, Vol. XIII, p. 66; Annals of Otol., Rhinol, and La/ryngol., 1913, Vol. XXII, p. 433. BoECHAED: Ueber psychologische Storungen bei einem Stirnhornabszess ; Archiv fiir Klin. Cfm-urgie, 1904, Vol. LXXIV, p. 103. BoBELius: Abszess im rechten Stirnlappen; Archiv fiir Ki/nderheilhunde, 1891, Bd. XXXII, p. 189. BousQUET: Abaces d^veloppfi dans le sinus frontal du c5te droit; Le Progrds Medical, 1877, Tome V, p. 972. Butzengeigee : Zur Cliirurgie des Stirnhirnabszesses ; Mimoh. Med. Wochen- schrift, 1911, No. 46, p. 2449. Caegill, L. v., Tubnee, Wm., and Thomas, St. Claie: A Case of Abscess in the Left Frontal Lobe Originating from Suppuration in Left Frontal Sinus; Pro- ceedings of the Royal Society of Medicine, London, 1907-08. Casamajoe: Brain with Double Frontal Abscesses; Medical Record., 1915, Vol. 87, p. 412. Cisneeos: Abscfes du lobe frontal; Revue Eehd. de Laryngol., 1905, XXV, p. 545. CoxJLTEB, E. J.: Notes on a Case of Cerebral Abscess Following Orbital Injury; Ophthalmoscope, 1909, Vol. VII, p. 393. Damaye: Absces staphylocoque du lobe frontal; Progris Medical, 1918, XXXIV, p. 402. Denker: Ehinogener Frontallappen Abszess und extradurales Abszess; Archiv fiir Laryngol. u. Rhinol., 1900, Bd. X, p. 411. Dmochowskt: Entziindliche Progresse des Antrum Highmori; ArchiA> fiir Laryngol., 1895, Bd. Ill, p. 255. Deeteuss: Rhinogene Gehirnaffektionen ; International Centralblatt fiir Ohrenr heilhunde, Bd. VI, p. 103. Eckstein: Beitrag zur Kasuistik der Komplikationen des Stirnhohleneiterun- gen; Zeitschrift fiir Laryngol., Rhmol., u. ihre Grenegehiete, 1912, Bd. V, p. 291. Elsbbibg, C. a.: Abscess of Frontal Lobe Following Orbital Cellulitis; Annals of Surgery, 1917, LXVI, p. 508. Elschnig: Der orbitogene Hirnabszess; Prager Med. Wochenschrift, 1914, Bd. XXXIX, p. 37. Fagqb, C. H. : Two Cases of Brain Abscess (One Frontal Lobe Abscess); Gu^'s Hospital Reports, 1909, Vol. LXIII, p. 79. Feeeeei: Empyema of Frontal Sinus, Osteomyelitis, Frontal Lobe Abscess; Personal Communication to Oerber; (See Komplikationen der Stirnhohlenent- ziindungen, 1909.) FBEtTDENTHAL, W. : A Case of Abscess of the Brain of Nasal Origin; Inter- national Journal of Surgery, 1908, Vol. XXI, p. 269. Fbeudbnthal, W. : Die intrakraniellen Komplikationen naaalen Ursprungs; Archiv fiir Laryngologie, 1909, Bd. XXII, p. 400. Gbbbbe: Die Komplikationen der Stirnhohlenentziindungen; Monograph, Berlin, 1909. Gaeipuy: Sinusite frontale. Abscfes du cerveau; Toulouse Medical, 1905, Tome VII, p. 142. APPENDIX III 379 Goodman, C: Brain Abscess; Medical Record, 1917, Vol. XCI, p. 699. GoBis: Absces extradural; sinusite frontale; Archives Internat. de Laryngoh, etc., 1905, Tome XXI, p. 404. Gbuening, E. i Orbital Cellulitis, Empyema of the Ethmoid Cells and the Frontal Sinus; Abscess of the Frontal Lobe; Medical Record, 1904, Vol. LXV, p. 215. GEtJNWAiD: Abszess des Frontallappens ; Mimch. Med. Wochensolvrift, 1895, Bd. XLII, p. 472. Hammesfahk: Stirnhirnabszess; Deutsche Med. Wochenschrift, 1907, No. 16, p. 659. Hanoi: Vaste absces du lobe frontal droit; Archi/v. Gin. de M4decine, 1890, Tome II, p. 599. Hansbebg: Casuistiache Mitteilungen ; Zeitsehrift fii/r Ohrmheilhmide, Bd. 44, p. 361. Heiman, Th.; Absces c6rebral; L'Oreille et ses Maladies, 1914, II, p. 1068. Heiman, Th. : Empyema antri Highmori et sinusum frontalium Abscessus cere- bri; Zeitsehrift fUr Ohrenheilkunde, 1897-98, Bd. XXXII, p. 41. Hekzfeld: Rhinogischer Stirnlappenabszess durch Operation geheilt; Berliner Klin. Wochenschrift, 1901, No. 47, p. 1180. Hinsdale, G.: Purulent Encephalitis and Cerebral Abscess in the Newborn; Am. Jour. Med. Sciences, 1899, Vol. 118, p. 280. Hirschbebc: Beitrag zur Lehre der Hirnabszesse ; Deutsche Archiv fur Klin. Med.; 1912-13, Bd. 109, p. 314. Hoffmann: Multiple Hirnabszesse nach doppelseitiger traumatischer Stirn- hohleneiterung ; Verhandlung d. Vereins siid-deutsoher La/ryngologen, 1905, p. 185. Hoffmann: Absces multiples du cerceau; Archiv. Internat. de La/ryngol., 1906, Tome I, p. 79. Hosch: Erfolge der Radikaloperationen der Sinusitis frontalis; Zeitsehrift fur Ohrenheilkunde, 1910, Bd. LXI, p. 347. Hubbaed, Th. : Report of Cases of Pyogenic Brain Diseases Associated with or Caused by Acute and Chronic Nasal Suppuration; Trans. Am. La/ryngol., Rhinol., and Otol. Soc, 1903, p. 129. Hued, L. M. : Discussion Dr. McCoy's paper — Chronic Pansinusitis, Epidural Abscess, Frontal Lobe Abscess, Meningitis and Death; Trans. Am. Laryngol., Rhinol., and Otol. Soc, 1910. Jacubasch, D. : Abszess im vorderen rechten Gehirnlappen ; Berli/ner KUn. Wochenschrift, 1875, Bd. XII, p. 505. Jessamon, L. W. : Brain Abscess as a Complication of Acute Infection of Nasal Accessory Sinuses; Laryngoscope, 1920, Vol. XXX, p. 147. Johnston: Personal Communication to Gerber. (See Komplikationen der Stirnhohlenentziindungen, 1909.) Keimee: Personal Communication to Gerber. (See Komplikationen der Stirn- hohlenentziindungen, 1909.) Kennedy, Foster: Abscess of the Right Frontal Lobe; Operation; Recovery; Journal of Nervous and Mental Diseases, 1911, Vol. 38, p. 691. Knapp: Beitrag zur Pathologic der Stirnhohlen; Archi/o fiir AugenheilTcunde, 1880, Bd. IX, p. 448. Koebel: Ueber Kombination von Otitis media mit rhinogenem Gehirnabszess; Beitrdge zur KUn. Ghiru/rgie, 1898-99, Bd. XXV, p. 256. Kohleb: Empyema des Sinus Frontalis; ChaHti-Annalen, 1892, Vol. XVII, p. 333. Kohlee: Abscess of Frontal Lobe Following Traumatism; Issenfreund, Eeil- hroun, 1879, Vol. XXI, p. 33. (Abstract, Holt, Archives of Pediatrics, 1898, Vol. XI, p. 99.) 280 BRAIN ABSCESS Kbeckl: Beitrag zur Pathologie und Therapie des chronischen Stirnhohlen- empyems; Munch. Med. Woohenschrift, 1894, No. 51, p. 1030. Lauebns, M. p.: Abscess of Brain with Frontal Sinusitis; Journal of Laryn- ■ gology, 1908, Vol. XXIII, p. 339. Lee, L. M.: Abscess of Frontal Lobe of Brain; Bomeopathio Eye, Ear and Throat Journal, 1897, Vol. III. Leegaard, Fbithjof: Cerebral Abscess of the Frontal Lobe Originating from the Frontal Sinus; Annals of Otol., Bhmol., and Laryngol., 1919, Vol. XXVIII, No. 1, p. 95. Linden: Fall von Gehirnabszess im Anschluss an ein Empyems des Sinus frontalis; International Centralblatt fur Laryngologie, 1901, No. 7, p. 349. LoMBAKD, Blooh, and Moulouguet : Un cas d'absces du lobe frontal du c6te oppose a une otite suppuree chronique; Annal. des Maladies de I'Oreille, 1914, Tome 90, p. 749. Lubbers : Hirnabszess, Osteomyelitis des Stirnbeins, Stirnhohleu Empyema ; Archiv fii/r Ohrenheilkunde, 1912-13, Bd. 90, p. 172. Maas: Zur Kasuistik und Therapie der Gehirnabszesse; Berliner Klin. Woohen- schrift, 1869, Bd. VI, p. 127. MacEwbn, Wm. : The Pyogenic Infective Diseases of the Brain and Spinal Cord. Abstract by T. Passmore Berens in Transactions of Am. Otol. Soc, 1913, Vol. XIII, p. 80. Mabtei: Absces van de voqrhoofs des kwab der hersenen; Nederlandsoh. Tijdschrift von Q-eneeskunde, 1910, II, p. 2302. Manasse: Ueber orbitale und cerebrale Komplilcationen bei akuten Neben- hohleneiterungen ; Verhamdlung des Vereins deutschen Laryngol., 1911-12, p. 621. Mayee: Beitrag zur Kenntniss der Sehstorung nasalen Ursprungs; Wiener Klin. Woohenschrift, 1907, No. 31, p. 938. McCoy, J. : Report of Two Cases of Brain Abscess in the Frontal Lobe Secondary to Ethmoid and Frontal Sinusitis; Tramsactions of Am. Laryngol., Rhinol., and Otol. 8oo., 1910; Armals of Otol., Bhinol., and Laryngol., 1910, XIX, p. 287. Mertiks, p. S. : Empyema of Frontal Sinus, Followed by Extradural Abscess and Abscess of the Frontal Lobe; Am. Jour. Med. Soienoes, 1904, Vol. 127, p. 684. Meubees: Ueber Vier in Anschluss an eiterige Nebenhohlenerlcrankungen ent- standene Komplikationen mit todtlichem Ausgang; Zeitschrift fur Ohrenheil- kimde, 1910, Vol. 60, p. 335. MiLLiGAN, W.: Suppurative Frontal Sinusijiis; British Medical Journal, 1905, I, p. 171. MuLLiN, W. v.: Abscess of Left Frontal Lobe Following Suppuration of Frontal Sinus; Annals of Otol., Bhinol., and Laryngol., 1918, Vol. XXVII, p. 667. NoNNE: Atypisch verlaufene Falle von Hirnabszess; Deutsche Zeitschrift filr Nervenheilkunde, 1907, Vol. 33, p. 316. Onodi: Ueber die okulo-orbitalen, intrakraniellen und cerebrallen Komplika- tionen nasalen Ursprungs; Medizin. Klinik, 1914, No. 17, p. 719. Patjnz: Ueber den rhinogenen Hirnabszess; Arohiv fiir Laryngol. und Bhinol., 1902-03, Vol. XIII, p. 427. Pfingst, A. C. : Brain Abscess; Its Cause and Pathology; Miss. Valley Med. Jov/f., 1918, XXV, p. 193. PlCQU^: Absces c^r^bral consiScutif ^ une otite moyenne suppuree; Annal. d. Mai. de I'Oreille, 1890, XVI, p. 437. PlCQirfi, L., and F^vbiee, C. : Absces intracraneur d'origine otique; Annal. d. Mai. ■ de I'Oreille, 1892, XVIII, p. 883. Piffl: Zur Kasuistik der hinogenen Stirnabszesse; Prager med. Woohenschrift, 1914, Vol. XXXIX, p. 39. APPBKDIX III 281 Pretsing: Neun Gehirnabszesse im Gefolge von Ohren- und NaseA-Erkrankun- gen; Archiv filr Ohrenheillcunde, 1900-1901, Vol. LI, p. 262. Raj'IN: Sinusite frontale; absces du cerveau; Lyon Medical, 1897, Tome 85, p. 236. Rawling, L. B.: Case of Chronic Abscess of the Frontal Lobe; Recovery Transactions of the Medical Society of London, 1907, XXX, p. 375. Rbdtenbachee : Hirnabszesse und Eiterung im Sinus frontalis nach Influenza Wiener Med. Blatter, 1892, XV, No. 13, p. 200. Reimek: Gehimabszess : Jah/rbuch fii/r Kinderheilhunde, 1877, Vol. XI, p. 38 Reinhaed: Stirnhohleneiterung und Stirnlappenabszess ; Miinch. Med. Wochen- sohrift, 1905, No. 46, p. 2245. Reis, W. : Ein Abszess in der Lamina cribrose des Sch. nerven; Archiv filr Ophthalmologic, 1904, LIX, p. 155. Renton, J. C. : Note on a Case of Cerebral Abscess Subsequent to Orbital Periostitis; Glasgow Med. Jour., 1886, XXVI, p. 68. RiSCHE: Ein erfolgreich operierter Fall von Hirnabszess nach Stirnhohlener- krankung; Zeitschrift filr Ohrenheillcunde, 1911, Vol. LXII, p. 231. • RoPKE: Ueber die Osteomyelitis des Stirnbeins im Anschluss an Stirnhohleflei-' terung, und iiber ihre intrakraniellen Folgeerkranliungen ; Y erhandlu/hgen der deutschen Otol. Gesellschaft, 1907, Vol. XVI, p. 162. Sachs, E.: A Case of Frontal Lobe Abscess; Jour. Nervous and Mental Diseases, 1911, Vol. 38, p. 693. SCHAEFEK: Ein Fall von ulceroser Entziindung im Bereieh der rechten Stirn- hiilfte; Prager Med. Wochenschrift, 1883, Vol. VIII, p. 189. Schilling: Ueber die Osteomyelitis der fiaclien Schadelknochen ; Zeitschrift filr Ohrenheillcunde, 1904, Vol. 48, p. 52. ( Erganzungshef t. ) ScHlNDLEB: Absces du cerveau suite d'inflammation du sinus frontal gauche; Archiv. de Med. et de Pharm. Milit., 1892, Vol. XX, p. 241. SCHOESTEIN: The Schorstein Lecture on Abscess of the Brain; Lancet, 1909, II, p. 843. ScHOUSBOB: Ein Fall von Empyema sinus frontalis mit Stirnlappenabszess; Transt. Danish Oto-Laryngol. Society, March, 1915. Internat. Centralblatt fur Laryngol., 1915, XXXI, p. 396. VON ScHEOEDEE: Retrobulbares Phlegmon; Peterburger Med. Wochenschrift, 1895, No. 6, p. 56. ScHWABACH: Beitrag zur pathologisohen Anatomie des inneren Ohres und zur Frage vom primaren Hirnabszess; Beitrage zur Ohrenheillcunde. Lucae Fest- schrift, 1905, p. 55. Seifeet: Sur les absces du lobe frontal; Revue Behdom. de Laryngol., 1905, No. 24, p. 689. SiLEX: Fall von Stirnlappenabszess; Berliner Klin. Wochenschrift, 1896, No. 51, p. 1140. SiLLAB: Abscess in Left Frontal Lobe; Edinburgh Med. Jour., 1889, Vol. XXXV, p. 178. SoLOWCEjczYK and Kabbovitski: Zur Kasuistik der Stirnhohleneiterungen mit intrakraniellen Komplikationen ; Zeitsorift filr Laryngol., Rhinol., und ihre Grenzgebiete, 1914, VII, p. 15. Steese, E. S. : A Report of Fifteen Cases of Abscess of the Brain ; Medical and Surgical Report of the Presbyterian Hospital, 1898, Vol. Ill, p. 211. Struycken : Hersenabsces tengevolge van sinusitis frontalis in ethmoidalis; Nederlandsch. Tijdschrift von Geneeskunde, 1917, Vol. LXI, p. 224. Sttjoky, J. A.. Multiple Abscess of the Anterior Surface of the Left Frontal Lobe of the Cerebrum, Complicated by Mastoiditis and Otitic Meningitis; Autopsy; American Practitioner and News, 1911, Vol. LXV, p. 33. Stuoky, J. A.; Traumatic Ethmoiditis — Cerebral Abscess; Annals of Otol., Bhmol, Laryngol., 1907, XVI, p. 364. 282 BEAIIT ABSCESS StdckT, J. A.: Further Clinical Observations— Anterior Frontal Lobes; Lanoet- Clinio, 1912, Vol. LXIX, p. 612. Symonds; Diagnosis and Treatment of the Nasal Accessory Sinuses; British Medical Journal, 1894, I, p. 1357. SzDLiSLAWSKi : Ueber die Entstehung von Gehirnabszeasen im Verlauf von eiteriger Augenhohlenentziindung; Przlglad Lekwrski (Polish), 1900, No. 28, p. 380. Zeitschrift filr Augenheilkunde, 1900, IV, p. 235. Talko: Erweichungsherd im Frontal-Lappen; Zeitschrift fiir Augenheilkunde, 1900, rV, p. 236. Tatlob, F. L.: a Case of Abscess of the Frontal Lobe of Traumatic Origin; "New York Medical Journal, 1908, Vol. 87, p. 891. Trautmann: Abszess des linken mittleren Stirnlappens ; Oha/riti-Annalen, 1900, XXV, p. 301. Teeitei.: Ueber Hirnabszesse nach Stirnhohleneiterung; Deutsche Med. Woohen- schrift, 1896, Vol. XXII, p. 758. Uffenoedb: Complicierte Falle von Nasenhohlenerkrankung; Zeitschrift fur Laryngologie, 1911, Vol. Ill, p. 597. Vangehtjchten : Absces volumineux du lobe frontal gauche; Bull. Acad. Royal de Belgique, 1913, June 28. Weichselbaum : Influenza und Komplikationen ; Wiener med. Woohensohrift, 1890, Vol. XL, p. 223. WEETHEni: Erkrankungen der Nasen Nebenhohlen; ArcMv fur Laryngol., 1900, Vol. XI, p. 204. WiENEB, A.: Abscess in the Frontal Lobe of the Brain after Chronic Frontal Sinusitis; Medical Record, 1910, Vol. 78, p. 715. White, J. A.; Discussion. Transactions American Laryngol., Rhinol., and Otol. Society, 1910. Williamson, R. T.: A Case of Abscess in the Eight Frontal Lobe of the Brain; Medical Chronicle, 1890-91, XIII, p. 423. Wilson: Abscess of the Frontal Lobe; International Oentralblatt fur Laryn- gologie, 1899, No. 4, p. 149. Australian Medical Gazette, 1898, October 20. Wyss: Gehirnabszess im Kindesalter; Jahrhuch filr Einderheilkunde, 1871, IV, p. 139. YouL: Abscess of the Brain in a Child; Lancet, 1847, I, p. 71. Zdekauer: Hirnabszess. Heilung durch Trepanation; Jahrhuch filr Kinder- heilkunde, 1893, Vol. XXXV, p. 297. Zemaistn: Endocranielle Komplikationen nach chroniacher Nebenhohleneiterung; Zeitschrift filr Laryngologie, 1913, Vol. VI, p. 545. ZiRM: Thrombosierung beider Sinus cavernosa; Wiener Klin. Woohensohrift, 1892, No. 27, p. 394. ZwiLLiNGKR: Intrakranielle und cerebrale Komplikationen der Stirnhohlenent- zilndungen; Archiv filr Laryngologie und Rhinologie, 1914, Vol. XXVIII, p. 27L INDEX OF AUTHORS Acland, T. D., 242 Adami, 133, 163 Albrecht, W., 210 Alzheimer, 13 Amoss, H. L., 28, 143, 147 Aperlo, G., 261, 264, 269, 278 Argot, G., 129, 135 Armltage, F. L., 73 Arnold, J., 72 Ayer, J. B., 28, 141, 153, 154 Bacon, 46 Ballance, A. A., 97, 242 Barany, R., 12, 176, 200 Barr, J. S., 236 Beck, K., 16, 237 Behr, 173 Belinoflf, S., 66 Berens, T. P., 18, 70, 72, 73, 120, 246, 250,. 253, 259, 260, 265, 270, 271, 275, 278 Bibrowicz, W., 76 Bing, R., 209 Black, H., 187 Black, W. D., 235 Blake, 46 Bloch, A., 18, 73, 120, 259, 260, 262, 280 Bodkin, H., 67 Boenninghaus, G., 32, 122, 235 Boesch, H., 233 BoUack, J., 171 Bolton, J. S., 209 Borchard, 278 Borelius, J., 256, 261, 263, 268, 278 Bouchez, F., 82 Bourguet, 97 Bousquet, 245, 252, 256, 258, 263, 269, 278 Braun, A., 236 Braun, E., 242 Brieger, 31 BriggB, G. N., 235 Brock, W., 238 Brown, W. G., 179 Browning, W., 32, 120 Bruhl, 239 Bryant, W. S., 9 Buhl, C. G., 146 Butzengeiger, C, 247, 254, 271, 278 Cadwalader, W. B., 75, 183 Campbell, 178 Capdeville, F., 223 Cargill, L. V., 254, 258, 266, 273, 278 Caaamajor, L., 18, 259, 260, 262, 278 Cassidy, 134 Cassirer, R., 77 Cayley, 70 Cisneros, 248, 251, 255, 262, 273, 277, 278 Clark, 200 Climenko, H., 18 Coates, G. M., 60 Condat, M., 82 Coulet, G., 237 Coulter, R. J., 247, 258, 262, 272, 278 Couteaud, 73, 74, 120 Crile, 164 Crowe, S. J., 102, 170, 198 Cushing, H., 5, 7, 8, 11, 30, 59, 133, 141, 180, 202 Damaye, H., 110, 262, 272, 278 Dandy, W. E., 5, 128, 188 Day, 151 Dejerine, 12 Dench, E. B., 197 Denker, A., 208, 249, 251, 255, 258, 267, 274, 278 DeStella, 236 D'Hoore, 234 Dick, 73 Dixon, G. S., 242 Dmoehowaky, 252, 278 Dortea, P., 236 Dreyfuss, 278 Dupuy, 220 Durand, 74 Eagleton, W. P., 25, 63, 73, 89, 97, 98, 99, 103, 141, 149, 151, 169, 170, 200, 201, 243, 244, 256, 275 Eckstein, 251, 256, 267, 275, 278 Effler, L. R., 83 Elaberg, C. A., 278 Elschnig, A., 124, 247, 253, 257, 265, 270, 271, 277, 278 Emerson, L., 32 Emge, 73 Essick, C. R., 16, 25, 28, 32, 129, 132, 140, 148, 153 Fagge, C. H.,, 248, 254, 266, 272, 278 Faunz, M., 208 Feinier, L., 162, 184, 195 Felton, J. B., 69 Felton, L. D., 28, 69, 143, 153 Ferreri, 262, 272, 278 283 284 INDEX OP AUTHOES Ferrier, 195 Fevrier, C, 280 Finnel, 222 Flatau, 236 Flexner, S., 28, 143, 147 Fliess, H., 233 Foerster, 207 Forgue, E., 238 Frankel, 76 Fraser, J. S., 185 Frazier, C. H., 7, 9 Freudenthal, W., 248, 253, 254, 264, 266, 270, 273, 275, 278 Friedmann, M., 16, 48 Friedrich, 106 Friesner, I., 242 Garipuy, 248, 255, 258, 266, 273, 278 Gerber, P. H., Ill, 124, 278 Girard, L., 93 Glegg, W., 187, 238 Goodman, C, 279 Gordon, A., 178 Goris, 248, 255, 273, 275, 276, 277, 279 Gowers, W. R., 73 Gradle, H. S., 172 Grey; E. G., 202 Gribbon, G. C, 221 Groth, W., 73 Gruening, E., 245, 251, 256, 263, 279 Grunert, K., 232 Grlinwald, L., 246, 253, 264, 271, 277, 279 Guilliani, G., 209, 210 Gull, W., 220 Hadden, W. B., 222 Hammesfahr, 248, 254, 266, 273, 279 Hanfield Jones, M., 223 Hanot, 276, 279 Hansberg, 279 Harbordt, 227 Hare, A. W., 226 Harrison, C. E., 227, 228 Hartley, 9 Hartmann, A., 225 Harvey, S. C, 11, 12 Haasln, G., 16, 62 Hedinger, A., 224 Hegener, J., 16, 106 Heiman, Th., 229, 246, 250, 253, 260, 270, 275, 277, 279 Heine, B., 25 Held, 151 Henderson, D. R., 185 Henderson, J., 73 Hepe, 94 Herzfeld, J., 249, 255, 267, 274, 275, 276, 279 Heuer, 5 Heusinger, 220 von Hibler, E., 17, 239 Hill, F. T., 198 Hill, L., 14 von Hinsberg, 25, 118, 120, 123, 233 Hinsdale, G., 279 Hirschberg, 0., 259, 265, 271, 277, 279 Hoffmann, R., 255, 261, 262, 266, 273, 279 Hohgren, G., 198 Holmes, 131, 134 Homen, E. A., 16 Home, J., 94 Horsley, 5, 200 Hosch, P. H., 246, 250, 253, 270, 275, 277 279 Hubbard, Th., 249, 261, 274, 279 Huguenin, 49 Hurd, L. M., 247, 251, 254, 272, 274, 277, 279 Hutton, F. T., 224 Isemer, F., 235 Jacques, P., 237 Jacubash, D., 245, 269, 279 Jansen, A., 227 Japha, A., 72 Jessamon, L. W,, 198, 208, 210, 249, 251, 256, 274, 276, 279 Jobson, G. B., 25 Johnston, 260, 272, 279 Jones, H. E., 102 Jones, I., 198 Karbowski, B., 244, 251, 258, 267, 281 Karsner, H. T., 238 Keimer, 248, 254, 266, 272, 279 Kelson, W. H., 237 Kenefiek, T. A., 227 Kennedy, F., 178, 208, 210, 261, 271, 279 Kenyon, 9 Kesohner, M., 210 Klauber, E., 174 Klessens, J. J. H. M., 82 Klippel, D., 27 Knapp, A., 32, 117, 234 Knapp, H., 36, 46 Knapp, 249, 256, 263, 268, 279 Knott, J. F., 72 Koch, P., 242 Koebel, 245, 251, 260, 268, 279 Koehler, 252, 261, 263, 268, 276, 279 Kolpin, 16, 77 Kopetsky, 151 Kopeynski, 243 Korner, 0., 16, 22, 77, 228 Kostlivy, 151 Krause,' F., 7, 41, 74, 76 Kreckl, 245, 252, 256, 268, 276, 280 Kutzinski, A., 70, 82 INDEX OF AUTHOES 285 Laiguet-Levastine, 179 Lambur, M. P., 248, 254, 260, 266, 272 Landau, M. E., 12 Lannois-Perretiere, 234 Laurens, P., 235, 280 Lebert, 49 Lee, J. M., 256, 261, 263, 268, 280 Leegaard, F., 121, 267, 280 Lemaitre, F., 54, 63 Leriche, E., 174 Lewinsohn, G., 173 Libert, E., 209, 210 Linck, 238 Linden, 249, 255, 267, 274, 280 Loebinger, A. S., 135 Lombard, 18, 73, 120, 259, 260, 262, 267. 280 Lessen, W., 72 Lubbers, K., 247, 253, 258, 265, 271, 280 Luc, 245, 252 Luciani, L., 194, 195, 202 Ludewig, 225 Maas, H., 245, 263, 269, 280 MacEwen, W., 16, 24, 46, 81, 86. 87, 97, 98, 261, 271, 275, 280 Mackenzie, 89, 228 Macklin, C. C, 16, 142 Macklin, M. T., 16, 142 Maffei, 246, 257, 270, 280 Maier, M., 72, 240 Mall, 97 Mallory, 52 Manasse, 46, 244, 246, 250, 251, 252, 257, 264, 267, 269, 276, 280 Martin, H. H., 102, 170, 198 Martland, H. S., 3 Marx, 70, 82 Masland, H. C, 12 Mayer, H., 163, 248, 254, 266, 273, 277, 280 Mayman, L., 16 McCoy, J., 247, 250, 254, 258, 265, 272, 280 McCrae, 133, 163 McKibben, P. S., 142 McRobert, E. G., 162, 184, 195 Menetrier, P., 74 Mertins, P., 264, 270, 275, 280 Meurers, 246, 253, 257, 258, 260, 262, 264, 270, 280 Meyer, R., 73 Meyers, L L., 193 Michaelsen, U., 240 Miegeville, 12 Milian, G., 208, 210 Milligan, W., 114, 226, 248, 251, 255, 273, 277, 280 Mills, C. K., 193 Mlngazzirn, G., 202 MiodowBki, F., 16, 24, 242 Moeller, 251, 256, 267 Mollison, W. M., 127 Moore, J. T., 70, 83 Moos, S., 221 Moulouguet, A., 18, 73, 120, 196, 259, 260, 262, 267, 280 Muck, 57, 58, 188, 231 Muirhead, W., 185 Miiller, E., 66, 229 MuUin, W. v., 246, 253, 265, 270, 280 Myers, I. L., 192 M^fgind, H., 67, 212 Nauwerck, 67 Neal, J. B., 160 Neumann, H., 48, 101, 102 Nichorster, H., 210 Niehsmann, Th., 212 Nonne, 120, 256, 260, 262, 267, 280 Nourse, 242 Okada, W., 231 Onodi, 115, 280 Orne Green, J., 230 Page, 134 Panse, E., 226 Paunz, M., 249, 255, 258, 274, 280 Piingst, A. O., 124, 249, 251, 267, 274, 280 Pick, L., 170 Picque, 244, 259, 260, 267, 280 Piersol, 24 Piffl, O., 124, 247, 253, 257, 270, 280 Pike, F. H., 197 Pitt, G. N., 226 Plant, 3 Pogany, E., 83 Poirier, 151 Politzer, A., 16, 234 Pollak, 242 Preysing, H., 23, 232, 244, 245, 251, 262, 263, 276, 281 Quimby, W. O. G., 18, 72 Rados, A., 173 Eafin, 245, 252, 268, 281 Eahn, H., 12 Randall, B. A., 227 Rauzier, G., 238 Eawling, L. B., 128, 222, 248, 254, 266, 273, 281 Redtenbacher, 245, 256, 268, 281 Reinhard, 225, 244, 249, 255, 266, 273, 275, 276, 277, 281 Eeimer, 245, 252, 258, 259, 263, 268, 269, 276, 281 Eeis, W., 258, 262, 273, 277, 281 286 INDEX OF ATJTHOKS Eeischig, 3 Eenton, J. C, 245, 256, 263 268, 281 Reynolds, C. E., 43, 73 Reynolds, F. E., 237 Richardson, C, 211 Rische, H., 247, 253, 271, 281 Roepke, 46, 248, 254, 259, 266, 273, 275, 277, 281 Roger, 238 Rogers, P. T., 163 Rohardt, W., 198 Rossi, G., 194 Rothholz, H., 224 Roulland, H., 74 Ruttin, E., 66, 102, 171, 242 Ryder, 172 Sachs, E., 262, 271, 281 Saelhof, C. C, 76 Sant^, H., 24, 46, 52 Sargent, 131, 134 Sautter, C. M., 163 Savariaud, 238 Schaefer, H., 246, 250, 257, 264, 269, 276, 281 Schaller, W. F., 243 Schick, F., 173 Schilling, R., 116, 281 Schindler, 252, 263, 281 Schorstein, 70, 74, 76, 260, 272, 281 Schott, 49 Schottmiiller, 3 Schousboe, 124, 251, 256, 267, 281 von Schroeder, 245, 256, 263, 268, 276, 281 Schulz, R., 222 Schulze, 232 Schwabach, D., 120, 258, 259, 260, 281 Schwarze, 226 Sehwartze, H., 220 Scott, 94 Seifert, 248, 255, 266, 273, 281 Sierra, A. M., 210 Silex, 245, 249, 252, 263, 281 Sillar, 245, 252, 268, 281 Skillern, P. G., 108 Smith, H. B., 7 Smith, S., 134 Smith, Th. C, 225 Solowcyczyk, A., 244, 251, 258, 267, 281 Spencer, F. R., 239 Sperling, 74 Stallard, J. H., 223 Steed, K., 132 Steese, 245, 251, 256, 259, 261, 267, 268, 281 Steinbrugge, H., 221 Stolz, 97, 171 Strauss, I., 3 Streit, H., 25, 118, 123, 140 Struycken, H. J. L., 246, 250, 252, 257, 264, 269, 281 Stucky, J. A., 251, 260, 261, 262, 266, 272, 273, 277, 281, 282 Sutphen, T. Y., 224 Syme, W. S., 242 Symonds, C. J., 245, 249, 250, 252, 256, 257, 264, 269, 276, 282 Szulislawski, 282 Talko, 282 Taylor, F. L., 258, 262, 272, 282 Texier, v., 243 Thigpen, Ch. A., 242 Thomas, St. Olair, 254, 258, 266, 273, 278 Tobey, G. L., 133 Topley, W. C, 16 Trautmann, 249, 255, 267, 274, 282 Treitel, 245, 252, 268, 276, 282 Troeltsch, 221 Truckenbrod, C, 227 Turner, L. A., 116, 237, 254, 258, 266, 273, 278 Tylor, C, 16, 73 von Uchermann, 49, 233, 239, 242 Uffenorde, W., 236, 246, 250, 252, 257, 264, 270, 275, 276, 282 Urbantschitsch, E., 66, 77, 82, 239 Vangehuchten, 249, 263, 282 Verhoeff, F. H., 172 Viete, H., 209 Viollet, P., 230 Voltolini, R., 220 Voss, P., 66, 235, 243 Wallace, C. S., 229 Warrington, W. B., 32, 168 Weed, L. H., 20, 28, 69, 72, 128, 132, 141, 142, 144, 147, 150, 153, 154, 172, 173 Wiegeforth, P., 28, 69, 128, 132, 141, 145, 147, 150, 153, 154, 172 Weichselbaum, 245, 252, 256, 263, 268, 276, 282 Weisenberg, T. H., 193 Wertheim, 260, 267, 274, 277, 282 West, 94 Westphal, 16, 48 Wheat, D. S., 163 White, J. A., 247, 254, 272, 282 Whitehead, A. L., 32 Whiting, P., 56 Wiener, A., 179', 246, 252, 270, 282 Williamson, 245, 249, 252, 256, 268, 282 Wilson, 197, 249, 255, 267, 274, 282 INDEX OP AUTHOES 287 Wittmack, 16 Wolbach, S. B., 102 Woodward, J. U., 229 Wright, 224 Wyss, O., 261, 269, 282 Youl, 245, 261, 263, 269, 282 Zdekauer, 256, 261, 268, 282 Zeller 229 ZemaAn, W., 123, 244, 247, 250, 253, 257, 263, 265, 271, 276, 282 Zeroni, W., 232 Zirm, 252, 256, 263, 282 Zwillinger, H., 116, 140, 282 INDEX OF SUBJECTS Abdominal reflexes, loss of, in frontal abscess, 209 Abscess, adjacent, see Adjacent abscess brain, see Brain abscess capsulated, 23 cerebellar, see Cerebellar abscess cerebral, see Brain abscess, and Cere- bral abscess double, see Double abscess extradural, see Extradural abscess frontal, see Frontal abscess idiopathic, see Idiopathic abscess intercurrent, see Intercurrent ab- intracerebellar, see Intracerebellar intracerebral, see Intracerebral ab- scess intradural, see Intradural abscess intrapiarachnoid, see Intrapiarach- noid abscess in lateral cisterna, 05 losing, 56 meningeal, see Meningeal abscess meningo-cerebral, 22 metastatic, see Metastatic abscess of middle fossa, see Middle fossa oyster shaped, 34 perisinus, see Ferisinus abscess second, 59 secondary, 59 subdural, see Subdural abscess temporo-sphenoidal, see Temporo- sphenoidal abscess traumatic, see Traumatic abscess Accessory nasal sinuses, operations for suppurative lesions of, 123 Adhesive inflammation of piarachnoid to dura, surgical signiflcance of, 50 Adjacent abscess, 17, 20, 68 After effects of brain abscess, 211 Anesthesia, 4 local, 5 Aphasia, in frontal abscess, 208 in temporo-sphenoidal abscess, 177 naming, 46 Aseptic meningitis, case of (VI), 33 Assistants must be trained, 4 Autolysis, in subnormal temperature, 164 Bleyle's hammer, 9 Bone, sacrifice of, 9 Brain, and see Cerebral abscess, see below Brain abscess, Cerebellar abscess, Frontal abscess, Temporo-sphenoidal ab- scess blood supply of, 24 elevation of, 44, 50 exploration into, 45 hemorrhage from, control of, 12 hernia of, see Hernia herniation of, see Herniation infection of, methods, 138 injury to from its own pressure, 29 inspection of, within dura, 42 necrosis of, superficial, 32 oedema of, sudden death from, 15 protective mechanism of, 137, 139, 147 additional references to, 153 by dura, 139 by subarachnoid spaces, 140 by subdural space, 140 removal of dead tissue from, 149 repair of, 149 sensitiveness of, to toxic influences, 147 suppuration within, limitation of, 148 Brain abscess, acute, 61 adjacent, 17 closure of, 65 exploring for, 65 methods of treatment, 62 pathology of, 61 surgical aims in, 62 surgical pathology of, 62 varieties of, 22 after effects of, 211 case of (VII), 35 (XXIX), with transient aphasia and paralysis, 185 classification of, according to loca- tion, 30 clinical, 21 chronic, adjacent, 17 closure of, 65 surgical pathology of, 47 varieties of, 21 complications of, 211 compression, secondary in, 58 diagnosis of, 155 differential diagnosis of, 211 evacuation of, complications after, 211 289 390 INDEX OF SUBJECTS Brain abscess from meningitis, 144 idiopathic, 18, 73 intercurrent, 17 metastatic, 17, 18, 25, 68, 69, 120 pathology of, references to, 16 results of, 211, 212 surgical classification of, 17, 19 surgical factors in, 28 surgical pathology of, 17 surgical principles in, 27 surgical technic in, 28 traumatic, 17, 19, 25, 121, 261 Capsulated abscess, 23 Capsule, formation of in metastatic abscess, 76 Cerebellar abscess, 84 additional bibliography, 242 adjacent, surgical classification of, 85 surgical principles in treatment of, 101 analysis of pathological condition in reported autopsies of 125 cases, 220 anatomical factors in, 86 associated with extradural abscess, 105 case of (I), delay in operating fatal, 3 case of (XIX), 99 case of (XXXI), with vague symp- toms, 203 cerebellar ataxia in, 194 cerebellar attitude, forced, in, 195 cerebellar convulsions in, 195 cerebellar paralysis in, 194 changing character of vestibular re- actions in, 199 classification of symptoms, 191 clinical classification of, 95 diagnosis of, 190 double, case of (XII), 60 exploration of, 103 exposure of behind sinus, 104 failure of inhibition in, 194 falling in, 198 following sinus thrombosis, 101, 103 herniation in exploration for, 86 hypermetria in, 194 immediate occasion of, 84 irregular shape of, 101 knee jerks in, 202 labyrinth in etiology of, 91 labyrinthine suppuration in, 94 labyrinthitis in diagnosis of, 190 lateral deviation of eyes in, 197 lateral sinus thrombosis in diagnosis of, 190 local symptoms from direct pressure, 201 obliteration of symptoms the result of cerebellax compensation, 194 Cerebellar abscess, origin of, 84, 91 past pointing, spontaneous in, 198 pathological factors in, 87 physiological factors in, 86 post-mortem findings in, 220 psychic disturbances in, 202 pupillary disturbances in, 201 rapid loss of flesh in, 202 routes of infection in, 88, 91 in 125 cases, 89 secondary to sinus thrombosis, 101, 102, 104 situation of, 105 speech defects in, 195 spontaneous nystagmus in, 197 suboccipital tenderness in, 202 surgical considerations in, 85 surgical requirements for explora- tion and evacuation, 105 surgical treatment of, 96 symptoms of, 191, 201 due to internal hydrocephalus, 203 ventricular puncture in, 104 vertigo in, 197 vestibular manifestations in, 196 vestibular reactions, changing char- acter of in, 199 induced abnormal, 198 reported cases of, 198 vomiting in, 202 yawning in, 202 Cerebellar ataxia, in cerebellar abscess, 194 Cerebellar attitude, forced, in cerebel- lar abscess, 195 Cerebellar compensation, cause of ob- literation of cerebellar symp- toms, 194 Cerebellar convulsions, in cerebellar ab- cess, 195 Cerebellar cortex, pressure on, with vestibular manifestations, 200 Cerebellar cortical localization, in re- lation to vestibular reaction, 200 Cerebellar function, impaired, manifes- tations of, 192 Cerebellar lesions, stages of, 193 Cerebellar operations, outrigger for, 7 Cerebellar paralysis, in cerebellar ab- scess, 194 Cerebellar symptoms from direct pres- sure, 201 Cerebellum, experimental ablation of, symptoms, 192 exploration of after destruction of labyrinth, 96 exposure of lateral lobes with ex- ploration and drainage behind lateral sinus, 96 IITDEX OF SUBJECTS 291 Cerebellum, incision and evacuation in front of lateral sinua, 96 infection of from bony caries or necrosis, 9i operative approach to, 95 physiology of, 192 Cerebral abscess, case of (II), delay in operating fatal, 3 coma in, 167 compression, blood pressure in, 166 ocular paralysis in, 167 papillcedema in, 168 projectile vomiting in, 167 pulse pressure in, 167 pulse slow in, 166 symptoms of, 165, 166 in frontal abscess, 207 Cerebral suppuration, chill, evidence of, 157 convulsions, evidence of, 161 disproportion evidence of, 158 evidence of, 157, 160 headache, evidence of, 157 is it possible, 156 is it probable, 156 malaise, evidence of, 158 meningitis, protective, evidence of, 160 positive evidences of, 160 subnormal temperature evidence of, 163 symptoms of, in frontal abscess, 207 vomiting, evidence of, 157 Cerebral tissue, factors peculiar to which demand surgical recogni- tion, 13 histopathology of, 13 susceptibility of to bacterial viru- lence, 146 Cerebral trauma, death from, 15 Cerebro-spinal fluid system, anatomy of, 141 impr^nability to infection, 142 infection of from blood stream, 144 Chest position, Sims', 6 Chill, evidence of cerebral suppuration, 157 Chisels, 9 Chronic brain abscess, after-treatment of, 59 drainage in, 57 Cisterna, lateral, abscess in, 95 Clamp, Heuer's temporo-museular, 9 Clips, spring, of Makkas, 9 Closure, of brain abscess, 65 of dura, 12 Coma, in cerebral compression, 167 in frontal abscess, 207 Complications of brain abscess, 211 Compression, secondary, in brain ab- scess, 58 Compressors, 8 Contralateral hemiplegia in frontal abscess, 209 in temporo-sphenoidal abscess, 181 paralysis in temporo-sphenoidal ab- scess, 181 in frontal abscess, 209 Control of hemorrhage, 7, 8, 9, 11, 12 Convulsions, in cerebral suppuration, 161 in frontal abscess, 207 in temporo-sphenoidal abscess, 184 Dead tissue, removal of, 149 Death, sudden, from cedema of brain, 15 Decompression, principles in technic of, 58 Delay in operating in cerebellar abscess fatal, case (I), 3 Deviation, lateral, in cerebellar abscess, 197 Diabetes insipidus in frontal abscess, 207 Diagnosis, of brain abscess in general, 155 of cerebellar abscess, 190 of frontal abscess, 206 of temporo-sphenoidal abscess, 176 Differential diagnosis of brain abscess, 211 Diploic vessels, control of hemorrhage from, 9 Disposition, change of in frontal ab- scess, 209 Disproportion, in cerebral suppuration, 158 Double abscess, 59 additional references to, 66 cerebellar, case of (XII), 60' Drainage, in chronic intracerebral ab- scess, 52 Dreamy state, in temporo-sphenoidal abscess, 184 Dura, adhesive inflammation of pia- rachnoid to, surgical significance of, 50 bulging of into perforation openings, 10 closure of, 12 control of hemorrhage from, 11 incision of, technic of, 29 herniation of brain following, 42 inspection of brain within, 42 protection of brain by, 139 vulnerability of, 139 Dural defects, in hernia cerebri, 132 Dural separators, 10 Eagleton's encephaloscope, 56 Elevation of brain, inspection by, 44 technic of, 44 technic following, 50 392 INDEX OF SUBJECTS Elevation of head, during operations, 7 Encapsulated adjacent intracerebral abscess of middle fossa, 51 Encephaloscope, Eagleton's, 56 Whiting's, 56 Eradication, in treatment of chronic intracerebral abscess, 51 Exploration of cerebellar abscess, 103 protection of piaracbnoid prior to, 44 site for, 46 within cerebral substance, 45 Exploring, for brain abscess, 65 instrument, 46 Evacuation, complications after, 211 difficulties of, 52 importance of thorough, 53 Exposure of temporo-sphenoidal lobe, 40 Extradural abscess, associated with cerebellar abscess, 105 relationship of with osteomyelitis, and intradural abscess, 110 Eyes, lateral deviation of in cerebellar abscess, 197 Facial paralysis of opposite side, in temporo-sphenoidal abscess, 181 Failure of inhibition, in cerebellar ab- scess, 194 Falling, in cerebellar abscess, 198 Fibrin paper, as a hemostatic agent, 11 Flap, osteoplastic, formation of, 9 Frazier's electric fraise, 9 Frontal abscess, 107 analysis of 140 reported cas^s of, 244 anatomical considerations, 107 aphasia in, 208 associated with complications, re- port of cases, 267 with epidural abscess, report of cases, 274 with extradural abscess, report of cases, 275 with meningitis, report of cases, 276 with osteomyelitis, analysis of cases, 258 with subdural abscess, report of cases, 275 bibliography of, 277 coma in, 207 contralateral hemiplegia in, 209 contralateral paralysis in, 209 convulsions in, 207 diabetes insipidus in, 207 diagnosis of, 206 additional references to, 210 disposition, change of, in, 209 extradural abscess in, 206 localizing symptoms in, 208 loss of abdominal reflexes in, 209 loss of smell in, 208 Frontal abscess, mental disturbance in, 209 metastatic, 120, 259 in opposite lobe, 260 of aural region, 260 operative intradural policy in, 123 orbital abscess in, 206 osteomyelitis in, 206 papilloedema in, 208 path of infection, in, report of cases, 262 pathological considerations, 107 principles of exploratory intradural operation, 123 relation of trauma to, 109 retrobulbar neuritis in, 208 surgical classification of, 112 symptoms due to association with cerebellum, 210 symptoms, of cerebral compression in, 207 symptoms of cerebral suppuration in, 207 traumatic, 121, 261 treatment of, 123 types of, 117 Frontal abscess, adjacent, 112 analysis of cases, 244 associated with osteomyelitis, 117 capsule in, 122 case of (XXI), 111 from ethmoidal disease, 249 from frontal sinus, 251 immediate occasion of, 121 infection by complicating osteo- myelitis, 116 infection by continuity of tissue suppuration, 115 infection by retrograde thrombo- phlebitis or perivasculitis, 116 infection by tissue suppuration and thrombophlebitis, 116 intracerebral, without macroscop- ical evidence of cortical involve- ment, 120 meningeal, subdural, 118 occurence of, 112 operative results in, 122 origin of infection in, 114 paths of infection in, 115 piaracbnoid, 119 situation of, 122 eurgical aims for operation for, 124 terminations of, 123 treatment of, 123 with orbital complications, 256 with stalk, 119 Frontal abscess, intercurrent with stalk, case of (XXII), 125 Frontal abscess, metastatic, 120, 259 Frontal bone, peculiarities of in rela- tion to frontal abscess, 107 INDEX OP SUBJECTS 393 Gtigll saw, 10 Gliosis, 13 Gradenigo's syndrome, 173 Gravity, utilization of in evacuation of brain abscess, 6 Hammers, 9 Hartley and Kenyon's perforators, 9 Head, elevation of during operations, 7 Headache, evidence of cerebral suppura- tion, 157 Head-rests, 7 Heidenhain'a sutures, 9 Hemianopsia, case of (XXVII), in temporo-sphenoidal abscess, 180 Hemiplegia, contralateral, in frontal abscess, 209 in temporo-sphenoidal abscess, 181 Hemorrhage, control of, 7, 8, 11, 12 from brain, 12 from diploic vessels during per- foration of skull, 9 from dura, 11 from interior of skull before dura is opened, 10 from pial vessels, 11 from scalp, 8 postage-stamp method of, 10 Hemostats not to be used, 11 Hernia cerebri, 127 case of (XXIII), 129 ease of (XXIV), following operation for temporo-sphenoidal abscess, 135 circulatory factors in, 129 dural defects in, 132 etiology of, 127 f ungating, 131 non-ulcerative, 131 physiological factors in, 131 prevention of, 132 protection in, 133 reduction of increased intracerebral pressure in, 134 surgical pathology of, 131 surgical treatment of, 132 ulcerative, 131 Herniation, in exploration for cerebel- lar abscess, 86 of brain on incision of dura in tem- poro-sphenoidal abscess, 42 puncture of opposite veniiiele for reduction of, 44 Heuer's temporo-muscular clamp, 9 Histological considerations, 13 History taking, importance of, before exploration, 1 prior to appearance of symptoms, 2 Homolateral ventricle, obliteration of in temporo-sphenoidal abscess, 42 Eorsley's wax, use of, 9 Hudson's perforators, 9 Hydrocephalus causing symptoms in cerebellar abscess, 203 Hypermetria in cerebellar abscess, 194 Idiopathic brain abscesses, 18, 73 Illumination, necessity for, 57 Immunization, 145 Induced "stupeur art^rielle," in pro- duction of papilloedema, 174 Infection, pathological processes in, 138 impenetrability of cerebro-spinal fluid system to, 142 latent, recrudescence of, 149 method of entry into brain, 138 prevention of, 137 varying degrees of sensitiveness to extension of, 148 Inflammation, adhesive, of piarachnoid to dura, surgical significance of, 50 Inhibition, failure of, in cerebellar ab- scess, 194 Inspection of brain within dura, 42 Intercurrent abscess, tertiary, 17 secondary to sinus thrombosis, 31, 102 Intracerebellar abscess, situation of, 104 Intracerebellar pressure, 86 direction of maximum, 87 Intracerebral abscess, 19 adjacent, of middle fossa, 51 with capsule, 47 with surgical treatment, 55 without macroacopical cortical in- volvement, 36 drainage of, 52 eradication of, 51 evacuation of, 52, 53 selection of eases, 52 stalk of, 19, 20 with capsule, 21 with capsule and stalk, 22 with stalk, 19 without cortical involvement discov- erable macroscopically, 23, 46 without limiting membrane, 22 Intracranial operations, general surgi- cal technic, 6 position of patient in, 6 Intracranial pressure, increased, diag- nosed by vestibular reactions, 199 influence of in papilloedema, 168 reduction of, 134 Intradural abscess, 19 relationship between osteomyelitis, extradural abscess and, 110 Intradural suppuration in middle fossa, exposure for in suspected cases, 40 394 INDEX OF SUBJECTS Intrapiarachnoid abscess, 20, 26, 32, 93 case of (XVIII), 92 extension of, 34 situation of, 104 Kenyon and Hartley's perforators, 9 Knee jerks in cerebellar abscess, 202 Kredel's plates, 9 Labyrinth, in etiology of cerebellar ab- scess, 91 Labyrinthine suppuration, in cerebellar abscess, 94 types of, 94 Labyrinthitis, case of (III), 15 in diagnosis of cerebellar abscess, 190 meningitis from, case of (XV), 71 secondary serous, 95 Lateral cisterna, abscess in, 95 Lateral deviation of eyes in cerebellar abscess, 197 Lateral sinus, anatomy of on cross section, 98 blood pressure in, 98 physiological and anatomical factors, 98 primary exposure of, 97 surgical obliteration of, 98 Limitation of field of operation, 7 Localized serous (protective) menin- gitis, 32 diagnosis of, 33 Location of lesion, influence of in papilloedema, 171 Losing abscess, 56 Lumbar puncture, dangers of, 29 Lymphatics, absence of and subnormal temperature, 164 Makkas, spring clip of, 9 Malaise, evidence of cerebral suppura- tion, 158 Marentz rongeur, 10 Meningeal abscess, 20, 22, 26 adjacent, of middle fossa, 32 adjacent subdural, 118 Meningitis, aseptic, case of (VI), 33 brain abscess from, 144 case of from disturbed meningeal protection (XXV), 144 from labyrinthitis, case of (XV), 71 localized serous protective, 32 diagnosis of, 33 protective, evidence of cerebral sup- puration, 160 suppurative, from cerebral abscess, case of (XXVI), 151 Meningitis, suppurative, with brain abscess, relation of to protective meningitis, 150 Meningo-cerebral abscess, 22 Mental disturbances in frontal abscess, 209 Metastatic abscess, 17, 18, 25, 68, 69, 120 additional references to, 82 case of (XXVIII), 182 classification of, 68 development of, 68 frontal, 120, 259 formation of capsule in, 76 frequency of, 72 limitation of by capsule, 76 location of, 74 multiple, 75 case of, 75 of otitic origin, case of (XVII), 77 of venous origin, 71 treatment, 76 Metastatic vascular occlusion, 69' Middle fossa, abscess of, 31 case of (XI), 46 adjacent meningeal abscess of, 32 adjacent secondary abscess of, con- siderations prior to operation, 37 cleansing and obliteration of abscess with stalk near surface, 56 following thrombosis of superior pe- trosal sinus or dural veins, 31 osteoplastic flap for exploration of, 41 Mills, naming center of, 46 Muscle, control of hemorrhage by, 11 Naming aphasia, 46 Naming center of Mills, 46 Nasal sinuses, accessory, operations for suppurative lesions of, 123 Necrosis, superficial of brain, 32 Nerve head changes, diagnostic deduc- tions from, 175 Neuritis, retrobulbar, in frontal ab- scess, 208 Neuroglia, 13 Neurological examination, guide for, 213 prior to appearance of symptoms, 2 Neurons, 13 Nystagmus, spontaneous, in cerebellar abscess, 197 Obliteration of homolateral ventricle in temporo-sphenoidal abscess, 42 Ocular paralysis in cerebral compres- sion, 167 CEdema of brain, from trauma of opera- tion, 15 INDEX OF SUBJECTS 29S CEdema of brain, sudden death from, 15 Oozing, control of, 11 Operating in cerebellar abscess, delay in fatal, ease of (I), 3 Operation, time for, 3 Operative technic, general, 6 additional references to, 12 Optic nerve, intracellular pathways of in papilloedema, 172 Osteomyelitis, adjacent frontal lobe ab- scess associated with, 117 relationship between extradural and intradural abscess and, 110 Osteoplastic flap, cutting of, 10 for exploration for abscess of middle fossa, 41 Outrigger, for cerebellar operations, 7 Oyster-shaped abscess, 34 Pain behind eye in temporo-sphenoidal abscess, 183 in teeth in temporo-sphenoidal ab- scess, 183 Papilloedema, etiology of, 169 in cerebral compression, 168 in frontal abscess, 208 increased intracranial pressure in, 168 induced "stupeur artfirielle" in pro- duction of, 174 influence of location of lesion in, 171 influence of parenchymatous fluids in, 172 interference with venous circulation in, 169 Paralysis and transient aphasia, case of brain abscess with (XJQX), 185 Paralysis of contralateral arm, in frontal abscess, 209 in temporo-sphenoidal abscess, 181 Parenchymatous fluids, influence of in papilloedema, 172 Past pointing, in cerebellar abscess, 198 in tempero-sphenoidal abscess, 187 Pathological considerations, 13 Pathological processes in brain, se- quence of, 159 Pathology of brain abscesses, 47 references to, 16 Patient, position of in intracranial op- erations, 6 Perforation of skull, 9 bulging of dura in, 10 control of hemorrhage during, 9 Perforators, 9 Petrous pyramid, cerebellar abscess from infection of, 91 Perisinus abscess, case of (XX), 103 Pia, blood vessels of, 24 Pial vessels, control of hemorrhage from, 11 Piarachnoid abscess, adjacent, 119 Piarachnoid, adhesive inflammation of to dura, surgical signLflcauce of, 50 protection of prior to exploration, 44 Plates, Kredel's, 9 Postage-stamp method of controlling hemorrhage, 10 Posterior fossa, surgical ajiatomy of, 84 Preparation, 1 Projectile vomiting, in cerebral com- pression, 167 Protection of brain, by dura, 139 by subarachnoid spaces, 140 by subdural space, 140 Protective mechanism of brain, 137, 139, 147 additional references to, 153 Protective meningitis, evidence of cere- bral suppuration, 160 Psychic disturbances in cerebellar ab- scess, 202 manifestations of toxic delirium in temporo-sphenoidal abscess, 185 Pulse, slow in cerebral compression, 166 Pulse pressure, in cerebral compression, 167 , Puncture, lumbar, dangers of, 29 ventricular, 29 for reduction of brain herniation, 44 in cerebellar abscess, 104 technic of, 10 Pupillary disturbances in cerebellar abscess, 201 Rapid loss of flesh, in cerebellar ab- scess, 202 Reflexes, loss of abdominal, in frontal abscess, 209 Repair of brain substance, 149 Results of brain abscess, 211, 212 Retina, intracellular pathway of, in papilloedema, 172 Retrobulbar neuritis, in frontal ab- scess, 208 Roentgen ray diagnosis in temporo- sphenoidal abscess, 187 case of (XXX), 188 Rongeurs, 9, 10 Searcher, 45 Second abscess, 59 Secondary and double abscesses, 59 Sensitiveness of brain to toxie influ- ences, 147 Separators, dural, 10 Serous labyrinthitis, secondary, 95 Sims' chest position, 6 396 INDEX OF SUBJECTS Sinus thrombosis, case of (V), 33 cerebellar abscess following, 101, 102, 104 treatment of, 103 in diagnosis of cerebellar abscess, 190 intercurrent abscess secondary to, 31, 102 Sinus wall, incision through, 103 Skull, cutting of osteoplastic flap, 10 perforation of, 9 control of hemorrhage during, 9 Smell, loss of, in frontal abscess, 208 Speech defects in cerebellar abscess, 195 Spontaneous nystagmus in cerebellar abscess, 197 Stalk, development of, 22 of intracerebral abscess, 19, 20, 22 "Stupeur ajtdrielle," induced, in papilloedema, 174 Subarachnoid space, elimination of bac- teria from, 145 protection of brain by, 140 Subdural abscess, 20, 24, 32 adjacent meningeal, 118 Subdural space, protection of brain by, 140 Subnormal temperature, autolysis in, 164 absence of lymphatics in, 164 evidence of cerebral suppuration, 163 Suboccipital tenderness, in cerebellar abscess, 202 Suction apparatus, 45 Sudden death from oedema of brain, 15 Surgeon, mental attitude of, 1 Surgical factors, 28 Surgical principles, 27 Surgical teehnic, general, 28 Temperature, subnormal, autolysis in, 164 absence of lymphatics in, 164 evidence of cerebral suppuration, 163 Temporo-muscular clamp, of Heuer, 9 Temporo-sphenoidal abscess, 31 additional references to, 66 adjacent, case of (XIII), 63 diagnosis of, 176 aphasia in, 177 case of (VIII, IX, X), 37, 38, 43 contralateral hemiplegia in, 181 convulsions in, 184 diagnosis of, 176 dreamy state in, 184 facial paralysis of opposite side in, 181 hemianopsia, case of (XXVII), in, 180 herniation of brain in incision of dura in, 42 Temporo-sphenoidal abscess, intradural teehnic in suspected adjacent cases, 49 localizing symptoms in, 176 localizing value of primary focus of infection in, 176 obliteration of homolateral ventricle in, 42 pain behind eye in, 183 pain in teeth in, 183 past pointing in, 187 pathognomonic symptoms in, 177 principles of operative treatment in, 40 psychic manifestations of toxic de- lirium in, 185 Roentgen ray diagnosis in, 187 case of (XXX), 188 symptoms, 183 uncinate symptoms in, 185 with stalk, 36 word deafness in, 178 Temporo-sphenoidal lobe, exposure of, 40 Thrombosis of cerebral vessels, case of (XIV), 70 Thrombotic nidus, origin of, 71 Tourniquets, 8 Toxic influences, sensitiveness of brain to, 147 Trauma, cerebral, death from, 15 Traumatic abscess, 17, 19, 25, 121, 261 frontal, 121, 261 Uncinate symptoms in temporo-sphe- noidal abscess, 185 Vascular occlusion, metastatic, 69 Venous circulation, interference with in papilloedema, 169 Ventricle, obliteration of homolateral in temporo-sphenoidal abscess, 42 puncture of opposite for reduction of brain herniation, 44 Ventricular puncture, 29 for reduction of brain herniation, 44 in cerebellar abscess, 104 teehnic of, 10 Ventricular reaction, in diagnosis of increased intracranial pressure, 199 Vertigo, in cerebellar abscess, 197 Vestibular manifestation, from pres- sure on cerebellar cortex, 200 in cerebellar abscess, 196 Vestibular reactions, changing char- acter of in cerebellar abscess, 199 INDEX OP SUBJECTS 397 Vestibular reactions, cerebellar cortical localization in relation to, 200 diagnosis of by increased intracran- ial pressure, 199 in cerebellar abscess, 198 reported cases of, 198 Vomiting, in cerebellar abscess, 202 Vomiting, in cerebral compression, 167 in cerebral suppuration, 157 Wax, Horsley's, use of, 9 Whiting's encephaloscope, 56 Yawning, in cerebellar abscess, 202 ■u.^m