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Cornell University Library 
 RC 360.B61 1921 
 
 Compendium of regional diagnosis in affe 
 
 3 1924 012 458 786 
 
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/cu31924012458786 
 
BING'S COMPENDIUM 
 
COMPENDIUM OF REGIONAL 
 DIAGNOSIS IN AFFECTIONS OF 
 THE BEAIN AND SPINAL COED 
 
 A CONCISE INTRODUCTION TO THE PRINCIPLES 
 OF CLINICAL LOCALIZATION IN DISEASES AND 
 INJURIES OF THE CENTRAL NERVOUS SYSTEM 
 
 BY 
 
 ROBERT BING 
 
 PRIVAT-DOCENT FOR NEUROLOGY IN THE UNIVERSITY OF BASLE 
 
 TRANSLATED BY 
 
 F. 8. ARNOLD, B.A., M.B., B.Ch. (Oxon) 
 
 SECOND EDITION 
 
 REVISED AND ENLARGED 
 
 WITH SEVENTY -THREE ILLUSTRATIONS 
 
 NEW YORK 
 
 REBMAM COMPANY 
 
 Herald Square Building 
 141-145 West 36th Street 
 
First pub/ ished, May 19II 
 
 New Edition, July, 1913 
 
 New Impressions, October, 1913 ; October, 1914 ; 
 
 December, I917; January. 1920; 
 
 November. 1921 
 
 Printed in Great Britain 
 
PREFACE TO THE SECOND EDITION 
 
 I CANNOT, I think, better express my thanks for the friendly 
 reception accorded by expert critics to the first edition of 
 my Compendium than by following out, so far as possible, 
 the suggestions for the improvement of the work which 
 have been brought to my notice . Some of my reviewers have 
 urged an enlargement of the general plan and scope of the 
 book as laid down in the preface to the first edition. To this 
 I have been unable to agree, since the practical utility of the 
 book to practitioners who are not neurologists must thereby 
 have been diminished. Though so short a time has elapsed 
 since the appearance of the first edition, a considerable 
 number of emendations and additions have proved to be 
 necessary ; apart from my own numerous observations, a 
 large number of new works dealing with the subject have 
 appeared to which it has been necessary to give careful 
 attention. The section dealing with the brain, for instance, 
 has required considerable modification (locahzation of motor 
 cortical areas, tumours of the cerebello - pontine angle, 
 aphasia, apraxia, hypophysis, epiphysis, Rontgen-ray diag- 
 nosis, etc.). I have been enabled by the co-operation of 
 my publishers not only to add some new figures, but also 
 to substitute improved illustrations for some of thosi 
 
 appearing in the former edition. 
 
 ROBERT BING. 
 
PREFACE TO THE FIRST EDITION 
 
 Whelb delivering a course of lectures on regional diagnosis 
 
 to medical men during the winter session 1907-08, I was 
 
 repeatedly urged by members of my audience to publish 
 
 a book which should give in a concise form, and one suited 
 
 to readers who are not neurologists, the substance of my 
 
 lectures. I was unable to fall in with the suggestion. There 
 
 is no lack of excellent textbooks dealing with the subject. 
 
 A short, practical vade-mecum of a didactic character has 
 
 not, however, to the best of my knowledge, been, up to the 
 
 present, available, and yet it seemed probable that such a 
 
 work would be by no means unwelcome to the physician 
 
 or surgeon called upon to localize a pathological process 
 
 affecting the central nervous system. It is from this point 
 
 of view that the present compendium took its origin. Its 
 
 chief task is to give a presentation of a subject generally 
 
 reputed difficult and compUcated, which shall be as clear 
 
 and simple as the author can make it, while not failing to be 
 
 accurate and comprehensive, and which shall furnish, even 
 
 to those who have special knowledge of neurology, an easily 
 
 and quickly consulted work of reference. In such a scheme 
 
 there is no room either for the putting forward of elaborate 
 
 theories or the discussion of controverted points. At the 
 
 same time I have nowhere shirked the attempt to give a 
 
 scientific explanation of clinical facts. In the main, only 
 
 such material has been put forward as is to be regarded as, 
 
 in the present state of our knowledge, firmly established. 
 
 Where this is not the case, attention is specially called 
 
viii PREFACE TO THE FIRST EDITION 
 
 to the fact that our knowledge on the point dealt with 
 is still incomplete. The names of authors are only given 
 where they have become part of neurological nomencla- 
 ture — e.g., Brown-Sequard's symptom-complex, Westphal- 
 Edinger nucleus, etc. Quotation from other authors is 
 limited to the few occasions on which I have directly 
 borrowed a table or a diagram. The illustrations are those 
 which served me as wall diagrams in my lectures. This 
 must be my apology for their frequently simple and sketchy 
 character, which, however, is more conducive to a rapid 
 apprehension and comprehension of the matter put forward 
 than would be the case with a less diagrammatic form of 
 illustration. 
 
 ROBERT BINQ. 
 
 Basle, 1909. 
 
INTRODUCTION 
 
 The object of that branch of the science of neurology 
 denominated " regional diagnosis " is, by inference from 
 the clinical phenomena called forth by a circumscribed 
 lesion of the central nervous system, to localize that lesion 
 — that is to say, to determine (without, in the first place, 
 any reference to its special nature^ its exact anatomical 
 situation. 
 
 Regional diagnosis bases its conclusions on the observa- 
 tion of disease symptoms arising from the injury or destruc- 
 tion of separate structures forming part of the central 
 nervous system. Inasmuch as all these structures (nerve 
 nuclei, nerve tracts, etc.) have clearly-defined situations in 
 the brain or the spinal cord, it is possible to deduce the 
 situation of a lesion from the combination of irritative and 
 paralytic symptoms found to be present in the given case. 
 Regional diagnosis, then, borrows its tools alike from 
 anatomy and from physiology. In essence, the science of 
 clinical localization is a collation and comparison of data 
 furnished by those two sciences. It is in fact, funda- 
 mentally, the applied anatomy and physiology of the central 
 nervous system. Its practical importance is immense. In 
 all lesions of the nervous system the prognosis depends 
 quite as much on the situation as on the specific anatomico- 
 pathological nature of the lesion, and, where surgical inter- 
 ference is in question, regional diagnosis is, of course, of 
 equally vital importance. 
 
TRANSLATOR'S NOTE 
 
 is a few cases references in German form part 
 of the plates. As their removal and replace- 
 ment by English equivalents involved difB- 
 culties and considerable expense, translations 
 have been given in the index. 
 
CONTENTS 
 
 PAGE 
 
 Preface to the Second Edition ..... v 
 
 Preface to the First Edition - - - - - vii 
 
 Introduction - ix 
 
 DIVISION I. : REGIONAL DIAGNOSIS OF LESIONS OF THE 
 
 SPINAL CORD 1 
 
 A. " Transverse " or Systemic Diagnosis (Querschnittsdiagnostik) 1 
 
 Chaptek I. 1. The Spinal Tracts - 2 
 
 2. Cells and Cell-Groups of the Spinal Cord 12 
 
 „ II. 1. The Spinal Sensory Mechanism - - 14 
 
 2. The Spinal Motor Mechanism - - 17 
 
 3. The Spinal Trophic Mechanism - - 20 
 
 4. The Spinal Vaso-motor Mechanism 21 
 Appendix : The Nervous Mechanism govern- 
 ing the Sweat Function - 24 
 
 „ III. 1. Localizing Value of Motor Disturbances 25 
 (o) Distinguishing Features of Paralysis 
 due to Affections of the Lateral 
 Columns 25 
 
 (6) Distinguishing Features of Paralysis 
 due to Affections of the Ventral 
 Horn 28 
 
 (c) Paralytic Phenomena due to Com- 
 bined Affections of the Lateral 
 Column and Ventral Horn 29 
 
 2. Localizing Value of Sensory Disturbances 31 
 
 3. Localizing Value of Combined Motor and 
 
 Sensory Disturbances 34 
 
 (o) Simultaneous Affections of Dorsal 
 
 and Lateral Columns 34 
 
 (6) Transverse Interruption of Spinal 
 
 Nerve Channels 35 
 
 (c) Unilateral Transverse Interruption of 
 
 Spinal Nerve Channels (Hemi- 
 
 section) - . - .38 
 
 Appfendix : Differential Diagnosis between 
 
 Intra- and Extra-Medullary Tumours 43 
 
xii CONTENTS 
 
 FAOE 
 
 B. " Longitudinal " or Segmental Diagnosis {Hohrrdiagnostik) ■ - 43 
 
 Chapter I. Anatomical and Physiological Principles of 
 
 Segmental Diagnosis - 44 
 
 II. 1. Segmental Diagnosis in Motor Paralyses : 
 Differential Diagnosis between Radicular 
 and Peripheral Paralysis 48 
 
 2. Segmental Diagnosis in Sensory Disturb- 
 
 ances : DifEerential Diagnosis between 
 Radicular and Peripheral Forms 63 
 
 3. Segmental Diagnosis in Reflex Disturbances 66 
 „ III. 1. Distinguishing Features of Lesions of the 
 
 Upper Part of the Spinal Cord an 
 
 2. Distinguishing Features of Lesions of the 
 
 Lower Part of the Spinal Cord ^3 
 
 Appendix : Topographical Relations between 
 
 the Spinal Cord and the Vertebral 
 
 Column - - - "82 
 
 DIVISION n. : REGIONAL DIAGNOSIS OP BRAIN LESIONS 85 
 
 A. Lesions in the Region of the Cerebral Axis or Brain-Stem - 85 
 
 Chaptbe I. The Structure of the Brain-Stem - - 89 
 
 „ II. 1. Genera! Rules for the Localization of Dis- 
 
 eases and Injuries of the Brain-Stem 102 
 2. Points in the Semeiology of the Nerves of 
 the Brain-Stem which are of Importance 
 in Regional Diagnosis (with Special 
 Reference to the DifEerential Diagnosis 
 of Central and Peripheral Affections) 117 
 
 (a) The Caudal Group of Nerves 1 1 7 
 
 (6) The Nerves of the Cerebello-Pon- 
 
 tine Angle - . - 126 
 
 (c) The Trigeminus - ^ 138 
 
 (d) The Nerves of the Ocular Muscles 146 
 
 B. Lesions of the Cerebellum • - - - - 154 
 
 C. Lesions of the Cerebrum, the Basal Ganglia, and the Hypophysis \ gS 
 
 Chapter I. Anatomico-Physiological Introduction 168 
 
 „ II. The Localizing Value of Motor and Sensory 
 
 Disturbances of Cerebral Origin . 173 
 
 [a) Cortical Affections - • -179 
 
 (6) Subcortical Affections ... 134 
 
CONTENTS xiii 
 
 PAGE 
 
 Chapteb III. The Localizing Value of Visual Disturbances igj 
 
 1. The Visual Tract 1 91 
 
 2. The Localization of Lesions of the 
 
 Visual Tract 194 
 
 ., IV. The Localizing Value of Disorders of Speech 197 
 ,. V. 1. The Localizing Value of Certain Rarer 
 
 Cerebral Symptoms 204 
 (a) Auditory and Olfactory Disturb- 
 ances of Cerebral Origin 204 
 (6) Apraxia 204 
 (c) Intellectual and Moral Abnormalities 207 
 
 2. Symptoms due to Lesions of the Basal 
 
 Ganglia - - 208 
 
 3. Symptoms due to Lesions of the Hy- 
 
 pophysis - - 209 
 
 Appendix : Cranio-Cerebral Topography ; 
 Rontgen-Ray LooaUzation of Cerebral 
 Tumours .... 211 
 
 Index- 215 
 
BING'S COMPENDIUM. 
 
 DIVISION I. 
 
 Regional Diagnosis of Lesions of the Spinal 
 
 Cord. 
 
 In attempting to localize a focus of disease or lesion of any 
 kind in the spinal cord, two points of capital importance 
 have to be kept in view, owing to the cylindrical or cord- 
 like form of the organ. In the first place, we must determine 
 whether the lesion is central or peripheral, anterior or 
 posterior, right or left, and over how large an area it has 
 interrupted the spinal nerve channels and destroyed the 
 spinal centres. In the second place, we wish to know at 
 what level, at what point of its extent, the cord, is affected 
 by injury or disease. We may speak, therefore, of a 
 "transverse" or systemic, and a "longitudinal" or seg- 
 mental, diagnosis of spinal affections, and wiU proceed now 
 to the consideration of their foundation principles. 
 
 A. Transverse or Systemic Diagnosis. 
 
 It is necessary to begin with an outline of the anatomical 
 conditions, which, however, may be very simple and brief, 
 seeing that our point of view is to be purely clinical and 
 utilitarian. A knowledge of the anatomy of tho spinal 
 cord, and especially of the anatomical nomenclature of its 
 parts, is, of course, assumed. 
 
 The broad division into white and grey matter corresponds 
 to a finer division into conducting nerve channels and 
 nerve-ceU - network. We must realize, therefore, in the 
 
 1 
 
2 BING'S COMPENDIUM 
 
 first place, the position and course of the former, and the 
 grouping and division of the latter (Chapter I.). If we 
 then bring into relation with the foregoing a survey of the 
 normal functions of these elements so far as they are known 
 to us (Chapter II.), certain regional-diagnostic conclusions 
 are seen to follow naturally from disturbance or inhibition 
 of those functions (Chapter III.). 
 
 CHAPTER I. 
 
 I. THE SPINAL TRACTS. 
 
 In works on descriptive anatomy the spinal tracts are 
 divided into " long " or " short." From a clinical point 
 of view, we must select another principle of division, and 
 group the tracts under the two following headings : 
 
 (a) Tracts whose cells of origin lie outside the sjnval cord. 
 
 These tracts merely pass through the cord, taking their 
 origin elsewhere — in the brain, for example, or in the spinal 
 ganglia. These tracts are liable to destruction, as the 
 result, not only of primary disease of the cord, but also of 
 cerebral and ganglionic lesions — in accordance with Waller's 
 law : "A nerve fibre can only maintain its anatomical 
 and physiological integrity so long as it remains in un- 
 disturbed continuity with a healthy nerve cell." These 
 tracts are called exogenous. 
 
 lb) Tracts whose cells of origin lie within the spinal cord. 
 
 To bring about destruction of these tracts throuThout 
 their whole extent, a lesion of the spinal cord itself is re- 
 quired, and, further, ot the grey matter of the cord, the 
 exclusive seat of the spinal nerve-cells. These tracts are 
 called endogenous. 
 
 A. EXOGENOUS TRACTS. 
 I. Descending or Centrifugal (see Fig. l). 
 
 1. Tracts descending from the Cerebral Cortex = Fasciculi 
 Cortico-Spinales = Pyramid Tracts. 
 
 The cells of origin of these tracts lie in the motor area of 
 the cortex cerebri ; the tracts themselves pass, their fibres 
 
LESIONS OF THE SPINAL CORD 
 Fig. 1. 
 
 ' ^ Tractus cortuo-spinalis latemll 
 ' ' Tractus tecto-spinalia 
 Tractus cortico-spiuallB anteri<9 
 
 ' ' Tractus Testibulo-spinaliB 
 ' ' Tractus rubro-spiuEdif 
 ) ' Tractus thalamo-spiDalis 
 
 Descending Exogenous Spinal Tracts. 
 
 Tractus cortico-8pinaleB=chief motor tracts. 
 
 Tractus subcortico-spinales=secondary motor tracts. 
 
4 BING'S COMPENDIUM 
 
 converging as they go, through the substance of the parietal 
 lobe to the internal capsule, traverse the posterior limb of the 
 latter, and continue their further course through the ventral 
 portions of the pedunculi and the pons to the medulla 
 oblongata. Here the fibres divide into two systems : 
 
 (a) The Lateral Pyramid Tracts = Fasciculus Cortico-Spinalis 
 Lateralis. 
 
 The greater number of the cortico-spinal fibres cross from 
 the pyramid of the medulla oblongata to the opposite side of 
 the spinal cord at the upper Hmit of the latter, and pass down- 
 wards in the lateral columns of the cord, till their neurons 
 find their terminal divisions in the cells of the anterior horn. 
 
 (^) The Anterior Pyramid Tracts = Fasciculus Cortico- 
 Spinalis Anterior. 
 
 A smaller number of the cortico-spLnal fibres pass down- 
 wards without crossing at the upper limit of the cord through 
 the anterior columns. These also find their termination in 
 the cells of the anterior horn, but before doing so cross from 
 one side to the other of the cord by way of the anterior com- 
 missure, thus undergoing a delayed, preterminal decussation. 
 
 2. Tracts descending from the Lower Brain Centres = 
 Fasciculi Subcortico-Spinales. 
 
 Under this head I include the following : 
 
 (a) Tractus Rubro-Spinals = Monakow's Bundle. 
 
 This springs from the red nucleus of the tegmentum 
 cruris cerebri. It undergoes decussation soon after its 
 origin, and passes downwards in the lateral column of the 
 lord. 
 
 (ft) Tractus Thalamo-Spinalis, 
 
 This arises in the thalamus, passes into the tegmentum 
 cruris cerebri, where its fibres join those of the rubro-spinal 
 tract, and accompany them in their decussation, and 
 further passage down the cord. 
 
 (7) Tractus Tecto-Spinalis, 
 
 Arises from the roof of the mid-brain {Tectum opticum), 
 decussates with its fellow beneath the aqueduct of Sylvius, 
 and, passing through the pons and medulla close to the 
 middle line, descends in ihe ventral column of the spinal coi-d. 
 
 (8) Tractus Vestibulo-Spinalis. 
 
 Is deirived from the nucleus of Deiters in the medulla 
 oblongata, which belongs to the system of the vestibular 
 
LESIONS OF THE SPINAL CORD 5 
 
 nerve. Passes downwards, uncrossed, iii the ventral column 
 of the cord, and ends among the cells of the ventral horn, 
 the probable seat of termmation of the subcortico-spinal 
 tracts in general. 
 
 II. Ascending or Centripetal Tracts. 
 
 The ascending exogenous tracts have their ceUs of origin 
 in the spinal ganglia. These cells are connected peripherally 
 by means of fibres running in the nerve trunks, with the 
 various peripheral organs, " nerve-endings," " terminal 
 corpuscles," " end-bulbs," " tactile corpuscles," " Pacinian 
 bodies," and so on, found in the skin, the mucous mem- 
 branes, the mesentery, the articular surfaces, and elsewhere. 
 Centrally the fibres from the cells of the spinal ganglia pass 
 by way of the posterior roots into the spinal cord. These 
 fibres may be divided, according to their further course 
 within the cord, into three sections (Fig. 2) . 
 
 (") Short Fibres of the Posterior Roots. 
 
 These pass directly through the marginal zone of the 
 posterior horn into the grey matter, where they end by 
 arborizing among the cells (1) of the posterior, (2) of the 
 anterior horn, on the same side of the cord. 
 
 {13) Medium Fibres of the Posterior Roots. 
 
 These pass through the segment of entry into the posterior 
 columns, and from thence into the substance of the dorsal 
 horn of the same side, ending in the column of Clarke. 
 
 (y) Long Fibres of the Posterior Roots. 
 
 These also pass, through the segment of entry, into the 
 posterior columns, but, in these, pursue their further 
 course in the direction of the brain, and terminate in 
 certain nuclei in the medulla, the nuclei of the dorsal 
 columns. 
 
 The two following anatomical peculiarities of these fibres 
 of the posterior columns have also pathological signifi- 
 cance : 
 
 (1) As the fibres from a particular posterior root pass 
 upwards in the dorsal columns, they are pressed more and 
 more towards the middle line by fibres of the same kind, 
 entering through the zone of entry of higher segments. 
 In consequence of this, in a transverse section of the 
 cervical cord, the fibres from the sacral roots lie nearest the 
 septum ; next to them, a little more externally, are ranged 
 
BING'S COMPENDIUM 
 
 the lumbar fibres, then the thoracic, and, finally adjacent 
 to the dorsal horns, the fibres from the cervical roots. 
 
 In this manner there is brought about in the cervical 
 cord a macroscopic separation between the long posterior 
 
 Fio. 2. 
 
 ^ llTMAfcHMUa ) 
 
 zvmcmiihiku ^, 
 
 ( VIA tmAlamm «TTJ 
 
 Kvrzi ftkAtnu. 
 
 iZ. Uusksl. 
 
 The Various Groups of Posterior Root Fibres and their 
 contintjations within the spinal coed. 
 
 root fibres from the lower half of the body (from the fourth 
 dorsal segment downwards), which are united in the column 
 of GoU, and those from the upper half of the body (from 
 the fourth dorsal segment upwards), which form the column 
 
LESIONS OF THE SPINAL CORD 7 
 
 of Burdach. Pig. 3 gives a diagrammatic representation of 
 this distribution of fibres. 
 
 Fig. 3. 
 
 Formation of the Posterior CoLrMNS. 
 
 G=Coluinn of Gcll (funiculus gracilis). 
 
 B=Column of Burdach (funiculus cuneatus). 
 
 a =LoDg posterior root fibres from the upper half of the body. 
 
 b=Long posterior root fibres from the lower half of the body. 
 
 (2) Each long posterior root fibre, before commencing 
 its passage brainwards in the dorsal column, sends off a 
 branch which passes for some distance in a downward or 
 
8 BING'S COMPENDIUM 
 
 caudal direction, also in the dorsal column. These descend- 
 ing elements of the posterior root system unite to form a 
 special tract, the so-called comma tract of Schultze. The 
 comma tract, therefore, contains at any given level only 
 fibres which have entered the cord at a higher level. For 
 instance, in the upper lumbar segments the comma tract 
 contains no lumbar fibres, but only fibres which have 
 entered higher up, and belong, in the given case, to certain 
 dorsal segments. 
 
 B. ENDOGENOUS TKACTS. 
 
 I. Centripetal Fibres of the Second Order {vide Fig. 2). 
 
 Under this head we include those tracts which connect 
 with elements of the posterior root system that have 
 already terminated in the cord, and provide for the further 
 conduction, towards the higher centres, of impulses received 
 through those elements. 
 
 They are — 
 
 1. The Spino-Cerebellar Tracts. 
 
 {a) The Dorsal Spino-Cerebellar Tract. 
 
 These fibres arise in the cells of the column of Clarke, 
 pass upwards in the dorsal periphery of the lateral column 
 of the same side to the meduUa, and from thence by the 
 restiform body to the cerebellum, ending in the vermis. 
 They form the connecting neurons between the above- 
 mentioned medium fibres of the posterior root system and 
 the higher centres. 
 
 (^) The Tract of Cowers, or Ventral Spino-Cerebellar Tract. 
 
 The cells of origin of this tract are situated in the lateral 
 portions of the substance of the ventral horn. Its fibres 
 pass upwards in the ventral periphery of the lateral column, 
 partly on the same side of the cord, and partly on the. 
 opposite side after crossing the anterior commissure. 
 After traversing the medulla and pons, they enter the 
 cerebellum by way of the superior peduncle, along which 
 they pass to the vermis. They form the connecting neurones 
 for the short fibres of the posterior root system. These 
 fibres are not given in Fig. 2. 
 
 2. The Spino-Thalamic Tract. 
 
 This tract also arises from cells in which terminate 
 short, fibres from the posterior roots. These cells, however, 
 
LESIONS OF THE SPINAL CORD 
 
 are situated in the dorsal horn. The fibres of the spiuo- 
 thalamic tract decussate by way of the anterior com- 
 missure, and pass upwards in the lateral column, terminating, 
 however, not in the cerebellum, but in the optic thalamus. 
 
 11. The So-called Intersegmental or Associating Tracts. 
 These tracts serve to connect the grey matter of succes- 
 sive segments of the cord. The names " proprio-spinal," 
 
 Fig. 4. 
 
 Ascending {Centripetal) Tracts. 
 I=Long fibres of the posterior 
 roots. 
 II=Spmo-cerebeIIar tracts (a, dor- 
 sal ; b, ventral 
 Gowers). 
 [II = Spino- thalamic tract. 
 
 - tract of 
 
 Descending {Centrifugal) Tracts. 
 
 l=Cortico-spinal tracts (a, lateral 
 pyramid tract ; 6, anterior 
 pyramid tract). 
 
 2-5 = Subcortico-spinal tracts (2, 
 rubro-spinal and thalamo- 
 
 spinal ; 
 
 vestibulo-spinal ; 
 
 4, tecto-spinal ). 
 
 5, Descendine; 
 fibres of the 
 dorsal column. 
 
 Topography of the Long Sphial Tkacts. 
 
 " intrinsic," or " spino-spinal " are given to their fibres. 
 They are found — 
 
 (1) In the Ventro-Lateral Column. 
 
 (2) In the Dorsal Column, scattered over its whole area, 
 interspersed with the long fibres of the posterior roots, 
 but especially numerous at certain points, which are hence 
 known as endogenous tracts of the dorsal rolumn. These 
 
10 BING'S COMPENDIUM 
 
 are — -The ventral tract of the dorsal column (" cornu- 
 commissural bundle "), in the neighbourhood of the com- 
 missure, and the medio-peripheral tract of the dorsal column 
 (" septo- marginal bundle"). The former is composed 
 chiefly of ascending, the latter mainly of descending, inter- 
 segmental fibres. 
 
 III. Root Fibres. 
 
 These take their origin in the cells of the ventral horn, 
 and pass by way of the anterior roots to the peripheral 
 nervous system, where they are distributed to muscles, or 
 connect with elements of the sympathetic system. 
 
 It will be advisable here to describe the topography of 
 the long spinal tracts, as sho^vn in transverse section. In 
 Fig. 4 the ascending tracts we have so far dealt with are 
 depicted on the left of the figure, the descending on the 
 right. 
 
 Lateral Cortico- Spinal Tract. 
 
 The area of this tract, the " lateral pyramid area," is 
 of greatest extent in the cervical cord, and diminishes 
 steadily as one passes downwards. This is due to the fact 
 that in each spinal segment en route a portion of the fibres 
 find their termination. In the upper portion of the cord 
 the area has the forui and position given in Fig. 4, in the 
 dorsal portion of the lateral column. From about the third 
 lumbar segment downwards, however, it is found at the 
 dorsal periphery of the lateral column. Thus, at this lower 
 level, it occupies the position which higher up belongs to 
 the lateral cerebellar tract. The latter is ab.^ent from the 
 caudal segments of the cord. 
 
 Anterior Cortico- Spinal Tract. 
 
 The ventral pyramid area or antero-lateral descending 
 tract borders the ventral median fissure on either side. 
 This area diminishes so rapidly in passing down the cord 
 that it is no longer discoverable in transverse sections of 
 the lumbar and sacral regions. 
 
 Ruhro-Spinal and Thalamo- Spinal Tracts. 
 
 These tracts have a common area which forms a ventro- 
 lateral continuation of that belonging to the lateral pyramid 
 tract. It can be traced into the lumbar cord. 
 
LESIONS OF THE SPINAL COED 11 
 
 Tecto-Spinal Tract. 
 
 The fibres of this tract are found in the ventro-Iateral 
 eolumn, in the zone bordering on the grey matter. 
 
 Vestibulospinal Tract. 
 
 This forms a narrow fringe at the periphery of the ventro- 
 lateral column. 
 
 Long Tracts of the Posterior Boots. 
 
 These occupy the area of the dorsal columns. At the 
 positions which have been described as " endogenous areas " 
 they are thinned out, being here more closely interspersed 
 with intersegmental fibres. The descending fibres form the 
 comma tract of Schultze. 
 
 Spino-Cerebellar Tracts. 
 
 These fringe the dorsal half of the lateral column. The 
 dorsal portion of this field forms the lateral cerebellar tract ; 
 the ventral, the tract of Oowers. These tracts are not found 
 at a lower level than the third lumbar segment. 
 
 Spina-Thalamic Tract. 
 
 This tract is situated in the lateral column, opposite the 
 base of the dorsal horn. Where the tract of Gowers is present, 
 the spino-thalamic tract is in close apposition to it medially. 
 
 In Fig. 4 those tracts which are constituted of compact 
 bundles of fibres are represented in black. More scattered 
 or interspersed tracts are figured by dotted areas. It 
 must be borne in mind, however, that even in those tracts 
 which consist mainly of closely associated fibres of the same 
 class a certain number of intersegmental fibres are present 
 (in the pyramid tracts, for instance, the ascending and 
 descending fhroe proprice endopyraniidales). Areas also 
 frequently overlap each other, so that, for instance, spino- 
 thalamic and thalamo-spinal fibres are intermingled. In 
 brief, there are in the spinal cord no perfectly homogeneous 
 tracts. 
 
12 
 
 BING'S COMPENDIUM 
 
 II. CELLS AND CELL-GROUPS OF THE SPINAL CORD, 
 
 A distinction is to be made between " tract " cells and 
 " root " cells (see Fig. 5). 
 
 (a) Tract Cells (CellulsB Funiculares). 
 
 From these cells arise the tracts which we have enumerated 
 An pp. 8 and 9, under the headings " Centripetal Fibres of 
 
 FiQ. 5. 
 
 Endoqenous Spinal Fibres and theik Cells of Oeigin. 
 1-6 =Root cells. 
 
 a-d=Cells of secondary neurones 'l~ . „ 
 a-e=CeUs of association fibres /Tract cells. 
 
 the Second Order " and " Intersegmental Fibres.'" They lie 
 scattered over the dorsal horn and a large part of the 
 ventral horn, and are in part erratic, or without any definite 
 groupmg, in part united into cell-complexes, of which the most 
 important is the column of Clarke, at the base of the dorsal 
 horn. 
 
LESIONS OP THE SPINAL CORD 
 
 13 
 
 (6) Root Cells (Cellulae Radiculares). 
 From these cells arise the anterior roots. They lie without 
 exception in the ventral horn, and are characterized by 
 their more or less definite grouping. In the lumbar and 
 cervical regions, for instance, where the expansion of the 
 grey matter is most considerable, one can distinguish an 
 antero- and a postero-lateral, an antero- and postero- 
 mesial, and finally a central group. Later we shall give 
 
 Fia. 6. 
 
 ^ A.- As^int 
 
 DlSTBIBFTION OF BLOODVESSELS AND NebVE CelLS 
 
 IN THE Transverse Section of the Cord. 
 
 Root cells : (1) Postero- 
 lateral group ; (2) an- 
 tero - lateral group ; 
 
 (3) antero-meaial group ; 
 
 (4) central group; 
 
 (5) postero-meBJ^ group. 
 
 more detailed consideration to these groups, which contain 
 nuclei and nerve centres. The most important are the 
 lateral groups, from which springs the chief contingent of 
 the anterior root fibres. 
 
 All the cell-groups of the ventral horn are distinguished 
 by their very copious blood-supply. While radial branches 
 from the vaso-corona, the arterial " wreath," which forms 
 the connection between the anterior and posterior spinal 
 arteries, and surrounds the spinal periphery, supply the 
 
14 BING'S COMPENDIUM 
 
 white substance and the greater part of the dorsal horns, a 
 special arterial trunk penetrates into the ventral horn, on 
 the right side or the left, according to the level. This 
 sulco-Oommissural artery forms, in the substance of the 
 ventral horn, a rich and intricate network, which holds 
 the ceU- groups of the anterior roots enweaved in its 
 meshes. Only in the most peripheral portion of the 
 ventral horn, close to the boundary of the white matter, 
 does the vaso-coronal system share in the nourishment of 
 the grey matter. We shall see that the existence of two 
 quite distinct arterial " territories " in one and the same 
 transverse section of the cord is a fact of the greatest 
 clinical significance. 
 
 CHAPTER II. 
 
 We now proceed to consider the physiology of the structures 
 which in the foregoing chapter we have looked at from 
 a purely anatomical point of view. We shall thus learn 
 what functions the separate components of the spinal cord, 
 its tracts and nuclei, subserve, and, conversely, shall be 
 placed in a position to infer, from the presence of definite 
 physio-pathological phenomena, lesions of definite areas in 
 the cord. 
 
 The spinal cord is an organ of fourfold physiological 
 significance, performing at once sensory, motor, vaso-motor, 
 and trophic functions. 
 
 It will be as well to group its elements for consideration 
 under the above four heads. 
 
 I. SENSORY APPARATUS OF THE SPINAL CORD. 
 
 Sensory impulses reaching our consciousness or sub- 
 consciousness, and due to occurrences within the sphere 
 of trunk or limbs, make their way into the cord through the 
 spinal ganglia and the posterior nerve roots. Corporeal 
 sensibility in the broadest sense of the term is only normal 
 therefore, in the presence of a normal and intact system 
 of posterior roots and connecting neurons. Corporeal sensi- 
 bility is not a term of single, sharply-defined meaning. In 
 i+s analysis of the conception, physiology distinguishes 
 between sensations of pressure, position, cold, warmth, pain, 
 motion, and so on. 
 
LESIONS OF THE SPINAL CORD 15 
 
 Clinical medicine does not go so far, but in its semeio- 
 logical investigation of corporeal sensibility, confines itself, 
 in the main, to the testing of four principal functions. 
 
 1. Tactile Sensibility. 
 
 This is tested by means of a pledget of cotton-wool, a 
 camel-hair brush, the finger, etc. Its diminution is termed 
 " tactile hypsesthesia," its abolition " tactile anaesthesia." 
 
 2. Temperature Sense. 
 
 In studying this we test the subject's distinguishing 
 power for cold and warm objects. The conditions of imper- 
 fect or absent temperature sense are known respectively 
 as " thermo-hypsesthesia," and " thermo-ansesthesia." 
 
 3. Sensibility to Pain. 
 
 Pricks with a needle, pinching a fold of skin, etc., will 
 enable us to form conclusions here. Diminution = hypalgesia ; 
 abolition = analgesia. 
 
 The foregoing may be grouped together under the heading 
 " Superficial Sensibility," the integument being in each 
 case the seat of the stimulations to be investigated. Patho- 
 logical increase of tactile or temperature sensibility is 
 described as " tactile " or " thermic hypersesthesia," 
 increased sensibOity to pain is termed " hyperalgesia." 
 
 4. Deep Sensibility. 
 
 By this term we understand the sum of the centripetal 
 impulses which reach our central nervous organs from 
 the muscles, tendons, bones, joints, etc. A portion of 
 these impulses crosses within the brain the threshold of 
 our consciousness, and makes us aware of the position of 
 our limbs, the amount of flexion or extension, abduction 
 or adduction at particular joints, the extent of purposive 
 movements, etc. "Hese also must be included the sensation 
 of vibration ("paUsesthesia "), felt when a vibrating tuning- 
 fork is placed on superficially situated parts of the honj 
 skeleton. Another portion, however, does not reach the 
 sensorium, but regulates subconsciously the motor mechan- 
 ism which is called into play in the carrying out of all 
 complicated and combined movements — e.g., standing or 
 
16 BING'S COMPENDIUM 
 
 walking. This portion provides for the preservation of 
 equilibrium, the harmonious performance of the function of 
 locomotion, the "synergetic " action of functionally related 
 groups of muscles, and so on. 
 
 More or less marked deficiencies in the sphere of the 
 deep sensibility serve to fill in the symptom pictures oi 
 ataxia, inco-ordination, asynergia, etc. As the sense oi 
 motion and of position possessed by our fingers plays the 
 chief role in the recognition of objects by touch with the 
 eyes shut, " astereognosis,"* or the inabihty to appreciate 
 form by means of palpation, is also an expression of dis- 
 turbed "deep sensibihty." Inability to feel vibration is 
 termed "paUansesthesia." 
 
 The fibres which serve for the conduction of sensory 
 impressions of the above four chief categories separate from 
 each other immediately after their entrance into the cord. 
 
 1. Tactile sensations are conducted towards the brain by 
 both long and short fibres of the posterior root system (c/. 
 pp. 5-10, and Fig. 2) — some on the same, some on the opposite 
 side of the cord, the latter via the spino-thalamic tract. 
 
 2. Thermal sensations. 
 
 3. Sensations of pain are conducted exclusively by short 
 fibres of the posterior root system to cells in the dorsal 
 horn, and from thence by the above-described centripetal 
 fibres of the second order, which ascend to the thalamus 
 in the opposite lateral column. 
 
 4. The deep sensibilityf makes use of two routes — {a) by 
 long fibres of the posterior root system and the dorsal 
 columns to the thalamus and brain ;. (6) by medium fibres 
 of the posterior root system, the column of Clarke and the 
 lateral cerebellar tracts, to the cerebellum. Both routes 
 ascend uncrossed. The cerebellar fibres serve for the con- 
 duction of subconscious tactile and co-ordinatory percep- 
 tions ; the cerebral for the same purpose, and, in addition 
 for the conduction of conscious perceptions of position and 
 motion to the cerebrum. 
 
 * As the word " agnosis " is generally used to denote loss of some per- 
 ception due to a defect or lesion in the psychical sphere, the aboUtion of 
 the power of distinguishing form due to disturbance of the deep sensibility 
 should be termed stereo-anassthesia " rither than " astereognosis." 
 
 ■f In the peripheral nervous system the fibres conveying impulses of the 
 deep sensibihty run in the nerves of the muscles, hence the deep sensibihty 
 is not impaired by lesions of the branches of the cutaneous nerves. 
 
LESIONS OF THE SPINAL CORD 17 
 
 IL MOTOR APPARATUS OF THE SPINAL CORD. 
 
 By motility, in its broadest sense, we understand, not 
 merely the phenomena of voluntary movement, but also 
 those of tonus and reflex. 
 
 (a) Voluntary Motion. 
 
 Psycho-motor impulses arise, in greatly preponderating 
 measure, from the motor centres of the cortex, and are 
 conducted to the spinal centres in the ventral horns along 
 the pyramid tracts. The cortico-spinal tracts are there- 
 fore to be regarded as the chief routes for motor impulses. 
 They are, however, assisted in their task by a number of 
 secondary tracts. 
 
 A lesion, therefore, putting the pyramid tracts completely 
 out of action, may cause, not complete paralysis, but merely 
 a serious diminution of motility, or paresis, the secondary 
 tracts actmg, up to a certain point, vicariously for the 
 pyramidal. These secondary tracts are those which we 
 have denominated subcortico-spinal tracts. Their centres of 
 origin (the red nucleus, the thalamus, the tectum opticum, 
 the nucleus of Deiters) have communications with the motoT 
 cortex, thanks to which, even in the presence of lesions of 
 the'pyramid tracts, some psycho-motor impulses succeed in 
 reaching the ceU-groups of the ventral horn by a circuitous 
 route. 
 
 The centres for the whole muscular system are situated 
 among the cell-groups of the ventral horns ; thus each 
 separate muscle is innervated from, and represented by, 
 a particular ganglion-cell group in the cord. The exact 
 principles governing localization in this connection will 
 be considered in detail when the subject of regional diagnosis 
 qua level, or segmental diagnosis (Hohendiagnostik), comes to 
 be dealt with. Here we have merely to state clearly that 
 destruction of the motor cells of the ventral horn leads to 
 complete paralysis of the muscles governed by them. 
 
 (6) Tonus and Reflex. 
 
 A mechanical stimulus, such as striking or rubbing, 
 acting on particular parts of the body, tendons, special 
 skin areas, etc., gives rise, under normal circumstances, to 
 correspondingly definite motor phenomena (contraction of 
 
18 BING'S COMPENDIUM 
 
 particular muscles). We speak of these as reflexes. Apart 
 from this, however, subconscious afferent impulses of less 
 intensity are continuously passing from every part of the 
 body, deep and superficial alike, to the central nervous 
 organs, and these bring about, also reflexly, a moderate 
 but continuous contraction of the whole muscular system. 
 This is known as muscular tonus. It may be defined as 
 " the particular degree of tension which gives to our muscles 
 the capacity for prompt response, by a contraction, to 
 a voluntary nervous impulse." That it is brought about 
 reflexly is shown by the fact that section of the posterior 
 roots — in other words, suppression of centripetal impulses — 
 places the muscles in a condition of complete atony. That 
 under normal conditions centripetal impulses are con- 
 tinuously at work producing muscular tonus in a reflex 
 manner, is proved by the fact that in healthy persons the 
 condition of tonus never ceases to exist even in sleep. The 
 muscular system of a sleeper is never so completely re- 
 laxed as that of a corpse, and it is only in the more 
 advanced stages of narcosis that tonus is completely 
 abolished. 
 
 It is plain from the foregoing that in the mechanism of 
 spinal reflex and spinal tonus we have both centripetal 
 and centrifugal components, on whose integrity depends 
 the normal bringing into play of these phenomena, so essential 
 to the correct performance of voluntary movements 
 (c/. Fig. 7). 
 
 The centripetal limb, so to speak, of the reflex and tonus 
 ftrc lies, of course, in the posterior roots, the only structures 
 through which centripetal tracts enter the cord. Equally, 
 of course, the centrifugal limb is furnished by the anterior 
 root system — i.e., the peripheral motor neurons. The 
 connection between the two is established by the terminal 
 splitting of certain of the posterior root fibres among cells 
 of the ventral horn. 
 
 These " reflex collaterals " belong to the short fibres of 
 the posterior root system. In addition to this simplest 
 form of connection, in which the whole refiex arc lies 
 at one and the same spinal level, there are also more 
 complicated forms in which there are further connecting 
 neurons between the centripetal and centrifugal limbs, 
 by which a stimulus may be conveyed from a posterior root 
 to an anterior root of a higher level, or to several anterior 
 
LESIONS OF THE SPINAL CORD 
 
 19 
 
 roots — perhaps even, by a detour, to the corresponding 
 anterior root, etc. These conditions, however, need not 
 detain us longer at this stage of our inquiry. 
 
 We know, however, that certain cortico-spinal fibres 
 also have their terminal ramification among the same motor 
 cells, in whose neighbourhood the " reflex collaterals " of 
 
 Fio. 7. 
 
 <'«-«■ >«i»\<La«.xe.lle. 
 
 cerebIrale 
 
 ScnEMATio Repeesentation of the Mechanism op Spinal Reflex. 
 
 Lesion of neuron A"l Abolition or diminution of reflex 
 „ B/ and tonus. 
 „ ,. C=Hyperreflex and hypertonus. 
 
 the posterior root system spHt up. These also have their 
 pari to perform in bringing tonus and reflex into play. 
 They fulfil the function of a governor or regulator, acting 
 inhibitorily, and never allowing reflex movements or tonus 
 to be developed beyond a certain definite and serviceable 
 degree. Without this inhibitory action of the pyramid 
 tracts the phenomena of reflex would not be so constant in 
 
20 BING'S COMPENDIUM 
 
 character as they a,re. When those tracts are destroyed, 
 tonus increases to such a degree as to be a serious hindrance 
 to the performance of voluntary movements, and we find 
 the slight concussions of the body produced in locomotion 
 liberate reflexes sufficiently powerful to produce a markedly 
 disturbing effect. 
 
 The following simple rules, therefore, may be laid down 
 concerning tonus and reflex : 
 
 Lesions of the anterior or posterior root systems cause 
 diminution or abolition of tonus and reflexes, lesions of the 
 pyramid system cause increase of tonus and reflexes. 
 
 III. THE TROPHIC APPARATUS OF THE CORD. 
 
 The circumstance that each nerve cell constitutes the 
 trophic centre for the nerve fibres arising from it — we recall 
 here the Wallerian laio mentioned on p. 2 — has, as a conse- 
 quence, the fact that the root cells of the cord govern the 
 nutrition of that part of the peripheral nervous system 
 which takes its origin from them — i.e., the motor nerves 
 throughout the body. In an analogous manner the in- 
 tegrity of the sensory nerves throughout the body is dependent 
 on that of the spinal ganglia. The trophic influence of the 
 cells of the ventral horn, however, is not confined to the 
 peripheral motor nerve fibres. The terminal motor 
 apparatus, the muscles themselves, are also subject to it. 
 When the cells of the ventral horn are destroyed, the muscles 
 innervated- by them undergo an atrophy which is described 
 as degenerative, to distinguish it from the simple atrophy 
 of disuse. It is characterized, from the point of view of 
 pathological anatomy, by a rapid disappearance of contractile 
 elements, and their replacement by a similarly rapid growth 
 of fat and fibrous tissue, and, clinically, by the reaction of 
 degeneration. 
 
 Where this latter comes to its complete development, 
 the galvanic and faradic irritability of the nerves is ex- 
 tinguished within about fourteen days. At the same time, 
 the irritability of the muscles to direct faradic stimulation 
 diminishes and disappears, while, on the other hand, their 
 irritabiUty to galvanic stimulation increases. The galvanic 
 contraction, however, instead of being prompt and lightning- 
 like, is slow and " creeping," and the contraction formula 
 so altered, that the anodal closing contraction takes place 
 
LESIONS OF THE SPINAL CORD 21 
 
 with an equal or a weaker current than does the kathodal 
 closing contraction. After about two months, however, 
 the direct galvanic irritability of the muscles begins also to 
 diminish, and after the lapse of a few more months is 
 extinguished. For an account of partial and modified 
 forms of the reaction of degeneration, works on electro- 
 diagnosis must be consulted. 
 
 The cells of the ventral horn exert a trophic influence ov^er 
 the bony skeleton also. When destroyed in a growing 
 subject, a more or less marked inhibition is noticed in the 
 further growth of the bones in the region of the affected 
 muscles. Abnormal brittleness of the bones may also 
 result under like circumstances. 
 
 It would seem that the trophic influence of the cells oi 
 the ventral horn is to ,a certain extent called into action 
 reflexly by elements of the posterior root system, inasmuch 
 as trophic disturbances of the skeleton and muscular system 
 are sometimes found to follow (though at a considerable 
 interval) destruction of the posterior roots. 
 
 IV. THE SPINAL VASO-MOTOR MECHANISM. 
 
 Vaso-motility, as is well known, is under the direct 
 governance of the sympathetic system. Experimental 
 physiology teaches that vaso-constrictor fibres arise from 
 the so-called " lateral " ganglion system or sympathetic 
 chain of ganglia; while, on the other hand, vaso-dilator 
 fibres arise from the " collateral " gangUon system — i.e., 
 from the other cell-complexes included in the tracts of the 
 sympathetic nerves. It is true that the existence of vaso- 
 dilator fibres has only been experimentally proved in the 
 case of certain special nerve trunks of the body and 
 extremities — e.g., the nervi erigentes and the sciatic. 
 Vaso-constrictor fibres, on the contrary, are to be found 
 generally distributed as components of the mixed spinal 
 nerves. We know accurately how they reach the latter: ii 
 is by way of the grey rami communicantes, which pass from 
 the separate gangha of the sympathetic chain to join them- 
 selves to the corresponding somatic nerves. 
 
 The ganglion cells, however, of the sympathetic chain, 
 of which vaso-constrictor fibres are to be regarded as the 
 axis cylinders, themselves constitute connecting neurons 
 for contrifugal offshoots of certain spinal cells. The latter, 
 
22 BING'S COMPENDIUM 
 
 the spinal centres for vaso-constriction, lie in the ventral 
 horns, and, for the most part, in their mesial cell groups. 
 Their ofEshoots issue from the cord with the anterior roots, 
 to pass along the white rami communicantes to the sym- 
 pathetic chain. These spinal vaso-motor centres, however, 
 are themselves governed by a bulbar vaso-motor centre, 
 situated in the neighbourhood of the upper olive, whose 
 stimulation is followed by a general vaso-constriction, 
 while general loss of vascular tone follows its destruction. 
 That, further, above this bulbar centre there must stand 
 still a supreme centre, in the higher brain, is shown (apart 
 from infrequent and somewhat conflicting experimental 
 work) by the fact that psychic emotions may have, as a 
 consequence, blushing or pallor. 
 
 We have endeavoured to present in schema form (Fig. 8), 
 and in accordance with the foregoing, the mechanism of 
 vaso-motility, with its four neurones — ^cerebro -bulbar, 
 bulbo-spinal, spino-sympathetic, and sympathetico-muscular. 
 Vaso-dilator fibres are not represented in the schema, as 
 they are not of general occurrence, but are only found ia 
 certain special regions. As a matter of fact, they are 
 practically ignored clinically. Broadly speaking, we regard 
 loss of vascular tone as due to vaso-constrictor paralysis, 
 and vaso-constriction as due to vaso-motor stimulation. 
 
 It is easy, then, to understand that lesion of the ventral 
 horn has, as a consequence, vaso-motor paralysis, if it brings 
 about a discontinuity between the third neuron system 
 of our schema and the central cell-group, and, further, that, 
 under certain circumstances, disconnection of the lateral 
 columns, by interruption of the bulbo-spinal connections, 
 will have the same efiEect. What these particular circum- 
 stances are we cannot state with precision from an anatomico- 
 pathological point of view, for we do not yet possess 
 exact topographic data concerning the tracts of the lateral 
 columns which are involved. 
 
 Spinal vaso-motor paralysis, whether produced by destruc- 
 tion of the vaso-motor centres in the ventral horn, or by 
 mterruption of vaso-motor fibres in the laternal columns, 
 seldom reveals itself, and then only in its earliest stages, 
 by redness and heat of the skin. A pictm'e of an apparently 
 opposite nature is more frequently presented, one that may 
 supervene on and replace the other, but may also develop 
 
LESIONS OF THE SPINAL CORD 
 
 23 
 
 without any obvious stage of redness. The integument, 
 in fact, in the regions innervated by the affected sections 
 of the cord, becomes cold and cyanotic. The cyanosis 
 
 
 I'IG. 8. 
 
 ■ I Ctntr. cereliroXe. 
 
 \j(X., 
 
 MEDULLA 
 
 HCenlir. Wtare. 
 
 TRUNCUS 
 SYMPATH. K 
 
 ECentr. SMlnolc. 
 
 IST CentK S^mjioit^ic. 
 
 ARTERIA 
 
 Diagram of the Mechanism of Vaso-Motility. 
 
 a = Cerebro-bulbar vaao-motor tract ; 6 = Bulbo-spinal vaso-motor tract ; c= Spino- 
 sympathetio vaso-motor tract ; c2=Sympathetico-inuscular vaso-motor tract ; 
 I-IV=Primary and subordinate centres ; E. A. = Radix anterior; E.P. = Radix 
 posterior; R.O.A. = Ramus communicans albus ; R. C. G. = Ramus communi- 
 cans griseus. 
 
 is explained by the chronic obstruction to the capillary 
 circulation which follows the removal of vascular tonus, the 
 coldness (which may amount to a diminution in temperature 
 of 10°) by the disturbance of nutrition due to the cyanosis. 
 
24 BING'S COMPENDIUM 
 
 APPENDIX. 
 
 The mechanism of perspiration is very similar to that of 
 vaso-motility. Here also we have cerebral, bulbar, spinal, 
 and sympathetic centres. The schema of Fig. 8 will serve 
 as a description of the nervous elements of the sweat 
 mechanism, if we merely substitute a sweat gland for the 
 bloodvessel. The spinal sweat centres seem, like the spinal 
 vaso-motor centres, to be scattered throughout the cord, 
 and to have their cells in the ventral horns, in the neighbour- 
 hood of the motor ganglion-cells. Their injury or destruc- 
 tion is followed by diminution or abolition of the sweat 
 secretion in the regions of the body involved — hyphidrosis 
 or anidrosis. One would meet with these phenomena 
 oftener than is at present the case were it the routine 
 practice in diseases of the spinal cord to employ diaphoretics 
 in the endeavour to detect abnormalities of the function. 
 
 CHAPTER III. 
 
 Having passed in review the various neuron systems of 
 the spinal cord both from an anatomical and a physiological 
 point of view, the clinical symptoms and symptom-groups 
 present in any given case should make it possible to answer 
 the question — Which of those neuron systems is destroyed 
 or damaged by a pathological process 1 — i.e., which parts 
 of the transverse section of the cord are involved in the 
 latter ? 
 
 Diseases and injuries of the cord announce their presence 
 as a rule either — 
 
 (a) By disturbances of motility ; or 
 (6) By disturbances of sensation ; or 
 (c) By a mixture of both the foregoing. 
 
 Motor and sensory conditions are the only diagnostic 
 guiding stars in the symptomatology of spinal diseases. 
 Trophic and vaso-motor phenomena come so far behind them 
 in significance, that, in questions of regional diagnosis, they 
 are only brought in as secondary arguments and in special 
 cases. 
 
LESIONS OF THE SPINAL CORD 25 
 
 I. THE REGIONAL DIAGNOSTIC SIGNIFICANCE OF 
 MOTOR DISTURBANCES. 
 
 Paralysis or paresis follows, as we have seen, interruptions 
 of continuity, either in the cortico-spinal or in the spino- 
 muscular neurons. 
 
 The former occur in the great majority of cases in the 
 lateral columns ; the latter have their seat exclusively in 
 the ventral horns and anterior roots. When, in spinal 
 affections, therefore, we meet with paralysis or paresis, the 
 first question we have to decide is this : Is it a lateral 
 column affection, or one of the ventral horn and anterior 
 roots ? In some cases, it is true, we have to consider the 
 possibility of a combination of the two conditions. 
 
 (a) Characteristic Features of Paralytic Affections due to 
 Lesions of the Lateral Columns. 
 
 (a) In the first place, the paralysis is here not complete, 
 but is rather of the nature of paresis ; for the anterior 
 pyramid tracts remain, and also the subcortico-spinal 
 tracts, which carry motor impulses from the brain, and 
 innervate the motor centres in the ventral horn by a cir- 
 cuitous route. Where the affection is one of the lateral 
 pyramid area alone, aU the subcortico-spinal tracts enu- 
 merated on pp. 4 and 5 come into play vicariously ; where, 
 however, the whole lateral column is affected, the anterior 
 pyramid tracts may be assisted by a portion of the tecto- 
 and vestibulo-spinal fibres. 
 
 (/3) The paresis affects in about equal degree all the 
 muscles of the affected extremity. In a given transverse 
 section of the lateral pjrramid area there are cortico-spinal 
 fibres lying in close contact with one another, whose terminal 
 ramifications are distributed over a wide stretch of the 
 motor-cell columns of the ventral horns. 
 
 (7) Rigidity and spastic stiffness of the paretic muscles 
 IS a noticeable feature, a consequence of the cessation of 
 tonus-inhibiting impulses from the cortex, which, as was 
 shown on p. 19, pass continuously along the pyramid 
 tracts to the cells of the ventral horn. It is easy to satisfy 
 oneself of the presence of this hypertonus by palpation, 
 
26 BING'S COMPENDIUM 
 
 testing the resistance to passive movements, etc. Ex- 
 citability to mechanical stimuli is also increased in the 
 paretic muscles, owing to the presence of hypertonus. 
 
 (S) There is an exaggeration of tendon and bone reflexes 
 in the sphere of the paretic muscles, which is analogous to 
 their general spastic condition, and susceptible of an 
 analogous explanation (c/. p. 19, Fig. 7). With this ex- 
 aggeration of reflexes, the phenomenon known as clonus 
 may often be demonstrated in the affected musculo-tendinous 
 mechanism. The phenomenon consists of a series of mus- 
 cular contractions rapidly following each other in the affected 
 muscles, and produced by a suddenly applied passive stretch- 
 ing of their tendons. By far the most frequently elicited is 
 the ankle-clonus (AchiUes tendon) ; patellar clonus is not 
 uncommon ; wrist, finger, and elbow clonus are rare. 
 
 The condition of the skin reflex is far more variable than 
 that of the tendon reflex. Exaggeration of skin reflex can 
 only be demonstrated in a certain proportion of the cases, 
 in which, owing to a pyramid lesion, the normal cortical 
 inhibition is suppressed. Occasionally, in contrast to the 
 exaggerated tendon reflex, the skin reflex is actually 
 diminished or absent. It wiU be sufficient briefly to state 
 the fact here ; in the section on segmental diagnosis 
 opportunity will offer to deal with this peculiarity more 
 fully. While, however, the degree of reflex which answers 
 a stimulation of the skin is of far less diagnostic value in 
 the determination of a lesion of the lateral column than is 
 the case with the phenomenon of tendon reflex, there are 
 certain pathological skin reflexes which are established in 
 the presence of lesions of the pyramid tracts, and which 
 give diagnostic information of great value. Of these, the 
 most important is Babinski's sign, in which irritation of 
 the sole of the foot calls forth a slow tonic hyperextension 
 of the great toe, sometimes accompanied by a simultaneous 
 plantar flexion of the other toes. In the second rank is the 
 reflex of Oppenheim, in Avhich the same phenomenon can be 
 brought about by a vigorous stroking of the skin on the 
 medial surface of the leg. As an instance of a pathological 
 tendon-reflex may be mentioned the Mendel-Bechterew phe- 
 nomenon (dorsal foot reflex) ; in lesions of the pjo^amid tract 
 percussion of the lateral portion of the dorsum of the foot 
 (Metacarpals IV. and V.) may cause a plantar flexion of the 
 
LESIONS OF THE SPINAL CORD 27 
 
 toes. Under normal conditions either no reflex is caused, or 
 there is a dorsal flexion. These "pathological reflexes " 
 are normally present in the infant during the first few months 
 of life, and this is probably due to the fact that it is only 
 after birth, during the early post-embryonal period, that 
 the pyramids become fuUy effective in function through the 
 clothing of their axis cylinders in a medullary sheath. No 
 satisfactory explanation of these phenomena has yet been 
 given. We can only suppose that the reflex stimulus, 
 when not controlled from above — i.e., by the cerebral 
 centres — forces its way into tracts which are normally 
 closed to it 
 
 (e) The same may be the case when a voluntary impulse 
 rather than a reflex stimulus is in question, so that a par- 
 ticular intended movement of the paretic muscles is accom- 
 panied by unintended movements. Thus it may be im- 
 possible to flex the lower limb on the trunk without bringing 
 about simultaneously a vigorous dorsal flexion of the foot 
 (tibialis phenomenon or StriimpelVs sign). Involuntary 
 hyperextension of the great toe may take place under the 
 same circumstances [toe phenomenon). In the hand we 
 have the radialis phenomenon (involuntary dorsal flexion 
 of the hand accompanying volar flexion of the flnger) ; 
 involuntary pronation may accompany flexion of the 
 forearm {pronation phenomenon), and so on. 
 
 (f) There is no atrophy of the affected muscles —none, 
 at least, except the late and never very marked " atrophy of 
 disuse " — for the muscles remain, in spite of interruption 
 of the pyramid tracts, in unbroken connection with their 
 trophic centres, the cells of the ventral horn. For the 
 same reason the muscle retains, with its anatomical integrity, 
 its electrical excitability. 
 
 (77) The signs of vaso-motor paralysis mentioned on p. 23, 
 coldness and cyanosis, may be present in the parts affected by 
 cortico-spinal paralysis . In such case the vaso-motor neuron 
 in the lateral columns is probably interrupted. This is, how- 
 ever, not by any means always the case, nor are vaso-motor 
 phenomena as a rule present in any marked degree. 
 
 The whole picture of paralysis due to affection of the 
 lateral columns — i.e., to interruption of the cortico-spinal 
 tracts — may be described as a spastic symptom-complex. 
 
28 BING'S COMPENDIUM 
 
 (6) Characteristics of Paralysis due to Aflections of the 
 Ventral Horn. 
 
 (a) The paralysis of the affected muscles is at first com- 
 plete. No other structures can take on vicariously the 
 work of injured motor neurons of the second order. As 
 time goes on, there may be restoration of function to a 
 certain degree (if, for instance, some of the originally 
 merely damaged motor cells succeed in restoring them- 
 selves) ; this restoration is, however, always incomplete 
 and always slow. 
 
 (/8) It is seldom that all the muscles of an extremity 
 are paralyzed as the result of a ventral horn lesion. This 
 fact might be inferred from the anatomical conditions. 
 We have seen above that in a transverse section the nuclei 
 for the separate muscles lie separated from one another, 
 scattered over an area of some extent, and are thus far less 
 liable to be destroyed simultaneously by one and the same 
 lesion than the closely compacted fibres, covering only a 
 small area, of the pyramid bundle. Our discussion of seg- 
 mental regional diagnosis will show us, further, that in longi- 
 tudinal sections of the ventral horns this peculiarity is still 
 more perfectly displayed, so that the nuclei of separate 
 muscles of the same limb may be centimetres apart from 
 each other. Lesions of this extent, however, are rare in spinal 
 pathology. 
 
 (7) The muscles affected are atonic (interruption of the 
 centrifugal limb of the tonus-reflex arc). Absence of 
 resistance to passive movements, looseness of articulations 
 owing to deprivation of muscular support, possibility of 
 enormous hyperextension, " professional contortionist " posi- 
 tions, marionette attitudes, betray this atony with sufficient 
 clearness. With this complete atony is associated suppres- 
 sion of direct mechanical excitability. 
 
 (S) The reflexes disappear (interruption of the centrifugal 
 limb of the reflex arc). 
 
 (e) There are no involuntary associated movements. 
 
 (^) Lesions of the ventral horn centres are very rapidly 
 followed by severe atrophy of the muscles in trophic depen- 
 dence on them. This degenerative atrophy is accompanied 
 by the " reaction of degeneration." 
 
LESIONS OF THE SPINAL CORD 29 
 
 (n) Vaso-motor disturbances are much more severe, and 
 appear much more frequently than is the case in cortico- 
 spinal paralysis. The important vaso-con stricter centres 
 are especially liable to come within the range of the lesion 
 In addition to marked coldness and cyanosis of the in- 
 tegument, lowering of blood-pressure (an evidence of loss 
 of tone in the arterial trunks) is also to be noticed. 
 
 The fact that the ventral horiis, whose situation is a much 
 more protected one than that of the pyramid tracts, and 
 whose position in a transverse section is not far removed 
 from that of the latter, should so often be the seat of patho- 
 logical processes, which those tracts escape, and thus give 
 rise to paralysis of purely peripheral (spino-muscular) 
 type, is to be explained by reference to the conditions of 
 spinal blood-supply described on pp. 13 and 14. Owing to 
 their separate vascular supply, the anterior cornua are, noso- 
 logically, to a large extent independent of the remaining 
 structures in the spinal transverse section. Owing to the 
 very richness of their vascularization, they are specially 
 liable to injury from noxious matters reaching them by way 
 of the blood-stream, and to morbid processes of a peri- 
 arteritic nature — e.g., poliomyelitis anterior. On the other 
 hand, the rich anastomosis of the sulco-commissural artery 
 protects the ventral horn as a rule from the ischsemic 
 degeneration which, in the angio-sclerotic processes of 
 syphilitic endarteritis, for example, is so rapidly destruc- 
 tive to the more sparingly arterialized lateral columns. 
 This selection for isolated attack, either of the central or 
 the peripheral motor neurons, is also often seen in systemic 
 degenerations ; both may, it is true, be attacked simultane- 
 ously, as the condition known as amyotrophic lateral sclerosis 
 sufficiently proves — indeed, such simultaneous lesions of 
 protoneurons and deuteroneurons come under observation 
 occasionally from the most diverse causes. 
 
 [c) Paralytic Phenomena due to Combined Lesions of 
 Lateral Columns and Ventral Horns. 
 
 That this " combined " form of paralysis "resembles " the 
 cortico-spinal type, in so far as the extent of the paralyzed 
 region is concerned, is easy to understand ; equally natural 
 
30 
 
 BING'S COMPENDIUM 
 
 is it that otherwise, and on the whole, the features of spino- 
 muscular paralysis should dominate the clinical picture. 
 The paralysis of most of the affected muscles is complete, 
 and atrophy and the reaction of degeneration set in. Up 
 to the point, however, at which atrophy brings about the 
 destruction of the muscle, and the reaction of degeneration 
 gives place to a complete absence of reaction, phenomena 
 of hyperreflex and hypertonus may betray the lateral 
 column degeneration lurking, so to speak, behind the 
 degeneration of the anterior horn. During these com- 
 paratively early stages the reflexes are exaggerated, as also 
 is the direct mechanical excitabiUty. Purther^where the 
 paralysis affects the foot — hyper-extension phenomena, 
 Babinski's and Oppenheim's signs, may be eUcited for a 
 time, as also the Mendel-Bechterew phenomenon (dorsal- 
 pedal reflex). 
 
 Spinal Paralyses. 
 
 (a) Lateral Column Type. 
 
 (6) Ventral Horn Type. 
 
 (c) Combined Type. 
 
 Paresis 
 
 Paralysis preponderat- 
 
 Paralysis prepondcrat- 
 
 General distribution 
 
 ing 
 Distribution to indi- 
 vidual muscles 
 
 Distribution general 
 
 Hypertonus 
 
 Atony 
 
 Indications of hyper- 
 tonus, later atony 
 
 Hyperreflex 
 
 Absence of reflex 
 
 Hyperreflex, giving nay 
 later to absence cf 
 reflex 
 
 Associated movements 
 
 No associated move- 
 
 No associated move- 
 
 frequent 
 
 ments 
 
 ments 
 
 Hyperexiension phe- 
 
 No hyperexteusion phe- 
 
 Occasionally hvperex- 
 
 nomena and dorsal- 
 
 phenomena nor 
 dorsal-pedal reflex 
 
 tension phenomena 
 
 pedal reflex 
 
 and dorsal -pedal 
 
 
 
 rsflex, disappearing 
 
 
 
 later 
 
 No degenerative mus- 
 
 Degenerative mus- 
 
 Degenerative mus- 
 
 cular atrophy 
 
 cular atrophy 
 
 cular atrophy 
 
 No reaction of degenera- 
 
 Reaction of degenera- 
 
 Reaction of dogonora- 
 
 tion 
 
 tion 
 
 ticn 
 
 Before we turn to a consideration of sensory symptoms, 
 brief mention must be made of certain motor " irritation 
 symptoms " (hyperkinesis) which point to the presence of 
 morbid conditions which, without leading to complete 
 destruction either in the cortico-spinal or the spino-muscular 
 neuron-complexes, are sufficient to bring about abnormal 
 dynamic phenomena. 
 
 1. The so-called " spinal epilepsy " of Brown-S6quard. 
 This by no means common phenomenon is the motor "irrita- 
 
LESIONS OP THE SPINAL CORD 31 
 
 tion symptom " of lesions of the lateral column. It is a 
 spontaneous clonus of the paretic extremities, coming on 
 in definite attacks, and causing a more or less violent 
 shaking of the extremities by alternate contraction of their 
 flexors and extensors. 
 
 2. The weU-known " fibrillary twitchings " which occur 
 in functional neurotic states, and can be brought on even in 
 normal subjects, by the application of cold, for instance, 
 are a frequently occurring motor irritation symptom of 
 lesions of the ventral horn. 
 
 II. THE REGIONAL DIAGNOSTIC SIGNIFICANCE OF 
 SENSORY DISTURBANCES. 
 
 It will be advisable here to refer to Pig. 2, and to recall, 
 in connection therewith, what was said on p. 16 concerning 
 the separate sensory tracts. It was pointed out that tactile 
 impressions pass to the brain by both the routes, L and K2 ; 
 that the latter, exclusively, serves for painful impressions 
 and for the temperature sense ; while, finally, impres- 
 sions of the deep sensibility are conveyed to our conscious- 
 ness or subconsciousness partly by route L to the brain, 
 and partly by route M to the cerebellum. 
 
 These facts being kept in mind, we may proceed without 
 further introduction to make the statements here following : 
 
 1. A lesion of the posterior roots abrogates or diminishes 
 sensibility in the region from which those roots receive 
 centripetal fibres. Disturbances of the sensibility of the 
 integument to tactile, painful, and thermal impressions 
 are combined with ataxic and astereognostic. (vide p. 16) 
 phenomena ; expressions of impaired deep sensibility.* 
 
 -2. Lesions of the grey matter interrupt the routes for 
 painful and thermal impressions, which, one and all, pass 
 through it. Lesions, also, which interrupt the spino- 
 thalamic tracts in the lateral columns may be followed by 
 analgesia and thermo-anaesthesia, or by diminution of 
 those respective functions (hypalgesia, thermo-hypsesthesia). 
 Whether in the two above-mentioned conditions the tactile 
 sense, which, as we have seen, makes use partly of the same 
 routes, is affected or not, depends on individual factors — 
 
 * Sensibility to vibration reacts with great delicacy to lesions of the 
 centripetal tracts. It may be diminished, or even completely abolished, 
 when all other symptoms of involvement of the posterior roots are absent 
 — e.g., in cases of neural progressive muscular atrophy. 
 
32 BING'S COMPENDIUM 
 
 i.e., on the compensatory powers of the posterior columns 
 in the affected subject. As a rule it remains intact. This 
 condition, in which sensibility to pain and the temperature 
 sense are abolished, while the other sensory powers remain 
 unimpaired, is known as " dissociated anaesthesia." When 
 fuUy and typically developed, it is pathognomonic of central 
 affections of the cord (hsematomyelia, central ghosis, syringo- 
 myelia, certain intramedullary tumours, etc.). 
 
 3. If, however, the tactile sense is entirely abolished, 
 both its routes, alike that through the posterior column 
 and that through the lateral column, must be interrupted, 
 save in the cases of posterior root lesion mentioned above. 
 In a lesion of the posterior column alone tactile sensibility 
 is impaired, but not abolished. If, in the upper portion of 
 the cord, the lesion affects only the column of Goll, the 
 impairment of tactile sensibility is confined to the lower 
 half of the body (c/. Fig. 3 and p. 6). 
 
 4. Ataxia points (apart from the above-mentioned root 
 lesions) to lesions either of the posterior columns or of the 
 spino-cerebeUar tracts. As a rule the clinical features of 
 the case enable us to distinguish between posterior column 
 ataxia and cerebellar ataxia. To give here a description 
 of these two conditions would take us too far ; they are, 
 besides, fuUy described in every textbook. Posterior 
 column ataxia, the ataxia of tabes dorsalis, is a familiar 
 clinical picture to every medical man. We will confine 
 ourselves here to enumerating the differential phj-sio- 
 pathological criteria. In cerebellar ataxia single move- 
 ments of the extremities are fairlj'^ well performed — with 
 much greater accuracy, at any rate, than is the case in 
 posterior column ataxia (tabes). On the other hand, the 
 power of co-ordinating these single movements, the power 
 of combined movement, or synergia, is very gravely inter- 
 fered with. Such combined movements play a most im- 
 portant part in the performance of the function of locomo- 
 tion, in the maintenance of the erect position, etc. Hence 
 the zigzag progression of the cerebellar ataxic, the swaying 
 of his body when attempting to stand upright, etc. That 
 a mixed lesion of the posterior columns and of the spinal 
 cerebellar tracts causes a particularly severe ataxia of 
 mixed character is shown by a study of Friedreich's disease. 
 
LESIONS OF THE SPINAL CORD 33 
 
 Sensory "Irritation Symptoms." 
 
 Morbid processes affecting the system of the posterior 
 roots at their entry into the cord or during the further 
 passage of their fibres brainwards may, before they bring 
 about the destruction of the structures attacked, give rise 
 to severe sensory disturbances. A characteristic feature of 
 these sensory phenomena is that they are referred, not to 
 the cord itself, but to the periphery — i.e., to that region of 
 the integument, musculature or periosteum in which are 
 situated the sensory end-organs of the " irritated " tracts. 
 Patients are better able to describe with accuracy the 
 course of these tearing and cutting pains when only single 
 roots or single pairs of roots are affected — as, for instance, 
 in the case of circumscribed new growths or tuberculous foci 
 in the spinal column, in pachymeningitis cervicalis hyper- 
 trophica, etc. The lightning pains of tabes dorsalis belong 
 also to this category. In the case of hsemorrhagic or 
 traumatic foci in the substance of the cord, the localization 
 of the pains is less defined. In such cases they affect, 
 as a rule, considerable areas of the body, as there is a 
 simultaneous irritation of many closely apposed fibres which 
 form the continuation within the cord of numerous pairs 
 of posterior roots. Occasionally, but very rarely, " root 
 pains " may be referred to parts of the integument which, 
 tested objectively, prove to be anaesthetic. This is the case 
 where posterior roots have been recently severed, and where, 
 consequently, the conduction of impulses from the periphery 
 to the centres is interrupted ; while from the central ends of 
 the torn roots impulses of an irritative nature may, for a 
 time (until Wallerian degeneration sets in) reach the sen- 
 sorium (anaesthesia dolorosa). The same may also occur 
 in recent lesions of the sensory tracts in the cord itself. 
 
 The parsesthesias and hj^ersesthesias are also to be 
 regarded as sensory irritation symptoms, corresponding, 
 however, to less extensive impairment of nerve function. 
 Under the former heading we have to deal with sensations 
 of an abnormal character arising spontaneously (formica- 
 tion, pricking, burning, etc.) ; in the latter case we have 
 excessive subjective reactions to ordinary appHed stimuh — • 
 
 3 
 
34 BING'S COMPENDIUM 
 
 a light touch or gentle stroking, for instance, may give rise 
 to sensations of severe pain. 
 
 When root pains accompany herpes zoster, we may locate 
 the lesion in the spinal ganglion. The physio-pathological 
 basis of the vesicular eruption is at present obscure ; but, 
 bearing in mind the mechanism afiected, it would seem 
 possible that connections with the sympathetic play some 
 part in the matter. 
 
 111. REGIONAL-DIAGNOSTIC SIGNIFICANCE OF MIXED 
 SENSORY AND MOTOR DISTURBANCES. 
 
 The most important and typical forms of such mixed 
 affection that we meet with in spinal pathology are — 
 
 1. Simultaneous affection of the lateral and posterior 
 columns. 
 
 2. Disease or injury affecting the cord in transverse 
 section. The lesion may be partial or complete. 
 
 3. Lesions interrupting the nerve channels of one lateral 
 haK of the cord (Halbseitenlasion). 
 
 (a) Simultaneous Affection of the Lateral and Posterior 
 Columns. 
 
 This type is not very rare, and may be produced in various 
 ways. In the first place, true systemic degenerations may 
 affect simultaneously the posterior columns and the pyramid 
 and lateral cerebellar tracts. Again, a chronic meningitis, 
 especially one of syphilitic origin, may be complicated by a 
 myelitis whose tendency is to pass inwards from the 
 periphery, and involve by preference the posterior and pos- 
 tero-lateral columns. Thirdly, affections of the arteries, of 
 sclerotic or luetic-endarteritic type, lead not infrequently 
 to an ischaemic tissue necrosis, which, spreading inwards in 
 wedgelike form from the periphery — a consequence of the 
 anatomical distribution of the branches of the vaso-corona 
 [vide Fig. 6) — attacks and destroys by preference the posterior 
 columns and the lateral pyramid and lateral cerebellar tracts. 
 
 In these cases, then, centripetal channels and the most 
 important centrifugal nerve fibre complex are, owing to 
 anatomical association with one another, simultaneously 
 ftttaokod It is easy, therefore, to understand that the 
 
LESIONS OF THE SPINAL CORD 35 
 
 clinical picture likely to be presented is one combining 
 ataxic and hypsesthetic phenomena with muscular paresis. 
 As we have seen, however, lesions of the centripetal system 
 are followed by hjj^potonus and hyporeflex ; while, on the 
 contrary, suppression of the cortico-spinal inhibition brings 
 in its train exaggeration of tonus and reflex. In mixed 
 lesions such as we are considering, therefore, influences of 
 diametrically opposite tendency are at work, and the result 
 will depend on the greater or less intensity of the morbid 
 process in the different structures affected. 
 
 If the pyramid lesion governs the picture, we get the 
 symptom-complex : 
 
 Spastic-Ataxic Paraplegia, with Disturbances of 
 Sensibility. 
 
 If, on the other hand, the pyramid lession is less important 
 than that of the sensory tracts, the picture presented may 
 be described thus : 
 
 Ataxia and Absence of Reflexes with Motor Impairment. 
 
 In cases of the latter kind the pathological skin reflexes 
 pathognomonic of pyramid lesions (Babinski's and Oppen- 
 heim's signs, and the. Mendel-Bechterew phenomenon) may 
 be very marked. The so-called " associated muscular move- 
 ments " may also be present, and thus clear evidence be 
 given that the posterior column lesion is accompanied by an 
 affection of the lateral columns. 
 
 (b) Transverse Division (Disease or Injury affecting the 
 Cord in Transverse Section), 
 
 Transverse division of the cord, a condition brought about 
 most frequently by fractures or dislocations of the vertebral 
 column. Pott's disease, etc., much more rarely by a trans- 
 verse myelitis, gives rise, when complete, to no difficulties of 
 diagnosis. In this case we have complete abohtion of sensa- 
 tion and of motion. The former extends to every sensory 
 function, as aU the centripetal tracts are put out of action. 
 The latter is also absolute, not paresis, but paralysis, for 
 there is interruption, not only of the pyramid tracts, but of 
 each and every connecting route between the organ of the 
 will and the spinal motor centres. 
 
 It is clear that sensibihty wiU be abolished in those rntegu- 
 mental areas whose nerves enter the spine at or below thf 
 
36 BING'S COMPENDIUM 
 
 site of the lesion, and, similarly, that the paralysis will affect 
 every muscle innervated from nerve cells of the ventral horn 
 at the level of the lesion or on its caudal side. Further and 
 more detailed data concerning this distribution will be given 
 when we come to the study of segmental diagnosis. Here 
 we need only make the preliminary statement that in a com- 
 plete transverse lesion of the cord in the upper cervical region 
 the simultaneous paralysis and anaesthesia affect the four 
 extremities and the trunk (tetraplegic type) ; if the dorsal 
 cord is divided, the lower extremities and the lower half of 
 the trunk are affected ; while if the lesion is in the lumbar 
 cord, only the lower Hmbs are affected (paraplegic type). 
 
 As regards the character of the paralysis, we should expect 
 it to take a spastic form (pp. 25-27) ; for below the seat of the 
 lesion the reflex arc is intact, and, owing to the lesion, it is 
 freed from cortico-spinal inhibition. In complete division of 
 the cord in its upper part, however, we find in almost every 
 case, at any rate in the early stage, complete muscular atony 
 and abolition of reflexes in the paralyzed regions. An attempt 
 has been made to explain this as an effect of shock. The ex- 
 planation is not satisfactory, however, for in the first place the 
 atony and absence of reflexes persist in many cases, and in 
 the second place they may be found in non-traumatic cases 
 (myelitis transversa). We will not enter here upon a detailed 
 consideration of the various theories that have been put 
 forward to account for the paradox. None of them admits 
 of strict proof. Two bear examination better than the rest. 
 According to the first, in division of the pyramid tracts, it 
 is necessary for the development, not merely of the spastic 
 condition, but of tonus and reflex also, that the other cen- 
 trifugal exogenous tracts should be intact. The second 
 theory would place the responsibility for grave interference 
 with the functions of the deeper-lying posterior roots and 
 ventral horn ceUs on the disturbances of the lymph and 
 blood circulations which accompany a total transverse lesion. 
 Personally, I incline to the latter of the two theories. 
 
 In transverse lesions of the cord, not only the skeletal 
 muscles, but also those of the bladder and rectum, are 
 affected. The subject of sphincter innervation will be 
 dealt with in the section on Segmental Diagnosis, where it 
 may ranst appropriately be considered under the head of 
 
LESIONS OF THE SPINAL CORD 37 
 
 affections of the sacral cord. Here we need only state that 
 in transverse division of the cord, wherever its seat, the 
 bladder and the rectum are withdrawn from the influence of 
 the will. Faecal retention sets in. As regards the bladder, 
 we have at first retention of urine. When, however, the 
 distension of the bladder reaches a certain point, it may 
 empty itself involuntarily by reflex action (incontinentia 
 intermittens). 
 
 We saw above (p. 23) that there are vaso-motor fibres in 
 the lateral columns. This explains the vascular dilatation, 
 due to vaso-motor paralysis, which one meets with in recent 
 cases of complete transverse division, in the paralyzed region. 
 Later, the condition (cold and cyanosis), described on p. 23 
 as marking chronic vascular relaxation may supervene. 
 The engorgement of the corpora cavernosa which is noticed 
 in these cases, is also due to vaso-motor disturbance, as, 
 likewise, the pronounced tendency to the rapid development 
 and extension of bedsores. 
 
 It is of very great importance, from the point of view of 
 prognosis, to distinguish partial from complete transverse 
 lesions. 
 
 The following distinguishing features should be kept in 
 mind : 
 
 1. In partial transverse lesions the paralysis is as a rule 
 not symmetrical, as in complete division ; and, further, in 
 contrast with the absolute incurability of the latter condi- 
 tion, there is a tendency during the first few weeks towards 
 some measure of recovery. The identity of distribution, also, 
 of motor and sensory disturbances which is noticed in cases 
 of complete division, is here generally absent, the motor dis- 
 turbances affecting, as a rule, a wider area. 
 
 2. Vaso-motor and sphincter abnormalities are present 
 only in slight degree. 
 
 3. Even when the lesion is situated at a high level, the 
 patellar reflexes are never permanently abolished. As a 
 rule they are exaggerated. A difference can often be 
 noticed between the two sides. 
 
 On the distal side of the lesion, sensory, and sometimes 
 also motor, irritation symptoms assert themselves (pains, 
 anaesthesia dolorosa, parsesthesise, hypersesthesia, epilepsia 
 spinahs, etc.). In complete division, on the other hand. 
 
38 BING'S COMPENDIUM 
 
 irritation symptoms are never present. As an irritation 
 symptom one must regard also the marked priapism, which 
 is to be distinguished from the simple engorgement of the 
 corpora cavernosa present in cases of complete division. 
 These matters also will be dealt with more fully in the 
 section on Segmental Regional Diagnosis. 
 
 (c) Unilateral Transverse Lesions (Halbseitenlasion). 
 
 The phenomena which f oUow unilateral transverse division 
 of the cord by trauma or disease are known as " Brown- 
 Sequard's symptom-complex." The term comprises the 
 following morbid phenomena, which show themselves in 
 those parts of the body distal to the site of the lesion. 
 
 (a) On the Same Side as the Lesion. 
 
 1. Motor paralysis. 
 
 2. Vaso-motbr paralysis. 
 
 3. Disturbances of " deep sensibility." 
 
 4. Hj'persesthesia for tactile impressions. 
 
 (/S) On the Opposite Side. 
 
 5. Disturbance of superficial sensibility — e.g., to painful 
 and thermal impressions. 
 
 We will consider the separate sections of the above syn- 
 drome in their order, with a view to a physio-pathological 
 explanation. 
 
 1. Motor Paralysis of the Same Side as the Lesion. 
 
 This affects the regions innervated from ventral horn cells 
 distal to the site of the lesion. Its development is easy to 
 understand. The central motor tracts, especially the lateral 
 pyramid tracts, convey to the spinal centres of the same 
 side voluntary motor impulses. The paralysis has naturally 
 a cortlco-spinal — i.e., spastic — character. In the isolated 
 cases in which, immediately after the hemisection, the 
 reflexes are weakened or abolished, this is only a temporary 
 phenomenon, either due to shock or admitting of the explana- 
 tions suggested on p. 36. Babinski's and Oppenheim's 
 signs and the Mendel-Bechterew phenomenon can generally 
 be demonstrated. 
 
LESIONS OF THE SPINAL CORD 39 
 
 2. Vaso-Motor Paralysis of the Same Side. 
 
 The skin is, in the early stages, reddened and warmer 
 than that of the opposite side. Later on this symptom 
 simply disappears, or a chronic condition of cold and cyanosis 
 takes its place. Physio-pathological explanation : Inter- 
 ruption of the vaso-constrictor fibres of the lateral column 
 of the same side (c/. p. 23). 
 
 3. Disturbance of Deep Sensibility on the Side of the Lesion. 
 
 That the sense of position is seriously interfered with, or 
 even entirely abolished, so far as the parts distal to and on 
 the same side as the lesion are concerned, and that even 
 when motility is restored to those parts, ataxia supervenes, 
 can be readily understood if one bears in mind the fact that 
 impulses of the deep sensibility are conveyed upwards 
 almost exclusively on the same side of the cord, in the pos- 
 terior columns and spino-cerebeUar tracts. 
 
 4. Superficial Hypersesthesia on the Same Side as the Lesion. 
 
 The explanation of this phenomenon is much less clearly 
 established, and many are the hypotheses that have been 
 put forward to account for it. Of these the most probable 
 seems the following : As tactile impressions normally pass 
 upwards, partly crossed (lateral columns), and partly un- 
 crossed (posterior columns), only the crossed fibres can, 
 after hemisection, convey impressions from the same side 
 as the lesion. These fibres have thus extra work thrown 
 upon them, and the cells of the dorsal horn, from which 
 springs the crossed spino-thalamic tract, pass on to the 
 latter " summated " stimuli, which at first — i.e., until the 
 organism has accustomed itself to the new condition (this 
 form of h3rper8esthesia is a transitory symptom) — are felt 
 as painful impressions. 
 
 6. Superficial Anaesthesia on the Opposite Side to the Lesion. 
 
 This always affects sensibility to painful and thermal 
 impressions, which is easily intelligible in view of their 
 exclusively " crossed " conduction. In typical cases tactile 
 sensibility is also, though less markedly, affected. This also 
 is explained by the anatomico-physiological conditions. 
 
40 
 
 BING'S COMPENDIUM 
 
 Tactile impressions are conducted to the brain partly, as we 
 have seen, crossed (lateral columns), and partly uncrossed 
 (posterior columns). In some cases, however, no tactile 
 anaesthesia or h3rpsesthesia can be demonstrated. In these 
 cases we must conclude that the uncrossed fibres in the pos- 
 terior columns succeed in taking upon themselves, with 
 
 FiQ. 9. 
 
 Bkowh-Sequaed's Symptom-Complex. 
 
 extraordinary rapidity and completeness, the work of theix 
 affected coadjutors in the crossed lateral columns. 
 
 In the majority of cases lesions such as we are considering 
 are situated in the dorsal region, and the condition produced 
 is spoken of as hemiparaplegia. Fig. 10 is a diagrammatic 
 representation of the symptomatology of such a case. The 
 
LESIONS OF THE SPINAL CORD 
 
 41 
 
 narrow zone of ansesthesia which is to be seen in the figure 
 immediately above the paralyzed, region is due to the sup- 
 pression of impulses from those posterior roots which enter 
 the cord at the site of the lesion. 
 
 Fig. 10. 
 
 Sensory 
 Disturbances : 
 
 _ Superficial 
 ~ ansesthesia. 
 
 Deep 
 ' ansesthesia. 
 
 Superficial 
 hypereesthesia 
 
 Bbown-Seqtjard's Symptom-Complex in Left Unilateral 
 Tp-ansveksb Lesions op the Cokd. 
 
 If the lesion is in the cervical region, the symptom-complex 
 is described as spinal hemiplegia. Mutatis mutandis, we 
 have here the same distribution of motor and sensory dis- 
 
i2 
 
 BING'S COMPENDIUM 
 
 turbances. In lesions of the lower lumbar and sacral cord 
 this is not so. In these regions the separate segments are 
 so closely pressed together that a lesion involving one lateral 
 half of the cord allows few sensory channels to pass beneath 
 it to the opposite side of the organ. Superficial anaesthesia is 
 therefore generally present on the injured and paralyzed as 
 well as on the uninjured side (vide Fig. 11). In very rare cases 
 a pathological process may lead to a unilateral irritation 
 instead of a unilateral abolition or diminution of function 
 
 Diagram to explain the Extended Homolateeal Anesthesia fotjnd 
 IN Hbmisection of the Cokd in the Lowee Ltjiibab and Saoeal 
 Regions. 
 
 in the spinal cord. In these cases spastic phenomena are 
 observed on the side of the lesion, and painful disturbances 
 of sensation on the opposite side ("spasmodynia cruciata"). 
 Finally, it should be stated that typical " classical " forms 
 of Brown-Sequard's syndrome are much rarer than atypical, 
 as we seldom have to do with a clean and complete unilateral 
 division, the lesion generally either not amounting to a 
 complete hemisection, or else passing over, and affecting 
 more or less the second side of the cord. 
 
LESIONS OF THE SPINAL CORD 43 
 
 APPENDIX. 
 
 The differential diagnosis between intramedullary and extra- 
 medullary intravertebral tumours occasionally presents 
 great difficulties. There is no symptom which is pathogno- 
 monic of the one while it decisively excludes the other. At 
 the same time the following criteria favour, in general, the 
 diagnosis of an extramedullary as opposed to an intra- 
 medullary tumour, and, as is well known, the operative prog- 
 nosis in extramedullary tumours is steadily improving as 
 the surgery of the nervous system advances : 
 
 1. Slow development of motor and sensory disturbances. 
 
 2. Tendency of the motor and sensory disturbances which 
 may be present to remain stationary so far as extension 
 upwards is concerned, while increasing in intensity. 
 
 3. Persistence of Brown-Sequard's syndrome, 
 
 4. A pesudo-neuralgic prodromal stage preceding symp- 
 toms of organic disturbance (root pains). Extramedullary 
 tumours are generally situated on the dorso-lateral spinal 
 periphery. 
 
 5/ Marked intensity of the spastic symptom-complex and 
 persistence thereof after paraplegia is fully established. 
 
 6. Presence of irritative motor symptoms (spastic phe- 
 nomena, spinal epilepsy). 
 
 7. Absence or only slight development of degenerative 
 atrophic paralyses. (The amount of muscular atrophy 
 present is often quite out of proportion to the very slight 
 alterations in electrical excitability.) 
 
 8. Sensitiveness of the vertebrae to pressure. 
 
 On the other hand, a typical and well-marked dissociated 
 anaesthesia points strongly to an intramedullary situation 
 for the tumour {videTp. 32), while a simple prevalence of dis- 
 turbances of common sensation and the temperature sense, 
 as compared with other sensory disturbances, is not un- 
 common with extramedullary growths (increased sensitive- 
 ness of common sensation and thermal fibres to pressure). 
 
 B. "Longitudinal" or Segmental Regional 
 Diagnosis. 
 
 The problems to be solved by " longitudinal " diagnosis 
 have been already defined on p. 1. We will here, however, 
 preface our presentation of the material facts with some 
 
44 BING'S COMPEKDIUM 
 
 preliminary general statements which should help towarda 
 a logical anv systematic grouping of those facts, and toward? 
 a clear understanding of their physio-pathological bearing. 
 
 CHAPTER I. 
 
 THE ANATOMICAL AND PHYSIOLOGICAL BASIS OF 
 SEGMENTAL DIAGNOSIS. 
 
 As is weU known, the whole body of the embryo arises from 
 separate component parts, or somites, ranged one behind 
 the other. The neural tube, later to become the spinal 
 cord, the integument, and the muscular system, all have 
 a similar origin. Each somite, then, contains a neurotome, 
 a dermatotome and a myotome, which are intimately con- 
 nected with each other. For each, embryonal spinal segment 
 sends, by way of its pair of anterior roots, motor fibres to 
 the corresponding muscle segments, and receives, in like 
 manner, from the corresponding skin segments, the centri- 
 petal fibres of its posterior roots. 
 
 In the fully developed organism the signs of segmental 
 origin are in most of the organs no longer visible. This 
 applies also to the greater part of the muscular system. 
 From four myotomes — A, B, C, D — lying one behind the 
 other, three muscles — I., II., III. — may, for instance, be so 
 formed that muscle I. shall consist of parts from A, B, C, 
 and D ; muscle II., of parts from B and C ; and muscle III., 
 of parts from B, C, and D. To take a concrete instance : 
 The biceps femoris is composed of elements from the two 
 last lumbar myotomes and the two first sacral myotomes 
 (L4, L5, Si, S2) ; so also the gluteus maximus. The semi- 
 tendinosus and semimembranosus, on the other hand, are 
 made up of elements from L4, L5, and Si, and the tibialis 
 anticus of elements from L4 and L5 only. Consequently, in 
 the developed organism the biceps femoris and the gluteus 
 maximus will receive their motor nerve fibres from the 
 anterior roots of spinal segments L4 — S2 ; while the " radic- 
 ular innervation " of the semimembranosus and semi- 
 tendinosus is Lj — Si, and of the tibialis anticus L4, L5. As 
 regards the peripheral innervation, however, of the muscles 
 in question, we find that the biceps femoris, semimem- 
 
LESIONS OF THE SPINAL CORD 
 
 46 
 
 branosuB, semitendinosus, and tibialis anticus, are supplied 
 by the deep peroneal branch of the sciatic ; the gluteus 
 maximus, on the contrary, by the inferior gluteal nerve. 
 Both the sciatic and the inferior gluteal, then, draw fibres 
 from the spinal root pairs L4 - 83, and analogous conditions 
 obtain in the case of all other peripheral motor nerves. 
 Each contains fibres from several anterior roots, and, con- 
 versely, each anterior root distributes its fibres among 
 several peripheral nerve trunks. This often exceedingly 
 comphcated interchange of fibres takes place in the so-called 
 
 Fig. 12. 
 
 Vorjerhorn 
 I 
 
 Radiculak and Periphekal Muscular Innervation. 
 
 Muscle A supplied by segments 1 and 2. 
 Muscle B supplied by segments 1, 2 and 3. 
 
 " plexuses," whose special features are given in every text- 
 book of anatomy. Here we will merely give a rough dia- 
 grammatic representation of the principle of radicular and 
 peripheral motor innervation (Fig. 12 . 
 
 In the above diagram we see also that the centres for the 
 separate muscles present themselves, in a longitudinal section 
 nf the grey matter of the cord, as nuclear columns lying side 
 by side, and one above the other. It is these columns 
 which, in a transverse section, are seen as the cell-groups 
 of the anterior horn, with which we made acquaintance 
 on pp. 12 and 13. 
 
46 BING'S COMPENDIUM 
 
 A careful study of the atrophy of spinal nerve cells super- 
 vening on amputations, on experimental destruction of 
 nerve fibres, or on decay of single muscles, has given us a 
 knowledge of the position of the more important muscular 
 centres within the ventral horn, which, though by no 
 means complete, is yet fairly sufficient for our clinical 
 requirements. 
 
 In general it may be said that the centres for the spinal 
 musculature are to be found in the dorso-mesial group, 
 those for the muscles of the proximal segments of the limb? 
 in the ventro-mesial, while the two lateral groups govern the 
 remaining segments of the extremities. The centres for the 
 coarser movements of flexion and extension are in the neigh- 
 bourhood of the periphery, while those for the finer move- 
 ments {e.g., of toes and fingers) lie nearer the central groups. 
 We may here again draw attention to the fact that the 
 latter contain the vaso-motor centres. 
 
 Complete paralysis and loss of tone in a muscle may be 
 caused, as is made plain in Fig. 12, not only by a lesion in 
 the cord which destroys its whole spinal nucleus, but also 
 by the destruction of its peripheral nerves. Anterior root 
 lesions, on the other hand, unless very extensive, merely 
 weaken, and do not completely paralyze, the muscle, owing 
 to the fact that, as a rule, the muscle is innervated from 
 several roots. It will be necessary, therefore, to state 
 as clearly as possible the distinguishing marks between 
 radicular and peripheral paralyses. 
 To return to the plexuses : 
 
 We have up to the present considered them with reference 
 only to their motor constituents. As, however, soon after 
 their exit from the cord, the posterior roots unite with the 
 anterior to form mixed nerves, the nerve trunks issuing 
 from a plexus on its distal side will contain, not only con- 
 tingents from several anterior roots, but also sensory fibres 
 from various spinal gangha or posterior roots. Further, 
 each separate spinal ganglion, as also each ventral horn 
 centre, sends fibres to several distinct nerve trunks. There 
 is this marked distinction, however : wliile the muscle acts 
 as a functional unit, so that we do not find portions thereof 
 paralyzed in consequence of lesions affecting some only of 
 its allotted anterior roots, we meet with quite diffe^^it con- 
 
LESIONS OF THE SPINAL CORD 
 
 47 
 
 Fig. 13. 
 
 Seam..s[ilnalia 
 ■paiices poster 
 
 Plexus. 
 
 .Nervus sensit.X. 
 
 Area cutanea 
 
 Argae cut. raoliculares . * 
 
 Eadiculae and Pbeiphekal Cutan-bous Innervation, 
 Note the overlapping of the contiguous root fields. 
 
48 BING'S COMPENDIUM 
 
 ditions when we come to consider the innervation of the 
 integument. 
 
 Notwithstanding the often intricate routes which they 
 have followed along the peripheral nerve trunks, the 
 sensory fibres are- always distributed to the extreme 
 periphery in such manner that the " complex " entering a 
 given posterior root supplies with affereni fibres a definite 
 integumental area. Such area is termed a " radicular 
 zone" or "root field." In it are reunited the sensory 
 fibres, which were originally united in a posterior root, 
 though they may have found their way to the periphery 
 along several nerve trunks. It might naturally be inferred 
 from the foregoing that the destruction of a single posterioi 
 root would cause an integumental anaesthesia of sharply- 
 defined boundaries. This is not, however, the. case, inas- 
 much as the separate radicular zones overlap each other 
 somewhat like the tUes of a roof, and thus each portion of 
 the integument is innervated from two posterior roots. 
 Only when two adjacent posterior roots or spinal ganglia 
 are destroyed does a " radicular " anaesthesia supervene. If, 
 however, a peripheral nerve is severed, we have an in- 
 tegumental anaesthesia of quite dififerent distribution, of 
 so-caUed " peripheral " tjrpe. The anaesthesia affects the 
 whole area of distribution of the injured nerve trunk, and 
 is made up, after the manner of a mosaic, of those portions 
 of separate " root " zones which go to the composition 
 of the nerve trunk in question. It is obvious, there- 
 fore, that the conditions underlying radicular are far simpler 
 than those underljdng peripheral innervation of the integu- 
 ment (vide Fig. 13). 
 
 CHAPTER II. 
 
 I. SEGMENTAL DIAGNOSIS IN MOTOR PARALYSES. 
 DIFFERENTIAL DIAGNOSIS BETWEEN RADICULAR 
 AND PERIPHERAL PARALYSES. 
 
 Atter the prehminary remarks in the foregoing chapter, 
 the following tables, in which the radicular innervation of 
 the muscles is given according to Villiger's latest classifica- 
 tion, require no comment : 
 
LESIONS OF THE SPINAL CORD 
 
 49 
 
 p 
 S 
 
 
 H 
 
 is 
 I 
 
 O 
 
 CQ 
 
 <i3 
 
 to 
 
 
 s 
 
 g 
 
 
 
 > 
 
 I 
 
 555 
 
 
 
 'a 
 
 o 
 
 H 
 
 & 
 
 XI 
 
 O 
 
 a 
 
 3 
 
 si 
 
 
 .±3 ^ c3 o 
 
 O ©- S S 
 
 02 tj a g 
 
 
 a 
 
 o 
 
 
 
 a 
 o 
 
 PM 
 
 a 
 
 O 
 
 Hi 
 
 .2 
 
 I 
 1 
 
 |3 
 
 §a 
 
 s 
 a 
 
 o 
 i-:| 
 

 Segmenial Innervation of Muscles of Upper Extremity. 
 
 Cervical Segments. 
 
 Thoracic 
 Segment). 
 
 5 1 6 1 7 1 8 
 
 1 
 
 t1 
 o 
 
 Supraspinat. 
 
 
 
 
 1 
 
 i 
 
 Teres min. 
 
 
 
 Deltoideus 
 
 
 Infraspinatus 
 
 Subscapularis 
 
 
 
 1 Teres major 
 
 < 
 
 1 
 
 i 
 
 Biceps 
 
 
 Brachialis 
 
 
 
 Coracobrachialis 
 
 
 Triceps brach. 
 
 
 
 AnconsBUs 
 
 
 Supinator long. | 
 
 
 
 Supinator brevis 
 
 Extensor carpi radial. 
 
 
 
 Pronator teres 
 
 
 Flexor carpi radial. 
 
 Flexor poUic. long. 
 
 
 Abduct, poll. long. 
 
 Extens. poll. brev. 
 
 Extens. poll. Ion?. | 
 
 Extens. digit, coram. 
 
 Extens. indicis prop. 
 
 Extens. carpi uln. 
 
 Extens. dig. "V prop. 
 
 
 
 Flex, digitor. sublimis 
 
 
 Flex, digitor. profnnd. 
 
 Pronator quadrat. 
 
 
 Flex, carpi uln. 
 
 Palmaris long. 
 
 
 1 
 
 Abduct, poll. brev. 
 
 
 
 13 
 
 i 
 
 Flex. poll. brev. 
 
 
 Opponens poll. 
 
 
 
 Flexor digit. \' 
 
 
 Opponens dig. V 
 
 
 
 Adduct. poll. 
 
 
 Palmaris brev. 
 
 
 Abductor dig. V 
 
 
 
 
 Lumbrioales 
 
 
 
 
 
 
 
 
 luterossei 
 
Segmental Innervation of Muscles op Lower Extremity. 
 
 1 TH,2 i I., 1 La r L, 1 I4 1 L5 1 Si 1 Sa 
 
 a. 
 
 1 Ileo-psoas 1 
 
 
 
 
 Tensor fasciae 
 
 GrlutSEUs medius 
 
 i 
 
 
 
 Glutffius minim. 
 
 Quadratus femoris 
 
 Gemellus inferior 
 
 
 1 
 
 
 
 Gemellus super. 
 
 
 1 
 
 Glutseus maxim. 
 
 
 
 Obturator intern. | 
 
 
 
 
 Piriformis ] 
 
 
 Sartorius 
 
 
 
 1 
 
 
 Pectineus 
 
 
 
 t 
 
 Adduct. long. 
 
 Quadriceps 
 
 Gracilis 
 
 Adductor brevis 
 
 
 Obturator ext. 
 
 Adduct. masn. 
 
 Adduct. minim. 
 
 Articularis gen. 
 
 
 
 Semitendinosus 
 
 
 
 Semimembranosus 
 
 
 
 Biceps femoris | 
 
 
 
 Tibialis ant. | 
 
 
 
 Extensor halluc. long. | 
 
 Popliteus 
 
 Plantaris 
 
 Extensor digit, long. 
 
 
 
 
 
 Soleus 
 
 
 
 Gastrocnemius | 
 
 
 
 Peroneus longus 
 
 1 
 
 i 
 
 Peroneus brevis 
 
 
 
 Tibialis postic. 
 
 1 
 
 Flexor dig. long. 
 
 
 
 Plexor halluc. long. ' 
 
 
 Extensor halluc. brev. | 
 
 
 Extensor digit, brevis 
 
 
 
 
 Flex. dig. brev. 
 
 ': 
 
 Abduct, hall. 
 
 Flex, halluc. brev. 
 
 Lurabricales 
 
 
 Abduct, hall. | 
 
 Abduct, dig. V. 
 
 Flexor dig. V br. 
 
 
 Opponens dig. V 
 
 Quadrat, plant. 
 
 
 
 
 
 
 Interossei 
 
52 
 
 BING'S COMPENDIUM 
 
 It is easy to see at a glance from the foregoing tables 
 what muscles are likely to be paralyzed by a lesion affecting 
 the ventral horns or anterior roots in any given segments 
 of the cord. To distinguish these " radicular " paralyses 
 from others of peripheral origin (from such, that is to say, 
 as are caused, not by the destruction of motor roots, but by 
 that of peripheral nerve trunks and branches), it is neces- 
 sary to bear in mind also the conditions of peripheral inner- 
 vation, as given in the following tables. In the first column 
 we have given the separate peripheral nerves, in the second 
 the muscles supplied by them, while in the third are given 
 the movements carried out by the respective muscles. 
 Ability or inability to carry out its appropriate movements 
 points, respectively, to the functional soundness or to the 
 paralysis, of the muscle under consideration. The power 
 of voluntary as well as of electrically excited contraction 
 must be tested. For the latter purpose a knowledge of the 
 electrical stimulation points given in all works on electro- 
 diagnosis is essential. 
 
 A. Plexus Cebvicalis 
 Nervi cervioales 
 
 N. phrenious 
 
 b. Plexus Beachialis 
 
 (Cs-Th^) 
 
 N. thoracic, ant. 
 
 N. thoracic, long. 
 
 N. dorsalis scap. 
 N. suprascap. 
 
 N. aubscapul. 
 
 N. axillaris s. cir- 
 cumflexuB 
 
 N. musculocut. 
 
 Musculi profundi colli 
 Mm. scaleni 
 Diaphragma 
 
 M. pect. maj. et min. 
 M. serrat. ant. maj. 
 
 M. levator scapul. 
 Mm. rhomboidei. 
 
 M. aupraspinatua 
 
 M. infraspinatus 
 
 M. latissimus dors.l 
 M. teres major / 
 
 M. subscapularis 
 M. deltoideus 
 M. teres minor 
 M. biceps brapK. 
 
 Flexion, extension, and 
 rotation of the neck. 
 
 Elevation of ribs (in- 
 spiration ). 
 
 Inspiration. 
 
 Adduction and forward 
 
 depression of the arm. 
 Fixation of the scapula 
 
 during elevation of 
 
 the arm. 
 Elevation of the scapula. 
 Elevation and drawing 
 
 inwards of the scapula. 
 Elevation and external 
 
 rotation of the arm. 
 External rotation of the 
 
 arm. 
 ( Internal rotation and 
 -! dorsal adduction of 
 (. the arm. 
 Internal rotation of the 
 
 arm. 
 Elevation of the arm to 
 
 the horizontal. 
 External rotation of the 
 
 arm. 
 Flexion and supination 
 
 of the forearm. 
 
LESIONS OP THE SPINAL CORD 
 
 53 
 
 N. musoulocut. 
 N. mediauuB 
 
 M. nlaaris 
 
 Nervus radialis 
 
 M. coracobrachialis 
 
 M. brachialis int. 
 M. pronator teres 
 M. flexor carpi rad. 
 
 M. palm. long. 
 
 M. flex, digit, sublim. 
 
 M. flex. poll. long. 
 
 M. flex, digit, prof, (ra- 
 dial portion). 
 
 M. abduct, poll. brev. 
 
 M. flex. poll. brev. 
 
 M. opponens poll. 
 
 M. flexor carpi uln. 
 
 M flex, digit, prof, (ul- 
 nar portion) 
 
 M. adductor poll. 
 
 Mm. hypothenaris 
 
 Mm. lumbricalea 
 
 Mm. interosaei 
 
 M. triceps braoh. 
 M. supin. longus 
 M. extensor carpi rad. 
 
 M. extensor digit, comm. 
 
 M. extensor digit. V 
 prop. 
 
 M. extensor carpi uln. 
 
 M. supinator brevis 
 M. abduct, poll, longus 
 
 M. extensor poll, brevis 
 
 M. extensor poll, longus 
 
 Flexion and adduction of 
 
 the forearm. 
 Flexion of the forearm. 
 Pronation. 
 
 Flexion and radial-flexion 
 of the hand. 
 
 Flexion of the hand. 
 
 Flexion of the middle 
 phalangesof the fingers . 
 
 Flexion of the terminal 
 phalanx of the thumb. 
 
 Flexion of the terminal 
 phalanges of the index 
 and middle fingers. 
 
 Abduction of the first 
 metacarpal. 
 
 Flexion of the first pha- 
 lanx of the thumb. 
 
 Opposition of the first 
 metacarpal. 
 
 Flexion and ulnar-flexion 
 of the hand. 
 
 Flexion of the terminal 
 phalanges of the ring 
 and little fingers. 
 
 Adduction of the first 
 metacarpal. 
 
 Abduction, opposition, 
 and flexion of the little 
 finger. 
 
 Flexion of the first pha- 
 langes, extension of 
 the others. 
 
 The same ; in addition, 
 spreading and closing 
 together of the fingers. 
 
 Extension of the forearm. 
 
 Flexion* of the forearm. 
 
 Extension and radial 
 flexion of the hand. 
 
 Extension of the first 
 phalanges of the fingers. 
 
 Extension of the first 
 phalanx of the little 
 finger. 
 
 Extension and ulnar 
 flexion of the hand. 
 
 Supination of theforearm. 
 
 Abduction of the first 
 metacarpal. 
 
 Extension of the first 
 phalanx of the thumb. 
 
 Abduction of the first 
 metacarpal and ex- 
 tension of the ter- 
 minal phalanx of the 
 thumb. 
 
 * The name " supinator longus " is incorrect, inasmuch as electrical excita- 
 tion experiments show that the muscle has no supinating, but, on the contrary, 
 a slight pronating action. For this reason a preferable name is that of 
 " brachio-radialis. This is in common use among anatomists, but has not 
 yet been adopted by olinicians. 
 
54 
 
 BING'S COMPENDIUM 
 
 Nervus radialis 
 
 C. Nervi Thokacales 
 
 T>. Plexus Lumbalis 
 (Th,,-L,) 
 Nerv. cruralis 
 
 Nerv. obturatorius 
 
 Plexus Sacealis 
 
 (L,,-S5) 
 N. glutseus sup. 
 
 N. glutseus inf. 
 N. ischiadicus 
 
 (a) N. peroneus : 
 (a) Prof. 
 
 (/3) Superf. 
 {b) N. tibialis 
 
 N. pudendns 
 
 M. extensor indie, prop. 
 
 Mm. thoracis et abdo- 
 minalis 
 
 M. ileo-psoas 
 M. sartorins 
 
 M. quadriceps 
 
 M. pectineuB 
 
 M. adductor longus 
 
 M. adductor brevis 
 
 M. adductor magnus 
 
 M. gracilis 
 
 M. obturator extern. 
 
 H. glutseus med.\ 
 M. glutseus min. / 
 M. tens, fasciae latse. 
 M. pyiiformis 
 
 M. glutseus max. 
 M. obturator int. "| 
 Mm. gemelli j- 
 
 M. quadratus fern. J 
 M. biceps femoris ^ 
 M. semitendinosus j- 
 M. semimembranosus J 
 
 M. tibialis ant. 
 
 M. extens. digit. long. 
 M. extens. hall. long. 
 M. extens. digit, brev. 
 M. extens. hall. brev. 
 Mra. peronei 
 
 M. gastroonemiu3\ 
 M. soleus / 
 
 M. tibialis post. 
 M. flex, digit, long. 
 
 M. flex, halluc. long. 
 
 M. flex, digit, brev. 
 
 M. flex, halluc. brev, 
 
 Musouli plantares pedis 
 leliqui 
 
 Mm. perinei et sphinc- 
 teres 
 
 Extension of the first 
 
 phalanx of the index 
 finger. 
 
 Elevation of the ribs, 
 
 expiration, compres- 
 sion of abdominal vis- 
 cera, etc. 
 
 Flexion of the hip. 
 Internal rotation of the 
 
 leg. 
 Extension of the eg. 
 
 Adduction of the thigh. 
 
 Adduction and external 
 rotation of the thigh. 
 
 Abduction and internal 
 rotation of the thigh. 
 
 Flexion of the thigh. 
 
 External rotation of the 
 thigh. 
 
 Extension of the thigh. 
 
 External rotation of the 
 thigh. 
 
 Flexion of the leg. 
 
 Dorsal-flexion and supi- 
 nation of the foot. 
 
 Extension of the toes. 
 
 Extensionof the great toe. 
 
 Extension of the toes. 
 
 Extension of the greattoe. 
 
 Dorsal-flexion and pro- 
 nation of the foot. 
 
 Plantar-flexion of the 
 foot. 
 
 Adduction of the foot. 
 
 Flexion of the terminal 
 phalanges, II — V. 
 
 Flexion of the terminal 
 phalanx of the great 
 toe. 
 
 Flexion of the middle 
 phalanges, II — ^V. 
 
 Flexion of the first pha 
 lanx of the great to 
 
 Spreading and closing 
 together of the toes 
 and flexion of the first 
 phalanges. 
 
 Closing of the pelvic or- 
 gans, co-operation in 
 the sexual act. 
 
LESIONS OF THE SPINAL CORD 
 
 5^ 
 
 The following point is now clear : If we have a simul- 
 taneous paralysis afEecting a group of muscles which are 
 supplied by the same peripheral nerves, we may infer a 
 peripheral lesion ; if, on the other hand, the group of muscles 
 
 Fig. 14. 
 
 Radicular Innebvation op the Muscles op the Abm. 
 White, Cj— Ce ; black, Cj— Cj. 
 
 affected is one possessing the same radicular innervation, a 
 spinal lesion is indicated. 
 
 In Figs. 14 to 21 we have represented the more important 
 muscles of the extremities in diagrammatic transverse 
 sections of the arm and forearm, thigh and leg, and by dis- 
 
56 
 
 BENG'S COMPENDIUM 
 
 tinctive shading, etc., have grouped the muscles in accordance 
 
 with their radicular and peripheral innervation respectively. 
 
 The following special examples may be cited : In paralysis 
 
 of the radial nerve in the forearm the extensors of the wrist 
 
 Fio. 15. 
 
 Sapln. 
 long. 
 
 PbBIPHSBAIi ImrSBYATIOH OP THE MuSCLES OS THI AbH. 
 
 White=mii3culo-cutaneous; blacks radial. 
 
 and of the fingers are affected in company with the supinator 
 longus ; while, on the contrary, in the so-called " fore- 
 arm type " of spinal paralysis, flexors and extensors of the 
 wrist and fingers are affected in common, and the supinator 
 /ongus generally escapes, because its radicular innervation 
 
LESIONS OF THE SPINAL CORD 
 
 57 
 
 reaches upwards to the fifth cervical segment. Again, 
 paralysis involving the deltoid and teres minor alone is a 
 somewhat frequently observed affection, pointing to disease 
 or injury of a peripheral nerve, its relative frequency being 
 due to the exposed position of the affected nerve, the circum- 
 flex, in its course round the humerus. Cases are also met with 
 
 FiQ. 16. 
 
 Cj— C7: 
 Flex. carp, rad, 
 Flex. poll. Ige, 
 PitOimtor teres. 
 
 C5-C8 : 
 Supinator l^s.' 
 
 C6-C7: 
 Supinator brevis. 
 Extensor carpi lad. 
 
 C7-D1: 
 Palmaris long. 
 Flexor digit, subl. 
 
 Flexor carpi uln. 
 Flexor digit, prof. 
 
 Cj-Cs : 
 Extensor carpi uln. 
 
 Extensor poUic. long. 
 
 Extensor digiti V. 
 Extensor digit, comm. 
 
 Radicttlar Inkbrvation of Forearm Mtjscles. 
 
 in which the deltoid only is affected, the teres minor escaping 
 owing to the fact that it receives fibres also from the supra- 
 scapular nerve. This circumscribed paralysis is never the 
 result of a spinal lesion. In the corresponding form of paral- 
 ysis of spinal origin, the " upper arm type," the scapular 
 muscles, the biceps, and the supinator longus, are also 
 affected. 
 This " upper arm type " of paralysis may be produced, 
 
5S 
 
 BTNG'S COMPENDIUM 
 
 not only by a radicular lesion afEecting the fifth and sixth 
 cervical roots, but also by a lesion of the primary plexus 
 trunk which is formed by a miion of these two roots, and 
 which is, owing to its superficial situation, extremely liable 
 
 Medianhs : 
 
 Palm. long. 
 Flex. dig. Bubl. 
 
 Flex. carp. rad. 
 
 Flex. poll. IgB 
 Pronator ter 
 
 Hex. dig. prof, 
 (ladial portion) 
 
 Ulnarts : 
 Flex, carpi uln 
 
 ,^]ex. digit, prof 
 (ulnar portion) 
 
 Radialis : 
 Supinat. long.. 
 
 Extens. carp. rad. 
 
 Supinat. brev 
 
 Extens. digit, com. 
 
 Extens. pull. Igf. 
 
 Extens. dig. Y 
 
 Extensor carp. uln. 
 
 Peripheral Innervation of Forearm Muscles. 
 
 to injury. This form is spoken of as " Duchenne-Erb plexus 
 paralysis." 
 
 By analogy with the above-named types, one speaks, in 
 discussing radicular paralyses, of " hand," " thigh," "leg," 
 
LESIONS OF THE SPINAL COED 
 
 59 
 
 and " foot " types, according to the limb segment chiefly 
 affected. 
 
 Where we have to deal with a lesion not merely affecting 
 at a given point in the cord the spinal muscular centres — 
 i.e., the ventral horns — but also the cortico-spinal neurons, 
 
 Fio. 18. 
 
 Adduct. long. 
 
 L2— L4: 
 Quadriceps 
 
 Gracilis 
 
 L3 — L^ 
 Adduct, magn. 
 Li-Si: 
 Semimembr. 
 
 . SemitendiD, 
 
 Eadiottlab InSbevation of Thigh Muscles. 
 
 we shall find paralyzed, not only those muscles which are 
 innervated from the injured roots, but also all those inner- 
 vated from anterior roots distal to the site of the lesion. 
 From the tables given on pp. 48-50, one may, for any given 
 transverse lesion, read off the complex of muscles that will 
 be paralyzed by taking all those to the right of, or included 
 
60 BING'S COMPENDIUM 
 
 in, the column of the affected segment. In the classical 
 cases of fracture or dislocation of the vertebral column, as 
 also in Pott's disease, importance from a clinical and diag- 
 nostic point of view attaches, not only to the muscle-complex 
 
 Fio. 19. 
 
 Femora Lrs: 
 Quadriceps 
 
 Sartorius 
 Obtubatorids: 
 Adductor long. 
 
 Adductor mago. 
 Qracilia 
 
 IsoHUSioua : 
 Semiiuenibran. 
 Semitendin. 
 Biceps 
 
 PbEIPHEEAL IlTNBRVATION OF ThIGH MuSCLBS. 
 
 involved in the paralysis, but also to the condition of 
 irritability affecting the parts innervated from the region of 
 the cord immediately above the lesion. 
 
 We may have, for instance, functional h3rperactiv-ty of 
 particular spinal centres, contracture of the muscles inner-i 
 
LESIONS OP THE SPINAL CORD 
 
 61 
 
 vated from them, and extremely character st c forced posi- 
 tions of the extremities. Where antagonist muscles suffer 
 simultaneously from irritative contracture, the originally 
 more powerful muscles prevail. A few examples will illus- 
 trate these points. 
 
 A transverse lesion at the first dorsal segment may cause 
 clawlike contracture of the hand, the mobility of the upper 
 
 U-W- 
 Tibialis ant. 
 
 L4-S1: 
 Ext, digit, long. 
 
 Ezt. hall, longi 
 
 L5— Si: 
 Peronej 
 
 .Tibialis post. 
 ,Flex. dig. long. 
 
 Gastrocnemius 
 
 RadicitI/AE Innervation or Leg Muscles. 
 
 extremity remaining otherwise perfect. This is due to 
 " irritation " of the flexors of the fingers, which are inner- 
 vated chiefiy from the last cervical segment. In a lesion of 
 that segment we have as a rule a forced semiflexion of 
 the forearm, due to irritation of the biceps and brachialis 
 centres, which lie immediately above the seat of the lesion. 
 Similarly, the forced abduction and external rotation of 
 
62 
 
 BING'S COMPENDIXJM 
 
 the arm, which is often noticed in association with a lesion 
 of the sixth cervical segment, is explained as being due to 
 a condition of irritation affecting the immediately proximal 
 centres for the supraspinatus, teres minor, deltoid, infra- 
 spinatus, etc. A specially typical case of the kind is the 
 spastic flexion of the hip (irritation of the ilio-psoas centres) 
 in lesions of the lower lumbar cord. 
 
 FiQ. 21. 
 
 N. Peroneus: 
 
 a) Profundus 
 
 Tibial, ant 
 
 Ext. hall. long. 
 
 Ext. dig. long. 
 
 (6) Superficialis 
 Peronei 
 
 N. Tibialis : 
 Tibialis post. 
 Flex. dig. long. 
 
 Soleua 
 Gastrocnemiut 
 
 Peripheral Innervation of Leo Muscles. 
 
 In incomplete transverse lesions of the cervical cord, the 
 paraplegia of the arms is sometimes more severe than that 
 of the lower limbs. This is due to the fact that, in the 
 lateral columns, the pyramid fibres for the upper extremities 
 are more external in position, and consequently more ex- 
 posed to injury, than those for the lower. 
 
LESIONS OF THE SPINAL CORD 63 
 
 IL SEGMENTAL DIAGNOSIS IN SENSORY 
 
 DISTURBANCES, AND DIFFERENTIAL DIAGNOSIS 
 
 BETWEEN RADICULAR AND PERIPHERAL 
 
 DISTURBANCES OF SENSATION. 
 
 Still more significant than in the case of motor disturb- 
 ances is the distinction between sensory disturbances of 
 peripheral and those of spinal or radicular causation. 
 Figs. 22 and 23, in which are given, on one side the integu- 
 mental innervation areas of the separate nerve trunks, on 
 the other the sensory " root fields," or radicular areas, make 
 this distinction and its importance plain at a glance. In 
 connection with the representation of the root fields in the 
 figures, it is to be borne in mind that the radicular areas 
 extend on either side of the line bearing the corresponding 
 segment numbers. It is plain from this that an area of 
 anaesthesia is only to be demonstrated chnically when at 
 least two posterior roots are involved. Most of the dia- 
 grams of segment innervation of the integument given in 
 works on neurology leave the above very important fact 
 out of consideration, and represent the separate radicular 
 areas as ribbon-like and sharply defined. I have adhered 
 to the Edinger schema, which gives much the best repre- 
 sentation of the actual conditions. 
 
 In undertaking operative measures, the site of the spinal 
 lesion must always be taken to be a segment higher than 
 would be concluded from the upper limit of the area of total 
 anaesthesia, if the overlapping of the root fields were left out 
 of account. 
 
 The special type of arrangement of the radicular zones 
 in the extremities, in which, in contrast to the circular 
 arrangement in the trunk, a longitudinal distribution pre- 
 vails, ia explained by reference to ontogenetic conditions. 
 In the embryo the extremities, as they sprout from the 
 trunk, draw with them the dermatotomes lying within their 
 range, and as the limbs develop more or less perpendicularly 
 to the axis of the trunk, the circular arrangement must, in 
 them, give place to the longitudinal. 
 
 It may be mentioned here that in lesions of the spinal 
 ganglia an eruption of herpes zoster frequently breaks out on 
 the radicular area of the affected posterior roots. No satis- 
 factory explanation of this phenomenon has as yet been given. 
 
84 
 
 BING'S COMPENDIUM 
 
 Fig. 22. 
 
LESIONS OF THE SPINAL CORD 
 
 65 
 
 FiQ. 23. 
 
66 
 
 BING'S COMPENDIUM 
 
 III. SEGMENT DIAGNOSIS IN REFLEX DISTURBANCES. 
 
 Reflex disturbances, as well as paralyses and disturbances 
 of sensation, play an important part in the regional diagnosis 
 (longitudinal) of spinal affections. Reflexes are abolished 
 at the level at which the " reflex arc " is broken. By co- 
 ordination of clinical and anatomico-pathological observa- 
 tions, we have arrived at a fairly exact knowledge concerning 
 the levels of the separate reflex arcs. The following table 
 gives in compact form the present state of our knowledge 
 on the subject. It is only in quite young individuals that 
 one can expect to be able to demonstrate all the reflexes. 
 After puberty the great majority of the reflexes given in the 
 table cannot be ehcited even in perfectly healthy individuals. 
 
 
 Tendon 
 
 
 
 
 
 
 and Bone 
 Reflexes. 
 
 Skin Reflexes. 
 
 Method o£ Starting. 
 
 Effect. 
 
 Localization. 
 
 1. 
 
 _ 
 
 Scapular 
 
 Stimulation of the 
 
 Contraction 
 
 C5-D1 
 
 
 
 reflex 
 
 skin over the 
 scapula 
 
 of shoulder- 
 blade 
 muscles 
 
 
 2. 
 
 Bioepa 
 
 
 
 A blow on the biceps 
 
 Flexion of 
 
 Cb-Cc 
 
 
 reflex 
 
 
 tendon 
 
 forearm 
 
 
 3. 
 
 Triceps 
 
 — 
 
 A blow on the triceps 
 
 Extension of 
 
 Ce-C^ 
 
 1 
 
 reflex 
 
 
 tendon 
 
 forearm 
 
 
 4. 
 
 Scapulo- 
 
 — . 
 
 A blow on the inner 
 
 Adduction 
 
 0,-0, 
 
 
 humeral 
 
 
 side of the lower 
 
 of arm 
 
 
 
 reflex 
 
 
 angle of the scapula 
 A blow on the styloid 
 
 
 
 5. 
 
 Radius 
 
 — 
 
 Supination 
 
 O7-C8 
 
 
 reflex 
 
 
 process of the radius 
 
 of forearm 
 
 
 0. 
 
 — 
 
 Palmar reflex 
 
 Irritation of the palm 
 
 Flexion of 
 fingers 
 
 C,-D, 
 
 7. 
 
 — 
 
 Epigastric 
 
 Stroking from nipple 
 
 Drawing in of 
 
 I>7-I>9 
 
 
 
 reflex 
 
 downwards 
 
 epigastrium 
 
 
 8. 
 
 — 
 
 Upper 
 
 Stroking skin of upper 
 
 Drawing in of 
 
 Da-Ds 
 
 
 
 abdominal 
 
 part of abdomen 
 
 abdominal 
 
 
 
 
 reflex 
 
 
 wall 
 
 
 9. 
 10. 
 
 
 ^""^^"^ I reflex 
 
 Stroking skin of 
 
 Drawing in of 
 
 1 
 
 
 middle and lower 
 
 abdominal 
 
 D,„— Dj, 
 
 
 parts of abdomen 
 
 wall 
 
 
 11. 
 
 — 
 
 Cremaster 
 
 Stroking the adductor 
 
 Elevation of 
 
 Li— Lj 
 
 
 
 reflex 
 
 region of the thigh 
 
 testis 
 
 
 12. 
 
 Patellar 
 
 — 
 
 A blow on the quadri- 
 
 Extension of 
 
 Lj— L4 
 
 
 reflex 
 
 
 ceps tendon 
 
 leg 
 
 
 13. 
 
 — 
 
 Gluteal reflex 
 
 Stroking the nates 
 
 Contraction 
 of glutei 
 
 L4-L6 
 
 14. 
 
 Achilles 
 
 — 
 
 A blow on the AohiUes 
 
 Flexion of 
 
 S^ — 8-2 
 
 
 reflex 
 
 
 tendon 
 
 foot 
 
 
 15. 
 
 — 
 
 Plantar reflex 
 
 Stroking of the sole 
 
 Flexion of 
 toes 
 
 Si-S, 
 
 10. 
 
 — 
 
 Anal reflex 
 
 Pricking the perineum 
 
 Contraction 
 of sphincter 
 
 s. 
 
 
 
 
 
 ani extemus 
 
 
LESIONS OF THE SPINAL CORD 67 
 
 The patellar reflex is constant under normal conditions, 
 and the Achilles reflex almost equally so. Much less con- 
 stant are the skin reflexes, of which, however, the cremaster, 
 abdominal, and plantar reflexes can be ehcited in the great 
 majority of healthy individuals. The utility of the skin 
 reflexes from the point of view of localization is, however, 
 much diminished by the fact that they may be abolished as 
 the result of lesions situated far above the level generally 
 accepted as that of the corresponding reflex arcs — as the 
 result even of cerebral lesions, for instance. It is therefore 
 generally admitted that the mechanism of skin reflexes is 
 far more complicated than that of tendon reflexes. The 
 centripetal fibres of the abdominal reflex, for instance, enter 
 the lower dorsal cord by way of certain posterior roots, 
 and its centrifugal fibres leave the cord by way of corre- 
 sponding anterior roots. In the majority of individuals, 
 however, the irritative impulse is perhaps not conveyed by 
 the direct reflex arc, as depicted in Fig. 7, but by the inter- 
 vention of connecting flbres (c/. p. 18) which pass some 
 distance, first in a frontal, and then, again, in a caudal, 
 direction. This hypothesis would serve to explain how it 
 is that a skin reflex may be abolished, not only by a lesion 
 at its corresponding segment level, but also in certain circum- 
 stances by one at a much higher level. We cannot at 
 present put forward further conjectures concerning this 
 very complicated mechanism ; it is a subject which calls 
 urgently for further elucidation. 
 
 CHAPTER III. 
 
 It remains for us, before closing our consideration of the 
 principles of regional diagnosis in spinal affections, to discuss 
 certain special symptom-complexes which give to lesions of 
 the cervical and upper dorsal cord on the one hand, and 
 to those of the conus terminalis, together with the cauda 
 equina, on the other, quite a special character, and one, 
 consequently, of great importance from the point of view of 
 regional diagnosis. 
 
68 BING'S COMPENDIUM 
 
 I. DIAGNOSTIC CHARACTERS OF LESIONS AFFECTING 
 THE UPPER PART OF THE SPINAL CORD. 
 
 [a) Oculo-Pupillary Symptoms.* 
 
 The development of these phenomena in lesions of the 
 cervical and upper dorsal regions is easily intelligible if we 
 bear in mind the anatomical and physiological conditions 
 of the parts {vide Fig. 24). 
 
 The upper part of the sjnnpathetic chain is represented, 
 as is well known, by the three sympathetic cervical ganglia 
 (ganglion cervicale superius, medium, and inferius). In the 
 last-named are motor cells whose cranially-directed axis 
 cylinders innervate the following muscles : 
 
 1. The dilator pupiUse. 
 
 2. The unstriped (involuntary) portion of the levator pal- 
 pebrse superioris. 
 
 3. The unstriped (involuntary) musculus orbitalis. This 
 (the remains of a powerfully - developed muscular layer 
 which is found in those mammals whose orbits have a wide 
 communication with the temporal fossa) passes across the 
 lower orbital fissure, and prevents the contents of the orbit 
 from sinking backwards. 
 
 These three sections of motor fibres are under the inner- 
 vatory influence of a nuclear group of cells situated in the 
 lateral horn of the last cervical and upper dorsal segments, 
 the centrum cilio-spinale. The connection is made through 
 the eighth cervical and first and second dorsal roots and 
 their rami communicantes. 
 
 The centrum cilio-spinale itself is under the influence 
 (probablj' through the lateral column) of a bulbar centre, 
 concerning the exact anatomy of which we have, it is true, 
 no certain knowledge. That this centre, however (so far, at 
 any rate, as its dilating neurones are concerned), is governed 
 from the cortex cerebri, is deduced, not only from experi- 
 mental observations, but also from observation of the dilata- 
 tion of the pupil which accompanies feelings of terror, pain, 
 the sexual orgasm, etc. There is even an ideo-motor 
 mydriasis, which may be brought about by a very vivid 
 mental conception of darkness. Thus, between the sym- 
 
 * A combination of these oculo-pupillary symptoms with the vaso-motor 
 Bocretory symptoms dealt with on pp. 71, 72, is known as " Horner's 
 gyraptom complex " (c/. Fig. 24). 
 
LESIONS OF THE SPINAL CORD 
 
 69 
 
 Fig. 24. 
 
 CJortex cerebr 
 
 Ggl. symp. cer7, int 
 
 DiAGKAM IN Explanation or the Sympathetic Symptom-Complex im 
 Lesions of the Uppee Past of the Cobd. 
 
70 BING'S COMPENDIUM 
 
 pathetic oculo-pupillary mechanism and the vaso-motor 
 mechanism described on pp. 21 and 22 there is a close agree- 
 ment in principle. In the one case, as in the other, we have 
 centres which may be ranged in four orders, with cerebro- 
 bulbar, bulbo-spinal, spino-sjTnpathetic, and sympathetico- 
 muscular connecting routes. 
 
 Interruption of the sympathetic oculo-pupiUary innerva- 
 tion announces itself, as will be readily understood from the 
 foregoing — 
 
 1. By a paral5rtic myosis (spinal myosis), in which the 
 pupU, contracted owing to paralysis of the dilating fibres, 
 no longer dilates, even when the eje is shaded from the hght. 
 The inequahty of the pupils (anisocoria) which accompanies 
 unilateral lesions of this mechanism is, therefore, much more 
 easily demonstrated in partial darkness than in a bright light, 
 as, in the latter case, the antagonizing sphincter pupillse inner- 
 vated by the oculo-motor nerve comes into action on both 
 sides. 
 
 2. By a narrowing of the space between the eyelids, due 
 to paralysis of the unstriped elevator muscle, the superior 
 tarsal. 
 
 3. In some cases by a sinking of the ej'eball into the orbit 
 (enophthalmus). This synnptom is due to paralysis of the 
 orbital muscle. It is clear that the foregoing symptoms 
 may be brought about by several different conditions — e.g. : 
 
 (a) By lesions in the region of the cervical sympathetic. 
 
 (13) By injury or disease in the region of the centrum 
 cUio-spinale (lowest cervical and upper dorsal cord). 
 
 (y) By lesions of the lowest cervical and the two upper 
 dorsal anterior roots and their rami communicantes. The 
 sympathetic oculo-pupUlary symptom-complex may there- 
 fore be an accompaniment of the so-called ".ower brachial 
 plexus-paralysis," or Klumpke's paralysis. This latter is due 
 to a lesion (the result o.' neoplasm, syphilitic meningitis, 
 injury, etc.) of the eighth cervical and first dorsal roots, and 
 its motor manifestations involve the small muscles of the 
 hand and the flexors of the forearm. The oculo-pupiUary 
 phenomena are an accompaniment of those cases in which 
 the roots are damaged on the proximal side of the point at 
 which the rami communicantes are given off. 
 
 (6) By lesions of the rest of the cervical cord, if the bulbo- 
 spinal connecting fibres are divided {vide Fig. 24). 
 
LESIONS OF THE SPINAL COED 71 
 
 Irritation of the centrum cOio-spinale is a rare condition. 
 It may accompany lesions of the dorsal cord immediately 
 below the centrum, and is marked by spasmodic mydriasis 
 (contracture of the dilator pupillse) and exophthalmos. 
 
 (b) Disturbances of Respiration. 
 
 These are due chiefly to pathological processes affecting 
 the region of the phrenic centre (Cg — C5). Damage to 
 this centre causes paralysis of the diaphragm — a condition 
 which, when fully developed, leads always to a fatal termina- 
 tion. If the phrenic centre is irritated by a lesion situated 
 in its immediate vicinity, the condition reveals itself by the 
 onset of hiccough, cough, dyspncea, and vomiting. Lesions 
 situated at a higher level are also accompanied by respiratory 
 disturbances, which are generally grave and indeed eventu- 
 ally fatal. Here, however, we have to do with a condition 
 of impairment of the neighbouring respiratory centres of the 
 medulla (distant effect). 
 
 (c) Affections of the Pulse. 
 
 A characteristic feature of lesions of the upper cervical 
 cord is a (frequently merely transitory) slowing of the pulse. 
 This also is due to the proximity of the meduUa, and is to 
 be regarded as a result of irritation of the vagus centre 
 therein situated. More rarely a persistent bradycardia, with 
 occasional attacks of general muscular spasm, is noticed 
 as a symptom of lesions of the upper cervical cord ; these 
 phenomena urgently require further investigation and ex- 
 planation, especially in regard to their relation to the con- 
 dition knoM'n as Adams-Stokes disease. It would appear, 
 however, that the absence of a dissociation between the 
 auricular and ventricular rhythm is characteristic of the 
 "neurogenic " form of persistent bradycardia as distin- 
 guished from the " cardiogenic." 
 
 (d) Vaso-Motor Secretory Disturbances. 
 
 Enormous elevation of temperature (109° to 111° F.) is a 
 very frequent accompaniment of injuries to "the cervical 
 cord. In rare cases (generally such as exhibit also a slowing 
 of the pulse) we find the temperature, on the contrary, 
 
72 BING'S COMPENDIUM 
 
 lowered (89° to 86° P.). In the present state of our know- 
 ledge we can only regard these disturbances as due to serious 
 impairment of a complicated heat - regulating mechanism 
 in the medulla. We are not at present justified in as- 
 suming the existence of special temperature centres in the 
 cord. 
 
 Different, again, are the conditions governing the vaso- 
 motor innervation of the face, which is often typically 
 affected in cervical lesions, and whose centres, like those of 
 the above-discussed oculo-pupUlary mechanism, we are able 
 to localize. We have here a mechanism whose lowest (most 
 peripheral) centres are in the cervical sympathetic, and in 
 immediate dependence on the nuclear groups of the cervical 
 cord. These cell-groups appear to He at the same level as 
 the centrum cUio-spinale ; they are not, however, to be found 
 in the lateral horn, but probably in the central cell-complex 
 of the ventral horn. The connection between the spinal 
 and the sympathetic centres is here also made by the anterior 
 roots of the eighth cervical and first and second dorsal seg- 
 ments and their white rami communicantes. 
 
 It would seem that secretory fibres for the sweat glands 
 of the facial integument run in close proximity to the 
 corresponding vaso-motor fibres, for in cases such as we 
 have described above, in which paralytic miosis, enoph- 
 thalmus, and narrowing of the ocular aperture, are present, 
 we often find, not only vaso-motor paralysis, marked in 
 early cases by heat and redness, and later by coldness of 
 the surface and cyanosis (vide p. 23), but also anidrosis of 
 the same regions (Horner's symptom-complex). As regards 
 these anomalies of perspiration, our knowledge of the 
 causation of the symptom-complex is not as yet exact, 
 and the difficulty of giving a completely satisfactory 
 account of the matter is increased by the fact that in 
 rare cases, instead of the usual anidrosis, we are confronted 
 with a condition of hjrperidrosis. This fact makes it, in 
 my opinion, probable that the spinal centre for facial 
 perspiration, though lying very near the centrum cilio- 
 spinale and the spinal vaso-motor centre for the face, is 
 nevertheless yet at a sufficient distance from them to be, in 
 some cases, merely irritated by the proximity of a lesion 
 involving them, while remaining itself uninjured. 
 
LESIONS OF THE SPINAL CORD 73 
 
 (e) Special Condition of Reflexes. 
 
 In " high " total transverse lesions of the cord — i.e., those 
 affecting the cervical and upper dorsal regions — the reflexes 
 are practically always totally aboHshed over the paralyzed 
 regions. On pp. 35 and 36 we have considered certain 
 attempts to explain this paradoxical phenomenon. 
 
 It goes without saying that in paralytic miosis the in- 
 constant cilio-spinal reflex is Mkewise absent. It consists 
 of a dilatation of the pupil produced by stimulation of the 
 skin of the neck on the same side. 
 
 The foregoing is subject to an important qualiflcation, 
 inasmuch as lesions in the region of the four upper cervical 
 segments generally cause immediate death (respiratory 
 paralysis, interference with the important vital centres in the 
 medulla), so that only in a small proportion of such cases 
 can the symptoms above described develop. 
 
 II. DIAGNOSTIC CHARACTERS OF LESIONS AFFECTING 
 THE LOWER PART OF THE SPINAL CORD. 
 
 As in lesions of the lowest portion of the cord — the 
 so-called " conus terminalis " — the characteristic clinical 
 symptoms are due to disturbance of the nervous mechanism 
 governing the bladder, the rectum, and the sexual function, 
 we have reserved for this portion of our work a connected 
 account of the mechanism in question. 
 
 {a) Innervation of the Bladder. 
 
 The spinal centres for the closing and the emptying of 
 the bladder — i.e., for the sphincter vesicae and the detrusor 
 urinsB — are situated in the grey substance of the third and 
 fourth, perhaps also of the fifth, sacral segments. The 
 motor fibres which originate in these centres pass to the 
 bladder by the pudendal nerve and the inferior hypogastric 
 plexus. In the latter are inserted ceU-complexes which, 
 belonging to the collateral ganglion system, represent the 
 peripheral or sympathetic centres for the bladder functions. 
 
 As the spinal centres are superior to the sympathetic, so 
 are they, in their turn, under the influence of cerebral 
 
74 BING'S COMPENDIUM 
 
 centres. Impulses from these centres, which are partly 
 subcortical in situation (corpus striatum and optic thalamus), 
 and partly cortical, reach the sacral cord probably by way 
 of the antero-lateral columns. Recently the existence of 
 routes for these fibres in the posterior columns also has been 
 maintained by certain investigators. Their views are, how- 
 ever, not as yet generally accepted. We may justifiably 
 conclude that the cerebral impulse has opposite e£Eects on 
 the sphincter and the detrusor respectively, causing relaxa- 
 tion of the former at the same time as it excites contraction 
 in the latter. 
 
 Not only centrifugal stimuli, however, flow towards the 
 sacral bladder centre. It receives centripetal stimuli also, 
 and these from the vesical mucous membrane itself. These 
 centripetal fibres, which enter the cord with the posterior 
 roots of the second, third, and fourth sacral segments, form 
 the aflEerent limb of a reflex arc, by the instrumentality of 
 which, when distension of the bladder reaches a certain 
 degree, evacuation { = sphincter relaxation + detrusor con- 
 traction) is brought about reflexly, without the co-operation 
 — nay, even in spite of the opposing action — of conscious 
 impulses. Sensory fibres, using the term in its narrower sense, 
 are distributed to the bladder waU, as well as the centri- 
 petal reflex fibres above alluded to. They pass upwards to 
 the brain, and give us the sensation of urinary pressure and 
 desire to micturate. 
 
 (6) Innervation of the Rectum. 
 
 The conditions here are quite analogous to the foregoing, 
 but somewhat simpler. Here, too, we have a centre in 
 segments : S3 — Si( — S5) ; here, too, efferent fibres in the 
 pudendal nerve and the inferior hjrpogastric plexus, in 
 which latter also are inserted sympathetic ganglia. Hero 
 again we have centripetal fibres, some of which pass to the 
 centre, forming the afferent limb of a reflex arc, while 
 others pass upwards to the brain and give the sensation 
 of rectal pressure and desire for defsecation ; here too, 
 flnally, we have efferent fibres in the antero-lateral (or 
 posterior ?) column, which convey voluntary impulses from 
 the brain. 
 
LESIONS OF THE SPINAX, CORD 75 
 
 The conditions are simpler than those obtaining in the 
 sase of the bladder in the following respects : 
 
 1. The efferent fibres last mentioned are of cortical origin 
 only. We are not entitled to affirm the existence of any 
 definite subcortical defsecation centres. 
 
 2. The conditions of innervation are less complicated, 
 inasmuch as only a sphincter action (contraction or relaxa- 
 tion) is involved ; there is no simultaneous influence on a 
 detrusor in an opposite sense. The function of a detrusor 
 is performed by the abdominal muscles acting voluntarily 
 under the influence of spinal centres situated at a higher 
 level. 
 
 (c) Innervation of Male Genital Organs. 
 
 The capacity for coition depends on the capacity for 
 (1) erection, (2) ejaculation. 
 
 Two factors play their part in erection : (a) The over- 
 filling of the corpora cavernosa. This is brought about by 
 a relaxation of vascular tone in the arteries of the penis, 
 which causes the flow of an increased volume of blood to 
 that organ. (6) This increase of volume is accompanied 
 by an increased firmness and sohdity, due to hindrance to 
 the venous outflow, which, again, is due to tonic contrac- 
 tion of the transversus perinei and of the bulbo- and ischio- 
 cavernosus muscles. 
 
 In ejaculation, clonic spasms of the two last-named 
 muscles come into play, commencing when, by means of a 
 reflex peristalsis of the ampulla vasorum deferentium, the 
 vesiculse seminales and the ductus ejaculatorii, the semen 
 has found its way into the membranous portion of the 
 urethra. 
 
 The relaxation of arterial tone, which plays so important 
 a part in erection, is due partly to inhibition of vaso- 
 constrictor, partly to stimulation of vaso-dilator centres. 
 These centres are partly spinal (Si — S3), partly sympathetic, 
 ceU-groups of the inferior hypogastric plexus. They are 
 connected, through the lateral column of the cord, with 
 the vaso-motor centres of the meduUa and the brain. 
 
 The centres controlling the tonic action of the transversus 
 perinei, bulbo- and ischio-cavernosus, aUuded to above, are 
 situated in the grey substance of the third and fourth sacral 
 
76 BING'S COMPENDIUM 
 
 segments, as also are those regulating their clonic action 
 in the act of ejaculation. The supranuclear neurons prob- 
 ably take their course in the lateral columns of the cord. 
 
 To the foregoing it may be added that, in addition to the 
 centripetal fibres from the genital integument which give 
 to the genital act somewhat of a reflex character, the 
 normal functioning of the male sexual apparatus requires 
 also centrifugal tracts which shall conve}' ps3-chical stimuh. 
 
 It foUows from these preliminary remarks that dis- 
 turbances in the innervation of the bladder, rectum, and 
 sexual apparatus, may be produced not only by lesions of 
 the terminal section of the cord, but also (owing to inter- 
 ruption of the supranuclear tracts) by injury or disease of 
 the cord at any level. 
 
 We must now state the distinguishing features which 
 enable us to make a differential diagnosis in a case of rectal, 
 vesical or genital disturbance, and to state whether the 
 lesion causing the disturbance is situated in the nuclear 
 (sacral) or supranuclear region of the cord. 
 
 1. Bladder Affections. 
 
 A. Lesion above the Centrum Vesico-Spinale. 
 
 Abolition of Cerebral ( Voluntary) Control over the Bladder and 
 of the Sensation of Urinary Pressure and Desire for Micturition. 
 — The reflex mechanism alone is concerned in the emptying 
 of the bladder. As a rule, therefore, we have a condition of 
 active or intermittent incontinence — "automatism of the 
 bladder" or incontinence a jet — in which, as soon as the 
 distension of the bladder reaches a certain degree, afferent 
 impulses from the stretched bladder wall bring about a reflex 
 and involuntary emptying of the viscus by a jet of urine. 
 
 Exceptionally — in certain cases of total transverse lesions, 
 for instance — this reflex emptying effect is also abolished. 
 The explanation of these cases is probably the same as was 
 put forward for an analogous condition of tendon reflexes 
 in certain cases of transverse division of the upper cord 
 (c/. pp. 35 and 36). In cases such as we are considering 
 we have retention of urine, which, unless help is given by 
 catheterization, may lead to rupture of the overfilled bladder. 
 
LESIONS OF THE SPINAL CORD 77 
 
 B. Lesions in the Region of the Centeitm 
 Vesico-Spinale (S3 — S4). 
 
 Permanent Relaxation of Both Sphincter and Detrusor. — 
 The clinical picture presented here is one of passive or 
 permanent incontinence — incontinence vraie. There is a 
 continuous dribbling of urine in most cases ; but if, as is 
 fairly frequently the case, the neck of the bladder possesses 
 a considerable degree of elasticity, it may withstand for a 
 while the pressure of the urine resting upon it. The con- 
 dition is then one of ischuria paradoxa, or incontinence 
 'par regorgement. When the engorgement of the bladder 
 reaches a certain point, and not until then, the urine begins 
 to dribble away. 
 
 In rare cases this elasticity is very considerable, and may 
 even lead to retention of urine instead of incontinence in 
 any form. 
 
 2. Rectal Affections. 
 
 A. Lesions above the Centrum Ano-Spinale. 
 
 Abolition of Voluntary Control of the Sphincter Ani, and 
 of the Desire for Defcecation.-— With this the reflex contrac- 
 tion of the sphincter is maintained. There is, in fact, 
 generally some degree of spasm of the sphincter, which 
 makes itself evident on introduction of the finger, and 
 affords clear proof of the supranuclear situation of the 
 lesion. In cases of total transverse lesions the reflex 
 contraction is sometimes abolished. 
 
 The clinical picture is that of rectal retention of 
 faeces. 
 
 B. Lesions in the Region oe the Centeum 
 
 Ano-Spinale (S3 — S4). 
 
 Permanent Paralysis of the Sphincter {Incontinentia Alvi). 
 — The incontinence is complete or incomplete, according to 
 the degree of elasticity in the sphincter. In incomplete 
 incontinence hard faecal masses may be retained. 
 
78 BING'S COMPENDIUM 
 
 3. Affections of the Genital Organs. 
 
 A. Lesions situated above the Centrum 
 
 GeNITO-SpIN ALE . 
 
 Vaso-constrictor paralysis, leading to engorgement of the 
 corpora cavernosa and increase in volume of the penis, is 
 here the most prominent symptom. Actual priapism — i.e., 
 complete and lasting erection — is only occasionally seen, 
 and never in cases of total transverse lesion. Where it is 
 present, a condition of tonic contraction of the transversus 
 perinei, bulbo- and ischio-cavernosus, due to irritation, is to 
 be assumed. Occasionally a condition of hyper-reflex in 
 the ejaculatory apparatus makes itseH apparent — a con- 
 dition in which the most trifling stimuh lead, if not to actual 
 ejaculation, at any rate to clonic contractions of the muscles 
 concerned in the act. 
 
 B. Lesions in the Region of the Centrum 
 Genito-Spinale (Si — Sj). 
 
 These throw out of action in most cases the whole 
 mechanism of erection and ejaculation, with complete 
 impotence as a result. Occasionally a condition of incom- 
 plete impotence or dissociated disturbance of the genital 
 function is found. In very circumscribed lesions (small 
 haemorrhages, sclerotic foci, etc.) we may have, for instance, 
 aboUtion of ejaculatory power and of the orgasm, while 
 capacity for erection remains. Such investigations as have 
 been made up to the present into the pathological anatomy 
 of these cases render it probable that the erection centre 
 is situated somewhat higher than the ejaculation centre 
 (Si — S3, S3 — S4, respectively). 
 
 Other Characteristic Features of Lesions of the Conus 
 Terminalis. 
 
 Chnically we include under the term " conus terminahs " 
 the three last sacral segments and the coccygeal seg- 
 ment. Pure conus lesions, which are not common, have an 
 extremely characteristic symptomatology. 
 
LESIONS OF THE SPINAL CORD 79 
 
 (a) Passive incontinence, ischuria paradoxa, or retention 
 of urine. 
 
 (6) Incontinence of faeces. 
 
 (c) Impotence, or dissociated disturbance of the genital 
 function. 
 
 Accompanying the foregoing, which we have fully dealt 
 with above, we have : 
 
 {d) Peri-ano-genital anaesthesia. 
 
 This occupies an area suggesting that occupied by the 
 leather patch in a pair of riding breeches. The area is 
 made up of the third, fourth, and fifth sacral segment areas 
 {vide left side of Fig. 23). 
 
 A further characteristic feature is the — 
 
 (e) Absence of any impairment of motility or reflex in 
 the muscles of the lower extremity, owing to the fact that 
 the segment innervation, even of the small muscles of the 
 foot, does not extend below the second sacral ; the same 
 applies to the Achilles reflex. 
 
 The pure conus syndrome is therefore not to be mistaken. 
 It is, however, found pure seldom, and under strictly circum- 
 scribed conditions only (intramedullary haemorrhages, smaU 
 gliotic foci, metastases, etc.). Where the conus is damaged 
 or destroyed by extrameduUary injuries or morbid processes, 
 the pure symptom-complex can only very rarely be de- 
 veloped, inasmuch as the formation of the cauda equina 
 commences from the third lumbar segment, and the conus 
 is entirely enclosed within the cauda. Only in exceptional 
 cases, therefore (of fracture or dislocation of the vertebral 
 column, for instance), can a pure conus lesion be caused — 
 c^ses, namely, in which the fibres of the cauda equina 
 succeed in escaping injury, and the conus alone suffers, in 
 spite of its central and protected situation. Cases have 
 been already observed in which fractures of the sacrum 
 or of the last lumbar vertebra have caused injury of the 
 centrally situated roots only, and, as these all spring from 
 the lower sacral segments, the pure conus symptom-complex 
 has developed. 
 
 The peculiar arrangement of the terminal spinal roots in 
 the cauda, due to the disparities in growth between the 
 vertebral canal and its contents {vide Fig. 25), is the cause 
 of many diflSculties in diagnosis. As in the cauda equina, 
 
80 
 
 BING'S COMPENDIUM 
 
 all the sacral and coccygeal and the three last lumbar roots 
 pass downwards together, from the termination of the cord 
 at the level of the first lumbar vertebra, until the issue of 
 each at its corresponding vertebral foramen, it is easy to 
 understand that an injury destructive of the cauda equina 
 about the junction of the third and fourth lumbar vertebrae 
 causes symptoms which are clinically hardly distinguishable 
 from those produced by destruction of the terminal segment 
 of the cord (through fracture of the first lumbar vertebra, 
 for example). It is, in fact, the case that, in disturbances 
 of innervation due to trauma in this region, examination 
 with a view to the discovery of deformities, visible or 
 ascertainable by palpation, and of areas of special sensitive- 
 ness to pressure, is of most assistance in forming a diagnosis 
 as to the level of the lesion — a matter of eminent importance 
 from a surgical point of view. It is quite otherwise in the 
 ccse of morbid processes such as maligna,nt, tuberculous, tj-nd 
 syphilitic growths. 
 
 The following table should be of some assistance in 
 differential diagnosis in these cases. Even with its aid, 
 however, one must be prepared for many an error in diagnosis. 
 
 Of tho Lower End of the Cord. 
 
 In some cases (with central foci of 
 disease) "dissociated" disturb- 
 ance of sensation — ^temperature 
 sense and sensibility to pain 
 affected, while tactile sensibility 
 is retained. 
 
 Spontaneous pains rare and gener- 
 ally slight. 
 
 Fibrillary twitohings in the para- 
 lysed muscles rare. 
 
 Distribution of symptoms almost 
 always symmetrical. 
 
 Ma rked tendency to sacral bedsore. 
 
 Of the Cauda Eq'ilna. 
 
 All forms of sensation always 
 affected {vide p. 31, posterior 
 roots). 
 
 Spontaneous pains (psoudo-neural- 
 gias, anaesthesia dolorosa, root 
 pains, vide p. 33), especially in 
 the perineum, over the sacrum, 
 in the bladder (generally very 
 severe). In "compression 'affec- 
 tions generally precede symptoms 
 of impaired function. 
 
 Fibrillary twitohings in the para- 
 lysed muscles (peroneal region) 
 frequent. 
 
 Distribution of symptoms 
 quently unsymmetrioal. 
 
 fre- 
 
 Somewhat slighter tendency to 
 sacral bedsore. 
 
LESIONS OF THE SPINAL COED 
 
 Fro. 25. 
 
 81 
 
 Segmeuta cerrlcaUa 
 
 Radices cervicales 
 
 Vfi^, thoracalii 
 
 Begmecta lumbalia- 
 
 Begm. aacralia 
 
 Badicea thoracales 
 
 .Radices lumbaln 
 
 Radices sacrales 
 
 TOPOGBAPHICAL COKEBLATIONS BETWEEN THE SPINAL SbOMBNTS, THE BODIES 
 OF THE VEETEBR^, THE SPINOUS PROCESSES, AND THE POINTS Or ExiT 
 
 OF THE Spinal Roots. 
 
 6 
 
82 BING'S COMPENDIUM 
 
 The peculiar features presented by total unilateral 
 lesions in the lowest region of the cord are dealt with 
 on p. 42. 
 
 APPENDIX. 
 
 Fig. 25 is intended to explain, inter alia, the relation of the 
 separate spinal segments and pairs of roots to their corre- 
 sponding vertebral spines. 
 
 Only in the uppermost cervical region is the origin of the 
 spinal roots at the same level as their place of exit from 
 the vertebral canal. The farther one proceeds downwards, 
 the greater is the displacement between the points at which 
 the roots spring from the cord and those at which they pass 
 out of the spinal canal. There are, of course, individual 
 pecuUarities, but in general it may be said that the first 
 dorsal segment is opposite the seventh cervical vertebra, 
 the first lumbar segment opposite the tenth dorsal vertebra, 
 and the first sacral segment opposite the first lumbar 
 vertebra. From the second lumbar vertebra downwards 
 the cord ceases, and only the roots of the cauda equina are 
 found in the spinal canal. 
 
 The foregoing statements have reference to the bodies 
 of the vertebrae. As Fig. 25, based on the data of Dejerine 
 and Thomas, shows, the relation to the spines of the vertebrae 
 is in many respects essentially different. 
 
DIVISION 11. 
 REGIONAL DIAGNOSIS OF CEREBRAL LESIONS. 
 
DIVJSION II. 
 Regional Diagnosis of Cerebral Lesions. 
 
 A. Lesions in .the Region of the Brain-Stem. 
 
 The structures which the neuro-pathologist groups under 
 the titles " cerebral trunk," " cerebral axis," or " brain-stem " 
 — i.e., the medulla oblongata, pons, cerebral peduncles, and 
 corpora quadrigemina — reveal their anatomical and physio- 
 logical interrelationship in the fact that they contain the 
 nuclear areas of origin of all the cerebral nerves except the 
 olfactory and the optic. We are fully justified, too, in 
 placing the two first pairs of nerves in a different category, 
 for they are not to be regarded as peripheral nerves analogous 
 to the ten other pairs, but as port.ions of the brain which, 
 during the embryonal period, have protruded themselves in 
 a cylindrical or tubelike form. 
 
 This anatomico-physiological characteristic of the brain- 
 stem determines also the chnical character of its lesions and 
 their semeiology, for disturbances of function in the areas 
 of origin of the cranial nerves, from the oculo-motor to the 
 hypoglossal, are the significant features of all affections of 
 the brain-stem. Nay, further, only by careful consideration 
 of these signs, of their method and order of appearance, and 
 of their combinations, can we succeed in localizing correctly 
 pathological processes within that region. 
 
 A knowledge of the morphology of the brain-stem and of 
 the points at which its nerves spring from it is assumed. 
 Figs. 26 to 28 may serve for recapitulation. Some detailed 
 description, however, of the internal anatomy of these 
 structures cannot be dispensed with, and, in view of what 
 
 85 
 
S6 
 
 BING'S COMPENDIUM 
 
 Fig. 26. 
 
 Vbntbal Aspect of the Beain-Stbm, showing Points of Embrobnob of 
 Cbanial Neeyb"). 
 
 Py. =Pyramis medullae oblongatse. 
 D. =Decuasatio pyramidum. 
 0.=01iva. 
 P.V.= Pons Varolii. 
 Ped.=PedunouluB cerebri. 
 XII.=NerTus hypoglossus. 
 Xl.=Nervus aocessorius Willisii. 
 
 X. =NervuB vagus. 
 IX. =Nervu3 glosso-pharyngeus. 
 VIII.=NervTia aouatious. 
 VII. =NerTus facialis. 
 VI.=Nervus abducens. 
 V. =Nervu8 trigeminus. 
 III.=Nervu3 ooulo-motorius. 
 
CEREBRAL LESIONS 
 
 FiQ. 27. 
 
 87 
 
 DOBSAL Aspect of the BEAnr-SiEM, with Fourth Vbsteicle laid open. 
 
 F.G.=Funiciilus Golli. 
 F.B. =FuniouIus Burdaohi. 
 F.l. =Funioulus lateralis. 
 Cl.=Clava medullae oblongatse. 
 C. 3.= Calamus soriptorius. 
 A.c.=:Ala cinerea. 
 R.l.=Beoes3us lateralis fossae 
 
 rhomboidese. 
 8. m.= Striae medullares. 
 E.t. =Eminentia teres. 
 L.c. =Loous coBruIeus. 
 C r. =Corpus restiforme s. en 
 cerebelli post. 
 
 C.o.m.=Crus cerebelli med. s. bra 
 chium pontis. 
 Br.o.=Brachium conjunctivum ?. 
 crus cerebelli anterior. 
 Li. =Lingula cerebelli. 
 V.m.a.=Velum meduUare anterius. 
 P.V, =Pons Varolii. 
 T.l. =Trigontim laquei s. lemnisci. 
 Ped.=Pedunoulus cerebri. 
 C.q.p.^Corpus quadrigeminum post. 
 C.q.a. ^Corpus quadrigeminum ant. 
 F. = Frenulum veli medullaris ant 
 IV. =Nervus trocUearia 
 
88 
 
 BING'S COMPENDIUM 
 
 has been said concerning the chief diagnostic feature of 
 affections involving this region, it is essential to acquire 
 an accurate knowledge of the topography of the origins and 
 terminations of the cranial nerves, from the third to the 
 tweKth, included within it. In addition, the course of the 
 chief motor and sensory tracts with which acquaintance has 
 been made in Division I. has to be borne in mind. We may, 
 however, pass over a mass of structural details which are, 
 for the moment, of no diagnostic significance. Thanks to 
 this limitation, the necessary study of the histology of the 
 
 Fio. 28. 
 gUEK SCHIMlTTE 
 
 o 
 
 - ''2 « 
 
 If* so 
 
 Lateral Aspect op the Brain-Stem. 
 
 The figure shows the levels at which the transverse sections (Querschnitte) 
 shown in Figs. 30 to 37 are taken. 
 
 brain-stem (Chapter I.) becomes comparatively simple, and 
 correspondingly so the deduction of general rules for the 
 localization of injuries and diseases affecting it (Chapter II.). 
 The description of certain more complicated anatomical 
 conditions relating to the course, distribution, and inter- 
 relationships, of nerve fibres, a knowledge of which is 
 necessary for the due appreciation, from the point of view 
 of regional diagnosis, of certain special symptom-complexes, 
 will, together with a consideration of the latter, be reserved 
 for the third chapter. 
 
CEREBRAL LESIONS 
 
 89 
 
 CHAPTER I. 
 
 STRUCTURE OF THE BRAIN-STEM. 
 
 Our illustrations (Figs. 29-37) are so arranged that the left 
 half illustrates a transverse section at a particular level of the 
 medulla, pons, or cerebral peduncle. The level at which 
 the section is made is seen in Fig. 28. On the right half is 
 a diagrammatic representation of those structures only 
 which are of importance for our discussion of regional 
 diagnosis in the ensuing chapter — the origins, terminations, 
 and intracentral tracts, of the cranial nerves and the great 
 
 Fio. 29. 
 
 F.G. =B'uiiioulus Golli ; F.B. =Funioulus Burdachi ; S.g. =Substantia gelatinoea 
 Bolandi; C.p.=Comuposteriue; C.a.=Comuanterius;R.cerv.a.=Radioee 
 oervioales anteriores ; Py.l.= Fasciculus pyramidalis lateralis ; Py.a.= 
 Fasciculus pyramidalis anterior ; Tr.sp.o.=Tractus spino-cerebellares. 
 
 motor and sensory tracts for the body generally. Pro- 
 gressing in a frontal direction from the cervical cord, we 
 shall describe each transverse section in turn. In this 
 manner the more compUcated conditions are led up to 
 naturally, and elucidated by the more simple. 
 
 1. Section through the Upper Cervical Cord (C^) 
 (Fig. 29). 
 
 The illustration represents the topographical anatomy of 
 the grey substance and of the white tracts, as fully described 
 in Division I. 
 
90 
 
 BING'S COMPENDIUM 
 
 2. Section through the Lower Portion of the Medulla 
 Oblongata (Level of the Pyramid Decussation) 
 
 (Fig. 30). 
 
 The general structural arrangement remains as in the 
 cord. The transverse section of the grey matter, however, 
 as is seen by a comparison with Fig. 29, gives evidence of a 
 considerable change. Especially noteworthy is it that the 
 dorsal horns have lost their connection with the periphery 
 of the cord, inasmuch as there is no longer any entry of 
 posterior roots. The grey matter is, consequently, ter- 
 minated dorsally by the substantia gelatinosa, which is 
 
 Fig. 30. 
 
 N.P.G. =Nucleus funiculi GoUi ; N.F.B.=Nuoleus funiculi Burdachi ; Py.= 
 FaaoiouluB pyramidalis ; Tr.sp.V.=Traotus spinalis trigemini ; XI. = 
 Nervus acoessorius. 
 
 here markedly developed. Fibres enter its ganghon cells 
 which come from a considerably higher level — namely, from 
 the pons — and belong to the trigeminus. These fibres form 
 the descending or spinal root of the fifth nerve, so called 
 because its fibres extend downwards to the upper end of the 
 cord. This spinal root is situated, somewhat Hke a cap, on 
 the external and posterior aspect of the substantia gelatinosa, 
 which may be regarded as its nucleus. 
 
 We miss the anterior roots also. On the other hand, a root 
 of the spinal accessory nerve — the motor nerve for the sterno- 
 mastoid and trapezius muscles — issues from a group of cells 
 at the base of the ventral horn. The point of exit of this 
 
CEREBRAL LESIONS 91 
 
 root is not in the line either of the anterior or the posterior 
 roots, but directly to the side of the medulla. 
 
 The situation and topography of the spino-cerebellar 
 tracts are the same as in the cord. So also with the posterior 
 columns. Within these, however, we have at this level two 
 cell-complexes — ^the nuclei of the column of Goll and of the 
 column of Burdach respectively. The fibres of the posterior 
 columns — i.e., the long neurons of the posterior root 
 system described on p. 5 — find their termination in these 
 nuclei, forming a connection there with sensory neurons 
 of the second order {vide p. 9). These, the bulbo-thalamic 
 tracts, are the axis cyUnders of the nudeiis funiculi Golli 
 and the nucleus funiculi Burdachi. They are depicted in 
 the next figure. 
 
 The most characteristic feature of this section (Pig. 30) 
 is, however, the decussation of the pyramids. From the 
 area on either side of the anterior median fissure, which, in 
 the upper part of the medulla oblongata, contains the whole 
 of the fibres of the cortico-spinal tracts, the majority of those 
 fibres cross over to the opposite lateral column, and descend 
 therein as the lateral pyramid tract. Only a small portion 
 of the fibres remains uncrossed, and maintains its position 
 close to the ventral median fissure as the ventral or direct 
 pyramid tract. 
 
 3. Section through the Medulla Oblongata at the Level Oi 
 the Posterior Hypoglossal Roots (Fig. 31). 
 
 The grey substance has here undergone still more signifi- 
 cant changes. The remnant of the dorsal horn (substantia 
 gelatinosa) is pushed fr,r to the side by the much-enlarged 
 nuclei of GoU and Burdach ; its relations to the spinal root 
 of the fifth nerve, however, remain the same as at a lower 
 level. From the nuclei of the posterior column the bulbo- 
 thalamic tracts pass across in a wide sweep to the other side 
 of the medulla, to occupy there the area known as the 
 " laqueus," "lemniscus," or "fillet" (sensory decussation, 
 decussation of the fillet). 
 
 The ventral horns no longer exist as such. They have 
 resolved themselves into separate ceU-groups. The nucleus 
 of the accessory nerve is situated as in Fig. 30, and from 
 the nucleus of the hypoglossal nerve issue the roots for the 
 
92 
 
 BING'S COMPENDIUM 
 
 motor nerves of the tongue, their course and arrangement 
 closely analogous to those of the spinal anterior roots. 
 
 Other structures of the grey matter are the olive and the 
 accessory olive, about which we shall have something to 
 say later. 
 
 The pyramids form large compact masses of fibres on either 
 side of the median fissure. The spino-cerebellar tracts, 
 traversed by the accessory nerve, occupy their old position 
 at the periphery of the lateral columns. 
 
 Instead of the dorsal median sulcus, a median fissure has 
 now been formed, which penetrates almost to the central 
 
 Fig. 31. 
 
 Tr.b.th.=Traotus bulbo - thalamioi ; L.=Laqueus 8. lemnisous; r.l.p.= 
 Fasciculua longitudinalia posterior; 0. =01iva; Oa.=01iva aooeBsoria; 
 XII.=Nervus nypoglossus. 
 
 canal. With the junction of the median fissure and the 
 central canal — i.e., with the formation of the so-called 
 calamVfS scriptorius — the fourth ventricle takes its com- 
 mencement. 
 
 Behind the area of the fillet is seen the dorsal longitudinal 
 bundle. It is not until this level is reached that it forms a 
 sharply-defined area in transverse section. Its fibres, how- 
 ever, reach far down into the cord. It is a collection of 
 " association " fibres connecting cerebral with spinal nuclei. 
 On account of its close relations with the nuclei of the ocular 
 
CEREBRAL LESIONS 
 
 93 
 
 muscles and the vestibular system {vide infra), it is generally 
 supposed that the dorsal longitudinal bundle is chiefly 
 engaged in maintaining muscular synergia ; the co-ordination 
 and co-operation necessary for a correct appreciation of our 
 position in space. 
 
 4. Section through the Medulla Oblongata (Lower Third of 
 the Fourth Ventricle, Origin of Vagus (Fig. 32). 
 
 The fourth ventricle has opened out. Immediately 
 beneath its floor Kes the nucleus of the hypoglossal nerve, 
 which in Fig. 31 lay much farther forward — in an axial 
 
 Fio. 32. 
 
 Tr.sp.o.d.=Traetus spino-cerebeUaris dorsalis ; Tr.3p.c.v. = Tract. spino-cereb. 
 ventr. ; X.=N'ervus vagus ; N.a.-= Nucleus ambiguus. 
 
 continuation, in fact, of the ventral horns. The sensory 
 nuclei are, of course, stiU farther back. Passing from with- 
 out inwards, we meet — (1) the nucleus of Burdach, here con- 
 siderably enlarged ; (2) the nucleus of Goll, here very small 
 — i.e., having already given most of its flbres to the formation 
 of the flllet ; (3) the sensory nucleus of the vagus, which is 
 seen in macroscopic preparations through the floor of the 
 ventricle, and gives to the region known as the ala cinerea 
 its grey colour. 
 The motor nucleus of the vagus (nucleus ambiguus vagi) 
 
94 BING'S COMPENDIXJM 
 
 is situated ventro-laterally to the nucleus of the hjrpo- 
 glossal, in the middle of the area occupied by the curving 
 fibres of the fillet decussation. The vagus trunk, made up 
 of sensory and motor fibres for larjmx, stomach, oesophagus, 
 heart, and lungs, passes out laterally from the medulla, 
 between the tract of Gowers and the lateral cerebellar 
 tract. While the former has kept its old position (dorso- 
 lateral to the oHve), the latter (tractus spino-cerebeUaris 
 dorsahs), moving in a dorsal direction, has already arrived 
 within the near neighbourhood of the nucleus of Burdach, 
 pushing itself between the periphery of the medulla and 
 the area of the descending root of the fifth nerve. The 
 nucleus of the latter — the substantia gelatinosa Rolandi — 
 hes, as in Fig. 31, between it and the region of the bulbo- 
 thalamic tracts. It is now, however, traversed by the 
 neuron-complex of the vagus. 
 
 As regards the dorsal longitudinal bundle, fillet, pyramids, 
 hypoglossal roots, and olive, their positions are not markedly 
 changed from those given in the foregoing transverse section 
 (Fig. 31). In addition to the median, we have now a dorsal 
 accessory ohve. 
 
 5. Section through the Medulla at the Broadest Part of the 
 Fourth Ventricle ; Origin of Glosso-Pharyngeal (Fig. 33). 
 
 The section has, in its dorsal portion, undergone a con- 
 siderable broadening, in consequence of the flattening and 
 opening out of the fourth veatricle. The nuclei of the dorsal 
 funiculi, too, now He beneath the floor of the ventricle, and 
 far to the side, in the so-called "recessus laterahs." No 
 separation can now be made between the nuclei of Goll and 
 of Burdach. We still see their last sparse neurons passing 
 across to the opposite fillet ; in the succeeding sections we 
 shall not meet the dorsal nuclei again. 
 
 Immediately to the median side of the dorsal nuclei there 
 emerges, at this level, the nucleus of the vestibular nerve {vide 
 infra). The hypoglossal nucleus and the motor nucleus of the 
 vagus are seen in the same relative positions as in the more 
 caudal sections. In the place of the sensory nucleus of the 
 vagus appears the glosso-pharyngeal nucleus, in which the 
 gustatory fibres from the posterior third of the tongue and the 
 sensory neurons from tho pharynx and the tympanic cavity 
 
CEREBRAL LESIONS 
 
 95 
 
 find their termination. The glosso-pharyngeal nerve pierces 
 the periphery at a point closely corresponding to that at which 
 the vagus passes through it in Fig. 32. It, too, traverses 
 the substantia gelatinosa, which is here considerably smaller 
 in section, and has withdrawn itseK inwards and upwards 
 from the descending tract of the fifth nerve; while the 
 latter has moved still farther from the periphery, in a dorso- 
 median direction. The tract of Gowers still occupies its old 
 position; the dorsal spino-cerebeUar tract, or direct cerebellar 
 tract of Flechsig, merges dorsally in the restiform body, 
 which, as the inferior peduncle of the Cerebellum, connects 
 
 Fio. 33. 
 
 N.vest. = Nucleus vestibularis ; IX.=Nervus glosso-pharyngeus ; C.r. = Corpus 
 restiforme ; N.f.p. = Nu3leus funiculorum posteriorum. 
 
 the latter with the medulla. The dorsal longitudinal 
 bundle, the pyramids, and the fillet, have not altered their 
 relative positions. The inner or dorsal accessory olivary 
 nuclei are now enclosed in the substance of the fillet. The 
 olives are here at their greatest development. 
 
 6. Section through the Caudal End of the Pons-, Origin of 
 Auditory, Facial and Abducens Nerves (Fig. 34). 
 
 In this section the pyramids are "caught" just before 
 their sphtting up into separate bundles among the transverse 
 fibres of the pons. Above the pyramid is the transverse 
 section of the upper end of the ohve. 
 
96 
 
 BING'S COMPENDIUM 
 
 'In the dorsal half of the section the area bordering the 
 median line, or raphe, is occupied by the fillet and dorsal 
 longitudinal bundle. 
 
 Towards the sides there is a continuous passing over of 
 fibres from the brain-stem into the cerebellum. Here, in the 
 restiform body, the neurons of the dorsal spino-cerebellar 
 tract are enclosed. The ventral portion, or tract of Gowers, 
 is still situated at the periphery, dorso-lateral to the olive. 
 Its wedge-shaped transverse section exhibits, as in some 
 of the previous sections, a point directed inwards. The 
 
 Fig. 34. 
 
 N. vest. = Nucleus restibularis ; N.coch.=NuoIeus coohlearis ; N.D.=NuoleuB 
 Deiterai ; VIII.=Nervus aousticus ; VII.=Nervus facialis; VI.=NervTia 
 abducens. 
 
 substantia gelatinosa and descending tract of the trigeminus 
 show little change from Fig. 33. 
 
 As in the latter figure also, the vestibular nucleus lies, 
 close to the surface, beneath the floor of the lateral portion 
 of the fourth ventricle. We now see the fibres of the 
 vestibular nerve, the portion of the eighth which serves 
 to maintain our sense of our position in space, passing 
 between the restiform body and the descending tract of the 
 fifth nerve to the vestibular nucleus. The actual auditory 
 nerve, or nervus cochlearis, has its nucleus in a rounded 
 projection on the lateral and dorsal aspects of the restiform 
 body (the acoustic tubercle). 
 
CEREBRAL LESIONS 97 
 
 Not guperlicially under the floor of the fourth ventricle, 
 but deep in the substance of the formatio reticularis of the 
 pfons, lies the motor nucleus of the seventh or facial nerve. 
 The intracentral course of this nerve is a pecuhar one. It 
 passes inwards and backwards towards the floor of the 
 fourth ventricle ; when close under the latter it winds 
 itseK round the superficially situated abduoens nucleus, and 
 turns back through the substance of the pons, emerging in 
 the immediate neighbourhood of the eighth nerve at the 
 cerebello pontine angle. As the second half of the loop 
 thus formed does not run in the same transverse section as 
 the first, but at a somewhat higher level, we have repre- 
 sented it by a dotted Une. A little higher still emerges the 
 sixth nerve or abduoens, which suppUes the external rectus 
 muscle of the eye. Its roots also are, for the same reason, 
 represented by a dotted Une. They emerge from the base 
 of the brain at the lower border of the pons, considerably 
 nearer the middle fine than those of the facial nerve. The 
 portion of the facial root which circles round the nucleus of 
 the abducens — the so-called " genu " or " knee " of the facial 
 root — forms the prominence known as the " eminentia 
 teres " on the floor of the fourth ventricle. 
 
 Near the vestibular nucleus, at the boundary of the 
 cerebellum, lies the nucleus of Deiters, which, it should be 
 remembered, is the origin of the vestibulo-spinal tract. In 
 order not to comphcate the figure, we have omitted the 
 connections between the nucleus of Deiters and the dorsal 
 longitudinal bundle, between the former and the vestibular 
 nucleus, and between the vestibular nucleus and the dorsal 
 longitudinal bundle. These connections are, however, 
 physiologically of great importance, as already stated 
 (pp. 92 and 93 : Co-operation of Ocular and Labyrinthine 
 Apparatus in Maintaining Orientation in Space). 
 
 7. Section through the Middle Third of the Pons at the Level 
 of the Point of Exit of the Fifth Nerve (Eig. 35). 
 
 The ventral portion of the pons (pars basilaris pontis) 
 shows, embedded in the mass of its transverse fibres (which 
 are for the most part connected with the cerebellum by the 
 middle cerebellar peduncle) the pyramid tracts cut across. 
 
 7 
 
98 
 
 BING'S COMPENDIUM 
 
 They do not now form a compact, single bundle, as in the 
 foregoing sections, but are split up into separate fasciculi. 
 
 In the dorsal portion of the pons, or the tegmentum 
 pontis, the dorsal longitudinal bundle is seen in its accus- 
 tomed position. The area of the fillet has now lost its 
 narrow, elongated form and become broader, and at the 
 same time distinctly shorter from back to front, so that the 
 bulbo-thalamic tracts and the dorsal longitudinal bundle 
 
 Fig. 35. 
 
 L.l. =Laqueiis lateralis; L.m.=Laqueusmedialis ; N.s.=Nucleiis sensibilis : 
 N.m.=Nuoleusmotorius ; V.=NerTUB trigeminus; Cr.c.a.=Crus cerebelli 
 anteiius. 
 
 are no longer in immediate contiguity. The former, in this 
 and the succeeding sections, are no longer synonymous, 
 without quaMfication, with the filet. They form now the 
 median fillet, while more laterally placed is the lateral 
 fillet, an area occupied by neurons of the central auditory 
 tract in their passage from the auditory centres in the 
 brain-stem to the mid-brain. 
 
 The nuclear conditions are at this level much simpUfied. 
 The trigeminus has a motor nucleus which lies in the same 
 
CEREBRAL LESIONS 99 
 
 sagittal plane as the nucleus of the facial, but some distance 
 from it, in a dorsal direction. From it arises the smaller, 
 motor portion of the trigeminus. It issues from the base 
 of the brain in company with the larger sensory portion 
 comprising the sensory nerves of the face. Their ganglion 
 cells lie, as is well known, in the Gasserian semilunar 
 gangMon ; their axis cylinders pass to the sensory nucleus of 
 the trigeminus, which lies at the side of the fourth ventricle, 
 beneath its floor, through which it glimmers with a bluish 
 appearance, which has gained for the area concerned the 
 name of locvs coeruleus. For the last time we meet with 
 the substantia gelatinosa Rolandi, into which trigeminus 
 fibres continue to penetrate right down to the cervical 
 cord. These fibres come from the descending tract of the 
 trigeminus, which is made up of fibres from the sensory 
 portion of the fifth, which, instead of entering the sensory 
 nucleus, turn in a caudal direction, and traverse the brain- 
 stem for a greater or less distance. 
 
 The bundle of Gowers has left its peripheral situation at 
 the cerebeUo-pontine angle to reach the dorsal portion of 
 the tegmentum at the anterior border of the pons. Our 
 section finds it about haKway through its journey. 
 
 8. Section through the Anterior Third of the Pons ; Exit 
 of the Trochlear Nerve at the Velum Medullare Anterius 
 
 (Fig. 36). 
 
 The basilar portion of the pons has increased greatly in 
 extent. The pjrramid bundles embedded in it are stiU more 
 scattered than in Fig. 35. On the other hand, the volume 
 of the dorsal portion or tegmentum has much diminished 
 simultaneously with the marked contraction in size which 
 the fourth ventricle has undergone beneath the superior 
 medullary velum. The tegmentum stiU encloses in its 
 substance the dorsal longitudinal bundle and the fillets 
 (median and lateral). The former still hes close to the 
 median hne, and near the floor of the ventricle ; the median 
 fillet is at the deepest part of the tegmentum, but has moved 
 somewhat in a lateral direction (the bulbo-thalamic tracts 
 are now leaving each other, and passing in the direction of 
 the optic thalami). The lateral fiUet has moved close up 
 to the lateral periphery and velum medullare, and is about 
 to pass into the inferior corpora quadrigemina. 
 
100 
 
 BING'S COMPENDIUM 
 
 The whole fillet area surrounds, like a crescent, that occu- 
 pied by the fibres which, with the superior medullary velum 
 between them, pass from the cerebellum to the corpora 
 quadrigemina . These fibres constitute the superior cerebellar 
 peduncle or brachium conjunctivum. The bundle of Gowers 
 has attached itself closely to this structure, ar i passes along 
 it, coursing backwards therefore, to the vermis cerebelli. 
 
 Within the superior medullary velum we see the decus- 
 sation of the trochlear nerves. The trochlear — the nerve ^ 
 which supplies the superior oblique muscle of the eye — is 
 
 Fig. 36. 
 
 IV.=Iirervu3 troohlearra. 
 
 distinguished from all other cranial nerves by its dorsal 
 emergence. Some investigators have put fonvard a phylo- 
 genetic explanation of this remarkable anatomical peculi- 
 arity of the trochlear, and suggest that it originally suppUed 
 a muscle of the " parietal organ." 
 
 The nucleus of the trochlear nerve is not seen in this 
 section. It hes farther forward at the proximal extremity 
 of the pons, btmeath the inferior corpora quadrigemina and 
 behind the dorsal longitudinal bundle. The manner in 
 which it sends its fibres round the ventricle, to decussate 
 with its fellow in the superior medullary velum, is indicated 
 by a dotted line. 
 
CEREBRAL LESIONS 
 
 101 
 
 9. Section through the Cerebral Peduncles and the Superior 
 Corpora Quadrlgemina (Exit of Oculo-Motor Nerve) 
 (Kg. 37). 
 
 In this section also we distinguish a pars basilaris (crusta) 
 and a tegmentum. The boundary between the two is 
 formed by the substantia nigra of Sommering. In the pars 
 basilaris, or crusta, run the pyramids, closed in on either 
 side by tracts of fibres which connect the cerebral cortex 
 and the pons — mesiaUy by the occipito-temporo-pontine, 
 laterally by the fronto-pontine tract. 
 
 Fig. 37. 
 
 III.=Nervus oculo-motorius. 
 
 In the tegmentum we see, immediately beneath the 
 ventricle, which has here narrowed and become the aqueduct 
 of Sylvius, the oculo-motor nucleus ^nucleus of third nerve). 
 We have represented the latter in a manner which does not 
 fuUy portray the somewhat compKcated anatomical con- 
 ditions it presents. We shall have to deal with these later, 
 but may confine ourselves here to the coarser anatomy of 
 the parts. In its course to the base of the brain, where it 
 emerges at the median border of the crusta, the oculo-motoi 
 nerve traverses the red nucleus of the tegmentum, whose 
 importance as the point of origin of Monakow's bundle has 
 been already alluded to (vide p. 4). 
 
102 BING'S COMPENDIUM 
 
 The oculo-motor nucleus, whose neurons supply the 
 sphincter iridis, the ciUaris muscle, and aU the external 
 muscles of the eye, except the external rectus and superior 
 obhque, has the closest relations with the dorsal longitudinal 
 bundle. The median fillet has moved still farther laterally 
 than in Fig. 36. We are now only a few miUimetres below 
 (caudal to) the point at which the mass of the bulbo-thalamic 
 tracts bury themselves in their goal, the optic thalamus. 
 
 CHAPTER II. 
 
 I. GENERAL RULES FOR THE LOCALIZATION OF 
 
 INJURIES AND DISEASES OF THE 
 
 BRAIN-STEM. 
 
 We must endeavour in the first place to deduce, from what 
 has been said in the foregoing chapter concerning the 
 anatomy of the brain-stem, the structural principles which 
 govern its formation, and have their correlative in principles 
 of localization of similar general applicability. 
 
 (a) The nuclei of the cranial nerves are almost all situated 
 in the dorsal part of the brain-stem. We may distinguish 
 three layers, of which the first two occupy the tegmentum of 
 the pons and cerebral peduncles. Most dorsally situated 
 — i.e., close beneath the floor of the fourth ventricle or 
 the aqueduct of Sylvius — He the nuclei of the hypoglossal, 
 vagus (sensory), glosso-pharyngeal, vestibular, abducens, 
 trigeminus (sensory), trochlear, and oculo-motor nerves. In 
 a more ventraUy situated laj^er are the nuclei of the acces- 
 sory and facial nerves and the motor nuclei of the vagus 
 and trigeminus. This layer is situated in the " formatio 
 reticularis." A stiU more ventral situation is occupied by 
 the cochlear nerve alone, in the " acoustic tubercle." 
 
 (b) The fibre-complexes of the cranial nerves pass from 
 their nuclei above mentioned to the base of the brain ; the 
 majority follow a direct course, but the route followed by 
 the vagus (motor) is somewhat circuitous, and that of tne 
 facial still more so. The trochlear nerve (fourth) is alone in 
 emerging dorsally (at the superior medullary velum) ; it is 
 exceptional in another respect also — namely, that, after 
 
CEREBRAL LESIONS 103 
 
 leaving their nucleus, its fibres undergo a complete decussa- 
 tion with their fellows of the opposite side. We shall have 
 something to say later concerning a partial decussation of the 
 oculo-motor fibres to which allusion has not yet been made. 
 An the other nerve roots of the brain-stem, both motor 
 and sensory, emerge uncrossed — i.e., on the same side as 
 their nuclei. 
 
 (c) Ventral, or rather ventro-mesial, to the region of the 
 cranial nerve nuclei — i.e., the floor of the fourth ventricle 
 and the formatio reticularis — lies the area occupied by the 
 sensory tracts for the trunk and extremities. We know that 
 this is termed the " fillet " (laqueus, lemniscus), and we 
 have seen that the greater part of this structure is made 
 up of the bulbo-thalamic tracts, which form connecting 
 neurones for the dorsal columns — i.e., for the long fibres of 
 the posterior spinal root system {vide pp. 5-8). They form 
 afferent channels therefore for deep sensibility and the tactile 
 sense (vide p. 16). We became acquainted also in Division I. 
 with short fibres of the posterior root system, which termi- 
 nate in the dorsal horn, and to which the spino-thalamic 
 tracts connect themselves. These spino-thalamic tracts, 
 which decussate soon after their origin, pass without further 
 decussation to the optic thalami, and mingle with the bulbo- 
 thalamic tracts after the fillet has been constituted by the 
 latter. They convey to our consciousness all painful and 
 thermal, and in addition some tactile, impressions. Accord- 
 ing to the present state of our anatomico-pathological know- 
 ledge on the point, it would appear that, in the portion of the 
 fiUet nearest to the raphe or middle line, only bulbo-thalamic 
 fibres are contained, so that, in lesions affecting exclusively 
 the most mesial portion of the fillet, the chief symptoms are 
 disturbances of the muscular sense in the trunk and ex- 
 tremities. Only when the lesion affects also the lateral part 
 of the fillet is it usual to find sensibility to pain and to 
 thermal and tactile impressions affected. The circumstance 
 tha': these may be affected also in lesions of the formatio 
 reticularis gives support to the view expressed by several 
 authors, that some portion of the spino-thalamic tract must 
 also pass through this region on its way to the thalamus. 
 While, in the caudal portion of the brain-stem, the fillet areas 
 of the two sides are in contact, from the mid-pons region 
 they separate farther and farther from each other. 
 
104 BING'S COMPENDIUM 
 
 (d) The pyramids occupy the most ventral region of the 
 medulla and the cerebral peduncle. Within the pons their 
 situation is less superficial. Here also they are split up into 
 numerous separate fasciculi by the interposition of the 
 transverse fibres of the pons. For them, as for the sensory 
 tracts for the trunk and extremities, the statement holds 
 that, while in close apposition to one another in the more 
 caudal portion of the brain-stem, they diverge from each 
 other more and more as one proceeds in a frontal direction. 
 This divergence begins in fact in the meduUa. 
 
 (e) At their passage from the internal capsule of the brain 
 into the brain-stem (cerebral peduncle), the pyramids com- 
 prise, besides the central motor tracts for the trunk and 
 extremities, those also for the muscles of deglutition and 
 the facial, laryngeal, and lingual muscles. At this level the 
 expressions " pyramid tracts " and " cortico-spinal tracts " 
 are by no means co-extensive, for the pjrramids include the 
 cortico-bulbar tracts also — i.e., the supranuclear tracts for 
 the trigeminus (motor), facial, vagus (motor), and hypo 
 glossal. These components, however, detach themselves 
 successively from the united " complex " during its passage 
 through the brain-stem, to connect, after crossing the middle 
 line, with their respective nuclei. 
 
 (/) Longitudinal fibre tracts encountered throughout the 
 greater extent of the brain-stem are — dorsally, near the 
 middle Une, the dorsal longitudinal bundle ; laterally, the 
 descending or spinal root of the trigeminus, with its nuclear 
 column, the substantia gelatinosa Rolandi. Jn the medulla 
 we have, at the lateral periphery, the united spino-cerebellar 
 tract ; while in the pons only its ventral portion (tract of 
 Gowers) is seen, following the course shown in Figs. 35 and 36. 
 
 If the foregoing structural features are kept in mind, there 
 will be no difficulty in understanding the regional diagnostic 
 principles which we here base upon them. 
 
 Owing to the small calibre of the medulla, very smaJl 
 lesions, affecting especially its more caudal regions, may 
 give rise to very marked symptoms, and especially to 
 symmetrical affections in which both sides of the body are 
 involved. Thus, a minute haemorrhage or area of softening 
 may cause complete paralysis of the tongue owing to the 
 very sMght distance which separates the hypoglossal nucleus 
 on one side of the medulla from that on the other. As the 
 
CEREBRAL LESIONS 105 
 
 brain-stem broadens steadily in a frontal direction, the 
 conditions necessary for the production of bilateral affections 
 are far less often present in the pons and the tegmentum 
 than in the medulla. The close apposition to each other of 
 the right and left fillet area, however, explains the fact that 
 in the caudal half of the pons bilateral affections in the 
 fillet region, leading to bilateral anaesthesia of the trunk and 
 extremities, are fairly frequently produced by smaU lesions. 
 In small mesial lesions in the pons, the anaesthesia as a rule 
 only extends to the deep sensibility (muscular sense). The 
 detailed account of the topography of the sensory tracts in the 
 pons given on pp. 103 and 104 furnishes an explanation of this 
 fact, as also of the fact that the more laterally the lesion is 
 situated in the fillet area, the more likely are the temperature 
 sen.se and sensibility to pain to be affected. The sensory 
 disturbances produced by unilateral interruption in the 
 fillet tract are, of course, contralateral, and take the form 
 chiefly of crossed hemiataxia, unless the interruption has 
 taken place in the most caudal part of the medulla, distal 
 to the " decussation of the fillet." 
 
 Homolateral hemiataxia (of cerebellar type, vide p. 32) 
 is caused by unilateral affections of the spino-cerebellar 
 tract or of the corpus restiforme. The subject will be 
 further dealt with in the section on the Cerebellum. 
 
 The pyramids are in such close apposition to each other 
 in the medulla, that minimal lesions may cause a condition 
 of tetraplegia. That this is not more frequently observed 
 is due to the fact that lesions of the oblongata are, owing to 
 the inclusion of many important vital centres in the vagal 
 nucleus, generally fatal. A very rare condition is that of 
 hemiplegia criiciata, which is produced by lesions situated 
 laterally at the pyramid decussation in such a position that 
 the tracts for the arm are interrupted before, those for the 
 leg after, they have passed to the opposite side. We have, 
 then, a contralateral ar^n and a homolateral leg paralysis 
 of central cortico-spinal type (vide Fig. 38). 
 
 In the basilar portion of the pons, in which the pyramids 
 are split into separate bundles by the numerous transverse 
 pontine fibres, small lesions may fail entirely to produce 
 symptoms, either because too few pyramid fibres are affected, 
 or because the pyramids have escaped altogether. 
 
 If, however, we keep in mind the case of a unilateral 
 
106 
 
 BING'S COMPENDIUM 
 
 pyramid lesion, (found most frequently in lesions of the 
 brain-stem), it is clear that an interruption of nerve channels 
 affecting the cortico-spinal tracts exclusively, must cause 
 the same symptoms, whatever its situation between the 
 cortex cerebri and the pyramid decussation. In order, 
 therefore, to diagnose with certainty a lesion of the brain- 
 stem, still more to arrive at accurate conclusions as to the 
 level at which it is situated therein, we have to depend 
 upon the disturbances of function affecting the cranial 
 
 Mode of Oeiqin of Crossed HEMiPLBcii. 
 + = Paralyzed. 
 
 nerves from the third to the twelfth, which in these cases 
 are practically never absent. 
 
 As a matter of fact, an interruption of the cortico-spinal 
 tracts only, by a focal lesion within the brain-stem, is 
 almost impossible. For these tracts, the central neurons 
 for the motor spinal nerves, have, mingled with them, as 
 already stated, down to the point at which the medulla 
 passes into the cervical cord, the central neurons for the 
 motor cranial nerves. This condition is represented dia- 
 grammaticaUy'in Fig. 39, in which are given the cortico- 
 bulbar tracts of the facial and hypoglossal nerves. 
 
 Let us consider the cases cf two lesions, either of which 
 
CEKEBKAL LESIONS 107 
 
 causes an interruption in the pyramid tracts. If the inter- 
 rupting lesion is situated in the medulla (A, Fig. 39), we 
 shall have a lingual paralysis as well as that of the ex- 
 tremities, the facial muscles remaining unaffected. If, how- 
 ever, the lesion is in the pons (B, Fig. 39), the facial muscles 
 as well as the tongue wiU be paralyzed. These cranial nerve 
 paralyses, accompanying cortico-spinal paralyses of the ex- 
 tremities, proclaim, as do the latter, by the absence of 
 degenerative atrophy and the reaction of degeneration, the 
 supranuclear situation of the lesion which brings them 
 about. We have, then, when endeavouring - to form a 
 diagnosis of the level of a lesion in the brain-stem, a very 
 important principle of localization, in the fact, that in supra- 
 nuclear lesions of the pyramids, the trophic influence of the 
 cranial nerve nuclei remains intact, notwithstanding the 
 paralysis of their corresponding muscles. 
 
 Foci, however, which affect a single tract only, as that 
 of the pyramid, for instance, are, in a structure of small 
 sectional area such as the meduUa, of extreme rarity, and 
 even in the more frontal portions of the brain-stem they 
 are by no means common. We have, then, in the great 
 majority of these cases, a mixed symptom-complex, and here 
 again symptoms of cranial nerve disturbance, accompanying 
 those of interference with the long tracts, form the index 
 to the localization of lesions of the brain-stem. We have 
 seen how closely packed is the brain-stem with the nuclei 
 of the cranial nerves. Small wonder, then, that in lesions 
 of that structure one or other of the nuclei is almost always 
 damaged. It is not necessary that the focus of disease shall 
 actually include them within its area. Neighbouring foci 
 may indirectly, by the action of pressure, by causing circu- 
 latory disturbances and so on, bring about serious impair- 
 ment of a nucleus. The paralysis, however, which follow? 
 the destruction of a motor nucleus in the brain - stem 
 presents always the peripheral character^ — -is accompanied, 
 that is to say, by degenerative atrophy and the reaction 
 of degeneration. So soon, therefore, as these conditions are 
 found in the facial muscles, the muscles of mastication or 
 deglutition, the lingual or laryngeal muscles, a supranuclear 
 situation for the lesion may be at once excluded. That in 
 any given case the paralysis of particular nerves furnishes 
 the most valuable diagnostic aid of all, in establishing the 
 
108 BING'S COMPENDIUM 
 
 level of the lesion, goes without saying. A tegmental lesion 
 which produces degenerative facial paralysis, but spares 
 tongue, oesophagus, larynx, and masseters, must be situated 
 
 Fig. 39. 
 
 (^cntrum corticale extrcmi- 
 tatum 
 
 Radix spinalis 
 
 iSirPBANUcxEAR Paralyses of Cranial Nerves in Pyeamid Lesions at 
 DiFrERENT Levels in the Brain-Stem. 
 
 about the level of our section (Fig. 34) — i.e., of the caudal 
 extremity of the pons — and cannot extend either frontally 
 to the region of the trigeminus or caudally to that of the 
 nucleus ambiguus and the hypoglossal nucleus. 
 
CEREBRAL LESIONS 109 
 
 A further guide, therefore, in determining the level of a 
 lesion of the brain -stem, is afEorded by the degenerative 
 paralysis which affects those motor cranial nerves whose 
 nuclei are involved in, or are in the very near neighbourhood 
 of, the lesion. 
 
 Atrophic paralyses of muscles suppUed by cranial nerves 
 may, however, be brought about, not only by lesions affecting 
 those nerves in their nuclei or roots, but also by lesions 
 which involve them in their course to the periphery. A 
 further criterion comes into play here— namely, the manner 
 in which atrophic cranial nerve paralyses are combined with 
 symptoms due to interruption of the long tracts in their 
 course through the brain-stem. In these cases we fre- 
 quently meet with some form of the condition known as 
 hemiplegia alternans, in which, as shown in Fig. 40, we have 
 cranial nerves affected on one side, and a simultaneous 
 interruption of motor and sensory tracts supplying more 
 distally situated regions. 
 
 We may distinguish several tj^es of hemiplegia alternans : 
 
 (a) In lesions of the cerebral peduncle we have, in 
 addition to the pyramid lesion, which causes a complete 
 hemiplegia of the opposite side (that is to say, one in which 
 the facial muscles, the tongue, and the muscles of the 
 extremities, are affected), an involvement of the roots of the 
 third nerve, which leads to an oculo-motor paralysis on the 
 same side as the lesion (hemiplegia alternans oculo-motoria, 
 or Weber's paralysis, Fig. 40, A). 
 
 (b) In lesions of the caudal half of the pons we may have 
 a hemiplegia alternans facialis produced in an analogous 
 manner (Millard-Gubler's paralysis). In this condition we 
 have facial paralysis on the same side as the lesion, and 
 paralysis of the extremities on the opposite side (Fig. 40, B). 
 If the area of the lesion is large enough to involve the sixth 
 nerve or abducens, as well as the facial of the same side, 
 we have the condition known as " Foville's paralysis." 
 
 * Lesions which, without disturbing the pyramid tracts, exert an 
 irritating action on the pars basilaris pontis by contiguity, and at the same 
 time in'.errupt the fibres of the ooulo-motorius, evoke motor irritative 
 phenomena (tremor) in the opposite extremities, with homo-lateral oculo- 
 motor piralysis. This is known as " Benedikt's symptom-complex." As 
 will be plain from Fig. 37v Jesions affecting one of the red nuclei are specially 
 likely to bring about the development of this syndrome 
 
110 
 
 JBING'S COMPENDIUM 
 
 (c) A rare condition, whose infrequency is sufficiently ex- 
 plained by the smaller calibre of the brain -stem at the 
 
 Fig. 40. 
 
 Centrum corticale extremi- 
 tatum 
 
 N oculo- 
 motor 
 
 Radix spinalis 
 
 Mode or Origin of Alternating Hemiplegias. 
 
 A = lesion in the cms cerebri giving rise to hemiplegia altemana oculo- 
 motoria ; B and 6 = lesions in the pons giving rise to hemiplegia altemana 
 facialis — in B with, in b without, degenerative atrophy of facial muscleB. 
 
 level of the medulla, is that of hemiplegia alternans hypoglos- 
 sica, in which half of the tongue is paralyzed on the same 
 side as the lesion, and the extremities on the opposite side. 
 
CEREBRAL LESIONS 111 
 
 While it is the rule that, in these " alternating " symptom- 
 complexes, the cranial nerve paralysis is of the peripheral, 
 degenerative type, cases do occur, in the facial form 
 (Millard-Gubler type), for instance, in which it, as well as the 
 paralysis of the extremities, is supranuclear in type. The 
 explanation of this fact can be gathered from a glance at 
 b (Fig. 40), where the lesion is seen to be so situated that 
 neither the facial nucleus nor its issuing root is involved, but, 
 instead, the central facial tract shortly before its entry into 
 the nucleus, and thus immediately after it has crossed the 
 middle hne and entered on the side of the lesion. 
 
 The trigeminus also, as well as the motor cranial nerves, 
 may take part in an alternating symptom-complex, in which 
 loss of sensation over one side of the face, including the 
 corresponding mucous membranes, is combined with hemi- 
 plegia of the opposite side. In such cases one will attempt 
 to localize the lesion according to the motor cranial nerve 
 paralyses which accompany the hemiplegia ; for a facial 
 anaesthesia of the kind may, so far as it alone is concerned, 
 be produced by any lesion of the brain-stem caudal to the 
 trigeminal nucleus. This possibility is due to the existence of 
 the spinal or descending root of the fifth and the substantia 
 gelatinosa. Lesions of these structures cause, it is true, no 
 Buch extensive disturbances of sensation as are produced by 
 those involving the chief sensory nucleus or the root fibres 
 which enter it. It is probable, indeed, that destruction of 
 the substantia gelatinosa in the meduUa causes sensory dis- 
 turbances only in the region supplied by the first branch of 
 the trigeminus. We cannot make this statement categoric- 
 ally, however, as, at present, observations on the point are 
 neither numerous nor conclusive enough to enable us to do 
 so. Where masticatory paralysis is also present, the situation 
 of the lesion may be placed, without hesitation, on the 
 affected side, and not at a lower level than the middle third 
 of the pons. 
 
 General corporeal sensibility may also be involved in one 
 of these alternating symptom-complexes. The lesion, for 
 instance, to which an alternating hemiplegia is due, may 
 involve the fiUet, in which case the hemiplegic portions of 
 the trunk and extremities exhibit sensory disturbances in 
 addition, or, again, the lesion, while sparing the pyramids. 
 
112 BING'S COMPENDItJM 
 
 may involve, simultaneously, both the fillet and the crania* 
 nerve nuclei or roots. 
 
 We have therefore to note, as a chief characteristic 
 of lesions of the brain-stem, a generally " alternating " 
 character of the motor disturbances present. Further, from 
 the point of view of "transverse" or systemic diagnosis, 
 the special peculiarities of the cUnical picture presented by 
 any given case of alternating hemiplegia may give us quite 
 unambiguous information concerning, not only the side on 
 which the lesion lies, but also its more ventral or more dorsal 
 situation and its extent — this according to the number of 
 cranial nerves involved, according to the involvement of 
 pyramid or fillet, or of both, and so on. 
 
 Some account may be given here of the more important 
 remaining deductions commonly used in the systemic 
 diagnosis of afEections of the brain-stem. That affec- 
 tions of the tegmentum (pontis), and such other affections 
 {e.g., tumours of the vermis) as injure the tegmentum by 
 pressure from without ; that such affections manifest them- 
 selves chiefly by signs of injury to the cranial nerves, goes 
 without saying, for it is in the tegmentum that these have 
 their nuclei. In these cases the dorsal longitudinal bundle 
 is, owing to its dorsal situation, apt also to be involved. 
 If this important association tract {vide p. 92) is only 
 slightly involved, we have nystagmus developed on looking 
 to the injured side ; if the destruction is complete, combined 
 movement of the eyes towards the side of the lesion becomes 
 impossible (conjugate paralysis). We shall return to these 
 facts and their explanation later on. 
 
 In so far as we have to do, in lesions of the tegmentum 
 pontis, with injury to the motor nuclei, the nuclear character 
 of the lesion is, of course, betrayed by the degenerative 
 character of the paralysis which ensues. If the lesion 
 extends to the deeper regions, sensory disturbances of the 
 trunk and extremities are superadded (fillet). Finally, 
 should it extend still farther in a ventral direction, the 
 pyramids become involved (spastic paralysis of the muscu- 
 lature innervated from points distal to the lesion). 
 
 No less important is a scrupulously careful observation of 
 the order in which the symptoms of nerve involvement 
 develop, where there is in question the diagnosis of some 
 
CEREBRAL LESIONS 113 
 
 morbid process at the base of the brain, such as a tumour 
 growing into the brain-stem or an aneurysm of the basilar 
 artery pressing upon it. In the latter case the first symptoms 
 likely to be observed (as wiU readily be deduced from 
 anatomical considerations) are those of more or less sym- 
 metrical bilateral involvement of the pyramids, to which 
 are added, later, signs of involvement of the fillet, and 
 nuclear paralyses of cranial nerves other than the third and 
 sixth (oculo-motor andabducens), which, owing to the mesial 
 emergence of their roots, may be the first structures to 
 present symptoms of disturbance. It is otherwise with 
 new growths of the base of the brain, whose starting-point is 
 generally the emerging nerve trunks or the meninges in their 
 neighbourhood. Here, therefore, a unilateral symptom- 
 complex is the rule, and injury to nerve roots is the most 
 significant, and almost always the earliest, symptom. 
 
 In these cases we often meet with " irritative symptoms," 
 which exhibit a close analogy with those discussed when 
 deaUng with the spinal cord. They generally take the form 
 of hyper sesthesiae and " root pains " in the area of the 
 trigeminus {vide p. 33). The " irritative symptom " of 
 the motor portion of the trigeminus is trismus, that of the 
 facial nerve, spasmodic contractions of the facial muscles. 
 We have also, fairly frequently, such sensory irritation 
 phenomena as tinnitus, vertigo, etc. These points, as also 
 the general symptomatology of the nerves of special sense 
 of the brain-stem, which has been purposely left out of 
 consideration up to the present, will be dealt with in the 
 next section. In affections of the base of the brain (circum- 
 scribed meningeal inflammations must here be considered, 
 as well as tumours, gummata^ and tuberculous deposits), the 
 facial, abducens, and oculo-motor are the nerves most fre- 
 quently affected. Of the last-named, the fibres to the 
 levator palpebrae are apparently the most vulnerable, for 
 oculo-motor involvement generally' makes itself known, in 
 the first instance, by ptosis. Destruction of the pyramids 
 is exceedingly rare ; symptoms of sKght impairment of their 
 function come on gradually (spastic conditions, Babinski's 
 reflex, etc.). Only in the region of the cerebral peduncle 
 have lesions of the base any strong tendency to cause 
 destruction of the pyramid* so that, in these lesions, hemi- 
 
 s 
 
114 BING'S COMPENDIUM 
 
 plegia alternans oculo-motoria, or Weber's syndrome, is 
 often observed. 
 
 Though we have spoken of " irritative " affections of the 
 nerves of the brain-stem as characteristic of basal lesions, 
 we must not lose sight of the fact that they may, though 
 much more rarely, accompany internal lesions of the brain- 
 stem, such as haemorrhages. Even the cerebellar irritative 
 phenomena which we shall have to discuss later may be 
 sometimes observed as distant effects of lesions in the pons 
 and medulla. 
 
 Only a few words need here be devoted to the subject of 
 lesions of the corpora quadrigemina. As we have here, 
 crowded together in a small space, a number of important 
 structures (ooulo-motor and trochlear nuclei, median and 
 lateral fiUets, the red nucleus of the tegmentum, which has 
 important relations both with the cerebellum and the spinal 
 cord, and finally, as we shall see later, an important portion of 
 the optic tract), lesions in this region cause, simultaneously, 
 pupillary paralysis, paralyses of the external muscles of the 
 eye (frequently symmetrical and affecting separate corre- 
 sponding muscles on the two sides), ataxia, deafness, dis- 
 turbances of vision — many and varied symptoms, in fact, 
 which we shall discuss in detail later on. 
 
 An early symptom of pressure on the region of the 
 corpora quadrigemina (as a consequence, for example, of 
 tumours in the anterior portion of the cerebellum) is vertical, 
 upward nystagmus, of which we shall have more to say 
 later. The onset of symptoms of excitation of the sexual 
 system, abnormal growth of hair and development of fat, 
 abnormal height and premature development of the genital 
 organs in young individuals, points to the pineal gland or 
 epiphysis as the seat of a tumour pressing on the corpora 
 quadrigemina. This syndrome is regarded as the expression 
 of an alteration in the internal secretion of the pineal 
 gland ("dyspinealism "). 
 
 We cannot more appropriately conclude this section of our 
 work than by the diagrammatic representation, in transverse 
 sections of the brain-stem, of a few concrete cases of focal 
 lesions, with their clinical symptoms appended. A study of 
 the diagrams and of the accompanying table will serve as a 
 brief and concise recapitulation of the foregoing material. 
 
CEREBRAL LESIONS il5 
 
 II. POINTS OF IMPORTANCE, FROM THE POINT OF 
 VIEW OF LOCALIZATION, IN THE SYMPTOMA- 
 TOLOGY OF THE NERVES OF THE BRAIN- 
 STEM, WITH SPECIAL REFERENCE TO THE 
 DIFFERENTIAL DIAGNOSIS OF PERIPHERAL 
 AND CENTRAL LESIONS. 
 
 It will be necessary, seeing that signs of disturbance of the 
 oratiial nerves from the third to the twelfth are of such 
 marked significance in the regional diagnosis of lesions of 
 the brain-stem, to deal in still greater detail with certain 
 points in their symptomatology. The discussion must in- 
 clude, in the first place, isolated features of importance and 
 significance in the niceties of localization, which we have 
 been obliged up to now to leave out of consideration, and 
 in the second, others which are of weight from the broader 
 point of view of differential diagnosis. We must, in the 
 case of a lesion affecting nerves of the brain-stem, but 
 situated externally to that structure, avoid, so far as 
 possible, the mistake of overlooking its peripheral character 
 and regarding it as central. Finally, it wiU not be super- 
 fluous to describe, more exactly than we have been able to 
 hitherto, the clinical phenomena corresponding to lesions of 
 the cranial nerves. 
 
 In accordance with the foregoing, therefore, the nerves of 
 the brain-stem may be grouped as follows : 
 
 {a) The caudal group : Glosso-pharyngeal, vagus, acces- 
 sory, hypoglossal. 
 
 (6) Nerves of the cerebeUo-pontine angle : Auditory and 
 facial. 
 
 (c) Trigeminus. 
 
 {d) Nerves of the ocular muscles : Oculo-motor, trochlear, 
 abducens. 
 
 (a) The Caudal Group. 
 
 Let us first describe in their order the symptoms caused 
 by lesions of nerves in this group. 
 
 The hypoglossal may be briefly described as the nerve 
 supplying the muscles of the tongue. Its share in the 
 innervation of the sterno-hyoid, sterno-thyroid, and omo- 
 hyoid muscles is merely apparent. In the ao-called " ansa- 
 
IIG BING'S COMPENDIUM 
 
 Fm. 41. FiQ. 42. 
 
 Fia. 43. 
 
 Fio. 44. 
 
 Fias. 41-45. — Vide Table on opposite page. 
 
CEREBRAL LESIONS 
 
 117 
 
 6 
 
 6 
 
 o 
 
 ■<* 
 
 6 
 
 ! 
 
 
 Right. 
 
 Left. 
 
 Head. 
 
 — 
 
 Paralysis of accessory and 
 hypoglossal nerves (de- 
 generative). 
 
 Trunk and 
 Extremities. 
 
 Ataxia and superficial 
 anaesthesia. ' 
 
 Ataxia. 
 
 Motility intact. 
 
 Head. 
 
 Paralysis of facial and 
 abduoens nerves (de- 
 generative) ; conjugate 
 paralysis. 
 
 — 
 
 TEtTNK AND 
 
 Extremities. 
 
 — 
 
 Disturbances of superficial 
 sensibility. 
 
 Motilitj 
 
 intact. 
 
 Head. 
 
 Paralysis of facial and 
 hypoglossal nerves (not 
 degenerative). 
 
 Trigeminal anajsthesia 
 and degenerative paral- 
 ysis of the masticatory 
 muscles. 
 
 Trunk and 
 Extremities. 
 
 Hemiplegia. 
 
 — 
 
 Sensibility intact. 
 
 Head. 
 
 — 
 
 Paralysis of facial and 
 hypoglossal nerves (nol 
 degenerative). 
 
 Trunk and 
 Extremities. 
 
 — 
 
 Hemiplegia. - Sensory 
 disturbances. 
 
 Head. 
 
 Paralysis of facial and 
 hypoglossal nerves (not 
 degenerative). 
 
 Ooulo-motor paralysis (de- 
 generative) 
 
 Trunk and 
 Extremities. 
 
 Hemiplegia- 
 
 — 
 
 Sensibility intact. 
 
118 BING'S COMPENDIUM 
 
 hypoglossi," by which this innervation is effected, course no 
 fibres from the brain-stem, but only fibres from the upper- 
 most cervical nerves which have gained the hypoglossal 
 trunk by anastomosis. Bilateral hypoglossal paralysis 
 causes, of course, total glossoplegia : motionless, obeying 
 gravity merely, the tongue lies sunken on the floor of the 
 mouth ; speech is unintelhgible, and deglutition^ and masti- 
 cation very difficult. In unilateral paralysis (hemiglosso- 
 plegia), on the other hand, the disturbance of motility is 
 relatively trifling ; eating and speech are either not affected 
 at all, or only shghtly so. This is, of course, due to the 
 marked reciprocal intertwining of the muscle fibres of the 
 two halves of the tongue. If, however, the tongue is pro- 
 truded, one notices, in consequence of the partially un- 
 opposed action of the genio-glossus of the sound side, a 
 deflection of its tip towards the paralyzed side. 
 
 The accessory nerve supplies, unaided, the sterno-mastoid 
 muscle, while, in its innervation of the trapezius, it is 
 assisted by the upper cervical nerves. Destruction of the 
 accessorius, therefore, causes complete paralysis of the 
 sterno-mastoid. In unilateral lesions, then, we have in- 
 ability to draw the chin fully over to the opposite side, while 
 in bilateral lesions there is a tendency for the head to fall 
 backwards. The paralysis of the trapezius is, on the con- 
 trary, not complete, and betrays itself chiefly by weakness 
 and incompleteness in extension of the arm. 
 
 The vagus is a mixed nerve. On the one hand, it supplies 
 the muscles of the palate, pharynx, larynx, trachea, bronchi, 
 oesophagus, stomach, and smaU intestine, with motor fibres, 
 sends inhibitory fibres to the heart, and vaso-motor fibres to 
 numerous bloodvessels ; on the other, it is the sensory nerve 
 for the dura mater, the external auditory meatus, the lower 
 part of the pharynx, the larynx, the bronchi, the oesophagus, 
 and the stomach. In these organs, therefore, terminate the 
 fibres from the cells of the two vagal ganglia, the ganglion 
 jugulare and the ganghon nodosum vagi, which are to be 
 regarded as analogues of the ganglia of the sensory spinal 
 nerves. A complete bilateral paralysis of the vagus has, 
 as wiU be obvious from the foregoing, no symptomatology, 
 because it causes instant death. On the other hand, both 
 partial bilateral and complete unilateral paralysis of the 
 vagus may come under clinical observation. In the latter 
 
CEREBRAL LESIONS 119 
 
 case we shall find unilateral paralysis of the palate, pharynx 
 and larynx. One-half of the soft palate hangs flaccid, 
 with the result that the voice is nasal in character. One 
 vocal cord is immobile in the median or cadaveric posi- 
 tion, for the muscles which close, as well as those which 
 open the glottis, are put out of action. Owing to powerful 
 compensatory efforts on the part of the other vocal cord, 
 the voice may remain normal ; generally, however, it is 
 somewhat hoarse, and is apt to break into a falsetto. The 
 interference with deglutition is, on the other hand, almost 
 always of a trifling character, for hemipharyngoplegia is, in 
 consequence of the fact that the flbres of the pharyngeal 
 muscles of one side interlace with those of the other, of no 
 great functional significance. Tachycardia, or quickening 
 of the heart's action, is but rarely observed in unilateral 
 vagus lesions, and the same may be said of respiratory 
 disturbances, such as slowing and irregularity of respiration. 
 In incomplete vagal paralyses only some of the symptoms 
 above mentioned are present, and in some cases these only 
 partiaUy developed. Thus, instead of complete paralysis of 
 a vocal cord, we may have merely a paralysis of the crico- 
 arytenoideus posticus, whose function is to open the glottis. 
 The result of this " posticus paralysis," especially when 
 bilateral, is interference with respiration, phonation remaining 
 unaffected. The converse condition, aphonia with normal 
 respiration, seems only to flourish on the soil of hysteria. 
 
 The glosso-pharyngeal is an almost exclusively sensory 
 nerve, whose cells are situated in the ganglion superius and 
 ganglion petrosum glosso - pharyngei. According to the 
 latest researches, only a small motor portion is, in addition, 
 to be credited to it, which portion supplies the stylo- 
 pharyngeus, an elevator of the pharynx. The glosso- 
 pharjmgeal conveys sensory impressions from the upper 
 part of the pharynx and from the middle ear, as also gus- 
 tatory perceptions from the palate and the posterior third 
 of the tongue. Loss of taste in the latter regions is accord- 
 ingly the most important symptom of its interruption ; 
 anaesthesia of the pharynx may be detected, but especially 
 noticeable is the abolition of pharyngeal and palatine reflex, 
 which, however, is only of significance for localization if 
 unilateral. Bilateral abolition of these reflexes occurs, as 
 is well known, in purely functional affections. The stylo- 
 
120 BING'S COMPENDIUM 
 
 pharyngeus is of so little importance as an elevator of the 
 pharynx, a function which it shares with the pharyngo- 
 palatine muscle, that no motor disturbance of importance ia 
 to be expected as the result of a paralysis affecting it alone. 
 
 As regards irritative symptoms in the region of the caudal 
 group of nerves, they are one and all without real impor- 
 tance from the point of view of localization. Some of them 
 are to be referred, in almost every case in which they occur, 
 to the neuroses, and do not justify the diagnosis of an 
 organic irritative lesion of the affected structures. This is 
 especially true of the different forms of glossospasm, tonic 
 and clonic, and of spasms of the muscles supplied by the 
 accessorius (spasmus nutans, etc.). Pharyngismus, and 
 laryngismus and cesophagismus also, are hardly ever to be 
 referred to a localized lesion of the vagus. When these 
 conditions do not depend on a general functional or organic 
 nervous disease (hysteria, tetany, tabes, hydrophobia, teta- 
 nus), they are as a rule reflex phenomena due to disease 
 of the affected portions of the respiratory and digestive 
 tracts. On the other hand, we are perfectly justified in 
 regarding bradycardia, Cheyne-Stokes respiration, and 
 cerebral vomiting, as irritative symptoms originating in the 
 vagus cells in the meduUa. (For example, the vomiting 
 caused by injections of apomorphine fails to take place if, 
 as in bulbar paralysis, etc., the vagus nucleus has itself 
 suffered damage, and, conversely, the bradycardia due to 
 vagus irritation — in contrast to that present in lesions of 
 the atrio- ventricular bundle in the heart — may be controlled 
 by an injection of atropine.) Nevertheless, significance from 
 the point of view of localization must be denied also to these 
 morbid phenomena ; they may, in consequence of the appar- 
 ently extraordinary sensitiveness of the vagus nucleus, come 
 on as the result of any intracranial affection which causes 
 pressure on the brain, whatever be its actual situation. They 
 are therefore generally — and rightly — ^reckoned among the 
 symptoms, not of focal, but of general diseases of the brain. 
 
 If, then, the irritative symptoms are to be withdrawn 
 from our consideration, it becomes aU the more important, 
 where symptoms pointing to morbid processes in the region 
 of the cranial nerves IX. to XII. are present, to determine 
 where interruption of their continuity has taken place — 
 whether between the cerebrum and the medulla (supra- 
 
CEREBRAL LESIONS 121 
 
 nuclear), or in the region of the bulbar nuclei (nuclear), or, 
 again, beyond these, in the peripheral portion of the nerve's 
 course (infranuclear). In the latter case it is practicable, 
 and, of course, immensely important, to distinguish between 
 intracranial and extracranial lesions. 
 
 Supranuclear lesions are, so far as motor symptoms are con- 
 cerned, to be diagnosed first and foremost from the absence of 
 degenerative atrophy and the reaction of degeneration in the 
 affected muscles. Importance is also to be attached to the 
 determination of an increased irritability to mechanical and 
 electrical stimuli. These points are of general application. 
 A special imprint is given to supranuclear paralyses of the 
 nerves we are now considering by the fact that their cortico- 
 bulbar innervation is a bilateral one. Each cerebral hemi- 
 sphere, that is to say, shares in the innervation of the nuclei 
 of both sides. This is particularly the case with the vagus, 
 and, in consequence, unilateral interruptions of the tracts 
 leading from the cortex to the nucleus ambiguus present no 
 cUnicaUy demonstrable disturbances, inasmuch as the one 
 hemisphere remaining in unbroken communication with the 
 nuclei of both sides suffices to maintain in functional 
 efficiency the pharyngeal and laryngeal muscles on the side 
 of the lesion as well as on the opposite side {vide Fig. 46). 
 
 If, then, we have before us a unilateral pharyngo- and 
 laryngoplegia we may, without waiting for an electrical 
 test, conclude against the supranuclear nature of the 
 paralysis. It is almost the same with the accessorius and 
 the hypoglossus. Thus it will be found that, in cerebral 
 hemiplegias, the functions of the sterno-mastoid are gene- 
 rally as little affected as are those of the glottis and the 
 mechanism of deglutition. Here then, also, we have com- 
 plete bilateral innervation from the cortex. The trapezius, 
 it is true, usually only escapes unilateral paralysis so far as its 
 upper or clavicular portion is concerned. Only this portion, 
 which is distinguished as the respiratory portion, seems, 
 therefore, to share in the bilateral cortical innervation, the 
 remainder of the muscle being dependent not only on the 
 accessory, but also on the upper cervical nerves. Finally, 
 unilateral nuclear and infranuclear paralysis of the hypo- 
 glossal causes no serious disturbance of motility, a conse- 
 quence, as stated on p. 118, of the reciprocal intertwining 
 of muscle fibres of the two halves of the tongue. In the 
 
122 
 
 BING'S COMPENDIUM 
 
 case of supranuclear lesious, the fact that each hypoglossal 
 nucleus is innervated from both cerebral hemispheres 
 (though predominantly from the opposite cortex), tells in the 
 same direction. It is therefore not to be wondered at that, 
 in cases of the latter kind — cerebral hemiplegia, for example 
 — ^the functional disturbances in the region of the hypoglossal 
 
 Fig. 46. 
 
 Cer.trum cortical 
 larj-ngis 
 
 Centrum coiticalft 
 laryngifi 
 
 Radices nervi vagi ad laryngem 
 
 Radices nervl vagri ad laryngem 
 
 The Laryngeal Centre in the Nucleus Ambiguus. 
 
 Diagram showing bilateral supranuclear innsrvation. 
 (A unilateral supranuclear lesion X cannot cause laryngeal paralysis.) 
 
 are very trifling, and, as a rule, only reveal themselves in a 
 deflection of the protruded tongue toward the paralyzed side. 
 Bilateral interruption of their supranuclear tracts causes, 
 as will be plain from the foregoing, a bilateral paralysis 
 or paresis of the nerves under review, with serious motor 
 impairment in the pharynx, larynx, and tongue. This im- 
 pairment resembles that observed in lesions of the bulbar 
 nuclei. The symptoms have therefore been spoken of as 
 
CEREBRAL LESIONS 123 
 
 " pseudo-bulbar-paralytic." They may be brought about 
 in two ways : (1) By simultaneous symmetrical interrup- 
 tion of cortico-bulbar tracts. (2) Unilateral interruption, 
 which, owing to the bilateral innervation of the affected 
 nuclei, leaves the functions of the latter undisturbed, is 
 complicated later on by a similar interruption on the other 
 side, and immediately " pseudo-bulbar " symptoms mani- 
 fest themselves, of course on both sides. 
 
 It will help to the presentation of a clear and coherent 
 account of the symptom-complex known as " pseudo-bulbar 
 paralysis," if we allow ourselves here a sKght digression. 
 We will anticipate somewhat by stating that the motor 
 trigeminus, thus the masticatory musculature, has, like the 
 vagus, a bilateral cortical innervation ; further, that uni- 
 lateral interruption of the cortico-bulbar tract for the lowest 
 portion of the facial (orbicularis oris) causes a hemiparesis 
 of the latter, but only a bilateral interruption can produce 
 a disturbance of the function of the lips, as organs of speech, 
 at all approaching in severity that observed in bulbar 
 paralysis (vide infra, p. 127). The nervous structures just 
 mentioned, then, suffer, in pseudo-bulbar paralysis, an 
 impairment of function quite analogous to that observed in 
 the caudal group of oblongata nerves. The chnical picture 
 presented by pseudo-bulbar paralysis (also called " glosso- 
 pharyngo-labial paralysis ") is, in consequence, extremely 
 characteristic, and is constituted as foUows : Speech is 
 drawhng or dragging, monotonous, sometimes aphonic. 
 Consonants are pronounced badly and with difficulty, so 
 that in severe cases speech is unintelligible. Vowel forma/- 
 fcion is less seriously interfered with. The breath is often 
 lost while speaking, so that several attempts have to be 
 made before a sentence is completed, and speech is semi- 
 explosive. According as the paralysis of the lips or that 
 of the palate is predominant, so we have prevaihng either 
 difficulty in forming labials or a nasal quahty of voice. 
 The motility of the tongue may be so impaired that it hes 
 motionless on the floor of the mouth ; generally, however, a 
 certain power of protrusion is left, but the movements to 
 one side or the other or the power of curving the sides in- 
 wards to form a tube, are affected, or repeated protrusion 
 soon leads to inability to continue the movement. (In 
 many cases the interruption of the bilateral cortical tracts 
 
124 BING'S COMPENDIUM 
 
 is only partial.) The movements of the palate are either 
 abolished or are slow and incomplete ; in the larynx, paresis 
 of the vocal cords seldom reaches the more severe degrees. 
 The muscles of mastication are generally more markedly 
 affected ; it is impossible to clench the teeth firmly, and 
 the mouth often remains half open. The paralysis of the 
 pterygoids reveals itself by incapacity for protrusion and 
 lateral movement of the lower jaw ; occasionally the muscles 
 which open the mouth are also paralyzed, and it is impossible 
 to open the mouth completely or against resistance. Very 
 significant symptoms are often noticed when the attempt 
 is made to take food. Here, in addition to the weakness 
 of the masticatory muscles, that of the muscles of the tongue, 
 lips, and cheeks, plays an important role. The food cannot 
 be pushed between the rows of teeth, falls out of the mouth, 
 has to be passed to the back of the mouth with the help of 
 the fingers, and so on. If, in addition, there is paralysis of 
 the palate and pharynx, portions of food find their way into 
 the larynx and the nose. In the less severe cases, however, 
 especially if the patient eats slowly and chooses solid or 
 only semi-liquid foods, the act of eating is carried out fairly 
 weU. The essential difference between these conditions and 
 those found in true bulbar paralysis is that in the former 
 the paralyzed muscles exhibit neither degenerative atrophy 
 nor the reaction of degeneration. It is, in fact, mutatis 
 mutandis, the same difference as exists between spinal pro- 
 gressive muscular atrophy and spastic spinal paralysis. A 
 condition of genuine contracture may, as a matter of fact, 
 gradually supervene in the lips, tongue, or palate, of 
 patients suffering from pseudo-bulbar paralysis. Exaggera- 
 tion of the masseter reflex is hardly ever absent, and re- 
 quires no explanation here. 
 
 We pass now to the nuclear paralyses of the caudal group 
 of nerves, which, as we have seen, are readily distinguished 
 from the supranuclear. The reaction of degeneration is 
 easily demonstrated in the tongue, the sterno-mastoid, and 
 separate bundles of fibres of the trapezius ; with somewhat 
 more difficulty in the palate and pharynx. In the larynx 
 only a highly skilled specialist wiU succeed in demonstrating 
 it with certainty ; in practice we must content ourselves 
 with the demonstration that powerful electrical stimulation 
 of the recurrent laryngeal nerve in the neck causes no 
 
CEREBEAL LESIONS 125 
 
 adduction of the vocal cords. In the tongue, which of all 
 muscles is the most easily inspected and palpated, we soon 
 notice loss of volume, abnormal wrinkUng of the surface, 
 softness, flabbiness, and fibrillary twitchings. 
 
 Not so simple is it to distinguish nuclear from infra- 
 nuclear lesions — that is to say, from those affecting the 
 nerves under consideration at some point or other of their 
 peripheral course. Electro-diagnostic tests for the reaction 
 of degeneration and the search for degenerative atrophy 
 ahke fail us here utterly, for, so far as those phenomena are 
 concerned, it is immaterial whether the nucleus is afEected 
 or its corresponding nerve trunk at some part of its periph- 
 eral course. If the nature and situation of the injury or 
 disease do not betray at once the infranuclear character of 
 the paralysis present, we must depend on a consideration of 
 the remaining symptoms for guidance. The medulla is so 
 small in volume that an isolated nuclear paralysis of either 
 the glosso-pharyngeal, vagus, accessory, or hypoglossal nerve 
 is hardly ever seen. Where, however, we have uncombined 
 affections of these nerves, motor and sensory disturbances, 
 for themost part of the type of " alternating " paralyses, are 
 generally also present. Further, the two hypoglossai nuclei 
 (right and left) are so close to one another that a nuclear 
 lesion generally causes bilateral paralysis of the tongue. A 
 fact of great importance is that, in nuclear as distinguished 
 from infranuclear lesions of this nerve, the hypoglossal 
 paralysis is combined with a paresis of the orbicularis oris 
 of the same side. We must conclude, therefore, that in the 
 innervation of the orbicularis oris, not only the facial, but 
 also the hypoglossal nucleus participates, the former send- 
 ing off fibres within the medulla to join the facial trunk. 
 
 Combined paralyses of the various nerves of the caudal 
 group may result also from lesions whose situation is infra- 
 nuclear, but intracranial (tumours, aneurysms, exudates, 
 etc., in the posterior cranial fossa). We find the character- 
 istic symptom-complex of palatal, laryngeal, and lingua* 
 paralysis ; the sterno-mastoid and trapezius are sometimes 
 affected,* but the orbicularis oris remains intact. For the 
 
 * A pharyn^o-laryngeal or glosso-pharyngo-laryngeal hemiplegia is 
 known as AvelH's " syndrome " ; if to it is added a homolateral paralysis 
 of the stemo-mastoid and trapezius, the symptom-complex is Imown as 
 Schmidt's. 
 
126 BING'S COMPENDIUM 
 
 rest, the basal situation of the lesion is indicated by the order 
 in which the symptoms develop {vide p. 113). 
 
 After their exit from the cranial cavity, the conditions 
 necessary for the simultaneous destruction of several of 
 the nerves under review are very rarely found. The 
 morbid process must have its seat high up in the neck, 
 and will generally lend itself readily to direct inspec- 
 tion, palpation, and Roentgenoscopy. As regards lesions 
 affecting single members of the caudal group of nerves at 
 some point of their peripheral course, these generally cause 
 only partial paralyses, as the nerve branches proximal to the 
 seat of the lesion of course escape. Thus, disturbances of 
 the mechanism of deglutition are very rarely found in extra- 
 cranial affections of the vagus ; if the nerve is injured in the 
 mediastinum (by tumours, aortic aneurysm, etc.), the picture 
 presented is generally one of paralysis of the recurrent 
 laryngeal only — immobility of the vocal cord in the mid- 
 position. Exactly the reverse is true of the hypoglossal 
 nerve. If it is affected at or below the point at which the 
 fibres from the upper cervical roots join the ansa hypoglossi, 
 we have symptoms which are otherwise foreign to the picture 
 of hypoglossal paralysis — namely, paralyses of the external 
 laryngeal muscles which are innervated from the ansa 
 (sterno-hyoid, ster no-thyroid, and omo-hyoid), recognizable 
 by the degenerative atrophy of the muscular layer covoring 
 the thyroid cartilage, and by the lateral displacement of the 
 larynx in the act of swallowing. 
 
 (6) The Nerves of the Cerebello-Pontine Angle. 
 
 (a) The Facial Nerve, 
 
 This nerve supplies all the facial muscles — ^including the buc- 
 cinator, but excepting the levator palpebrse superioris, which 
 is supplied by the oculo-motor nerve — from the occipito-fron- 
 talis down to the platysma myoides, and, in addition, the stylo- 
 hyoid, the posterior belly of the digastric and the stapedius. 
 
 A lesion interfering with the motor function of the facial 
 nerve causes facial paralysis, which, when unilateral, is known 
 as " monoplegia facialis, " when bilateral as " diplegia facialis." 
 It is also known as "Bell's paralysis." The paralyzed side 
 of the face is masklike, immobile, expressionless ; the naso- 
 labial fold is smoothed out ; the forehead cannot be wrinkled ; 
 
CEREBRAL LESIONS 127 
 
 the eye, in consequence of the paralysis of the orbicularis 
 oculi, cannot be closed (lagophthalmus) ; the angle of the 
 mouth hangs downwards. The falHng of the base of the 
 tongue betrays the paralysis of the stylo-hyoid and posterior 
 belly of the digastric, an abnormal acuity of hearing and 
 special sensitiveness to deep tones, {oxyahoia, hyper akusis), 
 that of the stapedius, whose function it is to close the fenestra 
 ovalis of the tympanic cavity with the plate of the stapes. 
 
 The facial trunk, however, brings with it from its place of 
 origin other centrifugal fibres, namely : 
 
 1 . Lachrymal Fibres. — These fibres leave the facial trunk as 
 it passes through the cranial wall (Fallopian canal), coming 
 off from the geniculate ganglion as the nervus petrosus super- 
 ficiahs major, and joining the nervus lachrymahs trigemini. 
 
 2. Salivary Fibres. — -Ihete form a complex known as the 
 " nervus intermeiius of Wrisberg " or as " Sapolini's 
 nerve " {cf. also infra, p. 143). These fibres also leave the 
 facial trunk in the FaUopian canal, but at a point only 
 just above the stylo- mastoid foramen. They also join 
 the trigeminal system, the resulting anastomosis forming the 
 chorda tympani, through which the salivary fibres of the 
 facial reach the nervus lingualis trigemini . 
 
 Between the points at which these two nerves {petrosus 
 superficialis major and chorda tympani) leave the facial trunk, 
 a further bundle of nerve fibres joins it, which belongs strictly 
 to another nerve, the trigeminal, and only runs for a short 
 distance with the facial, returning then to the trigeminus . Its 
 fibres are centripetal ; they are, in fact, the gustatory fibres 
 from the anterior two-thirds of the tongue. From the lingual 
 they pass along the chorda tympani to the facial trunk in the 
 Fallopian canal, where they join the motor and sahvary fibres 
 of the facial to form a common trunk. They pass upwards to 
 the geniculate ganghon, which they enter. The latter does not 
 therefore, strictly speaking, belong to the facial, for centrifugal 
 nerves have no ganglia.* From the ganghon these gustatory 
 fibres, accompanied by the lachrymal fibres of the facial, pass 
 along the superficial petrosal nerve to the trigeminus again . If 
 
 * According to the view which classes the N. intermedins as a mixed 
 n^rve, cdntaining gustatory as well as secretory fibres (vide note, p. 143 ), 
 the geniculate ganghon must be regarded as belonging partly to the 
 intermedins. 
 
128 
 
 BING'S COMPENDIUM 
 
 To the 
 N. lacrsmal. 
 trigem. 
 
 Back to the Trigeminus 
 
 To the N. lingualh trig. 
 
 ScUEMA SHOWIUO THE COUESE OF THE VARIOUS GeOUPS OF FlBEES IS TUB 
 
 Facial Tehnk. 
 
 A. = Aoustious. 
 F.=Facialig - 
 
 ■{— 
 
 = Motor fibres. 
 ins = Lachrymal fibres. 
 = Salivary fibres. 
 
 *i.=Gangl. genio - PB'WM' = Gustatory fibrea. 
 
 they are involved in a lesion during their short passage along 
 the facial trunk, the clinical sign of their interruption (loss or 
 diminution of taste in the anterior two-thirds of the tongue) 
 accompanies, though foreign to the function of the facial, 
 
CEREBRAL LESIONS 129 
 
 the ordinary signs of facial paralysis — " caught together, 
 hanged together." * 
 
 These peculiarities of the peripheral course of the facial 
 and its several components are represented diagrammaticaUy 
 in Fig. 47. The central, supranuclear course of the nerve 
 also presents some rather complicated features : 
 
 1. Those portions of the facial nucleus from which the 
 upper facial fibres arise — i.e., the frontal and palpebral 
 branches — are innervated, like the laryngeal centre in the 
 nucleus ambiguus represented in Pig. 46, from the cortex 
 of both cerebral hemispheres. The frontal muscles present 
 a true type of bilateral synergetic action ; the orbicularis 
 ocuU also is, under ordinary circumstances, always con- 
 tracted simultaneously on both sides ; the separate closing 
 of one eye is, as is well known, an action that has to be 
 specially learnt. The lower facial, on the other hand 
 (mouth and cheeks), has a crossed cortical innervation ; in 
 eating, mimicry, etc., corresponding muscles on the two 
 sides are very often quite unsymmetricaUy employed. 
 
 2. The hypoglossal nucleus sends some fibres to the portion 
 of the facial which supplies the orbicularis oris. When, 
 therefore, a labial paresis is associated with nuclear paralysis 
 of the hypoglossal, it is not necessary to assume an affection 
 of the facial, unless other signs of the same are present. 
 
 Fig. 48 illustrates the supranuclear innervation of the 
 facial. 
 
 The anatomico-physiological conditions presented by the 
 facial as above described, (a) in its central, (6) in its periph- 
 eral course, enable us to diagnose, from the cHnical picture 
 presented in any given case, the point at which an interrup- 
 tion of continuity in the facial system has taken place. We 
 have endeavoured to represent the matter in tabular form. 
 A recollection of what has just been stated, and an occasional 
 reference to Figs. 47 and 48, wiU make the table intelligible, 
 and render superfluous any detailed explanation thereof. 
 
 The irritative phenomena observed in the region of the 
 facial — spasmodic contractions, twitchings — ^have, as a rule, 
 
 * In regard to vaso-motor fibres in the facial trunk and others connected 
 with the sweat function, vide infra in the section on the Trigeminus, where, 
 also, the question of the entry of gustatory fibres from the chorda tympani 
 into the nuclear region of the N. *ntermedius is discissed (note, p. 143^, 
 
 9 
 
13U 
 
 BING'S COMPENDIUM 
 
 Fio. 48. 
 
 Centrum corti 
 cale facitii 
 
 Schema showing Central Innbevation of the Facial Nebvb. 
 
 ^3B ~ Upper facial. 
 mm^ =-- Lower facial. 
 
 y 
 
 no significance from the point of view of localization ; for in 
 the great majority of cases they are of functional, neurotic 
 character (tetany, spasmodic tics, etc.), or are reflex phe- 
 nomena having their originating stimulus in painful affeo- 
 
CEREBRAL LESIONS 
 
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132 BING'S COMPENDIUM 
 
 tions of the face, mouth, etc. Even if we assume an organic 
 cause for the spasmodic contractions in the region of the 
 facial which are observed in the initial stage of progressive 
 paralysis, we have as yet no certain knowledge concerning 
 the material lesion on which they may depend. On the other 
 hand, spasmodic facial contractions have been observed 
 as the result of pressure on the intracranial facial trunk by 
 tumours, aneurysms, etc. They may also be produced by 
 irritation of the nerve in its peripheral course, due to con- 
 tracting scars on the face — e.g., duelling wounds (Mensur- 
 verletzungen). Finally, we shall see later, when we come 
 to discuss the subject of cortical epilepsy, that such irritative 
 symptoms are a frequent consequence of irritative lesions 
 of the facial centre in the cortex. In late stages also of 
 incomplete facial paralyses, of whatever causation, spasmodic 
 contractions may come on in the paralyzed muscles. 
 
 (/3) The Auditory Nerve. 
 
 In the section on the Structure of the Brain-Stem different 
 portions of the cochlear and vestibular mechanism have been 
 dealt with separately as they have come under our notice. 
 We must now briefly consider, in its continuity, the course 
 followed by each of these components of the auditory nerve. 
 
 The cochlear nerve originates from cells in the spiral 
 ganglion of the cochlea. These are bipolar cells whose 
 peripheral extensions are in connection with the auditory 
 ^ells of the organ of Corti, while their central extensions 
 enter the cochlear nucleus in the cerebeUo-pontine angle. 
 Here, with connecting neurons of the second order, begins 
 the central auditory tract. The manner in which this 
 passes across to the fillet of the opposite side is shown in 
 Fig. 49. The fibres from the dorsal portion of the cochlear 
 nucleus (acoustic tubercle) make their way under the floor 
 of the fourth ventricle, where they form the strice meduUares 
 or acusticcB ; those from the ventral portion pass through 
 the base of the tegmentum pontis, where, in the olive, 
 connection is made with fresh neurons. These latter fibres 
 are known as the "fibres of the trapezium." Both sets 
 of fibres, after reaching the fillet, pass in the form of the 
 lateral fillet and fillet of Reil to the posterior corpus quadri- 
 
CEREBRAL LESIONS 
 
 133 
 
 £ 
 
134 BING'S COMPENDIUM 
 
 geminum and its intimately related corpus geniculatuia 
 mediale, from which structures the terminal fibres of the 
 whole neuron chain of the acoustic tract pass to the cortical 
 auditory centre in the temporal convolutions. 
 
 The vestibular nerve has its origin in the ceUs of the 
 vestibular gangHon, which are connected peripherally with 
 the sensory epithelium of the ampullae, utricle, and saccule. 
 Its terminal ramification takes place in the vestibular 
 nucleus. The cells of the latter, however, send fibres to the 
 neighbouring nucleus of Deiters of the same side, from which 
 they finally pass to the vermis cerebeUi (Fig. 49). 
 
 As is plain from the foregoing, the vestibular mechanism 
 is in the closest anatomical connection with the cerebellum. 
 Their co-operation, also, in the maintenance of equihbrium 
 and the sense of position in space, establishes between them 
 so close a physiological unity, that the symptomatology of 
 the vestibular system must be left to be dealt with later, in 
 the section on the cerebellum. 
 
 Here, therefore, we wiU concern ourselves only with the 
 actual nerve of hearing, the cochlear nerve. Impairment 
 of the function of the cochlear brings with it, of course, 
 deafness, partial or complete. As, however, deafness may 
 be due to affections of the conducting apparatus of the 
 middle and outer ear, which are entirely within the province 
 of the aurist, our first task will be to consider carefully the 
 characters distinctive of the so-called " nerve " deafness.* 
 
 The two most important distinguishing features of nerve 
 deafness are loss or diminution of the ability to hear by 
 conduction through the bones of the skuU, and diminution 
 in the power of tone perception. 
 
 The first of these conditions is most easily investigated 
 by determining the length of time during which (a) the 
 patient, (6) the normal-hearing observer, can perceive the 
 sound of a vibrating tuning-fork, the handle of which is 
 placed against the vertex, the teeth, or the mastoid process. 
 This is known as Schwabach's experiment. If nerve deafness 
 is present, we have a shortening of the period during which 
 
 * Between nerve deafness (sensu strictiori) — namely, that due to lesions of 
 the cochlear nerve or its supranuclear tracts — and that due to lesions of the 
 percipient structures in the cochlea, no symptomatological distinction can he 
 drawn. From the neurological point of view, therefore, the regional diagnosis 
 of lesions of the auditory mechanism must be regarded as wanting in precision. 
 
CEREBRAL LESIONS 135 
 
 the sound can be perceived by bony conduction, or, if the 
 deafness be complete, a total aboHtion of such perception. 
 In affections of the middle ear, on the other hand, the 
 tuning-fork, applied after Schwabach's method, is heard for 
 a longer period than normal. This test can, of course, only 
 be applied diagnostically if the affection of hearing is 
 bilateral. 
 
 Other tests easily and quickly apphed are Rinne's and 
 Weber's tests. 
 
 In Rinne's test a vibrating tuning-fork is held in contact 
 with the mastoid process of the subject under examination ; 
 when he ceases to hear it there, it is held close to his ear. If 
 the hearing is normal, the subject now hears the tuning-fork 
 again. This is spoken of as the " positive " result of 
 Rinne's test. In disease of the sound collecting and con- 
 ducting apparatus of the ear, nothing is heard in this second 
 stage of Rinne's test. This is the " negative " result. In 
 nerve deafness, on the other hand, one generally obtains 
 "positive Rinne," unless of course the impairment of 
 hearing has reached a high degree, in which case hearing 
 by air conduction is also markedly impaired or aboHshed. 
 
 In Weber's test, the inferences connected with which are 
 more clearly defined, a vibrating tuning-fork is apphed to the 
 vortex. A normal subject wiU hear the sound in both ears ; 
 if one ear be now stopped, he wiU " lateralize " the sound 
 to the side on which air conduction has been thus broken. 
 A patient with disease of the conducting apparatus " lateral- 
 izes " spontaneously to the affected side {"positive Weber"); 
 while, on the other hand, the patient with nerve deafness wiU 
 lateralize to the sound side (" negative Weber "). 
 
 Affections of tone perception are investigated by means 
 of the so-called " Galton's whistle.' ' Deafness for the higher 
 notes is characteristic of affections of the labyrinth and 
 auditory nerve tracts, as distinguished from those of the 
 middle and outer ear. In nervous deafness the hearing for 
 words with sharp consonants and clear short vowel sounds 
 is specially affected — e.g., "sister," "twenty," "fish," etc. 
 — ^while those with broader consonant and vowel sounds 
 ("brood," "hundred," "ears," "dawn," "worm," etc.) 
 are much better heard and understood. The opposite is 
 the case in non-nervous deafness. 
 
136 BING'S COMPENDIUM 
 
 That the diagnosis of nerve deafness is also made by 
 exclusion, after examination of the membrana tympani, 
 after finding that inflation by Politzer's bag produces no 
 improvement, etc , is of course well known. Opinions are 
 still divided as to the value of the curious symptom known 
 as " parakiisis Willisii " in the diagnosis of nerve deafness. 
 Many otologists hold that patients suffering from nerve 
 deafness hear better in noisy places ; others, however, main- 
 tain that the symptom may be present in uncomplicated 
 middle-ear diseases. 
 
 The irritative symptoms to be referred to the cochlear 
 nerve are of the nature of subjective noises in the ear 
 (tinnitus aurium). The noise may be of a roaring, buzzing, 
 or whisthng character, and may be located by the patient 
 in the interior of the ear, or may seem to be external. These 
 subjective phenomena are of httle help in localization, as 
 they are present also in many cases of middle-ear disease. In 
 ankylosis of the stapes, for example, there is generally severe 
 tinnitus, due to a continuous irritation of the neighbouring 
 organ of Corti. At the same time singing in the ears (the 
 note is generally of very high pitch), is so constant an accom- 
 paniment of nervous deafness, that some authorities have 
 held that, in any case in which there is no history of tinnitus, 
 the deafness may be regarded, from that fact alone, as in 
 aU probability not nervous in character. 
 
 Where, however, it is estabhshed that we have to deal 
 with a case of nerve deafness, it is only possible to infer with 
 certainty an affection of the auditory nerve trunk when 
 accompanjang symptoms point to a basal morbid process. 
 In such cases a simultaneous affection of the vestibular nerve 
 is most probable. (As wiU appear more fully later on, 
 affections of the vestibular nerve reveal, themselves by 
 phenomena of the nature of vertigo.) The facial and other 
 of the cranial nerves are Hkely, however, to be involved 
 as well, and symptoms referable to the oblongata, the pons, 
 and even the cerebellum, are hkely to show themselves in 
 a manner which gives a special character to affections of 
 the cerebello-pontine angle, and somewhat facilitates their 
 diagnosis. 
 
 We have here chiefly to deal with tumours, especially 
 fibromata and fibro-sarcomata, arising from the nerve 
 sheaths of the facialis and acusticus at their emergence. 
 
CEREBRAL LESIONS 
 
 137 
 
 Fig. 50. 
 
 Diagram of the Cbntbal Tbigemdius Tbaotb. 
 SenBOiy tracts, light ; motor tracts, thick. 
 
138 BING'S COMPENDIUM 
 
 The clinical picture developed by such tumours is dis- 
 tinguished by the following symptoms, for whose explana- 
 tion later sections must be referred to (trigeminus, nerves of 
 the ocular muscles, cerebellum, etc.): Inability to direct the 
 eyes towards the side on which the lesion is situated, nystag- 
 mus, the movements being directed towards the affected 
 side. Absence or diminution of reflexes and of sensation in 
 the sphere of the fifth nerve, nervous deafness, adiadocho- 
 kinesia on the affected side ; choked disc, cerebellar ataxia 
 and pains at the back of the head, often confined to the 
 affected side, or more strongly developed there. 
 
 (c) The Trigeminus. 
 
 We know that the trigeminus has an anterior, motor, and 
 a posterior, sensory root. While the latter, in strict analogy 
 with the posterior roots of the spinal cord, forms a ganglion — 
 the ganglion of Gasseri — the anterior or motor root passes 
 behind the ganglion to join the third of the three main 
 branches which issue from it, and to confer on it, in so 
 doing, the character of a mixed nerve. 
 
 In the Gasserian gangUon are situated the cells of origia 
 of the fibres of the sensory root. Of these, part terminate, 
 as is seen in Fig. 50, in the nucleus of the locus coeruleus, 
 while part make their way downwards as the spinal root 
 of the trigeminus, giving off as they go terminals which 
 enter the nuclear column known as the substantia gelatinosa. 
 
 From the two sensory nuclei {locus ccsruleus and svh- 
 stantia gelatinosa), the trigeminal neuron tracts of the second 
 order pass across the middle hne to the fillet of the opposite 
 side, in which they pass to the thalamus. Here finally 
 arises a tertiary neuron system which terminates in the 
 cortical sensory centre for the trigeminus. 
 
 It can be seen clearly from Fig. 50 that the supranuclear 
 or cortico-pontine innervation of the motor trigeminus is a 
 bilateral one. 
 
 The structures innervated with sensory fibres from th© 
 three main branches of the trigeminus are — 
 
 {a) The first or ophthalmic branch. 
 
 {a) The cutaneous area, marked 1 in Fig. 51. 
 (/3) Conjunctiva, cornea, and iris. 
 (7) The mucous membrane of the frontal sinuses 
 and the upper portion of the nose. 
 
CEREBRAL LESIONS 
 
 139 
 
 {b) The second or maxillary branch. 
 
 (a) The cutaneous area — 2, Fig. 51. 
 03) The mucous membrane of the antrum of 
 Highmore and the lower portion of the 
 
 nose. 
 
 (7) The mucous membrane of the upper jaw, 
 
 and the soft palate up to the pharyngeal 
 arch. 
 
 (8) The upper teelh. 
 
 Fio. 51. 
 
 The Sbnsoky Nerve-Sitpply of the Head. 
 
 {1. Ramus ophthalmicus. 
 2. Ramus maxillaris. 
 3. Ramus mandibularia. 
 White: Vagus. V.=Nervus aurioularis vagi. 
 
 I =N. occipitalis major. 
 Black : Cervical nerves^ 0'=N. occipitalis minor. 
 
 La =N. auricularis magnus. 
 
 (r^ The third or mandibular branch. 
 
 [a) The cutaneous area — '3, Fig. 51. 
 
 (y8) The mucous membrane of the cheeks, lower 
 
 jaw, floor cf the mouth, and tongue. 
 (7) The lower teeth. 
 
140 BING'S COMPENDIUM 
 
 Total or partial destruction of one of the three branches 
 leads, of course, to anaesthesia or hypsesthesia in the struc- 
 tures inneWated from that branch. Further, in lesions 
 of the ophthalmic branch, the conjunctival and corneal 
 reflexes are abolished, as also the sternutatory reflex evoked 
 by irritating the upper part of the nasal mucosa ; in lesions 
 of the maxiUary branch the sneezing reflex evoked by irrita- 
 tion of the lower nasal mucous membrane is abolished, as well 
 as the anterior palatal reflex. It must be borne in mind, 
 however, that the latter is inconstant, and is often absent 
 in functional neuroses. The same is true of the conjunctival 
 and corneal reflexes, and even the reflex excitabihty of the 
 nasal mucosa is subject to individual variations. For this 
 reason it is only to unilateral absence of these phenomena 
 that decisive significance can be allowed. It should be 
 remembered also that the pricking sensations felt on smeUing 
 ammonia or acetic acid are due to irritation of the sensory 
 nerve endings of the trigeminus in the nasal mucosa, and 
 have nothing to do with the olfactory nerve. They are 
 absent in trigeminal lesions, as are also the reflex symptoms 
 evoked by them (lachrymation, alterations in the pulse- 
 rate, catching of the breath, etc.). 
 
 The trigeminus, in addition to its ordinary sensory 
 .^unctions, acts as a nerve of special sense. The mandibular, 
 or rather one of its branches, the lingual nerve, conveys 
 gustatory sensations from the anterior two-thirds of the 
 tongue. We have described above (p. 127) how its fibres 
 pass, with the chorda tympani, to join the facial trunk, 
 in which they pursue a short course, leaving it again and 
 rejoining the trigeminal system. This reunion takes place 
 in the spheno-palatine ganglion of the maxillary branch, 
 with which branch the lingualis fibres pass into the Gas- 
 serian ganghon and the nuclear region of the trigeminus. 
 The question whether they remain there, or whether they 
 reach finally the glosso-pharyngeal, is of no cUnical im- 
 portance. 
 
 The structures innervated from the motor portion of the 
 third branch of the trigeminus are — 
 
 (a) The muscles of mastication. 
 
 (b) The anterior belly of the digastric and the mylo- 
 
 hyoid muscle. 
 
 (c) The tensor tympani and tensor veli palatini muscles. 
 
CEREBRAL LESIONS 141 
 
 Unilateral paralysis of the muscles of mastication is 
 ioiown as "monoplegia masticatoria." In this condition 
 lateral movement of the lower jaw is only possible towards 
 the paralyzed side, because only the pterygoids on the 
 sound side can act. With a finger placed on the masseter 
 and the temporal muscle, it is easy to satisfy oneself of the 
 absence of contraction in those muscles. In diplegia 
 masticatoria the lower jaw falls and aU lateral movement 
 ceases. Further, the mandibular reflex is abohshed — the 
 contraction of the masseter which can be evoked in most 
 normal individuals by percussing the finger placed along the 
 lower row of teeth. 
 
 Paralysis of the anterior belly of the digastric and of the 
 mylo-hyoid will produce, in some cases, a flaccid condition 
 of the floor of the mouth. Little is known of any special 
 symptoms due to paralysis of the tensor tympani and 
 tensor veli palatini. They remain latent in most cases. 
 Occasional^, however, it would seem that we have to 
 attribute to such paralysis anomalies in the position of the 
 palato-pharyngeal arch, and dysakusis for deeper tones. 
 
 Irritative phenomena in the sensory sphere are — Pains, 
 hypersRsthesise or anaesthesia dolorosa, the latter condition 
 being analogous to that bearing the same name described 
 in connection with the spinal cord (p. 33). In the motor 
 sphere we have tonic and clonic spasms of the masticatory 
 muscles. As regards the localizing significance of irritative 
 symptoms in the domain of the motor trigeminus, broadly 
 speaking, what was said in connection with the irritative 
 symptoms of the facial on pp. 129 and 132 applies here also, 
 save that, here, these phenomena are due less often to 
 functional neuroses than to infective morbid processes 
 (tetanus, meningitis, etc.). Pains in the region of the 
 trigeminus, too, lose much of their sigilificance from the 
 frequency of genuine spontaneous neuralgias. At the same 
 time the absence of neuralgiform phenomena in central 
 affections of the fifth nerve deserves special mention. 
 
 Besides the motor and sensory fibres above discussed, all 
 three branches of the trigeminus are joined, soon after their 
 exit from the cran-al cavity, by sympathetic fibres, which 
 accompany the branches and some of their sub-branches in 
 their further course. The junction of these sympathetic 
 
142 BING'S COMPENDIUM 
 
 fibres, arising from the plexuses accompanying the arteries 
 to the head, with trigeminus fibres, takes place at certain 
 gangHa in the course of the latter. These ganglia are — 
 
 1. For the ophthalmic branch, the ganglion ciliare ; its 
 roots arise from the plexus caroiicus internus. 
 
 2. For the maxillary branch, the ganglion spJieno-pala- 
 tinum, whose roots have the same origin. 
 
 3. For the mandibular branch, the ganglion oticum, whose 
 roots spring from the plexus meningeus medium. 
 
 4. In addition, the chief offshoot of the mandibular, the 
 lingualis, possesses a ganghon of its own, the ganglion 
 submaxillare, whose sympathetic roots are drawn from the 
 plexus maxillaris externus. 
 
 What, then, are the functions of these sympathetic fibres ? 
 
 In order to arrive at an answer to this question, we would 
 refer in the first place to Fig. 24, and to the account given 
 in that part of our work, of the sympathetic symptom- 
 complex for the head (vide p. 68 et seq.). The sympathetic 
 tracts depicted on the right of the figure — " ad musculum 
 tarsalem superiorem," " ad musculum dilatatorem pupillae," 
 " ad musculum orbitalem " — pass, the first two through the 
 gangUon ciliare, the last through the ganghon spheno- 
 palatinum. A destructive lesion here may lead, in the one 
 case to pupillary paralysis and narrowing of the palpebral 
 aperture, and in the other to enophthalmus. The tracts 
 " ad glandulas sudoriparas " and " ad vasa sanguinea " 
 must, however, communicate with aU three branches of 
 the trigeminus. For in interrupting lesions of these nerves 
 we find, in almost every case, in the anaesthetic parts, either 
 heat and redness (early cases) or coldness of the surface and 
 cyanosis (older cases), also anidrosis. It may be weU to 
 point out here that, occasionally, the same phenomena are 
 noticed in cases of facial paralysis, so that it would appear 
 that some of these sympathetic fibres may accompany the 
 facial trunk. 
 
 Among other fibres accompanying branches of the 
 trigeminus in their course, but of sympathetic origin, which 
 may be mentioned, are the fibres governing the secretion of 
 nasal mucus, which form part of the fibre-complexes of the 
 ophthalmic and maxillary branches. It is on interruption 
 of their continuity that the abnormal dryness of the nasal 
 
CEREBRAL LESIONS 
 
 143 
 
 mucosa depends, which accompanies paralysis of those 
 nerves, and leads, secondarily, to impairment of the sense 
 of smeU. 
 
 We have already seen that the salivary fibres of the 
 mandibular (Ungual branch), and the lachrymal fibres of 
 the ophthalmic (lachrymal branch), come from the facial 
 trunk, the former via the chorda tympani, the latter via 
 the greater superficial petrosal nerve. The connection 
 between the lachrymal fibres and the first or ophthalmic 
 
 Fio. 52. 
 
 Ecs 
 
 cialis 
 
 tmC 
 
 The Laoheymal Tract in the Facialis and Teigeminus. 
 
 branch of the trigeminus takes place through the above- 
 mentioned spheno-palatine gangKon and an anastomosis 
 between the first and second rami of the trigeminus, the 
 zygomatic nerve. It follows from the foregoing that tri- 
 geminus lesions situated on the cerebral side of the zygo- 
 matic nerve — lesions of the Gasserian ganglion, for example — 
 do not cause a drying-up of the lachrymal secretion. 
 Lachrymal paralysis only occurs when the lesion affects 
 the spheno-palatine ganghon itself, the immediately adjoin- 
 ing portion of the maxiUary ramus, the zygomatic, or the 
 
144 BENG'S COMPENDIUM 
 
 lachrymal nerve — in a word, some pait of the tract marked 
 black in Fig. 52. 
 
 On the other hand, a trigeminus lesion which reveals itself 
 by impairment of the salivary secretion can only be situated 
 quite peripherally in the system of the third ramus, for it 
 is through the junction of chorda fibres from the facial with 
 the lingual nerve that the latter first acquires salivary 
 functions. 
 
 Disturbances of taste in the anterior two-thirds of the 
 tongue may, however, be found — 
 
 1. In lesions proximal to the spheno-palatine ganglion, 
 provided that they involve the second ramus, the Gasserian 
 ganglion, or the common trigeminal trunk.* 
 
 2. In lesions of the lingual nerve distal to the junction 
 with the chorda tympani. 
 
 Where, however, such gustatory disturbances are found 
 associated with diminution in the secretion of sahva, but 
 without anaesthesia in the domain of the trigeminus or 
 paralysis in that of the facial {vide supra, p. 131), the chorda 
 tympani itseK must be the seat of the lesion, a not un- 
 common eventuahty in affections of the tympanic cavity. 
 
 It may be stated broadly that lesions of separate rami 
 or of peripheral branches of the fifth pair are quite rare ; 
 apart from injuries to the bones or the soft parts of the 
 face, we have as causes only tumours and tuberculous or 
 syphilitic affections of the bones through which the nerves 
 make their exit, or of their periosteal covering. The ramus 
 ophthalmicus leaves the cranial cavity through the superior 
 orbital fissure ; the ramus maxillaris passes first through 
 the foramen rotundum, later (as the infra-orbital nerve) 
 through the canal of the same name ; the foramen ovale 
 gives passage to the ramus mandihularis, whose terminal 
 branch, the inferior alveolar nerve, lies in the mandibular 
 canal. The points of exit of the three branches on to the 
 
 * As, after extirpation of the Gasserian ganglion, ageusiaof the anterior 
 two-thirds of the tongue is sometimes entirely absent, while in other oases 
 the power of taste is merely diminished, the conclusion is justified that in 
 such individuals a certain proportion of gustatory fibres from the geniculate 
 ganglion, instead of passing to the trigeminus by way of the superficial 
 petrosal nerve, join the intermediate nerve of Wrisberg (wide p. 127), and 
 enter its nuclear area. This portion of the facial must in these cases be 
 regarded as a mixed (sensory-secretory) nerve. 
 
CEEEBRAL LESIONS 145 
 
 face arc the supra-orbital, infra-orbital, and mental foramina 
 respectively. 
 
 Much more frequently the Gasserian ganglion and the 
 common trunk of the nerve are affected, almost always 
 unilaterally (meningitis gummosa, aneurysms of the internal 
 carotid, transverse basal fractures posterior to the sella 
 turcica, tumours of the hypophysis, etc.). In such cases 
 one finds, in addition to anaesthesia over the whole of one 
 trigeminal region, monoplegia masticatoria, the peripheral 
 origin of which is demonstrated by the onset of degenerative 
 atrophy and the reaction of degeneration. The atrophic 
 condition of the muscles shows itself in a falling in of the 
 temporal fossa and the masseteric region, and, consequently, 
 by an abnormal prominence of the zygomatic arch. The 
 occurrence of herpes zoster in the cutaneous region of the 
 fifth nerve points to affection of the Gasserian ganghon 
 (c/. the analogous phenomenon in affections of the spinal 
 gangha ; vide pp. 34 and 62). 
 
 At the base of the brain the trigeminal trunk and its 
 ganghon are seldom .affected alone by pathological processes, 
 but almost always in company with other cranial nerves. 
 Here also we have the same general distinguishing features 
 as in other basal affections. 
 
 Nuclear trigeminal affections are generally associated, 
 as has been stated, in a typical manner, with evidences of 
 involvement of other structures in the brain-stem. Where 
 lesions in the oblongata impair the functions of the tri- 
 geminus by involving the substantia gelatinosa or the spinal 
 root of the nerve, the participation of other nerve roots 
 and nuclei in the medulla in the alternating symptom- 
 complex points to the caudal situation of the trigeminus 
 lesion. 
 
 It must here be noted that, in affections of the most distal 
 portion of the substantia gelatinosa in the medulla, we have 
 disturbances of sensation in the frontal region ; if the lesion 
 be somewhat higher up, the temples and eyehds are affected ; 
 while a still more proximaUy situated lesion affects the nose 
 and cheeks. Thus, nuclear trigeminal anaesthesias present 
 locahzing conditions distinguishing them from those of a 
 peripheral nature, just as is the case with the spinal sensory 
 nerves. We are not yet in a position to map out the sensory 
 
 10 
 
146 BING'S COMPENDIUM 
 
 cutaneous areas corresponding to the different levels of the 
 nuclear column of the trigeminus (substantia gelatinosa) as 
 definitely as we can in the case of the spinal root fields. At 
 the same time, in partial affections of the fifth nerve, dis- 
 agreement between the actual distribution of the symptoms 
 and the innervation areas given in Fig. 51 must be taken as 
 proof of the central situation of the lesion. 
 
 As regards supranuclear lesions of the trigeminus, they 
 cause, if unilateral, no motor, but only sensory symptoms, 
 because of the bilateral cortical innervation of the mastica- 
 tory nuclei. The chnical picture of supranuclear masticatory 
 diplegia has been already drawn in the discussion of pseudo- 
 bulbar paralysis (pp. 123 and 124). 
 
 Thanks to the foregoing various points on which it is 
 possible to make definite statements, the locaUzation of 
 morbid processes and of injuries in the oourse of the tri- 
 geminus and its branches presents, in actual practice, no 
 great difficulties. 
 
 [d) The Nerves supplying the Muscles of the Eye. 
 
 We stated, in our preliminary remarks on the anatomy 
 of the brain-stem, that there were three nuclei for the 
 ocular muscles, those^ namely, of the abducens, trochlear, and 
 oculo-motor nerves. 
 
 While we have hitherto spoken of the latter as a single 
 structure, we have now to consider the somewhat com- 
 plicated conditions arising from the fact that the separate 
 muscles supplied by the oculo-motor nerve are represented 
 by separate nuclear groups in the area of origin. 
 
 The nuclear region of the oculo-motor contains, as is 
 seen in diagram in Fig. 53 — 
 
 1. A small-celled lateral nucleus, the nucleus of Edinger 
 
 and Westphal. 
 
 2. A large-celled lateral nucleus. 
 
 3. A small-celled mesial nucleus. 
 
 Of these the longest is the large-celled lateral nucleus. 
 It contains, ranged one behind the other (the nuclei are 
 represented in our figure in horizontal projection) — 
 
CEREBRAL LESIONS 
 
 147 
 
 Fig. 53. 
 
 Imhbrvation of the Ocular Muscles. 
 
 III=Ooulo-motor nerve. 
 IV=Trochlear nerve. 
 VI=Abducens nerve. 
 
148 BING'S COMPENDIUM 
 
 (a) The centre for the levator palpebrse superioris. 
 (6) ,, ,, rectus superior. 
 
 (c) „ ,, rectus internus. 
 
 {d) „ ., obHquus inferior. 
 
 (e) „ ,, rectus inferior. 
 
 The fibres from (a) and (6) arise exclusively from the 
 nucleus of the same side, those from (e) exclusively from 
 that of the opposite side, while those from (c) and (d) arise 
 from the nuclei of both sides. 
 
 The mesial nucleus is the centre for accommodation — i.e., 
 for the cihary muscle, whose contraction, as is well known, 
 loosens the zonula of the lens ; the Westphal-Edinger nucleus, 
 on the other hand, innervates the sphincter pupillce, and is 
 thus the antagonist of the pupil-dUating centrum cilio-spinale 
 in the lower cervical cord (vide p. 67). Like the fibres 
 from the latter centre, but unhko those from the large-celled 
 nucleus of the oculo-motor nerve, the fibres from the two 
 small-celled nuclei of the latter do not pass directly to the 
 muscles they supply, but connect with fresh neurons in 
 the cihary ganghon of the same side. These latter neurons 
 are sympathetic, in correspondence with the smooth or 
 " unstriped " character of the internal muscles of the eye. 
 
 Immediately caudal to the large-celled lateral nucleus is 
 the nucleus of the trochlear nerve, whose fibres, after under- 
 going a complete decussation, innervate the superior obhque 
 muscle. 
 
 Much farther in a caudal direction — i.e., in the caudal 
 region of the pons — hes the abducens nucleus. Its fibres 
 pass to the rectus extcrnus of the same side. They are, 
 however, connected by long collateral fibres with that part 
 of the oculo-motor nucleus of the same side which helps in 
 the innervation of the rectus internus of the opposite side. 
 These collaterals run in the dorsal longitudinal bundle. 
 
 What now are the functions of the external ocular muscles ? 
 
 1. The levator palpebrce elevates the upper eyelid. 
 
 2. The rectus internus and externus rotate the eyeball 
 round a vertical axis — i.e., inwards or outwards. 
 
 3. The rectus superior and inferior rotate it round a 
 transverse axis — i.e., upwards and downwards. 
 
 4. The obliquus superior and inferior rotate the bulb 
 round a sagittal axis ; the former rolls the upper, the latter 
 
CEREBRAL LESIONS 149 
 
 the lower, part of the circumference of the eyeball towards 
 the nasal waU of the orbit. 
 
 The following, however, is to be noted : Only the rectus 
 extemus and intemus have an uncompUcated action, the 
 one acting exclusively as an abductor, the other exclusively 
 as an adductor — therefore in strict antagonism the one with 
 the other. The actions of the other four muscles of the 
 bulb are, on the contrary, complex, the rectus superior and 
 inferior acting, in addition to their main function, a& 
 adductors ; while the two obliqui are, secondarily, abductors, 
 and possess, further, the superior a depressing, the inferior 
 an elevating, action on the eyeball. The statements made 
 above, therefore, with reference to rotation about a transverse 
 and a sagittal axis must be taken in a quaHfied sense. For 
 a more detailed treatment of this subject, reference should 
 be made to works on ophthalmology, as also for an account 
 of the more minute diagnosis of disturbances of function in 
 the ocular muscles (double vision, etc.). 
 
 In directing the eyes upon a given object, however, not 
 only do several muscles of the same eye work together, but 
 also muscles of the one eye with those of the other, and the 
 muscles may be associated in varying combinations accord- 
 ing to the movements to be executed. The rectus internus, 
 for example, is associated, in the movement of convergence, 
 with the hke named muscle, and, in looking to the side, with 
 the rectus extemus, of the other eye. That the cortical 
 centres for ocular movements are association centres, in 
 view of the statements made above, goes without saying. 
 The connections between these association centres and 
 the various subordinate parts of the oculo-motor nuclei on 
 both sides make the mechanism as a whole one of great 
 complexity, and one concerning which many points are 
 still obscure. The conditions of innervation governing the 
 apparatus for looking sideways are on the whole the simplest ; 
 the abducens nucleus, it would seem, acts also as a pontine 
 centre for ocular movements, or possibly possesses, in close 
 contiguity, a pontine centre of its own. The supranuclear 
 tract* conducts (vide Fig. 53) impulses from the cortical centre 
 in the opposite hemisphere to the ganghon cells of the ab- 
 
 * That is to say, the chief supranuclear tract ; for there is, in addition, an 
 accessory tract, arising from the cortex of the same side. 
 
150 BING'S COMPENDIUM 
 
 ducens nucleus ; the axis cylinders of the latter pass, in the 
 first place, to the rectus externus of the same side, and in 
 the second place, by means of their collaterals running in 
 the dorsal longitudinal bundle, cause contraction of the 
 rectus internus of the other eye. The cortical centre for 
 the movements involved in looking sideways effects, there- 
 fore, a rotation of hoih eyes towards the opposite side. 
 
 Just as fibres from the hypoglossal nucleus pass into the 
 lower nucleus of the facial, in order to participate in the 
 innervation of the orbicularis oris, so fibres from the oculo- 
 motor nucleus apparently enter the upper facial nucleus, 
 and take part in the innervation of the orbicularis palpe- 
 brarum. The grounds for this conclusion are — ( 1 ) The paresis 
 of the orbicularis which accompanies nuclear lesions of the 
 oculo-motor nerve ; (2) the upward turning of the eyebaU, 
 which takes place simultaneously with closure of the lids. 
 
 With regard to the symptoms which accompany lesions 
 of the innervation mechanism we have described above, 
 certain definite statements may be made. 
 
 In the first place, it is readily intelligible that paralyses 
 of isolated ocular muscles are most commonly noticed in 
 the rectus externus and obliquus superior, each of which 
 possesses its own exclusive nerve-supply (abducens and 
 trochlearis respectively). Paralyses of single muscles in- 
 nervated by the oculo-motor are much rarer, their occur- 
 rence presupposing extremely circumscribed lesions in the 
 nuclear region of the nerve. 
 
 Complete oculo-motor par&.lysis is accompanied by falling 
 of the upper eyelid (ptosis), which is not to be confused with 
 the narrowing of the palpebral aperture due to failure of 
 the sympathetic innervation of the musculus tarsalis superior 
 [vide pp. 68 and 142). The globe is rotated permanently 
 downwards and outwards (rect. ext. and obi. sup.), and, 
 in addition, the pupil is dilated and the eye permanently 
 adapted for distant vision (paralysis of the sphincter pupiUse 
 and musculus ciliaris). If the abducens and trochlearis are 
 also paralyzed, we have the condition known as ophthalmo- 
 plegia totalis, in which the eyes are looking straight for- 
 wards and are immobile. The small-celled nuclei for the 
 intrinsic ocular muscles are, as is seen in Fig. 53, separated 
 from the large-celled nuclei for the extrinsic musculature. 
 
CEREBRAL LESIONS 151 
 
 They may escape injury when the latter are destroyed, in 
 which case there results the condition known as ophtJialmo- 
 plegia externa ; or, on the other hand, they may suffer 
 destruction alone {ophthalmoplegia interna). 
 
 Where co-ordinated movements of several muscles are 
 impaired, we speak of conjugate paralyses. Thus, the patient 
 may be unable to look to the right or to the left, upwards or 
 downwards, or to move the eyes, convergently. In these 
 cases the association centres are involved. The simplest 
 form of these association paralyses is that presented by the 
 abducens, whose nucleus may be regarded as functioning also 
 as a pontine association centre. Nuclear abducens lesions 
 are in consequence followed, not by simple abducens paralysis, 
 but by inability to look towards the side of the injured 
 nucleus. It is only when the abducens fibres are interrupted 
 peripherally to their nucleus — i.e., after the collaterals to the 
 rectus internus nucleus of the oculo-motor have been given 
 off — ^that we have an isolated paralysis of the rectus externus. 
 
 The following rules may be laid down for localization of 
 lesions involving paralyses of the ocular muscles : 
 
 1 . Unilateral paralyses of o 3ular muscles, whether multiple 
 or isolated, are almost always of nuclear or infranuclear type. 
 The supranuclear innervation of the ocular muscles is pre- 
 ponderatingly bilateral, the conditions resembling those 
 described in the case of the laryngeal centre (vide Fig. 46 
 and p. 121). In general, supranuclear paralyses of the eye 
 muscles only occur in affections involving both hemispheres, 
 and in these only very seldom, as the cortico-nuclear fibres 
 under consideration do not travel in compact bundles, but 
 are much scattered in their course from the cerebral surface. 
 Paralyses of the eye muscles cannot therefore be included 
 in the clinical picture of pseudo-bulbar paralysis drawn 
 above (pp. 123 and 124). 
 
 Morbid processes involving a large extent of the cortex 
 on both sides are the most likely to cause bilateral ophthalmo- 
 plegias (meningitis).* An exception to the foregoing is 
 afforded by ptosis. Isolated crossed paralysis of the levator 
 
 * la contrast with the nuclear and infra-nuclear paralyses of ocular 
 muscles, in these supra-nuclear ophthalmoplegias reflex ocular move- 
 ments may be started from the labjrrinth (" caloric nystagmu3," vide infra, 
 p. 165). 
 
152 BING'S COMPENDIUM 
 
 palpebrse is not uncommon in unilateral cortical lesions, 
 from which it would seem that in a good many individuals 
 the cortical innervation of this muscle is predominantly 
 contralateral. 
 
 2. The cortical innervation for the most important asso- 
 ciated movement, the direction of both eyes to one side, 
 is, broadly speaking, a contralateral one. The cortico- 
 nuclear tract passes, as shown in Fig. 53, from a particular 
 portion (for the localization of this centre, vide infra in the 
 section on the Cerebrum) of the cortex of one hemisphere, 
 to the abducens or pontine centre of the opposite side. 
 This supranuclear tract crosses the middle line at a spot, 
 marked in our figure, which lies at the level of the anterior 
 border of the pons. If, now, this tract is interrupted by a 
 lesion proximal to the point of decussation, we shall have, 
 supposing the lesion to be on the right side, inability to look 
 to the left ; if, on the other hand, the lesion is situated in the 
 pons — thus distal to the crossing — the patient will be unable 
 to look to the right. The unopposed action of the sound 
 antagonists causes a deviation of both eyes — -in the first case 
 towards the right, in the second towards the left. In any 
 case, therefore, in which this " conjugate deviation " has 
 resulted from interruption of the cortico-nuclear tracts, the 
 patient, if the lesion is above the pons, looks towards the 
 side on which his lesion is situated ; if the lesion is in the 
 pons, he looks, on the contrary, away from the side of the 
 lesion. The rules for diagnosis of a pontine lesion have been 
 already fully discussed. Conjugate deviation is not a lasting 
 symptom, for, apparently, the accessory cortico-nuclear 
 connections of the same side may gradually take over the 
 work vicariously. 
 
 3. Nuclear paralyses of the oculo-motor are, in conse- 
 quence of the great extent of the nucleus, seldom total. The 
 sphincter pupillse and musculus ciliaris generally remain 
 unaffected. Paresis of the orbicularis palpebrarum points 
 to a nuclear as distinguished from an infranuclear lesion, 
 {vide supra, and compare the analogous relation between 
 the hypoglossal nucleus and the orbicularis oris). A nuclear 
 lesion of the abducens causes, as we have seen, not isolated 
 paralysis of the rectus externus of the same side, but con- 
 jugate paralysis affecting the rectus externus on the side of 
 
CEREBEAL LESIONS 153 
 
 the lesion, and the rectus internus of the other eye, the result 
 being conjugate deviation towards the sound side. In this 
 condition, it should be expressly noted, convergence is not 
 interfered with if the oculo-motor be intact. Further, 
 nuclear abducens paralysis-is accompanied by facial paralysis 
 of peripheral type, owing to the proximity of the " genu " 
 of the facial as it turns round the abducens nucleus. 
 
 4. In infranuclear paralysis of the oculo - motor, the 
 sphincter pupillse and the ciliary muscle practically never 
 escape, as their neurons are in the closest contiguity 
 with those for the external ocular muscles in the oculo- 
 motor trunk. Infranuclear abducens lesions cause isolated 
 paralysis of the external rectus, not conjugate paralysis 
 of that and the rectus internus of the other eye. 
 
 5. Hemiplegia alternans superior vel oculo-motoria, or 
 Weber's paralysis, is characteristic of infranuclear oculo- 
 motor affections (vide p. 109). The lesions are generally 
 situated within the brain-stem (peduncular oculo-motor 
 paralysis). They are, however, occasionally basal. In 
 Foville's paralysis (hemiplegia alternans abducento- facialis) 
 the abducens affection is generally also infranuclear. 
 
 6. The basal situation of a lesion giving rise to ophthalmo- 
 plegia is indicated, apart from the general signs of an intra- 
 cranial and the special signs of a basal affection, by the 
 simultaneous involvement of other cranial nerves (anosmia, 
 amaurosis, trigeminal anaesthesia, facial paralysis, nerve 
 deafness). Where we have progressive pathological pro- 
 cesses (gummata, tumours, meningitis), in the neighbourhood 
 of the oculo-motor emergence, ptosis is usually the first 
 symptom. Fractures of the base involve, most frequently, 
 the abducens, which occupies a very exposed position at the 
 summit of the pyramid of the petrous bone. 
 
 Of irritative symptoms affecting the ocular muscles, 
 nystagmus first deserves mention. This is the name given, 
 as is known, to rhythmic contractions of the ocular muscles, 
 which may come on in the position of rest (spontaneous 
 nystagmus), but are more frequently evoked by voluntary 
 movements of the muscles (intention tremor). Horizontal 
 nystagmus is the form most frequently observed. There are, 
 however, vertical and rotatory forms. Nystagmus is also 
 found as a consequence of congenital weakness of sight or of 
 
154 BING'S COMPENDIUM 
 
 such as comes on early, before the individual has thoroughly 
 learnt to " fix " the eyes ; further, as an occupation spasm, 
 in coal-miners. We shall have something to say about 
 nystagmus in the section on the Cerebellum. In the nystag- 
 mus caused by irritation of the inner ear (cold or hot 
 douching,* acute inflammations), the afferent impulses pass 
 by way of the connection between the nucleus of Deiters 
 and the dorsal longitudinal bundle. Tegmental lesions in the 
 neighbourhood of the latter may also give rise to nystagmus, 
 which is brought on in this case by looking to the side on 
 which the lesion is situated. Lesions near the abducens 
 nucleus may also cause nystagmus, and in rare cases a con- 
 jugate deviation, which is to be regarded as an irritative 
 symptom, the deviation being to the side of the irritated 
 nucleus. Of much greater importance and significance is 
 the conjugate deviation due to irritation, not to paralysis, 
 of the cortical centre. This will, however, be dealt with 
 later, when we come to discuss cortical locaUzation. 
 
 The symptomatology of the pupillary reflexes will be 
 considered in connection with affections of the optic nerve. 
 
 B. Lesions of the Cerebellum. 
 
 The cerebellum is, from an anatomical point of view, to 
 be regarded as a self-contained structure with well-defined 
 boundaries. In its capsule, formed by the posterior cranial 
 fossa and the tentorium, it represents a more or less inde- 
 pendent annexe to the rest of the central nervous system, 
 with which it is connected by three pairs of crura or peduncles : 
 
 1. The inferior peduncles (crura ad meduUam). 
 
 2. The middle peduncles (crura ad pontem, brachia 
 
 pontis). 
 
 3. The superior peduncles (crura ad cerebrum, s. ad 
 
 laminam quadrigeminam, s, brachia conjunctiva). 
 
 The inferior and middle peduncles convey chiefly afferent 
 
 or cerebelli petal fibres to the cerebellum, while the superior 
 
 * Syringing thi! ear with cold water causes in the healthy a nystagmus 
 towards the opposite side. If, on the contrary, hot water is used, the 
 movement is towards the side of the syringed ear (Barany's experiment, 
 "caloric nystagmus"). Difierences in temperature cause movements in. 
 the endolymph which have an irritative action on the nervous apparatus of 
 thelab-.'rinth. 
 
CEREBRAL LESIONS 155 
 
 peduncles or brachia conjunctiva are composed mainly of 
 efferent (cerebellifugal) fibres. 
 
 In the cerebellum itself anatomists recognize a number 
 of lobes, which, consisting as they do of cortical and medul- 
 lary substance, present, on transverse section, the charac- 
 teristic dendritic appearance known as arbor vitce cerebelU. 
 The largest mass of grey matter contained in the substance 
 of the cerebellum is the nucleus dentatus. Other cell-com- 
 plexes contained in the white centre of the cerebellum are 
 the nucleus fastigii, nucleus emboliformis, and nucleus glo- 
 bosus. Clinically, however, our division of the cerebellum 
 is a much simpler one, as we merely have to distinguish 
 between a mesial portion, the vermis cerebelU, and two 
 lateral portions, the hemispheres. If in any given case of 
 cerebellar affection we are able, in our diagnosis, to say with 
 certainty in which of these three parts the lesion is situated, 
 we must, in the present state of our knowledge, at least, be 
 very well content. 
 
 How comes it that our knowledge is here so incomplete ? 
 How are we to explain the contrast between our knowledge 
 of this organ and of the other parts of the central nervous 
 system that have come under our view — the spinal cord 
 and the brain-stem — for the investigation of whose patho- 
 logical processes we have at our disposal regional diagnostic 
 weapons of such precision that we are able to recognize and 
 to localize correctly lesions no greater than a millimetre in 
 extent ? 
 
 In the first place, anatomical conditions play some part 
 in the matter, for, in consequence of the enclosure of the 
 organ between the tentorium and the base of the skuU, the 
 injurious action of all pathological processes whose tendency 
 is to encroach on an already closely occupied space extends 
 to very large portions of the organ, the conditions here 
 being far more favourable for the production of remote 
 effects, than is the case in other parts of the central nervous 
 system. 
 
 While, however, anatomical conditions play their part, 
 the comparative difficulty of localization in cerebellar lesions 
 is much more largely to be ascribed to the relatively small 
 physiological importance of the organ. The cerebellum is 
 neither a motor nor a sensory organ, nor does it exhibit any 
 
156 BING'S COMPENDIUM 
 
 clearly-defined arrangement of centres for specitic functions. 
 It acts rather as an accessory apparatus, in close connection 
 with the cerebro-spinal axis, but in no way vying with it in 
 importance, exertiag a modifying influence on impulses 
 originated therein, but not originating impulses of its own. 
 In consequence, impairment of cerebellar functions due to 
 pathological processes may be, with comparative ease and 
 completeness, compensated for by the vicarious action of 
 other nerve centres, especially those of the cerebral cortex. 
 
 The cerebellum is a reflex apparatus whose function is the 
 preservation of equilibrium in standing and walking. It is, 
 therefore, not the seat of any independent function, but of a 
 certain reaction to centripetal impulses. 
 
 The centripetal impulses in question result from the con- 
 stantly changing positions of the body and of its parts in 
 relation to external objects. The centrifugal impulses 
 automatically evoked by them in the cerebellum, however, 
 govern and modify the voluntary movements called into 
 play by the cerebrum in such a manner as to secure the 
 preservation of equilibrium. To express the matter in 
 more precise terms, the cerebellum provides for the proper 
 co-operation of various groups of muscles (synergia), and 
 correctly graduates the strength of the nervous impulses 
 passing to them (eumetria). It acts, in a word, as a co- 
 ordinator and a moderator, and, by its action, insures that 
 the centre of gravity of the body shall be in stable equili- 
 brium while the body is standing erect, and that, in walking, 
 the equilibrium of the body shall be maintained, and there 
 shall be no tottering or staggering. 
 
 The afferent impulses which automatically start into 
 action this subtle regulating mechanism are brought to the 
 cerebellum by two routes, namely : 
 
 1. Via the spino-cerebellar tracts. We have here to do 
 with a part of the impulses included under the term " deep 
 sensibility," which come from the muscles and joints of the 
 vertebral column and the extremities, especially the lower (c/. 
 p. 16). The great majority of the fibres of the spino-cere- 
 bellar system arise from the lumbar and dorsal cord. In the 
 preservation of equilibrium, alike in standing and in walking, 
 the control of the legs and trunk is of the first importance. 
 
 2. Via the nucleus of Deiters, whose direct connections 
 
CEREBEAL LESIONS 157 
 
 with the cerebellum are shown in Fig. 49. The figure shows 
 also the tract which leads from the utricle and the saccule 
 to the nucleus in question — the vestibular tract. The 
 vestibular nerve, as the nerve for space perceptions, conveys 
 to the cerebellum information concerning the position of the 
 body, especially of the head, in surrounding space. Thanks 
 to the numerous association fibres between the nuclei of the 
 ocular muscles and the nucleus of Deiters, the cerebellum 
 is, also, however, kept informed of the position of the eye- 
 balls and the state of contraction of their muscles, if such 
 an expression may be used in the case of impulses of a sub- 
 conscious nature. The importance of these perceptive 
 impulses conveyed from the ocular muscles, in the estima- 
 tion of our position in space, is shown by the fact that their 
 state of contraction varies with every change of our position 
 with relation to external objects, plays an important part 
 in the estimation of distance, and so on. 
 
 We must now consider the tracts which convey efferent 
 impulses from the cerebellum to the organs of motion, and 
 thus act as motor limbs of the cerebellar reflex arc. It 
 may be stated, as a preliminary, that these efferent reflex 
 limbs are never formed by a simple neuron stretching from 
 the cerebellum to the motor cells, but always by a chain of 
 neurons, the most important connecting stations in which 
 are the nucleus of Deiters, the optic thalamus, and the red 
 nucleus of the tegmentum. 
 
 The nucleus of Deiters is thus not merely a sensory, but 
 also a motor nucleus. We have already (p. 17) made 
 acquaintance with the vestibulo-spinal tracts as a class of 
 subcortico-spinal tracts which, in pyramid lesions, convey 
 impulses to the cells of the ventral horn, so that the latter 
 are not entirely cut off from central innervation. Under 
 normal conditions, however, they act under the governance 
 of the cerebellum, and regulate the supply of nervous 
 impulses to the motor cells in the ventral horn. 
 
 In addition to the above, however, a portion of the centrif- 
 ugal fibres of the nucleus of Deiters, passing in a frontal 
 direction along the dorsal longitudinal bundle, connects with 
 the cells of the oculo-motor, trochlear, and abducens nuclei. 
 The cerebellum therefore provides, also, for synergia and 
 eumetria in connection with ocular movements. 
 
158 BING'S COMPENDIUM 
 
 Further, the optic thalamus and the red nucleus of the 
 tegmentum send, as we have seen, the thalamo-spinal and 
 the rubro-spinal tracts (Monahow^s bundle) to the cells 
 of the ventral horn. As, however, a strong contingent of 
 efferent fibres from the cerebellum passes through the 
 superior cerebellar peduncles {brachia conjunctiva), to the 
 cells of origin of these tracts, they are held to play a part in 
 the cerebellar regulation of motor impulses, analogous to 
 that of the vestibulo-spinal tracts. 
 
 The cerebellum, then, to summarize, provides, by means 
 of the spino-cerebellar tracts and the system of the nucleus 
 of Deiters, for the perception of the position of our body, 
 limbs, head, and optic axes ; while, by means of the vestibulo- 
 spinal, thalamo-spinal, and rubro-spinal tracts, and the 
 dorsal longitudinal bundle, it regulates the innervation of 
 our trunk, lirdb, and eye muscles, in such manner as to 
 secure a continuous and harmonious maintenance of equi- 
 librium in standing or walking. 
 
 Cerebellar ataxia, therefore, a typical disturbance of 
 co-ordination, is by far the most important symptom of 
 cerebellar affections. 
 
 In contrast with posterior root ataxia, in which all 
 movements exhibit loss of co-ordination, cerebellar ataxia 
 affects specially the larger movements, movements in- 
 volving wide co-operation among groups of muscles, espe- 
 cially of the trunk and lower extremities. Single move- 
 ments, such as flexion and extension of the foot, knee, and 
 hip, abduction and adduction of the thigh, may be correctly 
 executed. Their static and dynamic co-ordination, however, 
 is interfered with in such a manner as to produce a zigzag 
 gait, like that of a drunken man, while the power of stand- 
 ing in an erect posture is impaired by a more or less marked 
 tendency to stagger. The separate trunk and limb muscles 
 can no longer co-operate correctly in maintaining rest and 
 stability simultaneously. This cerebellar asynergia may 
 reveal itself also by a tendency, while walking forwards, for 
 the head and trunk to lag behind, to fall backwards — -a ten- 
 dency which may so seriously disturb the equilibrium of the 
 body, as to bring about a fall ; or, again, in rising from the 
 supine position, the legs may be lifted instead of the body, 
 and so on- 
 
CEREBRAL LESIONS 159 
 
 The upper extremities are, as a rule, only very slightly 
 affected in cerebellar ataxia ; in some cases they appear to 
 escape altogether. Some degree of uncertainty in the action 
 of grasping with the hand is, however, observed in most 
 cases. The upper extremities are little subject to the co- 
 ordinating influence of the cerebellum, for the reason that 
 they have little to do with the maintenance of equilibrium. 
 Occasionally, however, one can prove the existence of a 
 latent disturbance of co-ordination by a kind of artifice. 
 The patient is told to carry out in rapid succession move- 
 ments of antagonistic muscles — e.g., movements of prona- 
 tion and supination. If cerebellar ataxia be present, the 
 patient will often prove unable to carry out the order, to 
 bring about so subtle a co-operation between antagonist 
 muscles. This abnormality is termed adiadochokinesia 
 (S(a?oY97= succession). 
 
 The spino-cerebellar tracts form the afferent or centri- 
 petal limb of a reflex arc, regulative, not only of muscular 
 movements, but also of muscular tone. Their experimental 
 section causes, in addition to ataxia, hypotonus in the mus- 
 culature of the extremities on the affected side. It is not 
 to be wondered at, then, that, as a rule, cerebellar ataxia is 
 accompanied by cerebellar hypotonus. 
 
 This cerebellar hypotonus can be demonstrated, like the 
 spinal hypotonus due to lesions of the posterior root system, 
 by palpation, by testing with resisted movements, and by 
 the possibility, owing to loss of tone in antagonizing muscles, 
 of putting the limbs in abnormal positions (vide supra, 
 p. 18). While, however, as we have seen, spinal hypotonus 
 is accompanied by impairment or abolition of reflexes, 
 cerebellar hypotonus is independent of the condition of the 
 reflexes. After ablation of one lateral lobe of the cerebellum 
 in man (operation for cerebellar tumours), the reflexes, even 
 if absent immediately after the operation, soon return, 
 sometimes in exaggerated degree, the condition of hypotonus, 
 on the other hand, persisting. Somewhat different, indeed, 
 are the conditions obtaining in these "pure " cases of cere- 
 bellar lesion (comparable to those produced in animal experi- 
 mentation) from those found in cerebellar diseases which 
 encroach on space, and so cause pressure (e.g., tumours). 
 Here one finds, not infrequently, abolition of tendon reflexes, 
 
160 BING'S COMPENDIUM 
 
 especially of the patellar and Achilles reflexes. This is, 
 however, to be regarded as a remote effect. The increased 
 intracranial pressure is communicated to the dural envelope 
 of the spinal cord, and injures, as has been proved anatomi- 
 cally, the centripetal fibres for those reflexes at the point 
 where the posterior roots pass through the enclosing pro- 
 longation of the dura mater. This point is, as the pathology 
 of tabes dorsalis shows, to be regarded as a locus minor is 
 resistentice. It has been possible in some cases to prove, 
 histologically, the connection between pressure lesions of 
 this kind and ascending degenerations of the dorsal columns 
 of the spinal cord. 
 
 Cerebellar ataxia and hypotonus are most fully developed 
 in diseases of the vermis, in whose grey matter it is that the 
 spino-cerebellar tracts find their termination. In unilateral 
 or mainly unilateral cerebellar lesions, ataxia and hypotonus 
 may in some cases affect the trunk and extremities on the 
 same ,side only as the lesion ; in other cases, while not 
 entirely homolateral, they are much more marked on the 
 same side than on the opposite one. This also is fully 
 explained by the anatomical conditions, for the spino- 
 cerebeUar tracts, which, with the exception of a small 
 portion of the bundle of Gowers, undergo no decussation in 
 the cord, traverse the cerebellum also uncrossed. The 
 lateral cerebellar tract passes through the homolateral corpus 
 restiforme, and then roi-ind the homolateral nucleus dentatus ; 
 the tract of Gowers, through the homolateral superior cere- 
 bellar peduncle. The termination in the cortex of the vermis 
 takes place, it is true, for tlie most part after the middle 
 line has been crossed, but so near to the latter that the ter- 
 mination may almost be regarded as mesial {vide Fig. 54). 
 
 Through the efferent limbs of the refiex arc also, the 
 cerebello - rubro - spinal and the cerebello - vestibulo - spinal 
 tracts, each half of the cerebellum is connected with the 
 homolateral half of the spinal cord. It is true that each 
 cerebellar hemisphere is connected with the opposite red 
 nucleus of the tegmentum, but this decussation is counter- 
 vailed by the decussation, in the opposite sense, of Monakow's 
 bundle (vide Fig. 55). The cerebello-vestibulo-spinal tract, 
 however, undergoes no decussation in any part of its course. 
 
 It has been maintained rpoently, that the disorders of 
 
CEREBRAL LESIONS 
 
 161 
 
 locomotion observed in cases of cerebellar disease, are 
 characterized by a tendency to stagger towards the affected 
 side. The statement is not, however, of universal applica- 
 tion, the opposite tendency being found in some cases. 
 
 A pronounced cerebellar hemihypotonus may lead to a 
 true homolateral hemiparesis. The hypotonus suffices to 
 distinguish the latter from crossed cerebral hemiparesis, 
 which is, indeed, spastic in character. Babinski's sign also 
 is absent. 
 
 FiQ. 64. 
 
 CouBSE AND Termination or the Spino-Ceeebellae Tracts (Later ai. 
 Cerebellar Teact and Teact oe Gowbes). 
 
 Cerebellar ataxia is the cerebellar symptom par excellence. 
 Cerebellar hjrpotonus does not approach it in significance, 
 for the symptoms pointing to involvement of neighbouring 
 structures, which are often present in cerebellar affections, 
 may obscure it altogether. This is not the case with cere- 
 bellar ataxia, which may be unmistakably present side by 
 side with marked spastic manifestations. 
 
 If we regard cerebellar lesions from the point of view of 
 
 U 
 
l62 
 
 BING'S COMPENDIUM 
 
 aetiology, we shall find the possible causes numerous and 
 varied. Conigenital hypoplasias and other defects, sclerotic 
 contractions and atrophies, haemorrhage and softening, 
 injuries and abscesses, tumours, gummata, and tuberculous 
 deposits. It is clear that, of aU these affections, the total 
 and partial atrophies and aplasias will give the most typical 
 pictures of cerebellar impairment, seeing that here the 
 picture is not veiled by irritative phenomena and remote 
 
 Fia. 55. 
 
 Connection or the Cerebellar Hemispheres with the Corbbspondiso 
 Lateral Halves or the Spinal Coed by the Cerebello-Rubbo- 
 Spinal Tract. 
 
 effects. If all those cases are carefully eliminated, in which 
 there are present other affections of the central nervous 
 system in addition to the pure cerebellar lesion, we find that, 
 on the one hand, partial lesions, even when they involve the 
 destruction of a whole cerebellar hemisphere, may remain 
 latent ; while, on the other hand, lesions involving both 
 hemispheres lead to nothmg further than pure cerebellar 
 
CEREBRAL LESIONS 1G3 
 
 ataxia and — probably in every case — hypotonus, though, 
 unfortunately, in the earlier observations, attention was not 
 paid to this latter point. 
 
 None of the other symptoms, therefore, which play a part 
 in the diagnosis of cerebellar affections, and which we shall 
 now proceed to consider in detail, are to be regarded as 
 pathognomonic components of the cerebellar symptom- 
 complex. They may all be evoked by non-cerebellar lesions. 
 If cerebellar ataxia (whether alone or associated with hypo- 
 tonus), be absent, we are not entitled to make a positive 
 diagnosis of cerebellar disease. But not even these two 
 symptoms themselves can be regarded as pathognomonic, 
 for lesions of the cerebellifugal or cerebellipetal tracts out- 
 side the cerebellum itself may put its regulating function 
 out of action, whether the lesion be in the mid-brain, in the 
 pons, in the medulla, or even in the spinal cord (c/. Fried- 
 reich's disease). In the case of a reflex apparatus it may, 
 under certain circumstances, amount to the same thing, 
 whether the centripetal components, the centre, or the cen- 
 trifugal components, be the seat of interruption. 
 
 That vertigo, which, next to ataxic or ataxic-hypotonic 
 disturbances, is by far the most frequently-occurring symp- 
 tom of cerebellar disease, is not a true cerebellar phe- 
 nomenon, but a sign of disturbance of the vestibular system, 
 is shown both by clinical observation and by experiment. 
 The so-called " cerebellar vertigo " is, in character, very 
 closely allied to labyrinthine vertigo— one might say, indeed, 
 identical with it. Even when it occurs in diseases of purely 
 intracerebellar situation, it is to be regarded as an irritative 
 symptom, to be referred to the vestibulo-cerebellar tracts 
 which traverse the cerebellum and enter its cortical grey 
 matter (videFig. 49). Cerebellar vertigo is, like labyrinthine, 
 a so-called " systematic " vertigo, a rotatory vertigo, and, as 
 such, to be distinguished from the " asystematic " form, the 
 diffuse disturbance of perceptions relating to position in 
 space, which may be present in the most varied functional 
 nervous conditictos, in abnormal conditions of the cerebral 
 circulation, in sea-sickness, etc. The sensations here — i.e.-, 
 in cerebellar vertigo — are of rotatory displacements in a 
 particular direction between the patient and external 
 objects. These sensations, however, lead, reflexly or by 
 
164 BING'S COMPENDIUM 
 
 irradiation, to intense discomfort and feelings of malaise, 
 which may even go so far as to cause vomiting. We would 
 explain this phenomenon as follows : 
 
 The labyrinth performs its functions in reference to the 
 sense of position in space in the following manner : Tht 
 hydrostatic conditions present in the three semicircular 
 canals, which lie in the three chief planes, lead to the 
 development of nervous impulses in the vestibularis, and 
 these pass to the cerebellum by way of the vestibular 
 nucleus and the nucleus of Deiters. If, now, there is a con- 
 tradiction between the stimuli received from the vestibular 
 apparatus and the actual position of the body in space, the 
 messages received from the muscles and joints, eyes, etc., 
 will be, so to speak, " given the lie," and from this incon- 
 gruence result the vertiginous imaginary movements, and,, 
 indirectly, their painful accompaniments. 
 
 True vestibular rotatory vertigo may therefore be ob 
 served under the following conditions : 
 
 1. In affections of the labyrinth — e.g., haemorrhages 
 therein (Meniere's disease in the narrower sense), primary 
 labyrintihitis (so-called Voltolini's disease), etc. ; occa- 
 sionally, too, in middle-ear affections, as a remote effect. 
 
 2. In lesions of the vestibular trunk and the vestibular 
 nucleus (basal haemorrhages, tumours, haemorrhages in the 
 pons, gummata, etc.). 
 
 3. In intracerebellar affections. 
 
 The differential diagnosis between these conditions will, 
 as a rule, offer no difficulties, if careful consideration is given 
 to all the circumstances of the case. 
 
 In 1 and 2 we have, as a rule, accompanying auditory 
 disturbances, either paralytic or irritative (hardness of 
 hearing, deafness, tinnitus). Affections of the middle ear 
 are not difficult to recognize. Lesions affecting the peripheral 
 vestibular neuron, between the vestibular nucleus and the 
 labyrinth, exhibit, as a rule, in addition to the signs of 
 vestibular disturbance, the distinguishing characters of 
 basal or pontine lesions already enumerated. If, however, 
 we have to do with new growths, which, in the posterior 
 fossa, have, as stated, a marked tendency to produce remote 
 effects, these distinguishing characters are of much less 
 value, for cerebellar tumours injure pontine and basal 
 
CEREBRAL LESIONS 165 
 
 structures, just as, conversely, tumours of the trunk of the 
 acustious,* and in the pons, impair the functions of the 
 cerebellum. 
 
 It would appear from the latest pronoimcements of 
 English neurologists, based on a large mass of material, 
 that the direction of the imagined movements of external 
 objects, and of the patient himself, may supply an answer to 
 the question, " Intra- or extra-cerebellar ?" and, at the 
 same time, afford information as to the side on which the 
 morbid.process has developed. 
 
 If, for instance, with patients of sufficient intelligence and 
 power of self-observation, careful inquiry is made &s to the 
 direction of the imagined movements in attacks of vertigo, 
 results are arrived at which may be expressed in tabula* 
 form as follows : 
 
 Imagined Movements of External Objects of the Patient 
 
 In intracerebellar \ f-__, *!,. affected f ^^°^ *^^ affected towards 
 
 tumours [^ towards the sound ] ^^^ sound side 
 
 In extracerebellar i ., 1 from the sound towards 
 
 tumours J ( the affected side 
 
 Fig. 56 may here serve mnemotechnically. 
 
 Occasionally, in affections of the posterior cranial fossa, 
 which increase intracranial pressure by encroachment on 
 space, attacks of vertigo of the cerebellar or vestibular form 
 may come on. The vertiginous paroxysms are of extreme 
 severity, and are accompanied by symptoms of marked 
 violence (extreme ataxia, headache, excessive vomiting, 
 tinnitus, syncope, and nystagmus). 
 
 Nystagmus is, however, very often present in cerebellar 
 affections, apart from definitely " cerebellar " attacks. The 
 view formerly held was that the nystagmus, like cerebellar 
 vertigo, was caused by a lesion of that portion of the vestibular 
 nerve which passes through the substance of the cerebellum. 
 This, however, could not be established. It is true, indeed, 
 as we know, that irritation of the vestibular end apparatus, 
 the semicircular canals (by inflammatory affections of the 
 inner ear or by cold-water douching), may cause a transitory 
 nystagmus. " Cerebellar " nystagmus, however, must, it 
 would seem, be regarded as an irritative symptom, to be 
 
 * We have here chiefly to do with the so-called " tumours of the cerebello- 
 pontine angle," which spring from the nerve sheaths of the acusticus and facialis 
 at their point of emergence (chiefly fibromata). 
 
ICO 
 
 BING'S COMPENDIUM 
 
 referred to the dorsal longitudinal bundle, which, in conse 
 quence of its exposed dorsal position in the tegmentum, 
 immediately under the vermis cerebelli, is very liable to 
 irritation from neighbouring morbid processes. This form 
 of nystagmus seldom appears while the eyes are looking 
 straight forward ; it is, in general, only evoked by looking to 
 the side, and is, as a rule, most marked when the patient 
 looks to the side on which the lesion is situated. Usually 
 the movement is eqi'ally marked in the two eyes — "con- 
 jugate." Occasionally the movement of the optic axis is 
 wider on the affected side. 
 
 Fig. 56. 
 
 Imaginbd Movements in Vertigo. 
 
 a=in intracerebcllar, 6 = in extraccrebellar, tumours. 
 Aussenwelt = External objects. 
 
 Among other symptoms due to the action of cerebellar 
 lesions on neighbouring structures may be mentioned 
 paralysis of the abducens, perhaps also paralysis of associated 
 movements of the eyeball towards the affected side, which, 
 later, in consequence of the unopposed action of sound antag- 
 onists, leads to conjugate deviation of the eyes towards the 
 sound side. Paralysis of the trochlear nerve is a fairly regular 
 symptom of cerebellar lesions which have their seat in the most 
 frontal portions of the vermis. Often, too, in such cases, the 
 oculo-motor branches to the external muscles of the eye are 
 affected ; the intrinsic muscles remain almost always intact. 
 
 Irritative and paralytic symptoms in the domain of the 
 
CEREBRAL LESIONS 167 
 
 cranial nerves V. to XII. are, of course, chiefly to be 
 looked for in affections which encroach on space, and, as a 
 rule, come on earlier in extracerebellar than in intracere* 
 bellar affections. Disturbances of phonation, respiration, 
 deglutition, and articulation, may present a clinical picture 
 closely resembling that of bulbar paralysis. Sudden death 
 through pressure on the medulla has been repeatedly 
 recorded. Hemiplegia may be present on the side of the 
 lesion or on the opposite side, according as the pyramids are 
 subjected to pressure after or before their decussation. 
 
 Forced positions and forced movements (rotation of ths' 
 head or trunk to one -side or the other, turning of the body 
 about its long axis), are specially noticed in irritative affec- 
 tions (new growths, haemorrhages), when they involve the 
 superior or middle cerebellar peduncles. No rules can be 
 laid down as to the side towards which these twistings and 
 rotations take place, and their physio-pathological basis is, 
 at present, equally obscure. The latter statement applies 
 fully, also, to certain choreiform-athetotic movements af- 
 fecting the extremities of one side, which may be connected 
 with affections of the superior cerebellar peduncle of the same 
 side, and to the so-called Magendie's squint (skew deviation or 
 vertical divergence), which, coming on in association with 
 conjugate deviation, is said to indicate a lesion of the middle 
 peduncle. 
 
 Finally, we would draw attention to a number of symp- 
 toms which, in cases of increased intracranial pressure due 
 to neoplasm, justify the inference that the lesion is in the 
 cerebellum, or at any rate in the posterior cranial fossa : 
 
 1. The headache which afflicts patients with cerebellar 
 tumours is characterized by extraordinary persistence and 
 intensity. This is a consequence of the tight stretching of 
 the tentorium cerebelli, which is rich in sensory fibres. 
 The pain is referred chiefly to the occiput and the cervical 
 region, from which it may radiate as far as the upper part 
 of the back. It is also projected forwards to the forehead. 
 While, however, this frontal pain is diffused, the occipito- 
 nuchal is generally most acute on the side of the lesion. 
 It is often associated with more or less retraction of the head. 
 
 2. There is often local sensitiveness to pressure or per- 
 cussion in the occipital region, and occasionally a charac- 
 
168 BING'S COMPENDIUM 
 
 teris^ic pain is caused by upward pressure on the apex of 
 the mastoid.. In both cases the pain is felt on the side of 
 the lesion. 
 
 3. The condition of the fundus, known as "choked disc " 
 comes on very rapidly and in a very marked form, and 
 generally on both sides. Not infrequently it leads rapidly 
 to blindness. 
 
 4. If lumbar puncture be resorted to, pressure falls 
 rapidly, and the flow of cerebro-spiaal fluid very soon 
 ceases. Apparently the tumour suddenly presses the me- 
 dulla into the occipital foramen, and so blocks the com- 
 munication between the intracranial and the spinal fluid. 
 This involves such great danger for the patient (cases of 
 sudden death during the procedure have been recorded) 
 that, if a neoplasm is thought to be situated in or close 
 to the cerebellum, the use of this diagnostic method is 
 urgently contra-indicated. 
 
 C. Lesions of the Cerebrum, Basal Ganglia, 
 and Hypophysis. 
 
 CHAPTER I. 
 
 ANATOMICO-PHYSIOLOGICAL INTRODUCTION. 
 
 The organ for conscious psychic phenomena is the cerebral 
 cortex. It does not perform its tasks diffusely as a physio- 
 logical unit, but to different parts of its area are assigned 
 different fimctions. Both the efferent, centrifugal tracts, 
 which carry impulses from it, and the afferent, centripetal, 
 which convey stimuli to it, find their origin and termina- 
 tion respectively, in topographically defined areas of the 
 surface of the hemispheres — the so-called "cortical areas.'' 
 While Figs. 57 and 58 give the anatomical divisions of the 
 cortex cerebri, the fissures and convolutions ; the physio- 
 logical divisions, the above-named cortical areas, are repre- 
 sented in Figs. 59 and 60. 
 
 The cortical areas may be divided into — 
 
 1. Motor areas. From these arise the cortico-nu clear 
 tracts which innervate our whole voluntary musculature. 
 
CEREBEAL LESIONS 
 
 169 
 
 2. Sensory areas. In these end the various neuron 
 chains which serve as channels for the conduction of super- 
 ficial and " deep " sensory impulses (tactile, painful, thermic, 
 and those connected with the sense of motion and position 
 in space). Certain ganglion cells of these sensory cortical 
 areas, however, not merely receive and bring into relation 
 with our consciousness sensory stimuli, but also, in a sense, 
 store them up, producing memory pictures. The memory 
 pictures of the muscular sense — kincesthetic memory pic- 
 
 Anatomical Divisions of the Lateral Cebebbal StrBFACE. 
 
 P*, F^= first and S30ond frontal fissures; C= Central fissure; Ip. = Inter- 
 parietal fissure ; O', 0^=First and second occipital fissures; T*, T^=First 
 and second temporal fissures; B.h., B.a., B.p.,=Kamus horizontalis, 
 ascendens, and posterior fissurse Sylvii ; G.=Gynis. 
 
 tures — facilitate the performance of movements whose 
 previous performance is recollected. For this reason the 
 kinsesthetic and the motor areas coincide. When a kinses- 
 thetic perception reaches our consciousness, it is, thus, able 
 to translate itself at once into the appropriate movement. 
 The cortical areas for the superficial sensibility also coincide, 
 in the main, with the cortical motor zone (called, therefore, the 
 *'sensori-motor zone"). They, however, somewhat overlap it. 
 3. Cortical areas for special sense. These are the ter- 
 minal areas of the visual, auditory, olfactory, and gustatory 
 
i7o: 
 
 BING'S COMPENDIUM 
 
 tracts, and the " storing-up place '' for memory pictures 
 connected with these special senses. r-y 
 
 The simpler memory pictures (for tactile impressions, 
 tones, colours, forms, etc.), are subordinate to the more 
 complex (for the appearance of objects, for the spoken, 
 written, or printed word, etc.). Association fibres which 
 connect these different higher centres of perception with 
 each other raise the percepts into concepts, so that, for 
 instance, the reading of a particular word leads to th^ 
 understanding of its meaning, and, at the same time, also 
 awakens a concept of the object denoted by the word ; or. 
 
 Anatomical Divisions of the Mesial Ceeberal StrEPACE. 
 
 C. =Central fissure; C.m.=Suloiis oalloso-marginalis ; P.o.=Parieto-oooipital 
 fissure ; Clo. = Caloarine fissure ; O.t.=0coipito-temporal fissure. 
 
 again, so that the auditory perception of the ringing of a beU 
 awakens in us, not merely the concept of the " object," bell, 
 but also brings before us the word " bell," and at once places 
 at our disposal the kinsesthetic memory pictures required 
 for the pronunciation and writing of the word. Associative 
 connections between the various concepts built up of per- 
 cepts provide, finally, the foundation for our higher psychical 
 functions {Nihil est in intellectu quod non fuerit in senau)^ 
 Concerning the manner in which this is done, however, we 
 have at present no full anatomico-physiological knowledge. 
 In our Figs. 59 and 60 the various motor, sensory, and 
 
CEREBRAL LESIONS 
 
 171 
 
 special sense areas are distinguished from each other by 
 differences of shading. The physiological significance of the 
 portions of the cortex left unshaded is stUl obscure. Th^ 
 present state of our knowledge, however, justifies us in 
 claimitig for the frontal portion of those areas the formation 
 of concepts and their synthesis into intellectual personality, 
 while the unshaded temporo-occipito-parietal area contains 
 centres which are intercalated in the association tracts 
 
 Fig. 59. 
 
 Upper extremity Lower extrem'ly 
 Trunk 
 
 Head and eyes 
 
 Motor speech' 
 centre (left 
 side only) 
 
 Larynx 
 
 Mastication 
 
 Motor, Sensory, and Special Sbvsb Areas in the Cortex. 
 Motor area. 
 
 = Sensory area. 
 
 |ir-.^£r^ = Special sense area. 
 
 A. = AuditoTy; V. =Viaual cortical area; S.C. = Sensory speech centre (left side 
 only); a = Foot centre; 6= Elbow centre; c = Hand; ii= Fingers; e = 
 Shoulder; /= Upper facial; g'= Lower facial. 
 
 between the spheres of common sensation, sight, and hearing. 
 The cortical centre for taste is not represented in our figures, 
 for the reason that its localization is still matter of dispute, 
 and is, in fact, at present the subject of mere hjrpothesis. 
 Some place it in the inferior frontal convolution, others aUot 
 it a common area with the olfactory centre ; in the present' 
 state of our knowledge no decisive conclusion can be formed. 
 
172 
 
 BING'S COMPENDIUM 
 
 Among the association tracts which connect separate areas 
 of the cerebral cortex with one another, the so-caUed " com- 
 missural " tracts take a special place, inasmuch as they co- 
 OTdinate the action of symmetrically placed areas of the two 
 hemispheres. The largest commissural complex is the 
 corpus callosum ; the anterior commissure, however, also 
 forms an important transverse connection. 
 
 Among the neuron systems which, apart from the cortico- 
 cortical connections, enter into relation with the cerebral 
 cortex, the following deserve mention : 
 
 Fig. 60. 
 fyndenfeU 
 
 Motor, Sensory, akd Special Sense Areas in the Mesial Cortex. 
 ||||!||||!l!|||| | = Motor area. 
 I I = Sensory area. 
 
 f|^5fS| = Special sense area. 
 V=visual, 0. = olfaotory area. 
 
 1. Corticofugal. — (1) Cortico-Nudear — i.e., the supra- 
 nuclear fibres of the motor cranial and spinal nerves. The 
 latter = the cortico-spinal tracts. 
 
 (2) Oortico-Svhcortical. — These fibres pass, in part directly, 
 in part through intercalated centres, to the subcortical 
 centres, the thalamus, the red nucleus of the tegmentum, 
 the roof of the mid-brain, the cerebellum, etc. Their con- 
 necting neuron systems are, among others, the subcortico- 
 
CEREBRAL LESIONS 173 
 
 spinal tracts (thalamo-spinal, rubro-spinal, tecto-spinal, ves- 
 tibulo-spinal), whose significance as accessory motor tracts 
 we have discussed on pp. 4 and 5. 
 
 2. Corticopetal. — These are the terminal links of the 
 neuron chains for common sensation and special sense. 
 Their cells of origin lie in the subcortical centres — in the 
 thalamus, for instance, for the tracts from the sensory, spinal 
 and cranial nerves ; in the posterior quadrigeminal body 
 and the mesial geniculate body, for the auditory tract ; in 
 the thalamus and the anterior quadrigeminal body, for the 
 visual tract. 
 
 The arrangement of the great majority of the corticofugal 
 and corticopetal tracts is a very characteristic one. As 
 
 (1) most of the cortico-subcortical and corticopetal neuron- 
 complexes pass to the thalamus or come from it, and 
 
 (2) the cortico-nuclear tracts, with a contingent of the cortico- 
 subcortical, enter the internal capsule (which is enclosed 
 between the thalamus and the corpus striatum), there is a 
 radial convergence of fibres from a great part of the cortex 
 towards these two centrally-situated structures. It is in 
 this manner that the so-called " corona radiata " is formed. 
 
 That part of the corona radiata which merges itself in the 
 thalamus forms the " stalks " of the thalamus. The masses 
 of fibres, however, which go to form the internal capsule are 
 BO arranged that in a horizontal section we may distinguish 
 in the capsule an anterior and a posterior " limb " and a 
 genu, or " knee." As Fig. 61 shows, the various fibre 
 complexes of the internal capsule, differiag from each other 
 in place of origin and in function, are arranged in a definite 
 manner. At the " knee " lie the supranuclear facial tracts, 
 while behind them are ranged, in order, the pyramid divisions 
 for the hypoglossal and for the upper and lower extremities. 
 The posterior portion of the posterior limb is occupied by the 
 sensory tracts, and as at this point the two chief special 
 sense tracts, the visual and the auditory, branch off for the 
 temporal and occipital cortex, French anatomists have 
 bestowed upon it the very appropriate name carrefour 
 sensitif. The figure requires no further detailed explana- 
 tion. We would only point out, in addition to the fore- 
 going, that the fronto-pontine and the occipito-temporo- 
 pontine tracts (Fig. 37, p. 101) contain cortico-subcortical 
 
174 
 
 BING'S COMPENDIUM 
 
 fibres which originate in the cortical areas named, and pass 
 thence to the pons, having their terminal ramification among 
 certain groups of ganglion cells (the so-called " pontine 
 
 Inteknal Capsule and Corona Radiata. 
 
 T.=Thalamus; L.=Lenticulato nucleus; C. = Caudate nucleus; F.=Supra- 
 nuclear tract for the facial nerve ; H. = Supranuclear tract for hypoglossal ; 
 A. = Supranuclear tract for arm muscles ; B.= Supranuclear tract for leg 
 muscles ; S. =Sen3ory tracts (thalamo-oortical tracts) ; (i=Auditory tract to 
 the temporal lobe ; «= Visual tract to the occipitaJ lobe (tract of Gratiolet) ; 
 l=Fronto-pontine tract and corona radiata ; 2 = Occipito-temporo-pontine 
 tract and corona radiata. 
 
 nuclei "), which are scattered between the pontine fibres. The 
 pontine nuclei, however, send their axons to the cerebellum. 
 In this manner is established a control of the cerebellum by 
 portions of the cerebral cortex. 
 
CEREBRAL LESIONS 
 
 175 
 
 ■ It will be appropriate here to considet briefly tbef distribu- 
 tion of bloodvessels to the brain. The fact that the great 
 majority of focal lesions of the brain are of vascular origin, 
 and- that their situation" 'is 'generally in closfe relation with 
 the arterial distribution,' gives the matter a very special 
 importance. Two pairs of arteries supply the brain with. 
 bJoodi-^the internal carotids and the' vertebral arteries (c/. 
 Figs. 62-65). 
 
 Fig. 62. 
 
 A. Spin. 
 
 The Chief Arterial Trunks supplying the Beain. 
 
 The latter, after supplying the medulla, unite to form the 
 basilar artery, which supplies, not only the pons, but also, 
 by its branches the cerebellar arteries, the cerebellum. The 
 anterior cerebellar artery supplies the dorsal, and the middle 
 and posterior branches the ventral portions of the organ. 
 At the point where the crura cerebri diverge, the basilar 
 divides into the two posterior cerebral arteries, which, after 
 winding round the peduncles and giving off branches to the 
 corpora quadrigemiaa, supply the lower portions of the tern- 
 
176 BING'S COMPENDIUM 
 
 poral and occipital lobes. Each posterior cerebral artery 
 sends, finally, to the internal carotid of the same side, a 
 posterior communicating artery. 
 
 The internal carotid divides into two branches — the 
 anterior and middle cerebral arteries. As the two anterior 
 cerebral arteries are united by an anastomosis, the anterior 
 communicating artery, we have a complete arterial ring 
 
 Fig. 63. 
 
 Abterial Supply to the Cerbbbum and Basal Ganolia. 
 I - I = Area supplied by the anterior cerebral artery. 
 
 I I = Area supplied by the middle cerebral artery. 
 
 Illlllllll = Area supplied by the posterior cerebral artery. 
 
 C.i. = Internal carotid ; A.o.ni. = Middle cerebral artery j 1 = Lpnticulo- 
 optic artery; 2 and 3=Leutionlo-striate arteries; 3=Artery of cerebral 
 hemorrhage. 
 
 formed round the infundibulum and the optic commissure 
 (circle of Willis). The anterior cerebral arteries pass for- 
 wards in the great median fissure, and turn round the border 
 of the corpus callosum. They supply the anterior portion 
 of the frontal lobes and the mesial surface of the hemispheres, 
 as far as the parieto-occipital fissure. 
 
CEREBRAL LESIONS 
 
 177 
 
 Of these arteries, however, the most important from a 
 pathological point of view is the middle cerebral (c/. Fig. 63). 
 Its main trunk passes, as the Sylvian artery, to the Island of 
 ReU, where it splits up into its terminal branches. Previ- 
 ously, however, it gives off, at the base of the brain, perpen- 
 dicular branches to the optic thalamus, corpus striatum, and 
 internal capsule (Arteria lenticulp-optica and Arteriae len- 
 ticulo-striatse). One of the latter, which creeps along the 
 outer surface of the lenticulate nucleus to the internal capsule. 
 
 fio. 61. 
 
 Abtbrial Supply or the Lateral Cerebral Surface. 
 The middle cerebral artery and its divisions are shown on the area left white. 
 I I = Area supplied by the anterior cerebral artery. 
 
 = Area supplied by the posterior cerebral artery. 
 
 passes through the substance of the latter and terminates; 
 in the caudate nucleus, is the so-caUed " artery of cerebral 
 haemorrhage," so named because the majority of cases of 
 apoplexy are brought about by its rupture. These per- 
 forating basal arteries are, in contrast with the arteries of 
 the cortex, which anastomose freely with one another, so- 
 called " end arteries," and their embolic or thrombotic 
 plugging is, therefore, far more likely to be followed by 
 ischsemic degeneration of the parts supplied by them, than 
 is the case with the cortical vessels 
 
 12 
 
178 BING'S COMPENDIUM 
 
 Further, as is shown in Fig. 64, the arteria fissurse Sylvii 
 gives off, in its nourse, branches to the lower and middle 
 frontal convolutions, to the central convolutions, the supra- 
 marginal and angular lobes, and to the outer surface of the 
 
 Fig. 65 
 
 Aeteeial Stjpply of the Mesial Cbeebeal Surface. 
 
 = Area supplied by the anterior cerebral artery. 
 = Area supplied by the posterior cerebral artery 
 
 temporal lobe — thus, to the motor and sensory centre for 
 speech, to by far the greater part of the senso-motor 
 cortical area, and to the auditory centre in the cortex. 
 
 CHAPTER II. 
 
 LOCALIZING VALUE OF MOTOR AND SENSORY 
 DISTURBANCES OF CEREBRAL ORIGIN, 
 
 It is obvious, from the anatomical principles stated in the 
 foregoing section, that focal lesions of the cerebrum which 
 reveal themselves by motor and sensory disturbances, may 
 vary much in locality. 
 
 They may be situated, for instance, either in the cerebral 
 cortex, the corona radiata, or the internal capsule. 
 
CEREBRAL LESIONS 179 
 
 (a) Motor and Sensory Disturbances of Cortical Origin. 
 
 The motor areas in tlie cortex control, in virtue of the 
 decussation of the pyramid fibres which issue from them, the 
 muscles of the opposite side of the body. The connection of 
 cortical centres with the corresponding muscles of the same 
 side is quite subordinate. We have already had occasion 
 to point out that the muscles supplied by the upper part of 
 the facial, the muscles of mastication and deglutition, 
 the laryngeal muscles, the sterno -mastoid, and the upper 
 or " respiratory " portion of the trapezius, as also the 
 majority of the ocular muscles, share in this bilateral 
 cortical umervation. It may be added here that the same 
 holds good of the trunk muscles. This small category of 
 muscles, therefore, will escape paralysis in unilateral focal 
 lesions of the cerebrum. As, however, the great majority 
 of muscles have a purely contralateral innervation, we are 
 justified in giving the title " cerebral hemiplegia " to those 
 forms of paralysis due to interruption of the motor impulses 
 from a single hemisphere. 
 
 Where an interruption of the cortico-petal fibres pass- 
 ing from the thalamus to the sensory areas in the cortex 
 occurs, we speak, analogously, of cerebral hemi-ances- 
 thesia. 
 
 What enables us to distinguish motor disturbances due 
 to cortical lesions* from those due to. subcortical, especially 
 capsular, lesions, is, primarily, the circumstance that in the 
 former case the affected muscular area is, as a rule, a small 
 one. This is due to the great extent of the motor areas in 
 the cortex. It will hardly ever happen that a cortical 
 lesion will be equally and simultaneously destructive of the 
 whole surface of the central convolutions, the neigh- 
 bouring portions of the two upper frontal convolutions and 
 the paracentral lobule. The monoplegic type of supra- 
 nuclear (spastic) paralysis is, therefore, a distinguishing 
 feature of affections of this region of the cortex. Only as 
 regards cortical paralyses occurring in childhood, does this 
 statement require some qualification, as, here, a hemiplegic 
 type is not altogether unusual. Reference to Figs. 59 
 
 * The very rare " intrioortioal hemiplegias" due to diffuse affections 
 of the cortex will be dealt with later in CDnnection with the subcortical 
 disturbinces of motility and the atypical forms of cerebral hemiplegia. 
 
180 BESTG'S COMPENDIUM 
 
 and 60 will facilitate localization in monoplegias of orural, 
 brachial, facial, facio-brachial, and facio-lingual type.* The 
 facial paralysis is of course limited to the lower or unilaterally 
 innervated portion of its musculature. 
 
 Where we have to deal with tumours (the most frequent 
 cavse of cortical paralyses), the monoplegia usually takes 
 the form of a gradually progressive paresis. In haemor- 
 rhages we may have, at first, a hemiplegia (remote effect) ; 
 it soon, however, gives place to a pure monoplegia. Trans- 
 itory monoplegias, pointing to a temporary cessation of 
 activity in a particular portion of the cortex {fatigue 
 symptom), are often observed after epileptic and paralytic 
 seizures ; only lasting monoplegias are, therefore, to be 
 regarded as pointing to true lesions of the cortex. 
 
 Bilateral lesions of the senso-motor cortical area are 
 rare. They are most likely to depend on a diffuse cerebral 
 arterio-sclerosis. They naturally lead to diplegias, and il 
 the symmetrical lesions involve the region of the oper- 
 culum, with its masticatory, laryngeal and lingual centres 
 and the centre for deglutition, we have the symptom- 
 complex of pseudo-bulbar paralysis {vide pp. 123, 124). 
 Tumours of one paracentral lobule are very apt, by 
 pressure on the other, to cause paraplegia of the lower 
 extremities. 
 
 Sensory Disturbances due to Cortical Lesions. — ^The topo- 
 graphical coincidence of the motor zone with the greater 
 part of the sensory, especially with that for the deep 
 sensibility, leads to characteristic results in many of these 
 monoplegias. Thus, we have in the paretic extremity — 
 sometimes, it is true, only in a portion thereof — a hyp- 
 sesthesia which almost always affects the superficial much 
 less than the deep sensibility. Ataxia, impairment of the 
 sense of position in space and of the faculty of stereognosis 
 (vide p. 16), are to be expected in the first place. It may be 
 Btated as a general rule that these cortical disturbances of 
 sensation (as also cerebral disturbances of sensation in 
 general) are most marked at the ends of the extremities. f 
 
 * Slight lesions of cortical motor centres may cause, instead of a paralysis 
 or paresis, a motor apraxia {vide infra, Chapter V.). 
 
 t The circumstances under which cortical lesions cause disturbances of 
 sensation, whose topographical distribution recalls that of the radicular 
 areas, arc not yet thoroughly elucidated 
 
CEREBRAL LESIONS 181 
 
 That cortical lesions never cause complete anaesthesia, is due 
 to the fact that the sensory neuron terminations in the 
 cortical sensory zone are scattered, and there are no such 
 sharply defined areas for separate parts of the body, as in 
 the case of the motor functions. For this reason, too, small 
 lesions in the senso-motor zone may be entirely unaccom- 
 panied by sensory disturbances. On the other hand, 
 lesions outside the motor area, especially such as involve the 
 superior parietal convolution and the supramarginal gyrus, 
 may cause disturbances in the sensory sphere (ataxia, im- 
 pairment of the power of orientation in space, and astereog- 
 nosis affecting the opposite hand) ; we see in Fig. 60 that 
 here the sensory cortical area stretches out beyond the 
 motor. A staggering gait, due to ataxia of the trunk 
 muscles, so-called " cerebral ataxia," is observed in 
 lesions of the superior frontal convolution. Irritative 
 symptoms play as important a part in affections of the 
 senso-motor area as those betokening impairment of 
 function. They may be observed pure, or in association 
 with symptoms of paretic monoplegia. 
 
 In this connection we must place in the front rank of 
 importance irritative symptoms affecting the motor sphere. 
 
 The name " cerebral monospasm " is given to certain 
 tonic-clonic spasms which affect a hitherto normal or an 
 already paretic muscular area (facial, arm, hand, etc.), 
 leaving behind them a permanent paresis or a permanent 
 exacerbation of one already existing . 
 
 Attacks of Jacksonian or cortical epilepsy point to a 
 higher degree of cortical irritation. These attacks generally 
 begin as monospasms, which are at first, as a rule, of tonic 
 type. The spasm may, however, be clonic in character 
 ab initio, especially when the attack commences in the 
 sphere of the lower facial. In these cases the spasms are 
 not confined to the lower half of the face, as in an ordinary 
 cortical monospasm, but affect the arm, and finally the 
 leg, of the same side. If the attack commences in the arm, 
 it generally, when the whole arm has become involved, 
 spreads first to the face and then to the leg of the same 
 side. The succession leg, arm, face, is denominated the 
 " crural " type. It is important to observe carefully in which 
 muscles the first spasms of all, the so-called "motor aura," 
 
182 BING'S COMPENDIUM 
 
 come on, for this " signal " symptom is of determining 
 weight in the diagnosis of the situation of the cortical 
 lesion. If, for instance, the attack begins in the fingers of 
 the right hand — the contractions may at first affect the 
 thumb alone — the focus — most frequently a neoplasm, but 
 alst), possibly, a cicatrix, a foreign body, a small abscess, 
 or a circumscribed meningitis — will be situated in the left 
 posterior central convolution, at the point marked h in 
 Fig. 59. If the spasm commences at the left angle of the 
 mouth, the lesion is situated on the right side, at /. A 
 lesion here "irritates " the neighbouring pyramid cells, and 
 the irritation spreads gradually over the contiguous areas 
 of the cortex, like waves produced on the surface of water 
 by a stone. The muscles will be involved in an order 
 corresponding to the relative positions of their cortical 
 centres. In severe cases the Jacksonian spasms may pass 
 over also to the opposite limbs, and may be accompanied by 
 loss of consciousness. A very intense irritation may spread 
 to the motor area of the opposite hemisphere by way of the 
 commissural tracts, and, further, may deaden the higher 
 psychic centres, especially those in the cortex of the frontal 
 lobe. The bilaterally innervated muscles (frontal, palpebral, 
 masticatory, sterno -mastoid, etc.) are, in these cases, affected 
 simultaneously on both sides. 
 
 Unless the diagnosis is supported by the presence of 
 other symptoms — symptoms of cerebral pressure such as 
 slowing of the pulse, obstinate headache, choked disc, 
 cerebral vomiting, etc. — or unless a history of cranial trauma 
 helps to confirm it, cortico-epileptic attacks do not enable 
 one to infer with absolute certainty the presence of a lesion 
 in the cortical motor areas. For, in the first place, there is a 
 form of genuine epilepsy, which presents the typical Jack- 
 sonian symptomatology, the so-called "idiopathic hemi- 
 epilepsy " — it is true that more recent experiments and the 
 results of surgical procedures have shown that, as a matter 
 of fact, alterations in the region of the cortex underlie this 
 form (cysts, encephalitis) — and, in the second, intoxications 
 and auto-intoxications (alcoholism, absinthism, urcemia, etc.) 
 may evoke Jacksonian attacks by chemical irritation of the 
 motor cortex. All these conditions may also lead to tran- 
 sitory monoplegic or hemiplegic pareses. Only where the 
 
CEREBRAL LESIONS 183 
 
 latter are lasting in character do they furnish a fully valid 
 argument for the organic nature of a cortical irritation ; 
 the same applies also to those cases in which Jacksonian 
 epilepsy comes on in already paretic muscles. 
 
 Irritation of one particular portion of the cortex, the 
 base of the second frontal convolution, the area marked 
 " Head and eyes " in Fig. 59, reveals itself by a phenomenon 
 which has already been discussed in the section on the 
 inneivaticn of the eye musclts — viz.. Conjugate Deviation. 
 From the statements there made (pp. 148-153), it appeared 
 that, in contrast with other movements of the eyes, tho 
 mechanism for conjugate movement to one side or the 
 other is, in the main, unilaterally innervated. The supra- 
 nuclear tract which leads to the abducens centre in the. 
 pons, whose function it is to set in action, simultaneously, 
 the rectus externus of its own side and the rectus internus 
 of the other, takes its origin in a cortical centre in the 
 opposite hemisphere. A paralyzing lesion of this centre has 
 the same effect as one involving the supranuclear tracts 
 issuing from it, at any point before their decussation at 
 the anterior border of the pons ; i.e., it renders it impossible 
 to look towards the opposite side, and thus brings about, by 
 unopposed action of antagonists, a conjugate deviation 
 towards the side of the lesion (c/. Fig. 53). If now, on the 
 other hand, the cortical centre in question be irritated, 
 exactly the reverse takes place. The patient looks, not to 
 the side of the lesion, but away from it, or towards his spas- 
 modically contracted limbs, if, as often happens, a Jack- 
 sonian attack occurs simultaneously. Frequently the head 
 is turned spasmodically in the same direction as the eyes. 
 
 As a conjugate deviation towards the side of the lesion is 
 also observed after destruction of the angular gjrrus, it might 
 be thought that there was, here, a second ocular centre. This 
 is, however, not the case. The angular gyrus is, rather, 
 merely a thoroughfare for fibres which connect the visual 
 area in the cortex with the frontal centre for the ocular 
 muscles. No less important, from the point of view of 
 regional diagnosis, is the fact that conjugate deviation may 
 also occur as a result of lesions of the parietal lobe. 
 
 Irritative phenomena in the sensory sphere also accompany 
 affections of the senso-motor cortical area. Paraesthesias 
 
184 BING'S COMPENDIUM 
 
 have not infrequently been observed in the monoplegia 
 muscular area. Jacksonian attacks are very frequently 
 ushered in by such parsesthesias {sensory aura) ; more rarely 
 a lightning-like pain darts through the same area that 
 is afterwards affected by convulsions. Broadly speaking, 
 I owever, no very acute sensitiveness to pain is to be attri- 
 'luted to the cerebral cortex. The fearful headache from 
 ivhich so many patients with brain disease suffer, is not an 
 irritative symptom to be referred to the cortex, but is 
 rather to be ascribed to the extremely sensitive meninges. 
 If the state of tension in the latter, due to increased intra- 
 cranial pressure, be diminished by trephining or lumbar 
 puncture, the pains also abate. Exacerbation of the pain 
 on percussion of the skull over the central convolutions, 
 etc., is, however, sometimes observed in tumours of the 
 senso-motor area. 
 
 (6) Motor and Sensory Disturbances of Subcortical 
 Origin. 
 
 A result of the fan-shaped or conical arrangement of the 
 motor and sensory fibres in the corona radiata (rapid con- 
 vergence of pyramid fibres and divergence of thalamo- 
 cortical fibres), is, that the deeper the situation of a lesion 
 between the cortex on one side, and the internal capsule 
 and basal ganglia on the other, the more nerve tracts will 
 be destroyed by it in proportion to its size. 
 
 The crossed motor disturbances, therefore, due to lesions 
 in the corona radiata, are, contrary to those produced by 
 cortical and capsular lesions, of more than monoplegic, if 
 not of definitely hemiplegie, type. As, however, lesions in 
 the corona frequently interrupt the important commissural 
 tracts of the corpus callosum, their symptom-complex 
 sometimes includes the condition known as apraxia, 
 which is characteristic of lesions of that body {vide infra, 
 Chapter V.). 
 
 As regards sensory disturbances, their intensity and 
 extent is generally proportional to the depth below the 
 cerebral cortex at which the lesion producing them is 
 situated. 
 
 " Capsular " paralyses may next be considered. Among 
 
CEREBRAL LESIONS 185 
 
 Other causes, these are present in the great majority of 
 cases of cerebral haemorrhage due to rupture of the arteria 
 lenticulo-striata, of which special mention was made on 
 p. 177. Fig. 61 shows that in the posterior limb of the 
 internal capsule, all the motor tracts for the opposite side 
 of the body are closely packed together into a bundle of 
 relatively small calibre. Total hemiplegia is, therefore, in 
 by far the larger number of cases, the result of lesions of 
 this posterior limb of the capsule. We have, that is to say, 
 crossed paralysis of the lower facial, the hypoglossal, the 
 upper and the lower extremity. If the lesion extends to 
 the posterior third of the posterior limb, where the sensory 
 tracts, immediately after their emergence from the optic 
 thalamus, lie in a compact bundle, we have, in addition, 
 complete crossed Tiemianoesthesia. 
 
 Occasionally, however, the lesion is limited to the posterior 
 extremity of the internal capsule, the carrefour sensitif. 
 The simultaneous interruption, in such a case, of the sensory, 
 auditory, and visual tracts leads to the development of the 
 triad symptom-complex Jiemiancesthesia, hemianakiisis, and 
 hemiandpsia. It has been stated that hemianosmia and 
 hemiageusia {yevco, I taste), may also be present in these 
 cases, but no sufficient proof of the statement has been given. 
 Spastic paresis of the anaesthetic lower extremity is not 
 uncommon, as the pyramid fibres therefor are in close con- 
 tiguity with the anterior portion of the sensory neuron- 
 complex in the posterior third of the capsule. 
 
 The internal capsule is of such small dimensions that the 
 development of monoplegias is almost impossible, and they 
 are of extreme rarity in these cases. 
 
 We may now state briefiy the most important distinguishing 
 characteristics of cerebral hemiplegia. 
 
 1. As has been stated several times, the bilaterally in- 
 nervated muscles (mastication, deglutition, larynx, eyes, 
 trunk, and upper facial) escape. With regard to the upper 
 facial, however, a slight impairment of contractile power is 
 often noticed in the frontalis and orbicularis palpebrarum 
 of the side opposite to the lesion. The contra-lateral eye- 
 brow shows a tendency to droop, or the eye cannot be 
 kept closed so long as is the case with the homolateral. 
 
 2. Even in fuUj'-developed hemiplegias, different groups of 
 
186 BING'S COMPENDIUM 
 
 muscles are, as a rule, unequally affected. While, in a large 
 number of muscles, power of movement gradually returns, 
 others show, commonly, no sign of recovery {peronei, flexors 
 of knee, extensors of elbow, extensors of hand and fingers, 
 external rotators of arm, supinators of forearm). The arm 
 is, as a rule, much more severely affected than the leg. 
 In children the hand shows a much stronger tendency to 
 recovery than in adults. 
 
 3. The positions adopted by the extremities in conse- 
 quence of the preponderating action of the muscles which 
 recover their motility, are often, in later stages, fixed by 
 contracture. As a result, the foot is held in the position of 
 equino-varus, and the knee extended, so that, in walking, 
 the leg must be dragged forward, the foot describing a 
 lateral semicircle (circumduction, helicopody). . The arm 
 is fixed in adduction, the elbow in flexion, the forearm 
 in pronation, and the hand and fingers in flexion. These 
 contractures are thus produced : the ventral horn cells, 
 freed from the inhibiting influence of the pyramids, are 
 tonically stimulated by the impulses flowing in constantly 
 by way of the posterior roots, and a summation of these 
 stimuli occurs. The striking fact that it is certain deflnite 
 muscles which recover their motility, and are thus (thanks 
 to the supranuclear, hypertonic character of cerebral 
 hemiplegia), predisposed to contracture, depends on some 
 conditions of innervation, the anatomy of which is not yet 
 fully known to us. Probably the subcortico-spinal tracts 
 (p. 4) from the thalamus, the tegmentum, the nucleus of 
 Deiters, and the roof of the mid-brain, are in particularly 
 intimate relation with the ventral horn cells of these groups 
 of muscles, so that the reparatory efforts of the organism 
 bring them again, with comparative ease, under the influence 
 of the cerebral innervation, though by a circuitous route. 
 Cases of cerebral hemiplegia in which muscular groups other 
 than those mentioned gain the preponderance, and enter 
 into contracture, so that, for example, the leg is fixed in 
 flexion, form quite transitory exceptions. 
 
 4. The hypertonus of cerebral hemiplegia is accompanied 
 (unless there are complicating conditions which interrupt 
 the reflex arc ; cf. Cerebellar Tumours, p. 159) by exaggera- 
 tion of tendon reflexes. To this hyper-reflex, and to the 
 
CEREBRAL LESIONS 187 
 
 other pathological reflex phenomena {BahinsTci's, Mendd- 
 Bechferew and Oppenheim's signs, cloni, associated move- 
 ments, etc.), the statements made in the section on the 
 Spinal Cord apply (pp. 25, 26). The cutaneous reflexes, 
 especially the abdominal and the cremasteric, are, on the 
 contrary, almost always diminished, or even abohshed, 
 on the paralyzed side ; this symptom may be called to our 
 aid, when we have to deal with a patient who is lying un- 
 conscious after an apoplectic stroke, to determine on which 
 side the hemiplegic paralysis wiU be present when he awakens 
 from his coma. The explanation of this phenomenon is 
 by no means clear. In the section on Segmental Diagnosis 
 of Spinal Lesions we have attempted an explanation with 
 which we must, in the present state of our knowledge, con- 
 tent ourselves. The conjunctival reflex is also often absent 
 on the paralyzed side. 
 
 5. The paralysis is not degenerative in type. There are, 
 however, exceptional cases in which the so-called cerebral 
 atrophy sets in in the paralyzed, or even in the recovered, 
 muscles — an atrophy which cannot be referred to disuse, 
 and which is accompanied by diminution of electrical ex- 
 citabilitj?^, if not by the reaction of degeneration. Arthro- 
 pathies have also been occasionally observed. StiU more 
 rarely atrophy of bones on the paralyzed side has been re- 
 corded. More frequent than any of these trophic disturb- 
 ances are sympathetic disturbances of vaso-motility and of the 
 sweat function, for the physio-pathological explanation of 
 which we may refer to the section on the Spinal Cord 
 (pp. 22-24). 
 
 6. In hemiplegias resulting from cerebral haemorrhage, 
 fairly complete and rapid recovery from the paralysis often 
 takes place. This is the case when the haemorrhage has 
 not severed the cortico-spinal tracts, but has occurred in 
 their neighbourhood — in the lenticulate nucleus, for in- 
 stance. The condition of tension produced for a time in 
 the neighbourhood of the haemorrhagic focus, the collateral 
 oedema, etc., are, in such cases, responsible for the indirect 
 paralytic effects produced in the region of the motor tracts. 
 Only those pareses which are still present six to eight 
 months after the attack, are to be regarded as direct focal 
 symptoms, and to be estimated accordingly in prognosis. 
 
188 BING'S COMPENDIUM 
 
 7. Immediately after the "stroke," the tendon reflexes 
 are, as a rule, abolished, and the muscles become flaccid. 
 These are effects of shock. When, in spite of the coma, 
 the reflexes are exaggerated and the muscles spastic, we 
 are justified, in view of recorded experiences, in giving, with 
 considerable confidence, a diagnosis of hcemorrhage into the 
 lateral ventricle — a very grave condition. No satisfactory 
 explanation of this fact can at present be given. 
 
 Some atypical forms of cerebral hemiplegia deserve mention. 
 
 (o) The so-called hemiplegia sine materia. Cerebral hemi- 
 plegias which, apart from the typical case of haemorrhage, 
 may be caused by foci of softening, by tumours, by the 
 formation of cavities, sclerotic conditions, etc., have also 
 occurred occasionally without any lesion in the central ner- 
 vous system being discoverable on post-mortem examina- 
 tion. Many of these cases have been those of nephritic 
 patients who have died of uraemia. The ursemic poison 
 seems here to have, for some reason at present quite obscure 
 to us, exercised a paralyzing action on one side only, just 
 as it may exercise a unilateral irritating action and cause 
 Jacksonian convulsions. The earlier authors imagined an 
 arterial spasm of one side, and spoke of apoplexia serosa. 
 Other cases of so-called hemiplegia sine materia, recorded 
 in the older medical literature, depend probably on in- 
 adequate investigations, and are to be reckoned as examples 
 of local softening. 
 
 (6) The so-called lacunar hemiplegia. We have to do 
 here, not with a massive lesion which interrupts the cortico- 
 spinal tracts, but with disseminated, mostly miliary, lesions, 
 small areas of softening, and capillary haemorrhages, whose 
 physio-pathological basis is cerebral arterio-sclerosis. This 
 form of hemiplegia is marked by a great power of rapid 
 recovery and very slight liability to the development of 
 contractures, but also, on the other hand, by a pronounced 
 tendency to recurrence in the originally free hemisphere. 
 In the latter case a spastic-paretic condition comes on in 
 the bilaterally innervated muscles, and reveals itself by 
 phenomena suggestive of pseudo-bulbar paralysis. Sensi- 
 bility and cutaneous reflexes are, in this form, hardly 
 affected. Even if the onset be sudden, the symptoms are 
 not of severe type ; consciousness is generally retained or 
 
CEREBRAL LESIONS 189 
 
 only slightly clouded, and, if lost completely, the uncon- 
 sciousness is of short duration, generally less than an hour. 
 
 (c) Chronic progressive hemiplegia, which develops quite 
 gradually, either as the result of tumour growth in the 
 internal capsule or of advancing closure of bloodvessels due 
 to arterio-sclerosis. In the latter case it is distinguished 
 from lacunar hemiplegia by its progressive course and 
 absence of any tendency to recovery. Very rarely it may 
 happen that chronic morbid processes, such as cortical 
 atrophies {e.g., in epileptics), give rise to the development 
 of the clinical picture of this chronic progressive hemiplegia 
 by interrupting the connection between the pyramid tracts 
 (which themselves remain unaffected), and their related 
 cortical cells and ceU groups. This condition is known as 
 introrcortical hemiplegia. 
 
 {d) The so-called homolateral hemiplegia. A consider- 
 able number of cases have been recorded in medical 
 literature, in which the lesion has been found, not on the 
 opposite side to the paralyzed muscles, but on the same 
 side. In most cases of the kind we have to do with 
 faulty clinical or pathological observation. Thus, irritative 
 phenomena may appear in the paralyzed extremities very 
 soon after the stroke (vide infra), and be mistakenly regarded 
 as evidences of voluntary action ; while the opposite limbs 
 lie flaccid and inert, in consequence of the coma, and are 
 thought to be paralyzed. 
 
 Further, in the post-mortem examination, the attention 
 may be so drawn to a lesion of one hemisphere, which does 
 not involve the motor tracts at all, that less obvious lesions, 
 say in the pons or medulla of the opposite side, escape 
 observation altogether. WheiSj however, all allowances 
 have been made for these cases erroneously described as 
 cases of "homolateral hemiplegia," some cases remain which 
 are above suspicion. In some instances of the kind, absence 
 of the pyramid decussation, a comparatively rare anomaly, 
 has been proved. Further, a tumour may push one hemi- 
 sphere so far over to the opposite side that the substance of 
 the other is very seriously compressed and injured, and 
 rendered ischsemic in a high degree. 
 
 For the differential diagnosis between cerebral and 
 peduncular, pontine and bulbar hemiplegias, which are. as 
 
190 BING'S COMPENDIUM 
 
 a rule, distinguished by their alternating type, reference 
 may be made to the account of alternating hemiplegias 
 given on p. 109 et seq. The development of crossed hemi- 
 plegia, as the result of lesions at the level of the pjnramid 
 decussation, is explained on p. 105. Unilateral lesions 
 which cut across the cortico-spinal tracts at points still 
 farther caudal, reveal their spinal situation by the symptom- 
 complex of Brown-Sequard. 
 
 Irritative symptoms affecting the motor complexes of the 
 internal capsule are, in the main, late symptoms. When an 
 attack of apoplexy comes on, but especially at the moment 
 when embolic plugging of a vessel occurs, spasms may come 
 on in the muscles which are to be the seat of paralysis later 
 on, as the result of irritation of the area involved by the 
 embolus. They are not in any way pathognomonic, as they 
 may occur in irritation of the motor tracts in the crura 
 cerebri, the pons, the medulla, and the spinal cord. 
 
 AU the more typical, therefore, are the late irritative 
 symptoms which come on when a hasmorrhage has occurred 
 in the neighbourhood of the capsular motor tracts, and the 
 process of cicatrization has brought about a condition of 
 lait'ng irritation in the latter. We allude to unilateral 
 movements of the nature of chorea or athetosis which can 
 only in pure and typical cases be sharply differentiated 
 from each other. 
 
 In post-hemiplegic hemichorea, tne extremities are the sub- 
 ject of hvely jerking and shaking movements {" hemihallis- 
 mus "), which cease in sleep, but cannot be suppressed by 
 voluntary effort — are, in fact, exaggerated by any attempt 
 so to suppress them. In hemiathetosis post-hemiplegica, slow 
 movements occur in the hands and feet, but especially in 
 the fingers and toes. The movements begin with hyper- 
 extension, and recall the movements of the tentacles of a 
 cuttle-fish. They do not always cease during sleep, but they 
 can, to a certain extent, be suppressed by voluntary effort: 
 In many cases, however, the irritative symptoms noticed 
 constitute a mixture of hemichorea and hemiathetosis, or, 
 rather, a transition from the former to the latter The 
 Matter is possibly merely a variety of the former, the more 
 frequent variety ; for true unmixed hemichorea, as above 
 described, is a very rare condition 
 
CEREBRAL LESIONS 191 
 
 Lesions productive of hemiathetosis and hemichorea are 
 most frequently situated in the portions of the thalamus 
 bordering on the internal capsule, occasionally in the corre- 
 sponding portions of the lenticulate nucleus, more rarely in 
 the internal capsule itself, and here in the posterior third 
 of its posterior limb. The irritative symptoms usually com- 
 mence some months after the onset of the hemiplegia, 
 when some degree of voluntary rdovement has been re- 
 covered. A very rare condition is " hemichorea prcehemi- 
 plegica, "wlnich has been observed in some slow haemorrhages 
 into the optic thalamus. 
 
 Mention must here be made of the fact that, in rare cases, 
 choreic movements and athetosis are observed as results 
 of irritation of the motor cortex by a haemorrhage or 
 meningitis, and further that, as stated on p. 166, they may 
 be produced by lesions of the superior cerebellar peduncles 
 (brachia conjunctiva), in some manner as yet not under- 
 stood. 
 
 Childhood is a period especially liable to the development 
 of hemichorea and hemiathetosis. The latter symptom is 
 found in 50 per cent, of the cases of infantUe cerebral 
 hemiplegia. 
 
 A rare post - hemiplegic irritative symptom is post- 
 hemiplegic tremor, which resembles, sometimes the " inten- 
 tion " tremors of multiple sclerosis, sometimes the rhythmic 
 oscillatory contractions of paralysis agitans. 
 
 CHAPTER III. 
 LOCALIZING VALUE OF VISUAL DISTURBANCES. 
 
 1. The Optic Tract (vide Fig. 66). 
 From the retina, where they connect with the special sensory 
 epithelium, the so-called "rods " and "cones," the optic fibres 
 pass, in the optic nerve trunk, to the optic chiasma. Here 
 a partial decussation takes place, of such a nature that, of 
 the optic tracts leaving the chiasma, that on the right side 
 contains the fibres from the right halves of the two retinae, 
 while that on the left contains the fibres from the two left 
 halves. 
 
192 BING'S COMPENDIUM 
 
 The physiological result of this anatomical arrangement, 
 combined with the fact that the lens projects on to the 
 retina an inverted image of external objects, is that per- 
 
 (Field of Tiaion) 
 
 "Retk-rva.. 
 
 .rlm.a.re (Primary 
 
 ° .enthen. ■»'eual , 
 centres) 
 
 it iche (Eadiation 
 •^W Gratfolet) 
 
 VisuAi, Teact aid Pdi'IIi.ary Replex Teact. 
 
 ception of the left half of the field of vision is conveyed by 
 the right optic tract, and vice versa. 
 
 The fibres which cross at the chiasma come from the 
 mesial (nasal) portions of the retinae, and form the greater 
 part of the whole body of optic fibres. The lateral halves of 
 
CEREBRAL LESIONS 195 
 
 the fields of yision, whose impressions stimulate these decus- 
 sating fibres, are somewhat larger than the mesial, which are 
 restricted by the bridge of the nose. 
 
 Each optic tract carries the optic nerve fibres in a dorsal 
 direction, winds round the cerebral peduncle, and passes 
 to the primary visual centres of the same side, where the 
 fibres terminate. These centres are : the posterior portion 
 of the optic thalamus {pulvinar thalami), the lateral genicu- 
 late body, and the superior quadrigeminal body. 
 
 From the primary visual centres the stimuli received from 
 the retina are further conveyed in two directions : 
 
 1. The central visual tract, or bundle of Gratiolet, tractus 
 thalamo-occipilalis, passes to the cortical visual area of 
 the same side — i.e., to the cuneus — on the mesial surface 
 of the occipital lobe. The cortical visual centre of each 
 hemisphere, therefore, receives perceptions from the contra- 
 lateral halves of the fields of vision. 
 
 2. From the superior corpus quadrigeminum, nerve fibres 
 pass to the smaU-celled lateral nucleus {nucleus of Edinger 
 arid Westphal) of the oculo-motor nerve {vide supra, p. 146). 
 It is by means of these fibres that reflex contraction of the 
 pupil on stimulation of the retina by light is brought 
 about. The pupillary reflex arc is built up of four sets of 
 nerve fibres : {a) From the retina to the superior corpus 
 quadrigeminum ; (6) from the superior corpus quadri- 
 geminum to the Edinger-Westphal nucleus ; (c) from the 
 latter to the ciliary ganglion ; and (d) from the ciliary 
 ganglion to the sphincter pupillse. The connection (6) is 
 both crossed and homolateral ; that is to say, each corpus 
 quadrigeminum sends fibres to both Edinger-Westphal 
 nuclei. Illumination of a single eye, therefore, causes con- 
 traction, not only of its own pupil {direct reaction), but 
 also of that of the other eye {consensual reaction). The 
 nature of the lesion on which depends the form of sluggish- 
 ness of the pupillary reflex found in tabes and paralysis, 
 and known as the Argyll-Robertson phenomenon, is not yet 
 fuUy established. 
 
 ' From the cuneus, association fibres pass to the lateral 
 convex surface of the occipital lobe and the inferior parietal 
 lobe. As the cuneus is the perception centre for optic 
 ■fepressions, so are the latter areas of the cortex centres 
 
194 BING'S COMPENDIUM 
 
 for visual concepts and the storing up of memory pictures 
 of visualized objects. 
 
 2. Localization of Interruptions of the Optic Tract. 
 
 A knowledge of the anatomical conditions governing the 
 course and distribution of the optic fibres enables us in 
 
 Motcentrum 
 
 (Auditory centre) 
 
 Le.se ce.n.Cr(/m. 
 Cnur CinKs.'J 
 
 (Reading centre, left 
 Bide only) 
 
 (Visual memory centre) 
 
 ti enrinoLe,- (Visual cortex) 
 Schema tor Localization of Lesions oausino Visual Distuebances. 
 
 many cases, to determine, with considerable precision, the 
 situation of a focal lesion in the region of the optic conducting 
 tracts (c/. Fig. 67). 
 
 A. Lesions of the Optic Nerve. — Total destruction of the 
 optic fibres at a point peripheral to the chiasma (Fig. 67, 1) 
 produces, of course, complete blindness — amaurosis — of the 
 one eye. Pupillary reflexes are not evoked by the affected eye, 
 but may be by the other, whose perception of light is un- 
 
CEREBRAL LESIONS 195 
 
 impaired. If only a portion of the optic fibres is destroyed, 
 we have, instead of amaurosis, scotomata, narrowing of 
 the field of vision, etc., pathological phenomena we need 
 not consider more fuUy here, as they belong to the domain 
 of ophthalmology. 
 
 B. Lesions of the Chiasma. — {a) If the lesion involves 
 only the mesial portion of the chiasma (Fig. 67, 2), as is the 
 case in tumours of the hypophysis, hydrocephalus of the 
 third ventricle, dilatation of the infundibulum, and empyema 
 of the sphenoid antrum, it destroys the decussating fibres 
 which come from the nasal portions of the retinae. The 
 result is to blot out both temporal halves of the field of 
 vision, and to cause the condition known as bitemporal 
 heteronymous hemianopsia or hemiopia. Heterony-motis, 
 because the right eye is blinded for the right, and the left 
 eye for the left, half of the field of vision. 
 
 (6) If, on the other hand, the external portions of the 
 optic nerve decussation are destroyed, the mesial remaining 
 unaffected (Fig. 67, 3+ 3a) — a very rare condition which 
 may be brought about by aneurysm of both carotids, 
 symmetrical gummatous foci at the base of the skuU, perhaps 
 also by cysts of the hypophysis bulging laterally, etc. — we 
 have suppression of function in the outer portions of the 
 fundi oculorum, and, as a result, nasal heteronymous hemi- 
 anopsia. 
 
 (c) The reiult of destruction of one-haK of the chiasma 
 (Fig. 67, 2+3) is blindness on the side of the lesion, and 
 temporal hemianopsia in the other eye. 
 
 C. Lesions of the Optic Tract, the Primary Visual Centres, 
 and the Radiation of Gratiolet. — AU these lesions cause 
 homonymous lateral hemianopsia for the halves of the field 
 of vision contralateral to the lesion. Homonymous, because 
 either both right or both left halves of the visual field are 
 involved. 
 
 (a) If the lesion is peripheral to the point at which the 
 reflex fibres to the Edinger-Westphal pupillary nucleus are 
 given off (Fig. 67, 4), a ray of light thrown on to the blinded 
 halves of the retinae causes no contraction of the pupil 
 'hemianopic pupillary inactivity). 
 
 (b) If the lesion is central to the point at which the above 
 *flex fibres are given off (Fig. 67, 5), illumination of the 
 
196 BING'S COMPENDIUM 
 
 insensitive halves of the retinae does, on the contrary, cause 
 contraction of .the pupil (hemianopic pupillary reaction, 
 Wernicke's phenomenon). 
 
 D. Lesions of the Cortex of the Cuneus. — A unilateral 
 lesion (Fig. 67, 7) has, of course, if the whole visual area of 
 the cortex is destroyed, the same result as an interruption 
 of the corresponding thalamo-occipital fibres — -homonymous 
 lateral hemianopsia with retained pupillary reaction. If 
 only a part of one visual area be destroyed, a part only of 
 the contralateral halves of the visual fields is blotted out 
 — the so-called quadranthemianopsia. If the affection is 
 bilateral (Fig. 67, 7 + 7a) — tumours of the falx cerebri, 
 toxic disturbances of function in the cortex, such as uraemia 
 and saturnism — we have cortical blindness, in which the 
 pupillary reaction remains unaffected, and can be evoked in 
 both amaurotic eyes. 
 
 E. Lesions of the Convexity and of the White Matter of 
 the Occipital Lobe and of the Gyrus Angularis. — Bilateral 
 lesions involving the visual memory centres in the cortex, 
 or the association fibres which pass thither from the cuneus 
 (Fig. 67, 8 + 8a, 9 + 9a, 8 -h 9a, or 8a + 9), cause conceptual 
 blindness (" mind-blindness," " object-blindness ") — a, con- 
 dition in which patients can see objects as flat surfaces or 
 as solid bodies, but are unable to recognize them for what 
 they are. Where unilateral disease of the occipital lobe 
 causes conceptual blindness, we have to do with tumours 
 growing in one and pressing on the other occipital lobe. The 
 left angular gyrus has a special function. This is the centre 
 for recognition of the meaning of written signs, of " letter 
 pictures " — a centre which has close relations, not only with 
 the visual cortical area, but also with the cortical area for 
 the understanding of speech {vide Fig. 59). Lesions of the 
 angular gyrus (Fig. 67, 6) cause, therefore, alexia, word- 
 blindness, inability to read, sometimes, also, conjugate 
 deviation {vide supra, p. 182). 
 
 If the cuneate cortex is destroyed in one hemisphere, and 
 the occipital white matter or the cortex of the occipital 
 convexity in the other (Fig. 67, 7 -i- 9a or 7 + 8a), hemianopsia 
 is complicated by conceptual blindness ; for the unaffected 
 area for visual memory is put out of action, owing to the 
 fact that no stimuli reach it from the neighbouring cunew 
 
CERPJBRAL LESIONS 197 
 
 It should be added that, in the regional diagnosis of 
 visual disturbances, any accompanying symptoms, of a 
 different order, must be considered. It, for example, an 
 homonymous lateral hemianopsia comes on in the course of 
 a meningitis, we may infer that the contralateral cuneate 
 cortex is involved ; if , in a case of cerebral softening, we 
 have alexia with right-sided homonymous hemianopsia and 
 Wernicke's phenomenon, the inference is that a focus of 
 softening in the angular gyrus has, as not infrequently 
 happens, spread to the subjacent fibres of Gratiolet (Fig. 67, 
 6 + 6a) ; if, on the other hand, hemiansesthesia and hemi- 
 anakusis are present, the focus is to be looked for in the 
 carrefour sensitif (Fig. 67, 5 + 5a). 
 
 Direct observation of the optic nerves with the ophthalmo- 
 scope is of very little assistance in localization. All the 
 more importance, therefore, is to be attached to the con- 
 dition known as " choked disc," as a general symptom, 
 pointing to increase of intracranial pressure. With head- 
 ache, cerebral vomiting, vertigo, slowing of the pulse, and 
 disturbances of consciousness, it plays a leading role in 
 the symptom-complex of pressure on the brain. 
 
 CHAPTER IV. 
 
 LOCALIZING VALUE OF DISORDERS OF SPEECH. 
 
 Disorders of speech due to focal diseases or lesions of the 
 cerebrum must be distinguished as anarthric oraphasic. 
 
 The anarthric form, disturbance of articulation, depends 
 on lesions or the nervous mechanism governing the muscles 
 of speech. We meet it, therefore, in bulbar paralysis as the 
 result of nuclear, in pseudo-bulbar paralysis as the result 
 of supranuclear, lesions. The latter must be bilateral, as 
 all the muscles in question — so far, at any rate, as their 
 special speech function is concerned — are innervated from 
 both hemispheres. At what point, however, in the cortico- 
 nuclear nerve channels the bilateral interruptions may be 
 situated, whether in the opercula, the centrum semiovale, 
 the internal capsules, the cerebral peduncles, or the pons, 
 is, so far as the development of anarthric or dysarthric dis- 
 turbances of speech is concerned, a matter of indifference. 
 
198 BING'S COMPENDIUM 
 
 A description of this form of disorder of speech has been 
 given on pp. 123, 124. 
 
 Very different is the case with the aphasias, which we 
 classify as motor, or expressive, and sensory, or perceptive. 
 
 (a) In motor aphasia there is inability to translate ideas 
 or concepts into words. The patient is not dumb ; there 
 is no paralysis of his muscles of speech. Their ordered 
 co-operation, however, which is essential for normal speech, 
 has become impossible for him ; as, in childhood, he had to 
 learn gradually how to use the organs of speech to form 
 words, so, now, the kinsesthetic memory pictures for the 
 concepts mastered during the process of learning speech 
 have become lost to him. The distinction between this 
 form of disturbance of speech and the anarthric is expressed 
 most briefly and significantly in the French language : 
 " L'aphasique ne eait plus parler, I'anarthrique ne peut plus 
 parler." 
 
 (h) In sensory aphasia, not the power to speak, but the 
 understanding of speech, is lost. The patient hears the 
 spoken word perfectly, but can no longer understand it, as 
 it no longer evokes in the consciousness its corresponding 
 concepts. His mother-tongue sounds to him as a foreign 
 language of which he has learnt little or nothing, sounds 
 to a normal individual. He has lost his memory for the 
 meaning of words. Sensory aphasia is often accompanied 
 by paraphasia ; that is to say, the patient makes continual 
 mistakes in speaking, and uses, instead of the correct 
 words, others — perhaps of simUar sound. This is explained 
 by the fact that unconsciously we test, so to speak, inter- 
 nally the "ring " of each word before uttering it, by means 
 of our sensory speech centre. If this no longer functions 
 normally, the patient very readily uses incorrect words, and 
 is unable to recognize his mistake, as, in consequence of his 
 sensory aphasia, he does not understand his own words. 
 
 The motor speech centre (anterior centre, Broca's centre), the 
 storing-up place for the kinsesthetic memory pictures neces- 
 sary for ordered speech, is situated at the foot — i.e., in the 
 posterior portion — of the inferior frontal convolution, where 
 it borders the operculum (c/. Fig. 68), but extends probably 
 also into the neighbouring portions of the Island of Reil, 
 the second frontal convolution, and the pre-central gyrue. 
 
CEREBRAL LESIONS 199 
 
 The sensory speech centre {posterior centre, Wernicke's centre), 
 in which the tone pictures which render possible the under- 
 standing of speech are stored up, is situated in the left 
 superior temporal convolution (Fig. 68, W.). 
 
 If the anterior speech centre is destroyed by some morbid 
 process, motor aphasia develops, while destruction of the 
 posterior centre causes sensory aphasia. Should both 
 centres be destroyed, both the ability to speak and the 
 understanding of speech are lost, and we have the condition 
 known as total aphasia. 
 
 A 'priori it would be natural to suppose that destruction 
 of the nerve tracts coming from Broca's centre, or of 
 those passing to Wernicke's centre, would have the same 
 results as destruction of those centres themselves. It is 
 not so, however, and it is possible to distinguish between 
 cortical motor and sensory aphasia on the one hand, and 
 subcortical forms on the other. 
 
 A detailed account of the symptomatology of these 
 separate forms of aphasia would be out of place in an intro- 
 duction to the study of regional diagnosis. The following 
 statements on the matter will suffice : 
 
 As will be seen from Fig. 68, not only is the motor speech 
 centre (B) connected with the cortical centres for the labial, 
 lingual, and laryngeal muscles, and the sensory speech 
 centre (W) with thg auditory area in the cortex, but these 
 two centres communicate also by means of associatio: 
 fibres : (1) with one another ; (2) with the higher psychical 
 centres of the frontal cortex, the so-called " ideation 
 centres " ; and (3) with the cortical centres for writing and 
 reading (S and L). The gyrus angularis, the memory 
 centre for the recognition of written signs, whose destruction 
 causes alexia or word - blindness, constitutes a special 
 reading centre {vide supra, p. 196). A writing centre was 
 formerly placed at the foot of the left middle frontal convo- 
 lution ; this localization is now recognized as erroneous, and 
 the Asriting centre is regarded as identical with the centre for 
 the hand and fingers in the precentral gyrus (Fig. 59, c and d). 
 
 This network of association fibres is of significance in con- 
 nection with the psychical functions which we may briefly 
 denominate " inner speech." By this term we understand 
 all that must take place subconsciously in our brains before 
 
200 
 
 BING'S COMPENDIUM 
 
 we put a thought into words and express these words in 
 speech or writing, or before we gain full knowledge and under- 
 standing of the spoken or written expressions of others. 
 This "inner speech" develops autogenetically as follows: 
 The child first repeats words he hears, then attaches con- 
 cepts to them, then, when those concepts arise in his con- 
 sciousness, he reproduces the words himself ; later, in his 
 reading and writing lessons, connects sounds with the 
 symbols ehosen to express them, and so on. 
 
 Of primary importance for a true understanding of the 
 
 ^10. 68. 
 
 UndeiBtandlng 
 of writing. 
 
 The Cortical Speech Cbntkes and their Connections. 
 
 B = Brooa's ofsntre ; W= Wernicke's centre; L = Reading centre; S = Writing 
 centre ; a = Inferior frontal convolution ; 5 = Superior temporal convolution ; 
 c=Anterior central convolution ; (i=Angular gyrus. 
 
 question of aphasia is the fact that all the association fibres 
 concerned in the function of " inner speech " run in the 
 cerebral cortex, while those concerned in the act of speech 
 itself pass through the medullary substance. This is shown 
 diagrammatically in Fig. 69, from which it will be seen that a 
 cortical lesion of Broca's centre (A) must give rise to more 
 symptoms of disturbance of the speech function than a 
 subcortical lesion (B). For by the former the association 
 
CEREBRAL LESIONS 201 
 
 fibres for inner speech are interrupted, while the latter in no 
 way involves them. Thus subcortical motor aphasia is a 
 pure aphasia, a simple inhibition of actual speech, a mere 
 word-dumbness. Mutatis mutandis cortical sensory aphasia 
 is distinguished from subcortical, pure word-deafness, in a 
 similar way. It may be laid down therefore as a general 
 principle that cortical aphasias are never pure. 
 
 Agraphia and alexia are most marked in total aphasia. 
 
 Pm. 69. 
 
 3 
 1 Understanding 
 
 Writing. 2 of ape ech, 
 
 Reading. 
 
 t^^^^^^^ m.^ Centre for 
 
 Broca's H(MI^J^^^^^UU///IMMMl^^WSSSISBSWffil/ffi muscles of 
 
 centre. 1MM^^m:m^mil/llim/MIWmSiWnaiaMmU.milrl articulation. 
 
 In a Cortical Motob Aphasia (A). 1, 2, 3, and 4 are Interrttpi-bd ; in 
 A Subcortical Motor Aphasia (B), only 4 is Interrupted. 
 
 Here the patient has also lost the power either to use or 
 to understand the language of gesture and facial expression 
 (motor and sensory amimia). 
 
 The condition in which the individual has lost all power 
 of mutual understanding with his fellows is known as 
 Aaymbolia or Asemia. 
 
 The agraphia and alexia which accompany cortical sensory 
 aphasia are both very obvious. In cortical motor aphasia, 
 on the other hand, only the agraphia is as a rule at all severe ; 
 the power of reading is much less impaired, and in many 
 
202 lilNG'S COMPENDIUM 
 
 cases special methods are required for the detection of dis- 
 turbances of the function : printed words, for instance, may 
 be understood, but not written words, or the patient may be 
 unable to understand writing if the syllables are separated 
 from each other, and so on. The disturbance of speech 
 which characterizes cortical sensory aphasia is always 
 obvious, and is of the nature of paraphasia ; in cortical 
 motor aphasia, on the other hand, the patient is, as a rule, 
 not noticed to have any difficulty in understanding speech 
 unless his interlocutor speaks very quickly or uses compli- 
 cated sentences. 
 
 The case is different with aphasias due to subcortical 
 affections of the left frontal or temporal lobe, which do not 
 involve the cortex itself. In the former case (frontal), we 
 have pure motor aphasia ( = word dumbness) ; in the latter 
 pure sensory aphasia { = word deafness). In neither case is 
 there any defect in reading or writing ; "inner speech " is 
 intact ; only the power to speak or the power to understand 
 speech is lost. In pure word deafness, too, there is no 
 paraphasia, because the sensory cortical centre is able to 
 exert its usual stimulating and controlling influence over 
 the motor. In pure word-dumbness the patient, although 
 he is unable to give utterance to words, has, in contrast to 
 the patient with cortical motor aphasia, retained the corre- 
 sponding kinsesthetic memory-pictures, and is able to indi- 
 cate with his fingers the number of syllables in a sentence to 
 which he in vain endeavours to give utterance (Dejerine- 
 Lichtheim phenomenon). 
 
 With a view to obviating mistakes in locaHzation attention 
 must here be drawn to two further points : (1) Lesions 
 situated very superficially in the subcortical reigon — e.g., in 
 the white matter of an individual convolution — ^may, in 
 their effect, resemble cortical lesions, and give rise to 
 "mixed" aphasias. (2) Probably, also, incomplete disturb- 
 ances of the motor or sensory speech centres may excep- 
 tionally cause pure word-dumbness or word-deafness. In 
 such cases we may assume that the association fibres between 
 Broca's centre and the motor centre for the muscles of speech, 
 or between the cortical area for the cochlearis and Wer- 
 nicke's centre are interrupted intracortically, without 
 destruction of function in the affected speech centres. 
 
 The further study of aphasia in all its minutiae has, at 
 
CEREBRAL LESIONS 203 
 
 present, little relevance to the subject of regional diagnosis. 
 Special forms, such as transcortical aphasias, visual, tactile, 
 amnesic aphasias, etc., which are developed when Broca's and 
 Wernicke's centres are cut off from each other, from the corti- 
 cal centres for the higher psychical functions {ideation centres), 
 or from the sensory areas, cannot be ascribed to lesions of 
 ordinary type, but n^ust be regarded as depending on many 
 varied and variable interruptions of nerve tracts . The trans- 
 cortical aphasias are, further, probably for the most part 
 intermediate stages of cortical aphasias progressing towards 
 recovery. 
 
 The localization of the psychic speech mechanism in the 
 left cortex is the rule only in right-handed individuals. 
 Left-handed persons have their speech area in the right 
 hemisphere. At the same time, cases have been recorded 
 of motor aphasia in left-handed individuals as the result 
 of lesions of the left inferior frontal convolution. It is no 
 matter for surprise, therefore, and no argument against 
 Broca's teaching, if right-handed individuals occasionally 
 fail to become aphasic after destruction of the left inferior 
 frontal convolution ; they must be regarded as exceptional 
 individuals, whose speech centres are on the right side. 
 (It is, indeed, extremely probable that these cortical centres 
 were originally bilateral.) 
 
 From the point of view of localization, we may sum up 
 what has been said above concerning the study of disorders 
 of speech, as follows : 
 
 1. Motor aphasia points to a lesion of the posterior inferior 
 portion of the frontal lobe, on the left side in right-handed 
 individuals, and vice versa. 
 
 2. Sensory aphasia points to a lesion of the posterior 
 superior portion of the temporal lobe, on the left side in right- 
 handed individuals, and vice versa. 
 
 3. In the rare cases in which these aphasias are " pure " 
 i.e., uncomplicated by defects of "inner speech," of read- 
 ing and writing — a subcortical lesion, not very superficially 
 situated, may be diagnosed with a high degree of probability. 
 Exceptionally we may have to do with a minimal cortical 
 
 lesion. 
 
 4. The rule of a left-handed localization in right-handed 
 individuals, and vice versa, is subject to rare exceptions. 
 
204 BING'S COMPENDIUM 
 
 CHAPTER V. 
 
 I. LOCALIZING VALUE OF SOME RARER CEREBRAL 
 SYMPTOMS. 
 
 (a) Auditory and Olfactory Defects due to Cerebral 
 Lesions. 
 
 UniLATEEAii destruction of the auditory region in the 
 cortex (videFig. 59), or of the fibres passing to it from the 
 inferior corpus quadrigeminum and the mesial corpus 
 geniculatum, causes impairment of hearing or complete 
 deafness on the opposite side. This crossed hemianakusis, 
 which we have already alluded to as a symptom of lesions 
 in the carrefour sensitif, is but transitory in character, 
 a fact which forces us to the conclusion that each cochlear 
 nerve is in connection with both auditory areas in the 
 temporal cortex, though its relations with the contralateral 
 one are the more intimate. The conditions are thus rather 
 more complicated than would appear from Fig. 49. Perma- 
 nent cortical deafness is caused only by complete destruc- 
 tion of the auditory area on both sides. 
 
 As regards the olfactory cortical area in the uncinate 
 gyrus, it is certain that unilateral destruction thereof 
 causes no olfactory defect, and that anosmia is produced, 
 only by complete destruction of this area on both sides. 
 Of gustatory defects as symptoms of cerebral lesions nothing 
 is known. 
 
 (6) Apraxia. 
 
 By apraxia is meant a condition in which separate 
 movements of the extremities, especially of the hands, can 
 be carried out correctly, but the patient is unable to fit, so 
 to speak, his movements to his purpose. He has lost his 
 memory for the synergias and combinations of single move- 
 ments necessary for the effective and suitable use of an in- 
 strument, for gesture, for greeting an acquaintance, etc. He 
 puts his tooth-brush in his mouth like a cigar, and so on. 
 This condition has many analogies with motor aphasia. 
 
 Clinically, three distinct varieties of apraxia are recog- 
 nized : 
 
CEREBRAL LESIONS 
 
 205 
 
 1. Ideational apraxia, a condition which resembles ex- 
 treme absent-mindedness, and, as a general rule, only reveals 
 itself in the performance of complicated movements. The 
 power of forming in the ideational sphere a correct plan of 
 action suited to the movements to be carried out is inter- 
 fered with ; the voluntary impulses aie incorrect. The 
 underlying anatomical condition is some diffuse morbid 
 
 Fig. 70. 
 
 KanoL 
 
 N:»- 
 
 HandL 
 
 Thbbb Foci which may lead to Apraxia of the Left Hand. 
 (FoouB 1 causes paralysis of the right hand also.) 
 
 process, such as senUe dementia, progressive paralysis, or 
 diffuse cerebral arterio-sclerosis, so that this variety of 
 apraxia has no regional diagnostic significance. 
 
 2. Motor apraxia. In this form the movements of a limb 
 are carried out as if the patient were trying them for. the 
 first time ; coarse movements are very clumsily executed, 
 while finer manipulations (writing, threading a needle. 
 
206 BING'S COMPENDIUM 
 
 sewing, etc.) cannot be executed at all. The underlying 
 condition here is a lesion of the motor area governing the 
 affected limb, a lesion which, whUe not leading to paralysis 
 of the limb, effaces the kinaesthetic memory-pictures on 
 which its ordered movements depend. 
 
 3. Ideo-motor apraxia. In this form ideation and the 
 motor centres for movements of the limb with their kinaes- 
 thetic memory-pictures are both intact. Their connection, 
 however, with each other is interrupted. Simple move- 
 ments whose execution is, so to speak, laid down in memory- 
 pictures in the motor centre, are, therefore, executed cor- 
 rectly, but when forming part of a larger movement-sequence 
 they are brought in mal apropos, in incorrect relation with 
 other elements of the sequence. The " orders " of the 
 ideation centres no longer reach in correct form the motolr 
 centre for the limb, which has become to a certain extent 
 independent of general cerebral control. 
 
 Ideo-motor apraxia is found under two separate sets of 
 conditions : 
 
 Firstly, in general, when the senso-motor cortex, while 
 retaining its integrity, is cut off from other cortical areas, 
 especially from the centres for the storing up of verbal 
 and material concepts, in the temporal and occipital lobes. 
 Thus, lesions in the parietal lobe occasionally cause apraxia 
 of the opposite hand. The " apraxic " agraphia, which may 
 be present as one of the symptoms of such a lesion, is to be 
 distinguished, pathogenetically, from " aphasic " agraphia. 
 
 In the second place, apraxia of the left hand may be 
 observed when its senso-motor area in the right cortex, 
 whUe remaining itself intact, has lost its connection with 
 the senso-motor area of the left hemisphere. The left 
 hemisphere reveals, at any rate in right-handed individuals, 
 its functional superiority, in this respect also, that its senso- 
 motor area exercises a controlling influence over the activity 
 of that of its fellow. This control is exercised solely by means 
 of the commissural fibres of the corpus callosum. Apraxia 
 of the left hand is found, therefore, in lesions which sever 
 the callosal fibres or their prolongations, whether the inter- 
 ruption be in the corpus callosum itself* or in one of the two 
 
 * If the apraxia is associated with a bilateral hemiparesis without 
 hyper-reflex or Babinski's sign, it is probable that the interruption is 
 
CEREBRAL LESIONS 207 
 
 hemispheres. Thus, a lesion of the left centrum semiovale 
 may not only cause right hemiphlegia through interruption 
 of pyramid fibres, but, simultaneously, a left-sided apraxia, 
 owing to destruction of commissural fibres and consequent 
 removal of the right senso-motor area from the controlling 
 influence of the left {vide Fig. 70). 
 
 In the diagnosis of apraxia it is, of course, essential to 
 excluda : (1) word-deafness— i.e., to make sure that the 
 patient understands the directions given him ; and (2) ag- 
 nosia — i.e., to ascertain whether he recognizes objects cor- 
 rectly. One must also naturally be on one's guard against 
 mistaking ataxic, choreic, or athetotic movements for 
 apraxia. 
 
 The question of apraxia is not yet thoroughly cleared up ; 
 the whole subject, indeed, is still in process of investigation. 
 
 (c) Disturbances in the Spheres of Intellect and 
 Character. 
 
 Psychic disturbances are observed chiefly in lesions of 
 the anterior portions of the frontal lobe. The lesion must 
 be bilateral, or, if unilateral, it must be capable of producing 
 a sympathetic symmetrical affection of the opposite frontal 
 lobe (pressure from a tumour, etc.). In such a condition, 
 pronounced intellectual defect of a similar kind to that 
 found in progressive paralysis (in which there is marked 
 atrophy of the frontal brain) is apt to come on, and in 
 addition, especially in tumours, a tendency to make non- 
 sensical jokes (moria), with loss of moral sense and pleasure 
 in offensive behaviour. Unilateral affections of the frontal 
 lobes may be quite without symptoms. 
 
 situated in the corpus oallosum itself. In proportion to the more or less 
 median situation of the lesion is the intensity of the paresis alike or different 
 on the two sides ; there may also be a combination of unilateral hemiparesia 
 with contralateral motor irritative symptoms — e.g., convulsions or hemi- 
 chorea. Sensibility remains intact as a rule in oallosal lesions, as also the 
 function of the cranial nerves ; only when the most anterior portion of the 
 corpus oallosum is affected does one find a facial paresis produced. 
 
208 BING'S COMPENDIUM 
 
 II. SYMPTOMS DUE TO LESIONS OF THE BASAL 
 GANGLIA. 
 
 We are not, in the present state of our knowledge, able 
 to pronounce, with even an approach to certainty, that a 
 given lesion is situated in the corpus striatum {caudate or 
 lenticulate nucleus). Such sensory or motor disturbances, 
 as have been observed in lesions of these structures, must 
 be regarded as due to the action of the lesions on the 
 neighbouring internal capsule, seeing that identical symp- 
 toms may be produced by lesions in the neighbourhood of 
 the capsule, which are situated neither in the lenticu- 
 late nor the caudate nucleus. The fact that bilateral 
 lesions of the corpora striata may give rise to symp- 
 toms of pseudo-bulbar paratysis is also to be explained 
 by the hypothesis of a disturbing action exercised by the 
 lesion on neighbouring cortico-nuclear fibres. In cases of 
 symmetrical multiple softening lesions of both corpora 
 striata, due to arterio-sclerosis (in which similar lesions are 
 generally present in the optic thalami), a permanent incon- 
 tinence of urine has occasionally been observed, of the active 
 or intermittent type described on p. 76. At approximately 
 equal intervals, approximately similar quantities of urine 
 are suddenly voided, involuntarily, fn a jet. The power of 
 voluntary micturition is lost, and the bladder is never 
 emptied, there being always some " residual urine." The 
 subcortical innervation of the bladder in the corpus striatum 
 and the optic thalamus {vide supra, p. 74) is apparently 
 bilateral. 
 
 We have already stated that thalamus lesions, if situated 
 in the pulvinar, cause homonymous lateral hemianopsia on 
 the opposite side (p. 195) ; also that they usually lead, through 
 action on the internal capsule, to crossed partial hemiplegia, 
 on which foundation, hemiathetosis (exceptionally hemi- 
 chorea) not infrequently develops. The following, how- 
 ever, are to be regarded as direct symptoms of thalamus 
 lesions. 
 
 1. The abolition of certain psycho-reflexes. Occasionally, 
 Sor instance, the following paradoxic phenomenon is observed 
 
CEREBRAL LESIONS 209 
 
 in thalamus lesions : In involuntary laughter or weeping, 
 the lower facial muscles on the side opposed to the lesion re- 
 main stiff and immobile, the power to contract them volun- 
 tarily being at the same time quite unimpaired. As the 
 opposite condition is sometimes found in capsular hemi- 
 plegias, the inference is justified that we have here to do 
 with an interruption of a reflex arc as it passes through the 
 thalamus.* 
 
 2. A persistent crossed hzmianoesthesia, which is usually 
 much less marked for tactile, painful, and thermal 
 stimuli than for those connected with the deep sensibility 
 (" muscular sense "). The interference with the latter 
 causes unilateral ataxia and aster eognosis. 
 
 3. Exceedingly severe and continuous pains, occasionally 
 exacerbated, and very refractory to analgesics. These 
 central pains are referred to the contralateral half of the 
 body, the hemiansesthesia alluded to above being thus 
 given the impress of an hemiancesthesia dolorosa {cf. p. 33). 
 
 While the interference with psycho-reflexes, above de- 
 scribed, points to a lesion in the anterior^ portion of the 
 thalamus, the two last-named symptoms are more frequently 
 observed when the lesion is situated in the posterior half of 
 the organ. The character of the above-enumerated direct 
 thalamus symptoms, whether they be of paralytic or of u-ri- 
 tative type, corresponds with the function of the thalamus, 
 the great connecting station, so to speak, through which 
 practically the whole of the sensory tracts must pass before 
 diverging to the sensory area in the cortex. 
 
 III. SYMPTOMS DUE TO LESIONS OF THE 
 HYPOPHYSIS. 
 
 Tumours of the hypophysis usually lead, in the first 
 instance, and rapidly, to impairment of function in neigh- 
 bouring nerves. The closely contiguous optic chiasma is 
 particularly exposed to injury, and early disorders of the 
 visual function are common. The most characteristic is 
 heteronymous bitemporal hemianopsia. There may. how- 
 
 * Irritative lesions in the neighbourhood of this thalamic reflex centre may 
 perhaps lead to "forced laughter" and "forced weeping." 
 
210 
 
 BING'S COMPENDIUM 
 
 ever, be double amaurosis from complete destruction of the 
 chiasma, or unilateral amaurosis with hemianopsia of the 
 other eye from unilateral destruction. The production of 
 
 Fig. 7L 
 
 Topography of the Base of the Skull. 
 H = Hypophysis. I-XII = Cranial nerves. 
 
 these symptom-complexes has been discussed on p. 192-194. 
 The nerves of the ocular muscles, oculo-motor, trochlear, 
 and abducens, which pass close to the hypophysis on their 
 
CEREBRAL LESIONS 211 
 
 way to the orbit, are very readily paralyzed by pressure 
 from hypophysis tumours, as also is the first or ophthalmic 
 ramus of the trigeminus {vide Fig. 71). 
 
 In many affections of the hypophysis (haemorrhages, col- 
 loidal, or fibrous degeneration, tumours), the symptom- 
 complex known as " acromegaly " is developed (enormous 
 growth of the hands, feet, tongue, nose, and lower jaw). 
 In other cases, however, there is evolved the condition known 
 as " hypophysial eunuchism " or " degeneratio adiposo- 
 genitahs " (excessive growth of fat with arrested develop- 
 ment of the genitals and of secondary sexual characters, such 
 as pubic alteration of contour, axillary and pubic hair). It 
 would seem that acromegaly is the result of a pathological 
 over-stimulation of the hj^ophysis leading to an abnormal 
 increase in the special internal secretion of the gland, while, 
 on the other hand, degeneratio adiposo-genitalis is the ex- 
 pression of a secretory insufficiency on the part of the hypo- 
 physis. It must be borne in mind that many cases of 
 hypophysis tumours have been recorded in which neither 
 acromegaly nor hypophysial eunuchism was present. De- 
 tached adenomata of the hypophysis also (e.g., in the 
 sphenoid antrum) may lead to the development of acro- 
 megaly, while hj^ophysial eunuchism may be produced by 
 the action on the hypophysis of contiguous pathological 
 processes in the base of the skull. 
 
 Further symptoms which, when the general signs of 
 cerebral pressure are present, point to the hypophysis as the 
 seat of the lesion, are : obstinate somnolence, polyuria with 
 polydipsia (occasionally glycosuria), hydrorrhoea nasalis 
 (intermittent flow of clear cerebro-spinal fluid through the 
 nose). For a consideration of the question of Rontgen-ray 
 diagnosis in this connection, vide infra p. 214. 
 
 APPENDIX 
 
 CRANIO-CEREBRAL TOPOGRAPHY 
 
 Cranio-cerebral topography is of the utmost importance 
 in aU operative procedures on the brain. In operative 
 attacks on accessible morbid processes (superficial haemor- 
 rhages, tumours, abscesses, etc.), the choice of the situation 
 for trephining must, it need hardly be said, be based on 
 the localization of the lesion, whatever it may be. 
 
212 
 
 BING'S COMPENDIUM 
 
 It is of enormous practical importance to be able to fix 
 the position of the fissure of Sylvius and the central fissure 
 on the outside of the cranial wall; for, in the first place, cere- 
 bral surgery is, up to the present time, in the main a surgery 
 of the central convolutions and the temporal lobe, and, in 
 the second place, from the position of these two chief 
 fissures the position of the others can be deduced without 
 
 difficulty. 
 
 Fig. 72. 
 
 Projection of the Cerebral Fissurbs on the Surface of 
 THE Skull. 
 
 I = Coronal suture ; II = Sagittal suture ; III=Lambdoldal suture; IV=Temporal 
 suture; F' and F''=First and second frontal fissures; O* and 0^ = Flrst 
 and second occipital fissures; Ip. = Interparietal fissure; T* and T*= First 
 and second temporal fissures; 01m. = Cerebellum ; >c= Posterior border of 
 mastoid process. 
 
 Fig. 73 gives the position of the cerebral fissures with 
 reference to the external surface of the cranium. The two 
 vertical lines seen in the figure, the so-called " pre- and post- 
 auricular lines," are constructed as follows, with a view to 
 the determination of the position of the two chief fissures: 
 The former passes upwards from the anterior border of the 
 external auditory meatus to the vertex, being so drawn 
 as to meet the sagittal line connecting the root of the nose 
 and the occipital protuberance, at right angles; the latter 
 
CEREBRAL LESIONS 
 
 213 
 
 is drawn in an analogous manner, but from the posterior 
 border of the mastoid process. The points a and 6 divide 
 the pre-auricular Une into three equal parts; c bisects it. 
 If the trephine is applied between c and 6, the lower end of 
 the central convolutions will be reached, which in adults 
 generally lies about 7 centimetres above the auditory 
 meatus. The lower end of the central fissure often lies 
 directly under the pre-auricular line. In our figure it is 
 represented as reaching farther forward, for two types of 
 relation between the brain and the outer cranial wall may 
 be recognized-^a frontopetal type, as represented in our 
 
 Via. 73. 
 
 Projection of the Middle Meningeal Artery and the Tkansvbbsb 
 Sinus on the External Surface of the Skull. 
 
 figure, and an occipitopetal type, in which the different 
 fissures and convolutions lie rather farther back. 
 
 The post-auricular line crosses the upper end of the 
 central fissure. The fissure of Sylvius will be met with 
 about 1 to li centimetres below the lower end of the 
 central fissure. For some distance the Sylvian fissure lies 
 immediately beneath the squamous suture. Under the 
 parietal tuberosity lie, as a rule, the upper end of the fissure 
 of Sylvius and the supramarginate gyrus. 
 
214 BING'S COMPENDIUM 
 
 An indication for prompt surgical interference is afforded 
 by haemorrhages from the middle meningeal artery (after 
 fractures of the skull, etc.). This vessel, a branch of the 
 maxillary artery, enters the cranial cavity through the 
 foramen spinosum, and divides into an anterior and a 
 posterior branch. In order to ligature the common trunk, 
 the trephine must be applied immediately above the middle 
 of the zygomatic arch (c/. Fig. 73). The anterior branch is 
 reached by trephining at the intersection of two lines, one 
 of which is parallel to the zygomatic arch and two finger- 
 breadths above it, while the other is a vertical line drawn to 
 meet the first from a point just behind the zygomatic pro- 
 cess of the frontal bone. 
 
 Fig. 73 shows the superficial projection of the transverse 
 sinus, injury of which it is important to avoid in operations 
 on the cerebellum. 
 
 II. 
 
 The Rontgen rays play an important part in the localiza- 
 tion of cerebral tumours. Direct Rontgenoscopy of the 
 tumour is indeed impossible, unless the latter has undergone 
 some calcification. Valuable conclusions may, however, be 
 drawn from changes in the bones of the skuU revealed by the 
 rays. 
 
 The most significant of these changes are circumscribed 
 areas of involvement of the cranial waUs. Thus, tumours 
 of the h3^ophysis often erode the sdla turcica, those of the 
 cerebello-pontine angle the posterior surface of the dorsum 
 sellic, new growths of the cerebellum, the squamous portion 
 of the occipital, etc. On the other hand, circumscribed 
 thickenings of the cranial wall originating from the dura 
 mater are sometimes observed in the neighbourhood of 
 tumours. Occa^sionally we have both thickening and 
 erosion of bone substance. Again, a localized pushing out or 
 thinning of the cranial wall may be noticed over the site of 
 a tumour. Finally the VencB diploeticce, which are, normally, 
 hardly recognizable in Rontgen pictures, are occasionally 
 so much distended in cases of cerebral tumour, that they 
 appear as broad bands on the plate, the distension being 
 most marked in the neighbourhood of the tumour. 
 
INDEX 
 
 Abdominal reflex, 7 
 Abducens, 97 
 
 nucleus of, 97, 146 el seq. 
 
 paralysis of, 150, 166 
 Abscess, cerebral, 182, 211 
 Absence of reflexes, 20, 35 
 
 in cerebellar tumours, 159 
 Accessory nerve, 90, 92, 117, 118 
 nucleus of, 90, 91 
 paralysis of, 118 
 Achilles tendon reflex, 66 
 Acromegaly, 210 
 Adams-Stokes disease, 71 
 Adiadochokinesia, 159 
 Adiposo-genital degeneration, 114, 
 
 211 
 Agnosia, 16, 207 
 Agraphia, 201, 206 
 Ala cinerea, 93 
 Alexia, 199 et seq. 
 Amyotrophic lateral sclerosis, 29 
 Aneesthesia, IS 
 
 dissociated, 32 
 
 dolorosa, 33 
 
 peri-ano-genital, 79 
 Anakusis, 134 e^ seq. 
 Analgesia, 16, 31 
 Anarthria, 197 
 
 Aneurysms, 113, 126, 145, 195 
 Anidrosis, 24, 72 
 Anisokoria, 70 
 Ankle-clonus, 26 
 Anosmia, 153, 204 
 Ansa hjrpoglossi, 117, 118 
 Aphasia, 19T et seq. 
 Apomorphine, diagnostic injection 
 of, 120 
 
 Apoplexy, 177, 184 
 
 serous, 188 
 Apraxia, 184, 204 et seq. 
 Argyll-Robertson phenomenon, 1 93 
 Arteries, cerebral, 175 et seq. 
 
 spinal, 13, 14 
 Arterio-sclerosis, cerebral, 180 
 Associating tracts, 9 
 Astereognosis, 181, 209 
 Asjmergia, 16, 158 
 Ataxia, 16, 32, 105, 114, 180 
 
 cerebellar, 32, 158 
 
 "cerebral," 181 
 
 locomotor, 32 
 Athetosis, 167, 190 
 Atony, 18 et seq., 28, 36 
 Atropine, diagnostic injection of, 
 
 120 
 Auditory centre, 134 et seq., 169 
 
 nerve, 96, 132 et seq. 
 Aura, in Jacksonian epilepsy, 181, 
 184 
 
 "sensory," 184 
 Avelli's symptom-complex, 125 
 
 B 
 
 Babinski's sign, 26, 30, 38, 113, 187 
 
 Barany's experiment, 154 
 
 Basal ganglia, lesions of, 208 e< seq. 
 
 Bell's paralysis, 126 
 
 Benedikt's symptom-complex, 109 
 
 Biceps, 49 et seq. 
 
 Bladder, innervation of, 73, 74 
 
 symptoms, 76, 77 
 Blindness, conceptual, 196 
 Bogen = Arc 
 Brachialis intemus, 53 
 
 215 
 
216 
 
 BING'S COMPENDIUM 
 
 Bradycardia, 120 
 
 Brain, convolutions of, 168 et seq. 
 
 cortex of, 168 et seq. 
 
 haemorrhage into, 1 -'5 et seq. 
 
 lesions of base of, 113 
 
 tumours of, 113, 125, 132, 153, 
 180 et seq., 196, 207 
 Brain-stem, 85 et seq. 
 Broca's centre, 198 et seq. 
 Brown-Sequard's " spinal epilep- 
 sy," 31 
 
 symptom-complex, 38 et seq. 
 Bulbar paralysis, 124 
 Burdach, column of, 6, 7 
 
 nucleus of, 91 et seq. 
 
 Calamus soriptorius, 92 
 Capsule, internal, 173, 184 et seq. 
 " Carrefour sensitif," 173, 185 
 Cauda equina, 79, 80 
 
 lesions of, 80 
 Central convolutions, 168 et seq., 
 211 
 
 gliosis, 32 
 
 pains, 209 
 Centres for ocular movements, 149 
 
 etseq. 
 Centrum ano-spinale, 74, 77 
 
 cilio-spinale, 68 
 
 genito-spinale, 75, 78 
 
 vesioo-spinale, 74, 76, 77 
 Cerebellar ataxia, 32, 158 
 
 peduncles, 154, 155 
 
 tumours, 159, 164, 165 
 
 vertigo, 164 e< seq. 
 Cerebello-pontine angle, tumours of, 
 
 136, 165 
 Cerebellum, 153 et seq. 
 Cerebral convolutions, 168 e/ seq. 
 
 cortex, 168 et seq. 
 
 haemorrhage, 177, 185 et seq. 
 
 peduncles, 102 
 
 tumours, 113, 125, 132, 153, 
 180 etseq., 196,209 
 Chejme-Stokes breathing, 120 
 Chiasma, lesions of, 195 
 Choked disc, 168, 182, 197 
 Chorda tjrmpani, 127 
 
 Chorea in lesions of brachia con- 
 junctiva, 167 
 
 post-hemiplegica, 190 
 Circumduction, 186 
 Clarke, column of, 5, 8, 12 
 Clonus, 26, 187 
 Cochlear nerve, 96, 132 
 nucleus of, 96 
 Commissure anterior, 172 
 Conceptual blindness, 196 
 Conjugate deviation, 152 et seq., 
 166, 183, 196 
 
 paralysis, 151, 153 
 Conjunctival reflex, 140 
 Conus terminalis, 73 et seq. 
 Co-ordination, disturbance of, 16 
 Corneal reflex, 140 
 Comu-commissural bundle, 10 
 Corona radiata, 173 
 Corpora quadrigemina, lesions of, 
 
 114 
 Corpus oallosum, 172, 206 
 
 geniculatum, 134, 193 
 
 restiforme, 96, 160 
 
 striatum, 208 et seq. 
 Cortical ariiaurosis, 196 
 
 centres for ocular movements, 
 149 et seq. 
 
 epilepsy, 132, 181 
 Cranio-cerebral topography, 211 e< 
 
 seq. 
 Cremaster reflex, 66 
 
 D 
 
 Deafness, "nervous," 134 
 
 Deiters, nucleus of, 97, 157 
 
 Dejerine-Lichtheim phenomenon, 
 202 
 
 Dejerine - Thomas (spinal topo- 
 graphy), 81, 82 
 
 Deltoid, 52, 57 
 
 Deviation, conjugate, 152 et seq., 
 166, 183, 196 
 
 Dilatator pupillse, 68 
 
 Diplegia, cerebral, 180 
 facial, 126, 127 
 masticatory, 141 
 
 ' Dissociated anaesthesia, 32 
 
 defects of genital function, 78 
 
INDEX 
 
 217 
 
 Dorsal columns, 32 
 
 nuclei of, 91 et seq. 
 longitudinal bundle, 92 et seq., 
 
 112, 150, 154, 166 
 pedal reflex, 26, 30, 38, 187 
 Duchenne-Erb plexus-paralysis, 68 
 Dysarthria, 197 
 Dyspinealism, 114 
 
 E 
 
 Edinger's schema, 63 
 Edinger-Westphal nucleus, 146, 193 
 
 ttseq. 
 Ejaculation, 75 
 Elbow-clonus, 26 
 Emjnentia teres, 97 
 Empyema of sphenoid antrum, 
 
 195 
 Encephalorrhagia, 185 e< seq. 
 Endogenous areas of the dorsal 
 columns, 9 et seq. 
 spinal tracts, 2, 8 
 Enophthalmus, 70, 142 
 Epilepsy, Jacksonian, 180 e< seq, 
 
 spinal, 31, 37 
 Epiphysis, tumours of, 114 
 Erb's paralysis, 58 
 Erection, 75 
 Eumetria, 156, 157 
 Eunuchism, hypophysial, 210 
 Exogenous spinal tracts, 2 et seq. 
 Exophthalmus, 71 
 Eyelids, narrowing of aperture of, 
 
 70, 142 
 
 P 
 
 Facial nerve, 97 
 
 function of, 126 et seq, 
 genu, or knee of, 97 
 paralysis of, 126 et seq. 
 
 Fasciculus, v. Tract 
 
 Fasem= fibres 
 
 FibrsB propriae, 9 
 
 endop3^amida]es, 11 
 
 Fibrillary twitchings, 31 
 
 Fillet, 91 et seq. 
 
 Finger-clonus, 26 
 
 Fissure of Sylvius, position of, 
 211 
 
 "Foot" or pedal type of radicular 
 
 paralysis, 59 
 Forced attitudes, 61 et seq. 
 
 laughter, 209 
 
 movements, 167 
 
 weeping, 209 
 Foreign bodies in brain, 182 
 Foville's paralysis, 109, 153 
 Fracture of base of skuU, 145, 153 
 
 of spinal column, 35, 60 
 Friedreich's disease, 32, 163 
 Frontopetal position of brain, 212 
 
 G 
 
 Gtenglicn ciliare, 142, 148 
 Gasseri, 99, 138. 145 
 geniculatum, 127 
 jugulare vagi, 118 
 nodosum vagi, 118 
 oticum, 142 
 petrosum, 119 
 spheno-palatinum, 142 
 spinale, v. Spinal ganglia 
 spirale, 132 
 submaxillare, 142 
 superius glosso-pharyngei, 119 
 vestibuli, 134 
 Ganglionic chain of sympathetic, 
 
 21,22 
 Genital hyperplasia, 114 
 
 organs, innervation of 75 
 Glosso-pharyngeal nerve, 94 
 function of, 119 
 nucleus of, 94 
 paralysis of, 119 
 Glosso - pharjmgo - labial paralysis 
 (supra-nuclear), v. Pseudo-bulbar 
 paralysis 
 Glossoplegia, 118 
 Glossospasm, 120 
 Gluteal, 51 
 Glycosuria, 211 
 Goll, column or fasciculus of, 6 
 
 nucleus of, 91 et seq. 
 Gowers, tract or bundle of, 8 et aeq., 
 
 94 99, 160 
 Gratiolet, tract of, 193 
 Grenzstrang= Ganglionic chain ot 
 sympathetic 
 
218 
 
 BING'S COMPENDIUM 
 
 Grosshirn= Cerebrum 
 Gummata, cerebral, 113, 163, 195 
 
 H 
 
 Hsemato-myelia, 32 
 
 Hsemorrhage, cerebral, 186 
 
 " Hand " or manual type of radio 
 
 ular paralysis, 68 
 Headache in cerebellar tumours, 
 167 
 
 from cerebral pressure, 182 
 Helicopody, 186 
 Hemiageusia, 186 
 Hemianeesthesia, 179, 186, 209 
 Hemianakusis, 185, 204 
 Hemianopio fixation of pupil, 195 
 Hemianopsia, 185, 195 et seq., 
 
 208 
 Hemianosmia, 185 
 Hemiataxia, 105, 209 
 Hemiathetosis, 190, 208 
 Hemiballismus, 190 
 Hemichorea, post-hemiplegio, 190, 
 208 
 
 prsB-hemiplegio, 190 
 Hemi-epUepsy, 182 
 Hemi-glossoplegia, 118, 122 
 Hemi-hypotonus, 161 
 Hemiopia, v. Hemianopsia 
 Hemiparaplegia, 40 
 Hemiparesis, 161 
 
 Hemiplegia, 167, 179, 184 et seq., 
 208 
 
 altemans, 109 et seq., 153 
 
 cruciata, 105 
 
 homolateralis, 189 
 
 intracorticalis, 189 
 
 lacunaris, 188 
 
 spinalis, 41 
 Hemiseetion, 38 
 Hemmung= Inhibition 
 Herpes zoster, 34, 63, 145 
 Hinterstrang= Dorsal column 
 Hinirinde= Cerebral cortex 
 Homer's symptom - complex, 68, 
 
 72 
 Hydrorrhoea nasalis, 211 
 Hypsesthesia, 15 
 Hypakusis, 134 
 
 Hypalgesia, 16, 31 
 Hypersesthesia, 15, 33, 39 
 Hyperakusis, 127 
 Hyperalgesia, 15 
 Hyperidrosis, 72 
 Hyperkinesis, 30 
 Hyperthermia, 71 
 Hyphidrosis, 24 
 Hypogeusia, 128 
 Hypoglossal nerve, 91 et seq. 
 
 function of, 117 et seq. 
 
 nucleus of, 91 et seq. 
 
 paralysis of, 118 
 Hypophysis, lesions of, 209 e< seq. 
 
 tumours of, 146, 196, 209 
 Hyporeflex, 17 e< seq. 
 Hypotaxia, 18 
 Hypotonus, 11 et seq., 159 et seq. 
 
 Ileo-psoas, 61, 54 
 Impotence, 78 
 Incontinence of faeces, 77 
 of urine, 76 et seq., 208 
 Inco-ordination, 16 
 Intermedius Wrisbergi, 127, 144 
 Internal capsule, 173 e< seq., 185 et 
 
 seq. 
 Interossei, 50, 61, 63 
 Intersegmental tracts, 9 
 Irritative symptoms, motor, 30 et 
 
 seq., 113 et seq., 120, 129 
 
 et seq., 163 et seq., 181, 
 
 189, 208, 209 
 sensory, 33 et seq., 120 et 
 
 seq., 141, 183 et seq., 209 
 
 Jacksonian epilepsy, 132, 180 et sej. 
 
 Kern = Nucleus 
 Kinsesthetic centres, 169 
 Kleinhim = Cerebellum 
 Klumpke's paralysis, 70 
 Knee-jerk, 67 
 
INDEX 
 
 219 
 
 Labyrinth, 163, 164 
 
 Lachrymal nerve, 127, 143 
 
 Lagophthalmus, 127 
 
 Lahmung= Paralysis 
 
 Laryngismus, 120 
 
 Lateral colunms, lesions of, 25 et 
 
 seq. 
 Latissimus dorsi, 49, 52 
 Lenticulate nucleus, 191 
 Longitudinal bundle, dorsal, 92 et 
 
 seq., 112, 150, 154, 166 
 Lumbar puncture, 168, 184 
 Luxation of vertebral column, 35, 60 
 
 M 
 
 Magendie's vertical divergence, 
 
 167 
 Masticatory spasm, 141 
 Medulla oblongata, 90 et seq. 
 Mendel-Bechterew phenomenon, 26, 
 
 30, 38, 187 
 Meniere's disease, 164 
 Meningitis, 113, 145, 151, 153, 
 
 182 
 Millard-Gubler's paralysis, 109, 111 
 Mind-blindness, 196 
 Monakow, bundle of, v. Tract, 
 
 rubro-spinal 
 Monoplegia, 179 
 cruraUs, 180 
 facialis, 180 
 facio-brachialis, 180 
 faeio-lingualis, 180 
 masticatoria, 141 
 Moria, 207 
 
 Motor areas in cortex, 168 et seq. 
 Movements, involuntary associated, 
 
 27, 187 
 Muscles, fimction and innervation 
 
 of, 52, 54 
 Muscular atrophy, cerebral, 187 
 degenerative, 21, 28 
 neural progressive, 31 
 spinal, 28 
 centres, spinal, 44 et seq. 
 tonus, 18^ 
 Mydriasis, 71 
 
 N 
 
 Nucleus ambiguus, 93 
 
 ruber tegmenti, 101 
 Nystagmus, 112, 153, 165 
 
 Ocoipitopetal position of brain, 213 
 Oculo-motor nerve, 101 
 
 nucleus of, 102, 146 et seq. 
 
 paralysis of, 150 e^ seq. 
 Ooulo-pupillary symptoms in lesions 
 
 of cervical cord, 68 
 CEsophagismus, 120 
 Olive, 92, 95 et seq. 
 Ophthalmoplegia, 151, 166 
 Oppenheim's sign, 26, 30, 38 
 Optic tract, 191 e< seq. 
 Oxyakoia, v. Hyperakusis 
 
 Pachymeningitis cervicalis hyper- 
 
 trophica, 33 
 Pain, sensibility to, 15 
 Pains, "central," 209 
 Palatal reflex, 119 
 Pallsesthesia, 15 
 PaUanaesthesia, 16 
 Parsesthesiae, 33, 183 
 Parakusis Willisii, 136 
 Paralyses, 17 e< seq. 
 Paralysis, bulbar, 124 
 Paraphasia, 198 
 Paraplegia, 35 
 Paresis, 17 ei seq. 
 Patellar clonus, 26 
 
 reflex, 66, 67 
 Pectorales, 49, 52 
 P eduncles, cerebellar, 154 et se^ 
 
 cerebral, 101 
 Perception centres, 170 
 Peripheral innervation, 44 et seq 
 
 paralysis, 46, 48 et seq. 
 Petrosal nerve, superficial, 127, 
 
 143 
 Pharyngeal reflex, 120 
 Pharyngismus, 120 
 Pineal gland, 114 
 
INDEX 
 
 221 
 
 Spinal cord, physiology of, 14 
 
 epilepsy, 31 
 
 ganglia, 33, 63 
 
 paralysis, spastic, 25 et seq. 
 
 puncture, v. Lumbar puncture 
 
 tracts, 2 et seq. 
 
 tumours, 43 
 Bpino-cerebellar tracts, 8, 11, 94 et 
 
 seq., 156 
 Stereo-ansesthesia, 16 
 Stereognostic sensibility, 16 
 Strumpel's sign, 27 
 Substantia gelatinosa, 90 et seq. 
 Sulcus centralis, 212 
 Sweat centres, 24 
 
 function, disturbances of, 72 
 Sympathetic nerve, 21 et seq. 
 Synergia, 16, 93, 156 
 Syringo-myelia, 32 
 
 Tabes dorsalis, 32 
 Tachycardia, 119 
 Tegmentum, 98 et seq., 112 
 Temperature sense, 15 
 Temporo-occipito-parietal area, 171 
 Tendon reflex, 37, 66, 73, 159 
 Tetraplegia, 36, 105 
 Thalamus, 191, 208 
 Thermo-anaesthesia, 15, 31 
 Thumb, muscles of, 53 
 Tibialis phenomenon, 27 
 Tinnitus, 113, 136 
 Tonus, n et seq. 
 Total aphasia, 199 
 Tract, bulbo-thalamic, 91 et seq.. 
 102 
 cortico-spinal, 2 et seq., 10, 92, 
 172 
 anterior, 4, 10 
 lateral, 4, 10 
 fronto-pontine, 101, 173 
 ocoipito-temporo-pontine, 101, 
 
 173 
 posterior radicular, 5, 10 
 rubrospinal, 4, 10, 101, 158, 
 
 160 
 spino -cerebellar, 8, 11, 94 et 
 seq., 156 
 
 Tract, spino-cerebellar, dorsal, 8, 
 11, 94 
 ventral, 8, 11, 94 
 spino-thalamic, 8, 9, 11, 103 
 tecto -spinal, 4, 11 
 thalamo-occipital, 193 
 thalamo-spinal, 4, 10, 158 
 vestibulo -cerebellar, 163 
 vestibule -spinal, 5, 11, 97, 158. 
 160 
 Transverse division of spinal cord, 
 35 et seq. 
 myelitis, 35 
 Trapezium fibres, 132 
 Trapezius, 49 et seq. 
 Tremor, post-hemiplegic, 191 
 Triceps, 53 
 Trigeminus, 99, 138 
 nuclei of, 99, 138 
 paralysis of, 138 et seq. 
 spinal root of, 90, 138 
 Trismus, 113, 141 
 Trochlear nerve, 100 
 
 nucleus of, 100, 146 et seq. 
 paralysis of, 150, 166 
 Trophic centres, 20, 21 
 
 disturbances, 20, 21, 36 
 Tubercle acoustic, 96, 102, 132 
 
 of brain, 113 
 Tumour, cerebellar, 159 et seq., 164 
 etseq. 
 cerebral, 113, 125, 153, 180, 
 
 196, 211 
 extra- and intra-medullary, 43 
 
 Vagus, 94 
 
 function of, 118 
 nuclei of, 93 et seq. 
 paralysis of, 118 et seq. 
 Vaso-motor centres, 21 et seq. 
 
 disturbances, 23, 37, 71 et seq. 
 tracts, 21 et seq. 
 Vertebral column, injuries of, 34 
 
 topographical relations of, 
 to spinal cord, 81, 82 
 Vertigo, 136, 163 et seq. 
 Vestibular nerve, 96 et seq. 
 disorders of, 164 
 
222 
 
 BING'S COMPENDIUM 
 
 Vestibular nerve, function of, 134 
 
 lesions of, 163 
 Vibration, sensation of, 15, 31 
 Vaiiger's tables of radicular inner- 
 vation, 48 et seq. 
 Visual centres, 192 ei seq. 
 
 tract, 192 et seq. 
 Vocal cords, paralysis of, 119 
 Voltolini's disease, 164 
 Vomiting, cerebral, 120 182 
 
 W 
 
 Weber's experiment, 135 
 
 paralysis, 109, 114, 153 
 Wernicke's centre, 1 99 
 
 phenomenon, 196 
 Westphal-Edinger nucleus, 146, 193 
 Word blindness, 199 [et seq. 
 
 deafness, 202 
 
 dumbness, 202 
 Wurzel =Boot 
 
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