SYNOPSIS OF LECTURES 
 
 Diseases of ttie Nervous System, 
 
 DELIVERED AT THE 
 
 COLLEGE OF PHYSICL^NS AND SURGEONS, 
 
 MEDICAL DEPARTMENT OF COLUMBL\ UNIVERSITY, 
 
 NEW YORK. 
 
 BY 
 
 M. ALLEN STARR, M.D., Ph.D., LL.D., 
 Professor of Neurology. 
 
 New York: . 
 James T. Dougherty, Publisher, 
 
 409 & 411 West Fifty-ninth Street. 
 
COPYBIGHT, 1904, 
 
 BY 
 
 JAMES T. DOUGHERTY. 
 
Digitized by the Internet Archive 
 
 in 2010 with funding from 
 
 Open Knowledge Commons 
 
 http://www.archive.org/details/synopsisoflectuOOstar 
 
SYNOPSIS OF LECTURES 
 
 UPON 
 
 DISEASES OF THE MERYOUS SYSTEM. 
 
 A KNOWLEDGE of the Structure and functions of the central 
 nervous system is an essential preliminary to the study of its 
 diseases. The human nervous system is the most complex of all 
 nervous structures, and is the culmination of the process of evolu- 
 tion. It will aid in the understanding of its structure if the 
 various stages in its evolution are known. 
 
 The Evolution of the Nervous System. 
 
 The simplest form of a nervous system consists of a single 
 mass of gray matter with a sensory and a motor nerve. 
 
 The mass of gray matter receives impulses sent from the 
 surface by the sensory fibre, acts in response to the impulse, and 
 the action is transmitted to a motor mechanism by the motor 
 nerve. 
 
 Example. The closure of an oyster-shell when the oyster 
 feels any object touching its sensory surface. Parallel action in 
 human system — any spinal reflex — e.g., knee-jerk. 
 
 Several such single masses may be joined to one another, 
 each with its sensory and motor nerve. The masses receive im- 
 pulses in succession and act in succession. 
 
 Example. Wave-like motion of a jelly-fish or caterpillar. 
 
 A compound type of nervous system consists of several sub- 
 ordinate masses joined together and presided over by a single 
 higher mass, which is joined to each of the lower masses. The 
 higher mass receives impulses from the lower masses, not directly 
 from the surface. It sends impulses to the motor mechanisms 
 through the lower masses, not directly. It secures a certain defin- 
 ite succession and combination of action in the lower masses. 
 
4 DISEASES OF THE NERVOUS SYSTEM. 
 
 Examples. The nervous system of a frog experimentally de- 
 prived of its hemispheres, capable of automatic acts of swim- 
 ming-. The automatic act of respiration in man. In man the 
 facial, laryngeal, intercostal, thoracic, and diaphragmatic re- 
 spiratory muscles act in definite succession and rhythm in the 
 act of breathing; and this act is presided over by a single centre 
 in the medulla controlling the lower medullary and spinal centres. 
 
 The higlicst type of nervous system is the complex type. 
 There are the lower centres as in the sim/ple type. There are 
 higher centres controlling the lower centres, as in the compound 
 type. There is a supreme mass controlling both the others. 
 
 This is the form found in all vertebrates, and the degree 
 of evolution in the highest or supreme mass determines the place 
 of the animal in the scale of intelligence. 
 
 In man the supreme mass is the cerebral cortex, the next 
 lower or automatic centres are the optic thalami and corpora stri- 
 ata, including gray masses in the cerebral axis ; the lowest or 
 reflex centres are the cranial nerve nuclei in the cerebral axis 
 and the gray matter of the spinal-cord segments. 
 
 These distinct gray masses are joined with one another in all 
 possible combinations by means of the white nerve tracts, which 
 pass in all directions around and within them. 
 
 Read Herbert Spencer, ' Principles of Psychology," Part I., Chaps. I. -IV. 
 Charles Mercier, "The Nervous System and the Mind," Part I. 
 
 The Neurone. 
 
 The primary elements of the nervous system are neurones, 
 and the nervous system from the simplest to the most complex in 
 the order of evolution consists of a collection of such neurones of 
 greater or lesser complexity. 
 
 The neurone consists of : 
 
 (ist) A cell body whose shape and size vary at different 
 parts of the nervous system. 
 
 (2d) Dendrites or protoplasmic prolongations of the cell 
 body which divide and subdivide as they extend outward from it 
 much like the roots of a tree. The surface of these dendrites is 
 rough, appearing like moss under the microscope on account of the 
 
DISEASES OF THE xXERVOUS SYSTEM. 5 
 
 presence of fine granules. Nervous impluses are collected by 
 these dendrites and transmitted to the cell body. Fine filaments 
 have been demonstrated passing from each dendrite through the 
 cell body and entering the axon. 
 
 . (3d) The axon or axis-cylinder process of the cell body is a 
 single long, projecting fibre passing outward from the cell body 
 and transmitting impulses from the cell body to a distance. The 
 neuraxon gives ofif fine collateral branches in its course and 
 terminates as do its collaterals in a fine brush-like end. This 
 brush is supposed to come in contact with the gemmules of the 
 dendrites of other neurones so that connection between different 
 neurones is possible. The axon is made up of many fine fibrillje 
 which, as already stated, have come through the cell from the 
 dendrites. The cell body controls nutrition of the dendrites and 
 axon so that when it is destroyed they atrophy. Golgi divides 
 neurones into two types. In the first type the axon extends to a 
 distance and ends in a single brush. In the second type the axon 
 divide into numerous branches near the cell body and ends in a 
 network of fibres. 
 
 Tlie Structure of a Neurouc. — A fine trabeculum or frame- 
 work appears to be filled with semifluid protoplasm, which proto- 
 plasm is used up by action of the neurone, thus leading to altera- 
 tions in size in accordance with the amount of work performed. 
 The normal cell body shows under straining with meth}l blue a 
 granular appearance, and these granules are termed chlorophyl 
 bodies and appear to have a -regular arrangement within the cell. 
 The protoplasm within the trabeculse does not stain. In a de- 
 generated cell marked changes in the staining capacity and an 
 irregularity of arrangement of the chlorophyl bodies are noticed. 
 
 J^aricties of Neurones. — Neurones have been divided accord- 
 ing to their function into : (ist) Centrifugal, which are either 
 (a) motor, (b) secreting^ (c) trophic. (2d) Centripetal, or 
 sensory. (3d) Intrinsic, or association. Neurones have also 
 been divided into a series according to their position, into (i) 
 primary neurones whose cell body lies in the central nervous 
 system or in the ganglia, and whose axon extends thence to some 
 peripheral portion of the body, e.g., to a muscle, to a gland, to 
 
6 DISEASES OF 'l"HE NERVOUS SYSTEM. 
 
 the skin; (2) secondary neurones whose body Hes in the central 
 nervous organs and whose axon extends thence to some other 
 part of the central nervous organs to terminate about a primary 
 neurone. These neurones may lie in the cortex and brain or in 
 the basal ganglia or medulla. 
 
 All simple reflex acts involve the transmission of impulses 
 through primary neurones only. 
 
 All transmission of voluntary motor impulses, or conscious 
 sensory impulses, involves the action of both primary and sec- 
 ondary neurones. 
 
 The human nervous system has two distinct portions: (i) 
 the cerebro-spinal sy.'^tem, and (2) the sympathetic nervous sys- 
 tem. 
 
 ( i) The cerebro-spinal system includes: (o) a peripheral 
 portion, comprising the nerves, (b) a central system, comprising: 
 (i) the spinal cord and cranial nerve nuceli ; (ii) the cerebellum 
 gray masses of the medulla, pons, crura cerebri, corpora quadri- 
 gemina, optic thalami and corpora striata; (iii) the cerebral 
 cortex. 
 
 (2) The sympathetic nervous system is subdivided into: 
 (a) Two great cords containing ganglia, which lie on the sides 
 of the vertebral column and are joined to the spinal cord on one 
 side and to the plexuses on the other; (b) Three pervertebral 
 plexuses, the cardiac, solar, and hypogastric, which are masses 
 of ganglia connected with the viscera; (c) ]\lany peripheral 
 plexuses connected with various organs; (d) Terminal mono- 
 cellular ganglia scattered through the viscera; (e) Sympathetic 
 nerve-fibres joining the plexuses and ganglia together and con- 
 necting them with the cerebro-spinal system. 
 
THE PERIPHERAL NERVES AND THEIR DISEASES. 
 
 Structure of the nerves. Bundles of nerve-fibres — large or 
 small. 
 
 Structure of a nerve-fibre: i. Axis cylinder, a long process 
 of some nerve-cell. 2. Medullary sheath of myelin — a fatty in- 
 sulator,, interrupted at the nodes of Ranvier. 3. Connective-tis- 
 sue sheath of Schwann, with its nucleus. Nerve-fibres are bound 
 into bundles by connective tissue ; endoneurium, perineurium. 
 The sympathetic nerve-fibres have no medullary sheath. 
 
 Fig. 1.— a Normal Nerve, 
 
 All nerve-fibres branch during their course in the central 
 nervous system, sending out "collaterals," but do not branch in 
 their peripheral course. They arise from a nerve-cell. They ter- 
 minate in fine brush-like expansions which are spread out in the 
 skin, or on a muscle, or around another nerve-cell. 
 
 Nerves are divided into motor nerves and sensory nerves, 
 according to the mechanism to which they are attached. Motor 
 nerves convey impulses outward, sensory inward. Motor nerves 
 grow outward from large nerve-cells in the spinal cord. Sensory 
 nerves grow from cells in the posterior spinal ganglia, which send 
 one branch to the surface, and the other into the spinal cord. 
 
 Neuritis. 
 
 Neuritis may occur in a single nerve, or in a plexus. 
 Causes. — Injuries, strains, pressure, compression in fractures, 
 rheumatism, gout, cold. 
 
 Pathologw — I. Parenchymatous neuritis, congestion and exu- 
 
8 DISEASES OF THE NERVOUS SYSTEM. 
 
 dation in nerve-trunk; swelling and degeneration of individual 
 fibres ; ( I ) axis cylinder broken and disintegrated in fatty mass ; 
 (2) medullary substance separated into segments and fatty 
 globules, and mingled with granules and nucleated cells; (3) 
 connective-tissue sheath shrunken and empty. Nuclei multiply. 
 Products of degeneration liquefy and are absorbed. 
 
 Fig. "2. — Neuritis. 
 
 Fig. 3. — Neuritis. 
 
 Fig. 4. — Neuritis. 
 
 Regeneration occurs by growth of new fibres outward from 
 th.e healthy stump into the old sheath. 
 
 2. Interstitial neuritis. The connective tissue of the endoneu- 
 rium and perineurium increases in volume and the nerve-fibres 
 are compressed by the congested vessels and by the new tissue. 
 These forms usually occur together in non-traumatic cases. 
 
 Syiuptoins. — Weakness or paralysis with atrophy and reac- 
 tion of degeneration in muscles supplied by nerves involved. Re- 
 action of degeneration (R. D.) is a change in the action of the 
 nerves and muscles to the electric currents. The response of the 
 nerve to both currents is lost. The muscle loses its faradic reac- 
 tion. The galvanic reaction is changed, the muscle responding 
 more actively to the closure of the positive pole (anode) than to 
 that of the negative pole (kathode). Pain numbness or anzesthesia 
 in skin supplied by nerve involved. Vasomotor and trophic 
 changes in the distribution of nerve involved. Coldness from 
 
DISEASES OF THE NERVOUS SYSTEM. 9> 
 
 sluggish metabolism; glossy skin; oedema; pain and tenderness at 
 seat of inflammation in interstitial cases, and along the nerve 
 trunk. 
 
 Course. — Slow spontaneous recovery when continuity of 
 nerve is preserved. Otherwise, no recovery. 
 
 Treatment. — If nerve is broken unite divided ends. Rest the 
 part injured but exercise the muscles paralyzed by electricity and 
 massage. Use liot applications, sedative lotions. Protect from 
 cold by cotton batting. Morphine for pain. 
 
 ^Multiple Neuritis. 
 
 Multiple neuritis is an inflammatory or degenerative disease 
 of the peripheral nervous system varying in extent and intensity 
 and affecting symmetrical parts of the body. 
 
 The motor nerves may be involved alone {e.g., in lead and 
 mercury poisoning), or the sensory nerves alone (e.g., in coal- 
 gas poisoning),, or both may be involved together {e.g., in al- 
 coholic neuritis). The distal parts of the nerves are commonly 
 affected to a greater extent than the central parts. Hence the 
 symptoms appear chiefly in the distal parts of the extremities. 
 
 The pathological process is the same as in simple neuritis 
 and may be parenchymatous alone, or interstitial alone, or both. 
 
 Fig. 5— Neuritis contracted with normal nerve. 
 
 Etiology.-^i. Toxic cases: Alcohol, lead, arsenic, bisulphide 
 of carbon, copper, mercury, phosphorus, coal gas, coal tar drugs. 
 
10 DISEASES OF THE NERVOUS SYSTEM. 
 
 2. Infectious cases: Diphtheria, typhoid, typhus, scarlet fever, 
 -measles, malaria, leprosy, small-pox, erysipelas, gonorrhea, 
 grippe, and beri-beri. 
 
 3. Rheumatic cases : Exposure to cold, overexertion. 
 
 4. Secondary to anemia, gout, tuberculosis, syphilis, sep- 
 ticaemia, general malnutrition, and diabetes. 
 
 Syjiiplouis. — Acute or subacute onset with fever, 103°- 
 104° F., and general febrile symptoms — sometimes without fever, 
 
 Sensory Synipto)iis. — First to occur. Pain — sharp, severe, 
 located in limbs, increased by motion or pressure : muscular and 
 nerve tenderness, sensitiveness. 
 
 Parsesthesise — Burning, tingling, numbness, band about legs 
 and body. 
 
 Anaesthesia — In tips of fingers and toes, extends up limbs. 
 
 Ataxia — In fine movements and loss of sense of position. 
 
 Motor Syiiipfoiiis. — Paralysis, in extensors, dropped wrist 
 and foot, general inability to walk or move in bed ; contractures ; 
 cranial nerves may be paralyzed, causing symptoms in face and 
 eyes. 
 
 Atrophy — Rapid in onset. R. D.. or diminution in electric 
 contractility ; loss of deep reflexes ; no paralysis of sphincters. 
 
 Trophic Syuiptoms. — A'asomotor paralysis ; glossy skin ; 
 oedema ; abnormal growth of nails and hair : sweating profuse ; 
 no bedsores ; urticaria. 
 
 Certain cases present peculiar features in their course. 
 
 I. AlcoJwIic Xcurifis. — {a) Paralytic type. Rapid onset is 
 the rule, with delirium and delusions, subsequently imperfect 
 memory of recent events. Severe paralysis in extremities with 
 very great pain : anaesthesia very marked in hands and feet, also 
 tremor and tenderness; dropped wrists and feet; or (b) Ataxic 
 type. Sharp pains are soon followed by great ataxia in legs and 
 hands, by anresthesia and partial paralysis ; but no loss of control 
 of bladder or rectum. In both forms there is danger of heart 
 failure or death from exhaustion, due to complicating gastritis. 
 Usually there is rapid increase of symptoms for three or four 
 weeks, and then, after a stationary period of two months, a slow 
 progress to recoverv, the duration b^'ing from six to twelve 
 "months. 
 
DISEASES OF THE NERVOUS SYS'I'EM. 11- 
 
 2. Lead Xcnritis. — Onset with intestinal colic, lead line on 
 gums. Paralysis causing dropped wrists, without sensory dis- 
 turbance in hands. Deltoids next paralyzed. May affect all 
 muscles of arms and legs, and go on to sensory symptoms with 
 delusions, but this is rare. 
 
 Gradual recovery, when poison is eliminated, in four months. 
 
 3. Arsenical Cases. — Gastric disturbance at outset. Then 
 paralysis with ataxia, tremor, atrophy, and great numbness, but 
 little pain ; legs and arms equally affected. Skin darkened. Re- 
 covery in two to six months, depending on original severity. Con- 
 tractures. 
 
 4. Coal-Gas Cases. — Subacute and slight, chiefly sensory, 
 numbness for a long time in fingers, hands, and feet. 
 
 5. DipJifherific Cases. — Severe paralysis of all extremities, 
 usually without sensory disturbance, cranial nerves frec[uently 
 affected. It begins in uvula, and swallowing and talking become 
 difficult. Eyes are often turned. Ataxia is marked in some cases. 
 Never pain. Progress to recovery usual in three months. 
 
 6. Epidemic Form. (Beri-beri.) Occurs in Brazil, India, 
 Borneo, Japan, PhiHppines. Several types : acute pernicious, 
 chronic oedematous, chronic atrophic. Too rare to need attention 
 here. (See Organic Xervous Diseases. Starr. Chap. VIII.) 
 
 Diagnosis of Multiple Neuritis. — From anterior poliomyelitis : 
 by pain, tenderness along nerves, sensory symptoms, distribution 
 of paralysis, symmetrically. From locomotor ataxia : by rapid 
 onset and paralysis, preservation of control of bladder, and 
 absence of Argyle-Robertson pupil. From myelitis : by absence 
 of affection of bladder and rectum, by absence of bedsores, and 
 lack of tenderness of spine to heat, and by distribution of symp- 
 toms in periphery. 
 
 Prognosis. — Good in large majority of cases; slow recovery; 
 bad when heart becomes rapid and respiration poor. 
 
 Treatment. — Rest in bed. Warm applications to limbs by 
 packs. Rubbing with oil ; gentle massage if possible. Prevent 
 deformities and contractures by proper position of limbs. Elec- 
 tricity, galvanism through nerves and to muscles after acute 
 stage. Baths, warm, 98° F., for half-hour several times daily. 
 
n DISEASES OF THE NERVOUS SYSTEM. 
 
 Attention to diet, nourish well, fatty food, cut off alcohol in 
 all cases. 
 
 General and nerve tonics ; iron, quinine, strychnine, glycero- 
 phosphate of lime and soda 
 
 In acute stage, sodium salicylate, gr. x., q. 3 hr., and seda- 
 tives, morphine, phenacetine. 
 
 In chronic stage, arsenic ^V gr. t.i.d., cod-liver oil. 
 
 Neuralgia. 
 
 Neuralgia is a painful affection of the sensory neurone,, 
 sometimes functional, sometimes due to organic changes in the 
 sensory ganglia. 
 
 Causes. — Same as neuritis. 
 
 Symptoms. — Spontaneous pain of intense character in the 
 course and termination of a single nerve. The pain occurs in 
 paroxysms, is not continuous like neuritis. Painful points, tender 
 to pressure may be found, but the entire nerve is not tender as 
 in neuritis. Herpes Zoster often accompanies neuralgia. 
 
 Varieties as numerous as the Jicrvcs. Trigeminal, Brachial 
 Intercostal Sciatic most common. 
 
 Prognosis. — Good except in organic cases and in trigeminal 
 and sciatic, where recurrence is the rule. 
 
 Treatment. — Remove cause,, if found. Locally heat, counter- 
 irritation, salicylates, coal-tar drugs, opium, gelsemium, division 
 of nerves, exsection of ganglia. 
 
DISEASES OF THE XERVOUS SYSTEM. 
 
 13 
 
 THE SPIXAL CORD AND CRAXIAL-XER\^E NUCLEI. 
 
 The spinal cord in man is made up of thirty-one segments — 
 each of which consists of a mass of gray matter joined to a pair of 
 spinal nerves. There is no apparent line of boundary between ad- 
 jacent segments, the cord being a long cylindrical organ. But in 
 snakes and rabbits the area of gray matter is much larger opposite 
 the entrance of nerves than between them, and in fishes there is a 
 visible boundary between adjacent segments. 
 
 Each segment presents a symmetrical arrangement of its two 
 halves. Each half consists of a central mass of gray matter 
 surrounded by white tracts. Each gray mass has an anterior horn, 
 a central mass, and a posterior horn. To each horn nerve-fibres 
 are joined, making the anterior and posterior nerve-roots. The 
 two halves are separated from one another in front by the anterior 
 fissure, and behind by the posterior septum. They are joined to- 
 gether by the anterior white commissure and by the gray commis- 
 sure in which lies the central canal of the cord. The functions of 
 each segment are shown in the table on page 14. 
 
 '.tlOO^* 
 
 Fig, 6.— Cross Section of Spinal Cord. (Gowers) 
 
14 
 
 DISEASES OF THE NERVOUS SYSTEM. 
 
 2d and 3d 
 Cervical. 
 
 4th Cervical. 
 
 5th Cervical. 
 
 6th Cervical. 
 
 rth Cervical. 
 
 Sth Cervical. 
 
 1st Dorsal. 
 
 2d and 12th 
 Dorsal. 
 
 1st Lumbar. 
 
 2d Lumbar. 
 
 ;id Lumbar. 
 4th Lumbar. 
 
 5th Lumbar. 
 
 Ist and 2d 
 Sacral. 
 
 .3d Sacral. 
 
 4th and .jth 
 Sacral. 
 
 Sterno-mastoid. Tra- 
 
 pezius. 
 
 Scaleni and neck. 
 
 Diaphragm. 
 
 Diaphragm. 
 
 Deltoid. 
 
 Biceps. Coraco - bracli- 
 ialis. 
 
 Supinator Lougus. 
 
 Rhomboid. 
 
 Supra- & infra-spinatus. 
 
 Deltoid. 
 
 Biceps Coraco.-brachialis 
 
 Brachialis anticus. 
 
 Supinator longus. 
 
 Supinator brevis. 
 
 Deep muscles of shoul- 
 der blade. 
 
 Rhomboid. Teres minor. 
 
 Pectoralis (clav. part). 
 
 Serratus magnus. 
 
 Brach. anticus. 
 
 Pectoralis (clav. part). 
 
 Serratus magnus. 
 
 Triceps. 
 
 Extensors of wrist and 
 fingers. 
 
 Pronators. 
 
 Triceps (long head). 
 
 Extensors of wrist and 
 fingers. 
 
 Pronators of wrist. 
 
 Flexors of wrist. 
 
 Subscapular. 
 
 Pectoralis (costal part). 
 
 Latissimus dorsi. 
 
 Teres major. ( 
 
 Flexors of wrist and 
 fingers. 
 
 Intrinsic muscl«s of 
 liand. 
 
 Extensors of thumb. 
 
 Intrinsic hand muscles. 
 
 Thenar and hypothenar 
 eminences. 
 
 Muscles of back and ab- 
 domen. 
 
 Ereetores spinae. 
 
 Ilio-psoas. 
 Sartorius. 
 Quadratus lumb. 
 Transversalis. 
 
 Ilio-psoas. Sartorius. 
 Flexors of knee (Remak) 
 Quadriceps femoris. 
 Quadriceps femoris. 
 Inner rotators of thigh. 
 Adductors of thigh. 
 Abductors of thigh. 
 Adductors of thigh. 
 Flexors of knee (Ferrier) 
 Tibialis anticus. 
 fJlutei. 
 
 Biceps femoris. 
 Semi-tendinosis. 
 f)utward rotators. 
 Flexors of ankle. 
 Long flexor of toes. 
 Tibialis post. 
 
 I'croneus longus. 
 Intrinsic muscles of foot 
 
 Sjiliincter ani et venicae 
 
 Hypochondrium. 
 
 Sudden inspiration pro- 
 duced by sudden pressure 
 beneath the lower border 
 of ribs. 
 
 Pupil 4-7 cervical. 
 
 Dilatation of the pupil 
 produced by irritation 
 of neck. 
 
 Scapular. 
 
 Sth Cervical to 1st Dorsal. 
 
 Irritation of skin over the 
 scapula produces con- 
 traction of the scapular 
 muscles. 
 
 Supinator Longus. 
 
 Tapping its tendon in 
 wrist produces flexion of 
 forearm. 
 
 Triceps. 
 
 5th to 6th Cervical. 
 
 Tapping elbow tendon pro- 
 duces extension of fore- 
 arm. 
 
 Posterior wrist. 
 
 6th to Sth Cervical. 
 
 Tapping tendons causes 
 extension of hand. 
 
 Anterior wrist. 
 
 7th to Sth Cervical. 
 
 Tapping anterior tendon 
 causes flexion of wrist. 
 
 Palmar. 7thCerv.-lst Dor. 
 
 Stroking palm causes clos- 
 ure of fingers. 
 
 Epigastric. 4th-7th Dorsal. 
 Tickling mammary region 
 causes retraction of epi- 
 gastrium. 
 Abdominal. 7th-llth Dorsal 
 Stroking side of abdomen 
 causes retraction of belly. 
 Cremasteric. lst-3d Lumbar 
 Stroking inner thigh caus- 
 es retraction of scrotum. 
 
 Patella tendon. 
 
 Striking tendon causes ex- 
 tension of leg. 2d-4th 
 Lumbar. 
 
 Gluteal. 
 
 4tli-5th Lumbar. 
 
 Stroking buttock causes 
 dimpling in fold of but- 
 tock. 
 
 Achilles tendon. 
 
 Over - extension causes 
 rapid flexion of ankle, 
 called ankle clonus. 
 
 Babinski reflex. Scratch- 
 ing sole of foot causes 
 retraction of great toe. 
 
 Plantar. 
 
 Tickling sole of foot caus- 
 es flexion of toes and 
 retraction of leg. 
 
 Bladder and rectal centre. 
 
 Sensation. 
 
 Back of head to vertex. 
 Neck. 
 
 Neck. 
 
 Upper shoulder. 
 
 Outer arm. 
 
 Back of shoulder and 
 
 arm. 
 Outer side of arm and 
 
 foreaiTn. 
 Anterior upper t w o- 
 thirds of arm. 
 
 Outer side of arm and 
 
 forearm. 
 Inside and front of 
 
 forearm. 
 
 Inner and back of arm 
 and forearm. 
 
 Radial distribution in. 
 the hand. 
 
 Forearm and hand; me- 
 dian and ulnar areas. 
 
 Ulnar distribution to- 
 hand. 
 
 Skin of chest and ab- 
 domen, iu bands run- 
 ning around and down- 
 ward corresponding to- 
 spinal nerves. 
 
 Upper gluteal region. 
 
 Skin over groin and 
 front of scrotum, and 
 narrow band down the 
 front of the thigh and 
 leg. 
 
 Inner side of thigh. 
 
 Outer side of thigh. 
 
 Inner side of thigh and 
 
 leg to ankle. 
 Inner side of foot. 
 
 Lower gluteal region 
 back of thigh. Leg 
 and foot outer part. 
 
 Leg and foot except in- 
 ner side. 
 
 Perineum and back of 
 scrotum. Anus. 
 

DISEASES OF THE NERVOUS SYSTEM. lo. 
 
 The Anterior Horns of the Spinal Cord. 
 
 These vary greatly in size and shape in various segments,, 
 being large opposite the entrance of the cervical and lumbo-sacral 
 nerves and thus causing the cervical and lumbo-sacral enlarge- 
 ments of the cord. 
 
 Their size and shape depend upon the number of groups of 
 cells found at different levels ; for the horns are made up of cells 
 — large, polygonal cells with nucleus and nucleolus — collected 
 into distinct groups. 
 
 Some groups of cells lie on the edge of the horn, making pro- 
 jections of the gray mass into the white columns. These groups 
 are found in all the higher vertebrates and are not peculiar to 
 man. Other groups lie within the horn and these are peculiar to 
 naan and the higher apes. Each group of cells presides over the 
 action of a muscle and maintains its tone and nutrition, so that all 
 motor impulses to the muscle, whether reflex, automatic, or vol- 
 untary, proceed from the group of cells. The outer groups gov- 
 ern muscles of flexion, extension, pronation, and supination of the 
 larger joints. The inner groups govern the small muscles of the 
 fingers and toes. Hence the outer groups are said to preside over 
 fundamental motions and the inner groups over accessory 
 motions. 
 
 The thumbless monkev has no inner groups in the cervical 
 region. These are present in monkeys with thumbs and in man. 
 When the inner groups are destroyed by disease, the finger mo- 
 tions are paralyzed. 
 
 In each segment there may be from two to eight groups of 
 cells. Any group may extend through several segments. If a 
 single segment is destroyed by disease several muscles will be 
 paralyzed. But no muscle will be totally paralyzed unless its en- 
 tire group of cells is destroyed. Total paralysis with complete 
 atrophy in a muscle indicates destruction of the entire group of 
 cells which govern the muscle. If the group extends through 
 several segments the paralysis implies disease in all the segments. 
 The table shows the situation in the various segments of the 
 group of cells governing the various muscles, so far as these have- 
 been determined. 
 
16 DISEASES OF THE NERVOUS SYSTEM. 
 
 Anterior Poliomyelitis. 
 
 Anterior Poliomyelitis is a disease limited to the anterior 
 horns of the spinal cord. It may be acute or chronic. 
 
 Acute anterior poliomyelitis is a common disease of childhood 
 known as infantile paralysis. It occasionally occurs in adults. 
 Chronic anterior poliomyelitis is an uncommon disease of adult 
 life or old age, known as atrophic paralysis. 
 
 Acute Anterior Poliomyelitis. Etiology. — Occurs chiefly be- 
 tween 2 and 5 years, when exertion is greatest, in the summer, 
 June to September, when exposure is greatest to heat, occasion- 
 ally after falls and after fevers ; it is probably an acute infectious 
 disease in two-thirds of the cases. In the other third it is prob- 
 ably due to hemorrhage from or to thrombosis in a spinal blood- 
 vessel. 
 
 Pathology. — Lesion is an acute inflammation of the entire 
 gray matter of the anterior horn, the cells and interlacing fibres 
 being affected. The cells become swollen, undergo degeneration, 
 and liquefy, and then shrivel and atrophy. The fibres are sepa- 
 rated from their cells and atrophy. The neuroglia is infiltrated 
 with inflammatory corpuscles. The capillaries are distended and 
 frequently rupture. The process may go on to complete destruc- 
 tion of the cells or may be arrested at any stage. 
 
 If it is arrested early, repair may ensue and the cells regain 
 their former appearance. If it goes on, the result is a diminution 
 in the size of the horn, a change in its shape, and a contraction of 
 the entire cord at the level of the lesion. 
 
 As a rule the entire anterior horn is at first involved, but the 
 permanent destruction is limited to one or two groups of cells on 
 one side only. 
 
 Inasmuch as each motor nerve-fibre comes from and is a part 
 of the motor cell, the nerve-fibres degenerate when the motor- 
 cells are destroyed. Atrophy of the motor nerve-roots and motor- 
 nerves from the anterior horns to the muscles is therefore part of 
 the lesion in anterior poliomyelitis. The deformity of the spinal 
 cord at the level of the lesion and the atrophy of the nerve-trunks 
 are due in part to these changes in the nerve-fibres. 
 
DISEASES OF THE NERVOUS SYSTEM. 17 
 
 The muscles which are paralyzed atrophy rapidly, and when 
 recovery does not occur they remain small. 
 
 While no special groups of cells are known to control the 
 nutrition of the bones, it is found that if the gray matter near 
 the central region of the segment is destroyed by the disease, the 
 bones are much retarded in their growth. Hence in a severe case 
 of infantile palsy the limb affected is smaller than other limbs in 
 all its parts. But trophic changes in the skin, such as sores, glossy 
 skin, or gangrene, do not occur. Through the anterior horns pass 
 fibres from the central region which control the vascular tone and 
 metabolic processes. Hence in lesions of the anterior horn symp- 
 toms due to the destruction of these fibres ensue, viz., sluggish 
 circulation, cyanosis, and lowered temperature, with imperfect 
 nutrition. 
 
 Sy)uptoms. — Sudden onset with fever lOo" to 103° F., occa- 
 sionally without. Febrile symptoms : Headache, loss of appetite, 
 nausea, vomiting, diarrhoea. Restlessness : often convulsions and 
 delirium. The fever rarely continues more than two to three 
 days. Pain in the back and limbs is complained of when child is 
 old enough to talk. 
 
 Paralysis appears suddenly. Sometimes is found in the 
 morning : is complete and extensive either in one limb or more ; 
 legs oftener than arms, 4 to i ; one limb more than the other. 
 ^Maximum is reached in tirst week. Remains stationary for two 
 to six weeks and then improves. Result is recovery, which is 
 partial ; some muscles remain paralyzed. The aff'ected limb atro- 
 phies rapidly. Atrophy is most intense in the muscle permanently 
 weak. There is a change in the electric reactions in the paralyzed 
 muscles. R. D. Loss of faradic excitement in two weeks or 
 sooner. Increase at first, then decrease, in galvanic excitability. 
 ^Muscles contract slowly instead of quickly, more forcibly to the 
 positive than to the negative pole. 
 
 The nutrition of the entire limb suft'ers : bones small and 
 growth impaired: fat is less firm, and skin is cold; but no bed- 
 sores appear. The sphincters are not aff'ected. The reflex action 
 is lost at the level aff'ected, not changed elsewhere. 
 
 Course. — There is a progressive improvement which begins 
 
18 DISEASES OF THE NERVOUS SYSTEM. 
 
 within two months, but usually some muscles remain paralyzed 
 and atrophied, and the joints moved by these may become de- 
 formed ; spine curved. The muscles most frequently affected are : 
 The peronei and tibialis anticus in the leg — hence talipes equinus 
 and varus ; the muscles of the calf and anterior part of the thigh ; 
 the deltoid, biceps, supinators, and spinati in the arm — hence sub- 
 luxation of humerus ; the muscles of the hand and forearm. 
 
 General health is unaffected. 
 
 In adults acute anterior poliomyelitis presents the same 
 symptoms, but fever is less severe and pain is greater in muscles. 
 Extent of initial paralysis is greater. Occasionally the onset is 
 slow, so that case is called subacute, developing in two to four 
 weeks progressively, remaining for a time stationary and then 
 subsiding. 
 
 Diagnosis. — From acute rheunaatism in infants. Rheuma- 
 tism may produce immobility of joints. It also causes pain, red- 
 ness, swelling of joints, and tenderness. 
 
 Prognosis. — Good as to life. 
 
 As to recovery, at end of tzvo weeks test faradic reaction. 
 The muscles in which it persists will recover entirely. 
 
 At end of three months test again. The muscles in v/hich it 
 has returned will recover partially. 
 
 At end of six months test again. The muscles which do not 
 respond will never recover entirely, but if galvanic reaction is 
 good may improve. 
 
 As to use of limb, it depends on growth of bone ; e. g., short 
 leg; on development of deformity and contractures; e.g., talipes. 
 
 Treatment. — In acute stage : Cup or blister the spine and 
 keep quiet. Give ergot and bromide, and antipyretics. 
 
 In chronic stage : Rubbing, warm clothing, galvanism to the 
 muscles, interrupted, continuous. Strychnine ^^ g- to •g'-g- t.i.d., ac- 
 cording to age. Prevent or remedy deformities by apparatus or 
 surgical operation. 
 
 Chronic Anterior Poliomyelitis. — Progressive muscular atro- 
 phy occurs in adults between thirty and fifty years ; is a rare 
 disease. 
 
DISEASES OF THE NERVOUS SYSTEM. 
 
 19 
 
 Etiology. — Falls and injuries, exposure to damp and cold, 
 alcoholic and sexual excesses, lead poisoning (?), 
 
 Syuipfonis. — Gradually increasing atrophic paralysis, several 
 months in onset, preceded by fatigue and weakness and loss of 
 weight. Aluscles become flabby, then atrophied and paralyzed. 
 
 It begins in legs and extends upward (peroneal type). 
 
 It may begin in hands and then extend to shoulders and in- 
 vade the back (Aran-Duchenne type). 
 
 Finally, all the muscles of the body, including face and 
 tongue, may be affected. The tendon reflexes are lost. 
 
 There are fibrillary twitchings in muscles. 
 
 There are electrical changes which vary in dififerent cases ; 
 usually R. D. is found. 
 
 The circulation is poor in the limb, skin cold and blue. 
 
 There is no sensory disturbance except slight numbness. 
 
 There are no visceral symptoms, no disturbance of bladder 
 and rectal control. Bedsores do not develop. 
 
 Course. — Gradual increase after a long period of stationary 
 state. Sometimes a steady progress to bulbar paralysis and death. 
 
 Treatment. — Similar to chronic stage of acute anterior polio- 
 myelitis. 
 
 Cranial-Nerve Nuclei. 
 
 The groups of cells in the cerebral axis (medulla oblongata, 
 pons Varolii, and crura cerebri) which give origin to the motor 
 cranial nerves lie party on the floor of the fourth, ventricle (XII., 
 
 Fig. 7. — Longitudinal Section Showing the Relative Position of the Cranial Nerve 
 
 Nuclei (Edinger). 
 
20 DISEASES OF THE NERVOUS SYSTEM. 
 
 VI., IV., III.), and partly deep beneath the floor in the formatio 
 reticularis (XL, IX., VII., Vm.). These groups of cells are quite 
 homologous to the groups in the anterior horns of the cord, and 
 are subject to diseases whose pathology is the same of that of 
 poliomyelitis. 
 
 Bulbar Paralysis — or Glosso-Labio-Laryngeal Paralysis, 
 
 (Rare). 
 
 Symptoms. — Slowly progressing paralysis with atrophy in 
 the muscles supplied by the motor cranial nerve nuclei. 
 
 1. Disturbance of speech. Alalia, tongue letters, R L D T, 
 due to paralysis of XII. nerve nucleus. Atrophy and tremor of 
 tongue with paralysis. Chewing, swallowing impaired. 
 
 2. Muscles of lips and face become weak and thin, due to 
 paralysis of VII. nerve nucleus. Alalia extends to lip letters, P B 
 V F. Atrophy and tremor of lips with paralysis. Whistling, 
 facial expression impaired. Saliva runs and is increased. 
 
 3. Muscles of pharynx and larynx affected, due to paralysis 
 of the IX. and XI. nerve nuclei. Food regurgitates or cannot be 
 swallowed ; reflex action impaired ; larynx unprotected ; voice 
 monotonous, low ; cough impossible. 
 
 There is no change of sensation or of taste. 
 Pulse sometimes rapid, 100 to 130. 
 Duration, two to five years. 
 Death from inanition, pneumonia, heart failure. 
 
 Ophthalmoplegia. 
 
 This is a rare disease, due to an atrophy of the nuclei of the 
 nerves moving the eyeball or to hemorrhage into them. 
 
 The muscular apparatus of the eye consists of external mus- 
 cles moving the eyeball : Recti and obliqui and levator palpebrse. 
 Internal muscles moving the iris : Dilators and constrictors. Each 
 of these may be affected alone or together. 
 
 _ , , , 1 . ( externa. 
 Ophthalmoplegia ] .^^^^^^ 
 
 Ophthalmoplegia Externa. Symptoms. — Gradually increas- 
 
DISEASES OF THE NERVOUS SYSTEM. 21 
 
 ing loss of "power in all the muscles of eyeball. One or more 
 muscles at first, then others, till all are affected. 
 
 Result, ptosis. \'arious forms of strabismus, nystagmus, and- 
 finally immobility of eyeball. Double vision. 
 
 Ophthalmoplegia Interna. Symptoms. — Loss of reflex to- 
 light. Occurs, as a symptom in locomotor ataxia and general 
 paresis. 
 
 Diag)iosis. — From paralysis of single nerves, III. nerve or 
 VI. nerve,, by the fact that such disease is unilateral and all the 
 muscles supplied by the single nerve are involved, others remain- 
 ing unaffected, and by the fact that the pupil is always affected. 
 
 Progressive ^Muscular Dystrophy. 
 
 This is a primary muscular disease which results in atrophy 
 and paralysis. It is commonly mistaken for chronic anterior 
 poliomyelitis or progressive muscular atrophy, but dift'ers from 
 this in causation, symptoms, and pathology. 
 
 Causation. — It is an hereditary aft'ection, or a disease of de- 
 velopment or of nutrition. It develops in several children in same 
 family with same or various types. 
 
 Pathology. — The lesion is an essential and primary change 
 in the muscle fibres. 
 
 1. Individual fibres become hypertrophied. 
 
 The nuclei of the muscle fibres are increased in number. 
 The vacuoles appear as evidence of degeneration and fibres split 
 up. At the same time there is an increase in connective tissue 
 about the muscle fibres. Sometimes there is a development of fat 
 between the muscle fibres. 
 
 2. Subsequently to the hypertrophy and sometimes without 
 it, atrophv of the muscle fibres occurs with same development of 
 fat and connective tissue or without it. 
 
 Appearance during hypertrophy is a very fat limb in which 
 muscles are really w^eak ; during atrophy is a very thin limb in 
 which muscles are very weak or even totally paralyzed. 
 
 Symptoms. — In all forms there develops a progressive sim- 
 ultaneous weakness and atrophy of the muscles affected, going 
 
22 DISEASES OF THE NERVOUS SYSTEM. 
 
 on slowly to complete paralysis. The consequences of such par- 
 alysis are evident in size, posture, and deformities, use, motion, 
 and gait. No fibrillary twitching z's. progressive muscular atro- 
 phy. No R. D. I's. chronic anterior poliomyelitis. No sensory 
 disturbance, bladder, or rectal, or trophic skin changes. 
 
 Various types of the disease classified by Erb : 
 I. Infantile muscular dystrophy. 
 
 1. Hypertrophic in type. 
 
 Pseudo-hA'pertrophy — fat only. 
 True hypertrophy, muscle also. 
 
 2. Atrophic type. 
 
 In limbs only. 
 In limbs and face also. 
 II. Adult muscular dystrophy, with similar classes. 
 
 I. Infantile Muscular Dystrophy. — Hypertrophic Form, 
 
 1. Pseudo-hypertrophic Paralysis. — Children aged from two 
 to eight affected, males more than females. Only twenty-five per 
 cent, occur after twenty years. Several in one family. 
 
 Begins with difficulty in gait. Cannot walk, go up-stairs, or 
 get up. Muscles of back atrophied, and calves of legs hypertro- 
 phied. Also infraspinatus and deltoid hypertrophied. Other 
 muscles atrophy, pectorales, latissimus dorsi, triceps, and muscles 
 of thighs. 
 
 Posture, shoulders far back. Gait is waddling, and mode of 
 rising by climbing up the legs due to paralysis of extensors of hip 
 is characteristic. Finally, inability to sit up from paralysis of 
 trunk. 
 
 After paralysis has occurred shortening of muscles follows, 
 and deformities, talipes equinus, and curvature of spine develop. 
 
 No R. D. Knee-jerk normal, then weak. Sensation and 
 sphincters not involved. 
 
 Death is due to some intercurrent malady, occurs between 
 twelve and twenty years of age. 
 
 Treatment. — Massage. Thyroid extract. 
 
 2. True Hxperfrophic Paralysis (juvenile muscular dystro- 
 
DISEASES OF THE NERVOUS SYSTEM. 23 
 
 phy). Develops in children six to ten. Several in a family. Be- 
 gins with progressive weakness of muscles. 
 
 Muscles affected with hypertrophy are deltoid, infraspinatus, 
 muscles of forearm, sartorius, gastrocnemii. 
 
 Muscles which atrophy are : pectorales, latissimus dorsi, ser- 
 ratus magnus, biceps, coracobrachialis, supinator longus, adduc- 
 tors of thighs, glutei and back muscles ; finally, calf and peronei. 
 
 Gait, posture, and deformities are characteristic. No fibril- 
 lary contraction. No R. D. Knee-jerk slowly diminished. No 
 disturbance of sensation or of sphincters. 
 
 3. Atropine Type in Body and Limbs (hereditary muscular 
 atrophy). Same features, except entire absence of hypertrophy. 
 Develops from eight to ten years. 
 
 4. Atrophie Type in Limbs and Faee (infantile muscular 
 atrophy; Landouzy-Dejerine type). Face is often first affected. 
 
 When face is involved the zygomatic muscles are affected 
 first ; loss of naso-labial fold ; flat mask-like face ; lower lip pro- 
 jects ; orbicularis is affected; lips open; labials can't be spoken. 
 Sometimes orbic ; palpebrse weak. Facial muscles atrophy slowly. 
 The other muscles of the body are affected in succession much 
 later, pectorals, latissimus dorsi, biceps, and triceps. Deltoids 
 may be hypertrophied. Back muscles and extensors of thighs are 
 invaded. 
 
 Gait, posture, same as in other types. 
 
 Any of these types may go on to another type. 
 
 II. Adult Muscular Dystrophy. 
 
 Any of these forms may occur in adults. Usually a family 
 history can be obtained. Usually develops about age of eighteen, 
 sometimes not till thirty. Some muscles are hypertrophied, others 
 atrophied as in infantile types. 
 
 The Central Gray Matter of the Spixal Cord and its 
 
 Diseases. 
 
 The portion of gray matter lying behind the anterior horn, 
 and adjacent to the central canal of the spinal cord and extending 
 
24 DISEASES OF THE NERVOUS SYSTEM. 
 
 backward to the posterior horn, is made up of gelatinous gray 
 substance and of scattered nerve-cells with a plexus of fibres. 
 It contains one long column of flask-shaped cells — the column of 
 Clarke — in its posterior median part ; and an irregular column of 
 small cells in its lateral part — the intermedio-lateral column. The 
 majority of these cells differ from the cells of the anterior horn, 
 in not having a long axis-cylinder process which enters a nerve. 
 They have numerous branching processes, some sending a long 
 branch to the other side through the anterior commissure, others 
 sending a branch out into the antero-lateral column where it bifur- 
 cates, turning up and down, and in its course gives off collaterals, 
 which enter the gray matter at various levels. These cells thus 
 form an associated system within the cord. 
 
 The function of the central gray matter is to preside over, i, 
 vasomotor tone ; 2, nutrition of all parts ; 3, visceral activity,, in- 
 cluding digestion and excretion, and the activities regulated by 
 the sympathetic system. 
 
 1. Vasomotor innervation is a reflex matter requiring centres 
 with sensory and motor-nerves. Gaskell has proven that these lie 
 in the central gray matter and are joined by fine nerve-fibres 
 which pass in the nerve-roots through the two horns of the cord. 
 The regulation of the flow of blood in accordance with the need 
 of an organ is governed here. 
 
 2. The proper degree of metabolism necessary for nutrition 
 in the skin, bone, and joints and muscles, or for repair of tissue, 
 is under the control of nerves whose centres are in the central 
 gray matter. 
 
 3. The sympathetic system of nerves presides directly over 
 digestion, circulation, secretion, and excretion, but is in turn con- 
 trolled by spinal centres which lie in the entire length of the 
 
 • spinal cord in the central gray matter. 
 
 The central gray matter receives sensory impulses of pain 
 and temperature sense, and transmits these for some distance on 
 their way upward after they reach it through the posterior nerve- 
 roots ; each segment- of the cord being related to its own part of 
 the surface, as shown in the table. 
 
 All these functions are disturbed in diseases of the central 
 gray matter. 
 
DISEASES OF THE NERVOUS SYSTEM. 25 
 
 Syringomyelitis. 
 
 Pathology. — This is a rare disease, usually of congenital 
 origin, characterized by a development of gliomatous tissue in the 
 gray matter around the central canal, which subsequently ex- 
 tends outward, involving the entire central gray matter, and then 
 degenerates and is absorbed, leaving a cavity in the spinal cord. 
 Such a cavity may extend through a part of the cord, or through 
 its entire length ; varying in size at different segments and thus 
 destroying more or less of the gray matter. Its usual situation is 
 in the the lower cervical and upper dorsal regions. The disease 
 may invade the anterior horns of the cord, causing the symptoms 
 of chronic anterior poliomyelitis. It may invade the posterior 
 horns and columns, causing symptoms of posterior sclerosis. 
 Sometimes spinal gliosis develops in adult life and goes on to 
 the formation of a cavity. Sometimes long perforating hemor- 
 rhages occur in the cord, and when the clot is absorbed a cavity 
 remains. Sometimes local softening in the cord leads to the 
 formation of a cavity. Any disease destroying the central gray 
 matter of the cord causes the symptoms of syringomyelitis. 
 
 Symptoms. — i. Loss of the sensations of temperature and 
 pain while the sensations of touch and location are retained. The 
 distribution of this sensory disturbance depends on the location 
 of the disease, e. g., if the left hand and forearm only are thus 
 affected, the disease must be limited to the left side of the cervical 
 region of the cord in its lower third, which receives sensations, 
 from these parts. Such disturbance of sensation may be exten- 
 sive, involving irregular areas of the body. It is never symmet- 
 rical on both sides. 
 
 2. Vasomotor and trophic symptoms. Cyanosis, oedema, 
 blueness of extremities, with lowering of temperature, ulcers, bul- 
 lous eruptions, sweating, thickened or glossy skin, defective 
 growth of the nails, great brittleness of the bones leading to re- 
 peated fractures, and joint affections, also progressive atrophy of 
 the muscles. These occur usually in one limb only. 
 
 3. Disturbance in and loss of control over the action of blad- 
 der and rectum, and loss of sexual power, are present when the 
 lumbar region of the spinal cord is invaded. 
 
•36 DISEASES OF THE NERVOUS SYSTEM. 
 
 4. Paralysis of the spinal muscles with curvatures of the 
 spine. 
 
 Course of the disease is chronic, with slow progress till the 
 symptoms are developed, often including the symptoms of chronic 
 anterior poliomyelitis. It then remains stationary, but if it ad- 
 vances upward and invades the medulla, death may occur at any 
 time from paralysis of the heart and respiration. 
 
 The prognosis is bad and no treatment can stop the course. 
 
 When tumors destroy the central gray matter or hemor- 
 rhages occur in it, the same terminal symptoms may be expected 
 as in syringomyelitis. 
 
 The Posterior Horns of the Cord. 
 
 This portion of the cord is made up partly of gelatinous mat- 
 ter which occupies its extremity, and partly of a fine plexus of 
 nerve-fibres, in which small cells are irregularly scattered. The 
 function of the posterior horn is to receive the impulses coming 
 in through- the posterior nerve-roots, and to transmit such im- 
 pulses in various directions. These are the sensations of touch, 
 temperature, pain, pressure, and location, and of the muscular 
 sense. 
 
 Each nerve of sensation gives off numerous branches on 
 ■entering the cord, and finally terminates in a brush-like expansion 
 of nerve-fibrils which surrounds some nerve-cell, or in the plexus 
 of nerve-fibrils which make up a fine felt-like tissue in the pos- 
 terior horn. Any fibre after entering the posterior nerve-root 
 may pass directly into the posterior horn, or may turn up or down 
 in the white matter near the horn at some level other than that 
 of its entrance. The posterior horns are continuous upward 
 (through the medulla and pons) with the ascending root of the 
 fifth nerve. The diseases of the posterior horn will be considered 
 with diseases of the posterior roots and columns, as they uni- 
 formly coincide. 
 
DISEASr':S OF THE NERVOUS SVS'fEM. 27 
 
 The White Columns of the Spinal Cord and their 
 Diseases. 
 
 The gra}- matter of the spinal cord is surrounded by white 
 tissue made up of anterior and posterior nerve-roots and of nerve- 
 fibres passing up or down the cord for longer or shorter distances. 
 The white columns contain therefore : 
 
 1. Fibres joining the skin, joints, muscles, and viscera to the 
 gray matter of the spinal cord and entering the various segments 
 through the anterior and posterior nerve-roots. 
 
 2. Fibres connecting the various segments with one another. 
 
 3. Fibres joining the various segments with the brain. 
 
 The white matter can be divided into different columns by 
 observing the process of development — different columns develop 
 at dift'erent periods of foetal life ; or by studying the process of 
 disease — different diseases select different columns. 
 
 These columns and their diseases are as follow^s : 
 
 The Motor Coluj/;ns. 
 
 1. Anterior median eoliiniii. 
 
 2. Lateral pyramidal column. 
 
 .At the lower limit of the medulla each anterior pyramid di- 
 vides into two parts ; one part passes directly on into the anterior 
 median column of the cord : the other part crosses over to the 
 opposite lateral column of the cord, lying near to the grav matter 
 in the angle between the anterior and posterior horn. As the 
 fibres making up these columns pass down the cord, they turn 
 into the anterior grav horns of the diff'erent segments — each col- 
 umn becoming smaller the low^er it goes. The anterior median 
 column is exhausted at the lower dorsal cord, and therefore does 
 not exist in the lumbar region. The lateral pyramidal column 
 extends to the lowest segment of the cord. These columns trans- 
 mit motor impulses from the motor cortex of the brain and from 
 the motor ganglia of the brain to the spinal motor centres. These 
 columns also contain fibres whose origin is in the pons and the 
 cerebellum, which pass with the motor fibres from the brain, 
 and terminate in the anterior horns of the cord. 
 
28 
 
 DISEASES OF THE NERVOUS SYSTEM. 
 
 They also contain fibres of association 
 passing- between various segments of 
 the cord. All these sets of fibres de- 
 generate downward. The area of de- 
 generation is less in extent when the 
 lesion is in the brain than when it is in 
 the cord itself. 
 
 Lateral Sclerosis. 
 
 Lateral sclerosis is a chronic sclerotic 
 process affecting the lateral pyramidal 
 colums of the spinal cord. 
 
 It may be primary and is then bi- 
 lateral. 
 
 It may be secondary to other dis- 
 eases in the brain or cord which sepa- 
 rate the fibres of the motor tract from 
 their centres of origin and nutrition in 
 the brain cortex. Such diseases are: 
 
 1. Tumors, softening or hemorrhage 
 in the brain, destroying the motor tract 
 in one hemisphere, in which case the 
 secondary sclerosis is found in the ante- 
 rior median column and the opposite 
 pyramidal tract. 
 
 2. Congenital maldevelopment of 
 the brain and hydrocephalus, affecting 
 both motor tracts, in which case both 
 anterior median and both lateral col- 
 umns are sclerotic. 
 
 3. Any lesion in the spinal cord, 
 either unilateral or bilateral, or com- 
 pression of the cord by disease of the 
 vertebrae, in which case the sclerosis 
 
 Fig. 8. — The Motor Tracts. Py, lateral pyramidal; AM, anterior median column, both 
 from right pyramid of medulla to motor neurones of anterior horn, whence motor 
 nerves (w) pass to muscles; s, sensory nerve entering posterior horn and posterior 
 root zone of the column of Burdach (B), and sending fibres to (a) association- 
 neurones; (c) comniissuralilcurones, and also to motor neurones, in anterior horn; 
 h, fibres of lateral tract consisting of association-fibres between various segments. 
 
DISEASES OF IHE NERVOUS SYSTEM. 29 
 
 -only appears below the level of the lesion, and its extent is 
 greater in area than in 1 or 2 
 
 Pathology of Sclerosis. — i. An increase in the thickness of 
 the connective-tissue framework which supports the nerve-fibres. 
 2. A primary degeneration or a secondary destruction of the axis 
 cylinder in each nerve-fibre, resulting in its swelling, segmenta- 
 tion, fatty degeneration, and final absorption. The result is to 
 reduce the number of fibres in any column of the cord, or even to 
 destroy them entirely, the place of the fibres being filled by con- 
 nective tissue. 
 
 Symptoms of Primary Lateral Sclerosis, or Spastic Paraple- 
 gia. — A weakness and stififness in motion, beginning in the legs 
 and ascending, finally involving the arms. The muscles affected 
 do not atrophy rapidly, as their spinal centres are not diseased. 
 Their reflex and mechanical excitability is increased, as the spinal 
 centres are no longer inhibited by brain impulses. Hence in- 
 creased knee-jerk and ankle clonus are present. They become 
 rigid from the increased spinal activity. Hence the gait is at first 
 "spastic" (toes drag, knees overlap,, motion stiff) ; finally, when 
 paralysis is complete, the legs are drawn up, knees overlapping 
 and so rigid as to be incapable of passive motion. There are no 
 electric changes in the muscles. 
 
 The action of the bladder is imperfectly controlled, and 
 finally involuntary emptying of the bladder at intervals or reten- 
 tion of urine occurs. Constipation is obstinate. In some cases 
 of primary lateral sclerosis the bladder and rectum are not affect- 
 ed. The vascular tone is decreased toward the close of the dis- 
 ease and nutrition is impaired. There are no sensory symptoms. 
 
 Course of the Disease. — The symptoms develop slowly and 
 increase until, after many years, permanent paralysis has de- 
 veloped. 
 
 Secondary Lateral Sclerosis presents the same symptoms on 
 one or both sides, but the symptoms develop more rapidly accord- 
 ing to the nature of the primary disease. 
 
 Diagnosis between lateral sclerosis and anterior poliomyelitis : 
 
 Lesion in pyramidal tracts. Lesion in anterior gray horns. 
 
 Paralysis usually on both sides Paralysis may be limited to an\' sin- 
 equally, in legs, or in legs and gle limb, and rareh^ affects both 
 arms, never in arms alone. limbs equally. 
 
30 DISEASES OF THE NERVOUS SYSTEM. 
 
 All muscles are about equally af- Certain groups of muscles only are 
 
 fected. No muscles are entirely affected. Others escape wholly. 
 
 normal. 
 
 Muscular tone is heightened. Muscular tone is diminished. 
 
 Tendency to rigidity appears. Muscles are relaxed. 
 
 Reflex excitability is increased. Reflex excitability is lost. 
 
 Atrophy is absent, or is slight; Atrophy is always present in the 
 
 and merely due to disuse, hence paralyzed muscles. It advances 
 
 is gradual in progress. It af- rapidly, and may become ex- 
 
 fects the entire limb. treme. 
 
 Electric contractility is unchanged. Electric contractility is changed. 
 
 Reaction of degeneration is pres- 
 ent within two weeks of the on- 
 set. 
 
 Vascular tone is diminished; cyan- J'ascular tone is diminished, but 
 
 osis and oedema may occur. oedema does not occur. 
 
 Paralyzed limb is cold, and sweat Paralyzed limb is cool, but sweat is 
 
 may be increased. not increased. 
 
 Trophic disturbances in the skin Trophic disturbances in the skin do 
 
 are not infrequent. not occur. 
 
 The control over the bladder and The control over the bladder and 
 
 rectum may be diminished or lost. rectum is not impaired. 
 
 Treatinciif. — None. [Read Strumpell on spastic spinal par- 
 alysis and on compression myelitis.] 
 
 Amyotrophic Lateral Sclerosis. 
 
 This is a chronic disease affecting the entire motor system of 
 the spinal cord and cerebral axis, both the groups of cells in the 
 anterior horns and medulla and pons, and also the lateral pyra- 
 midal columns in the cord and in the medulla and pons being 
 affected together. The extent of the sclerosis is greater in the 
 cord than in primary lateral sclerosis, as the white column 
 which lies between the pyramidal tract and the gray matter (the 
 lateral limiting column) is also sclerotic in this disease. The 
 changes in the anterior horns are the same as in chronic anterior 
 poliomyelitis. 
 
 Symptoms. — The symptoms present features similar to those 
 of chronic anterior poliomyelitis and of extensive secondary later- 
 al sclerosis. W'eakness, paresis, and atrophy begin in one or both 
 arms and hands and increase slowly. The muscles of the hands 
 and the extensors of the wrists, the deltoid and triceps, are the 
 muscles chiefly affected. The electric contractility is diminished, 
 and finally reaction of degeneration appears. The muscular irri- 
 
DISEASES OE THE NERVOUS SYSTEM. 31 
 
 lability and reflexes are much increased. Finally contractures 
 result. 
 
 Gradual onset of spastic paraplegia in the legs occurs a few 
 months after the arms are affected. Spastic gait develops with 
 increased reflexes. In the final stage the legs are totally para- 
 lyzed. There are no sensory disturbances, and bladder and rectum- 
 are usually under good control. 
 
 After several years symptoms of bulbar paralysis gradually 
 develop, with paresis and atrophy of face, tongue, and throat, 
 and death occurs from respiratory paralysis. Occasionally the 
 bulbar symptoms appear early. 
 
 The course is a slow one. The disease may be arrested, but 
 recovery is impossible. 
 
 Diagnosis from myelitis of the cervical region and from 
 syringomyelitis by the absence of sensory symptoms ; from ante- 
 rior poliomyelitis chronica by increased mechanical and reflex 
 excitability in muscles atrophied, and by development of spastic 
 gait. 
 
 Treatment. — None. 
 
 The Sensory Columns. 
 
 3. Posterior Lateral Column, or Column of Burdach. 
 
 4. Posterior Median Column, or Column of Goll. 
 
 5. Marginal Column, or Column of Lissauer. 
 
 These columns are made up chiefly of sensory fibres which 
 enter the cord in the posterior nerve-roots. They also contain 
 fibres of association between different segments of the cord. Their 
 subdivision will be better understood b}^ a study of the course of 
 the posterior nerve-roots. 
 
 The posterior nerve-roots contain fibres which arise from the 
 cells of the posterior spinal ganglia. Each spinal ganglion cell 
 has two branches, or two divisions of one branch ; one going out 
 to the surface, the sensory nerve ; the other going in to the cord, 
 the posterior nerve-root. The cell in the ganglion nourishes both 
 branches, and if either branch is separated from its cell it degen- 
 erates in its entire length. The sensory cranial nerves (X., IX.,. 
 V.) arise from similar gangHa (jugulare, Gasserian). 
 
 The posterior nerve-root enters the cord opposite to the apex 
 
32 
 
 DISEASES OF THE NERVOUS SYSTEM. 
 
 of the posterior horn and then divides into two bundles, a median 
 bundle and a lateral bundle. 
 
 (1) The median bundle containing 
 large fibres enters the column of Bur- 
 dach, forming- its root-zone or lateral 
 zone. Here a few fibres turn down- 
 ward into the segment next below 
 (forming the comma-shaped bundle of 
 Schultze) and end in the posterior horn; 
 but the large majority of fibres turn 
 upward to go to higher segments. 
 Some of these soon enter the inner side 
 of the posterior horn (short fibres). 
 These lie near the horn in the lateral 
 zone. Others pass up through several 
 segments (medium fibres). These lie 
 nearer to the median line and in the 
 upper cord are adjacent to the column 
 of Goll, forming the middle .zone of the 
 column of Burdach. The remainder 
 pass all the way up to the medulla (long 
 fibres), lying at first in the hinder zone 
 of the column of Burdach and later 
 forming the column of Goll. For as 
 each root, from below iipward, enters 
 the cord, it displaces inward and back- 
 ward the fibres already ascending; so 
 that the higher the level the larger the 
 number of ascending fibres. In a 
 cross-section of the cord in the upper 
 cervical region the long fibres which 
 have come from thelumbo-sacral region 
 occupy the column of Goll, the sacral 
 fibres lying behind the lumbar; the long 
 fibres from the dorsal region occupy the 
 hinder zone of the column of Burdach ; 
 
 Fig. 9. — The Columns of Burdach and Goll are shown on the left side of the cord. The 
 association-fibres of the cord joining the various segments with each other of various 
 lengths are shown passing through all the columns. The oval column of Flechsig is 
 shown in the lumbar and sacral regions, also called the descending septo-marginal 
 tract. 
 
DISEASES OE 'JHE NERVOUS SYSTEM. iVd 
 
 the long- fibres from the cervical region occupy the middle zone 
 of the column of Burdach. It is evident that there is no phvsio- 
 Jogical distinction between the columns of Goll and Burdach. In 
 the anterior part of both columns near the g'ray commissure lie 
 association fibres and commissural fibres. It is thus evident that 
 the median bundle of posterior nerve-root fibres constitutes the 
 columns of Burdach and of Goll. 
 
 The final termination of these fibres is as follows : Each fibre 
 on entering the cord bifurcates, a short branch turns down, a 
 long branch turns up. The long branch in its course upward 
 gives oil collateral branches which pass into the gray matter of 
 the posterior horn, and finally the branch itself ends there. In all 
 cases the termination is by means of a brush-like expansion of 
 nerve-fibrils. The short fibres end in the fine network making 
 up the substantia gelatinosa of Rolando in the posterior horn, and 
 about the cells of the posterior and central gray matter. The 
 jnedium fibres end in a network which surrounds the cells of the 
 column of Clarke in the central gray matter. A few fibres pass 
 forward to the anterior horn and to the opposite side through the 
 posterior gray commissure. The long fibres pass up to the nuclei 
 gracilis and cuneatus in the medulla. 
 
 (2) The lateral bundle of the posterior nerve-root consists of 
 both large and small nerve-fibres. Many of these pass directly 
 into the gray matter of the posterior horn, where some end in a 
 network of fibres about the cells of the gelatinous substance, or 
 ■deeper in the horn; and others pass forward and cross over in 
 the gray commissure to the opposite side, where they turn out- 
 ward into the antero-lateral column or backward into the column 
 of Goll. The smaller fibres bifurcate on entering the cord and 
 turn down and up, forming the column of Lissauer, in which 
 they pass but a short distance and then turn into the horn. This 
 column is of uniform size through the cord, and hence cannot con- 
 tain any long fibres. 
 
 6. Aiitcro-latcral Ascending Tract or Coliiiiin of Gon'crs. — 
 In the antero-lateral column of the cord lying on the periphery 
 just in front of the direct cerebellar column is a small tract which 
 ascends through the cord and enters the formatio reticularis of 
 
B4 
 
 DISEASES OF THE NERVOUS SYSTEM. 
 
 the medulla, where it appears to end in 
 the gray cells of this formation. It be- 
 gins in the lumbar region, and increases 
 in size as it ascends, receiving fibres 
 from the cells of the central gray mat- 
 ter. It degenerates upward. It has 
 been supposed to convey sensations of 
 temperature and pain upward after they 
 have passed through the central gray 
 matter. 
 
 7. Direct Cci'ebcllar Cohnnn. — This 
 column lies on the lateral periphery of 
 the cord just outside of the pyramidal 
 tract and behind the antero-lateral as- 
 cending tract. It is very small in the 
 upper lumbar region, becomes larger in 
 the dorsal region, and is of consider- 
 able size in the cervical region. Its 
 fibres come from the cells of the col- 
 umns of Clarke in the central gray 
 matter. It passes into the restiform 
 body in the medulla and through this 
 into the cerebellum, where it ends in 
 the vermiform or middle lobe. It is 
 supposed to convey sensations of equi- 
 librium in the act of walking. 
 
 It is evident that the sensory fibres 
 from the posterior nerve-roots are dis- 
 tributed to many different columns of 
 the spinal cord, and even in the medulla 
 have numerous different connections. 
 This anatomical fact may be associated 
 with the physiological fact that one 
 sensation is capable of producing sev- 
 eral different effects, c.g.^ a burn causes 
 a reflex withdrawal of the part burned, 
 
 Fig. 10. — On the right side the termination of Sensory Nerves about the Cells of 
 Clarke's Column (C) and about the Intrinsic Cells (e) is shown. From C fibres pass 
 up in D C.the direct cerebellar column. From e fibres pass over to the column of 
 Cowers (G). On the left side the termination of sensory fibres about intrinsic cells 
 (x) is shown. From x fibres cross to the antero-lateral column and ascend. 
 
DISEASES OF THE NERVOUS SYSTEM. 35 
 
 vascular changes, and a process of repair, sensations of heat, 
 touch, and pain, accurately localized, followed by conscious effort 
 to protect the part : e. g., stumbling in the act of walking causes 
 reflex balancing movements involving motions of the entire trunk 
 and arms to reestablish the centre of gravity or protect against 
 fall, also conscious sensation of unstable position, possibly vertigo, 
 quickened respiration, action of ocular muscles and head to ob- 
 serve danger, sensation of contact, possibly pain, in the toes, and 
 corresponding vascular changes locally, and finally voluntary ef- 
 fort to correct position after an appreciation of all the various 
 sensations received. 
 
 We distinguish conscious sensations of contact, temperature, 
 pain, muscular sense, including pressure and position, and uncon- 
 scious sensations, which set up reflex and automatic acts, vascular 
 changes, variation in thermic and nutritive processes, and changes 
 in muscular tone. These all enter by the posterior nerve-roots, 
 and set up activities in the central nervous system. 
 
 Locomotor Ataxia. 
 
 This is a chronic disease of the sensory part of the nervous 
 system, the posterior nerve-roots and the posterior columns of the 
 cord being diseased. It is also called tabes dorsalis, or posterior 
 spinal sclerosis. 
 
 Pathology. — There is a degenerative neuritis of the posterior 
 nerve-roots, and sometimes of the sensory part of the peripheral 
 nerves. There is a sclerosis of the posterior columns of the spinal 
 cord, beginning in the lateral or root-zone of the column of Bur- 
 dach and in the column of Lissauer, extending thence to the mid- 
 dle zone of the column of Burdach, then to the column of Goll, 
 and finally to the hinder zone of the column of Burdach. Thus 
 both posterior columns are eventually diseased in their entire 
 extent. The disease usually begins in the lumbo-sacral region and 
 extends upward through the cord. It is many years before it 
 invades the cervical region or destroys the entire area of the pos- 
 terior columns. The terminal network of nerve-fibres in the pos- 
 terior gray matter, and especially about the column of Clarke, is 
 destroyed by the disease. 
 
36 DISEASES OF THE NERVOUS SYSTEM. 
 
 Theories of the disease : ( i ) It is a primary sclerosis of the 
 posterior columns of the cord. (2) It is a sclerosis of the root- 
 zone, due to disease of the vessels entering this zone. (3) It is a 
 primary disease of the cells of the posterior spinal ganglia, with 
 secondary degeneration of the sensory fibres entering the cord 
 from the ganglia, and compensatory sclerosis in their course. 
 
 Etiology. — It is a disease of adult life, persons under twenty- 
 five rarely being aftected, and it is rare among women. The chief 
 predisposing cause is syphilis, which precedes it in seventy per 
 cent, of the cases. The exciting causes are great physical exer- 
 tion, exposure to cold and wet, and alcoholic and sexual excesses. 
 
 Symptoms. — The symptoms of the disease are very numer- 
 ous, but appear in succession. They may be classified according 
 to the time of their appearance. There is a stage of pain, a stage 
 of ataxia, and a stage of paralysis. 
 
 Symptoms in Stage of Pain. 
 
 Paraesthesise. Numbness, formication, sensation of dead ex- 
 tremities, cotton or pins in soles of feet and fingers, coldness, 
 itching of anus and scrotum or of other parts. 
 
 Pain. Short, sharp, cutting, boring. Deep pain ; comes in 
 attacks, one second to one-half minute repeated, or in severe at- 
 tacks for several hours or days with intermissions, rarel}- con- 
 tinuous attacks. Begins in thighs and legs. Pain is a prominent 
 symptom early, but may continue through all stages. It may be 
 mistaken for rheumatism or sciatica, but its character is different. 
 It is the same as in alcoholic multiple neuritis, but there tender- 
 ness exists. There is no relation between intensity of pain and 
 degree of ataxia. As disease advances upward the pains extend. 
 Pain may be absent or insignificant in some cases, especially in 
 cases beginning with optic-nerve atrophy. 
 
 Pain in the small of the back and loins of an aching character 
 may occur. 
 
 Girdle sensation or sensation of tightness and pressure in- 
 tense and severe, about the legs and body. This ascends grad- 
 ually as the disease advances. 
 
 Loss of knee-jerk, called \\'estphars symptom. 
 
 Imperfect control of bladder. Slow urination. Slight drib- 
 
DISEASES OF THE NERVOUS SYSTEM. 37 
 
 bling, and hasty urination. I'^inally control is very imperfect and 
 may be painful. This may be a dangerous complication, since 
 death from cystitis occurs. 
 
 Impotence ; occasionally priapism and sexual excitement pre- 
 cede this. 
 
 Constipation ; usually obstinate throughout. 
 
 Loss of pupil reflex to ligbt, the reaction in accommodation 
 being preserved — Argyle-Robertson pupil. 
 
 Contracted pupil, "myosis spinalis," is frequent but not 
 constant. 
 
 Syiiiptoiiis in Stage of Ataxia. 
 
 In addition to those of first stage there develop : 
 
 An?esthesia and analgesia. Sense of pain impaired and de- 
 layed. This may be tested with faradic brush. It prevents in- 
 juries from being perceived; hence ulcer of foot and Charcot 
 joints occur as complications. Hence, guard against accidents in 
 giving hot baths, blisters, etc. 
 
 Hyperalgesia. Sensation of pain may be produced by any 
 touch, and pain is felt severely. This occurs in a few cases early 
 in the disease. 
 
 Change in temperature sensation. Cold felt keenly and heat 
 less than normal. 
 
 Complete anaesthesia develops late in the disease and in the 
 extremities. 
 
 Hypotonia ; an undue mobility of joints from lack of tone in 
 muscles. 
 
 Impairment of muscular sense. Muscular sense is the sense 
 by which the situation and movements of the limbs are appre- 
 ciated, and pressure and weight are felt. Not same as effort sense. 
 Imperfect perception of weight and pressure is a symptom ob- 
 served late. Situation of limbs is imperfectly -perceived. Hence, 
 one means of perfect guidance of limbs is removed. Hence, pa- 
 tient walks badly in the dark, and cannot touch objects accurately 
 with eyes closed ; hence he watches his own motions — aiding his 
 muscular sense by sight. Therefore a blind ataxia is the most 
 helpless of all. 
 
 Ataxia is imperfect co-ordination of muscular action. For 
 
38 DISEASES OF THE NERVOUS SYSTEM. 
 
 every compound act a regular succession and proper degree of 
 motions are needed, e.g., closure of fist, walking. This regula- 
 tion is largely automatic and is carried on in subcortical centres, 
 which receive unconscious sensations through the posterior nerve- 
 roots. It may be voluntary, by an effort of attention, and is so at 
 first, for all motion, and always for highly complex motion, e.g., 
 writing. Hence ataxia of movement may occur in many diseases. 
 It is a prominent symptom in locomotor ataxia. 
 
 Romberg's symptom — swaying when standing with eyes 
 closed. 
 
 Ataxic gait — legs wide apart, feet lifted too high, and planted 
 too forcibly, steps being of irregular length and body imperfectly 
 balanced. 
 
 Imperfect use of hands in dressing, writing, etc. Irregular 
 contraction of muscles on effort. Imperfect muscular tone. 
 
 Tests of ataxia. Stand with eyes closed,, walk, turn suddenly 
 or walk backward ; touch heel to toe, or heel to knee ; touch finger 
 to nose or both fingers with eyes closed ; pick up pin ; button 
 clothes. 
 
 Syniptonis occasionally present, due to complication of neu- 
 ritis in various nerves. Optic-nerve atrophy, with progressive 
 blindness, develops in ten per cent, of the cases. Optic disc looks 
 white, then gray. Arteries appear small and walls thin. Visual 
 field is contracted for colors and for light. Finally total blindness 
 occurs. 
 
 Paralysis of the ocular muscles. 
 
 VI. n. paralysis ; convergent strabismus, with contracted 
 pupil. 
 
 III. n. paralysis; divergent strabismus, with dilated pupil and 
 ptosis. Nystagmus rarely occurs. 
 
 Deafness develops in a few cases from atrophy of auditory 
 nerve. 
 
 Crises — (i) gastric; sudden vomiting with pain, for several 
 hours, even for days. Great prostration follows. Rectal feeding 
 necessary. Intestinal and rectal crises with diarrhcea and tenesmus 
 have been ol)served. (2) Laryngeal; sudden and severe cough, 
 with spasm of larynx and suffocation. (3) Cardiac; attacks of 
 
DISEASES OF THE NERVOUS SVS'IEM. 39 
 
 angina pectoris. All clue to a complicating peripheral neuritis in 
 pneumo-gastric nerve. These symptoms are quite exceptional. 
 
 Trophic disturbances are more common in stage of ataxia. 
 
 Charcot joints. Knee, elbow, ankle, wrist. Enormous swell- 
 ing with effusion without pain. Erosion of ends of bones and 
 destruction of articulation. Due to injury. 
 
 Perforating ulcer of foot, caused by a corn, or a subcutaneous 
 hemorrhage, or a caries of bone neglected. 
 
 Rarefication of the bones with production of fractures. 
 
 Irregular muscular atrophies develop late in the disease. 
 
 Herpetic eruptions and pemphigus. 
 
 These are due to a combination of causes, chiefly to a loss of 
 pain sense which prevents injuries from being perceived, or to a 
 complicating peripheral neuritis. 
 
 Syinpfoins in Stage of Paralysis. 
 
 General nutrition remains good, but ataxia becomes so ex- 
 treme as to render patient helpless and confine him to bed. 
 
 Control of bladder completely lost, and urine dribbles con- 
 stantly. 
 
 Accidents produce injuries, and trophic disturbances follow. 
 
 Hence patients die of bedsores, cystitis, exhaustion, or of 
 complicating penumonia. 
 
 Course of the disease is chronic through' the three stages, 
 lasting twenty to forty years. 
 
 Usual mode of onset is with pain, loss of knee-jerk, bladder 
 trouble, impotence, and ataxia. 
 
 Occasional modes of onset: (i) blindness, loss of knee-jerk, 
 imperfect gait, numbness, but no pain. 
 
 (2) Gastric crises at intervals, loss of knee-jerk, then pain 
 and ataxia. 
 
 (3) \'arious forms of strabismus, myosis. then ataxia of 
 arms. 
 
 There are remissions in the symptoms and complications may 
 subside, but no true arrest occurs or recovery, after the stage of 
 ataxia has begun. 
 
 Diagnosis. Early, by means of pains, fatigue, loss of knee- 
 jerk, and Argyle-Robertson pupil. Late, by ataxia and bladder 
 disturbance. 
 
40 DISEASES OF THE NERVOUS SYSTEM. 
 
 Diagnosis from multiple neuritis. See page 11. 
 
 Treatment. Moderate exercise, avoiding all fatigue. Good 
 general diet without special restrictions, which weaken patient. 
 Spinal douches, tepid or cool, never extreme. Massage. Practise 
 in fine movements to overcome ataxia. Medicines — arsenic,, 
 nitrate of silver, ergot. Anti-syphilitic remedies. 
 
 Treatment of pain by antipyrine, etc., gelsemium, opium,, 
 faradization, hot applications. Of crises by counter-irritation and 
 morphine. Of optic atrophy by strychnine. Of trophic disturb- 
 ances by rest and apparatus. 
 
 Combined Sclerosis. 
 
 This is a Sclerosis of the Lateral and Posterior Columns. 
 (rare). 
 
 (i) Congenital cases. Friedreich's Hereditary Ataxia is due 
 to defective development of the lateral and posterior columns. It 
 occurs in several members of a family, and is hereditary. 
 
 Symptoms. — As the children grow up they are found to be 
 awkward. They walk badly, and do not use arms well. Reflexes 
 are lost, exceptionally exaggerated. Dull pains in legs, not light- 
 ning in character. Deformity in feet. No bladder symptoms, 
 and no trophic changes, and no crises. Ataxia is marked and goes 
 on to actual paralysis. Speech may be thick and nystagmus pres- 
 ent. The condition is a chronic one, lasting during life. Chil- 
 dren often become imbecile. 
 
 (2) Acquired cases'. Ataxic Paraplegia of Cowers. 
 
 Etiology. — Occurs in males chiefly, between thirty and forty 
 years of life. Not. after syphilis, but after exposure to cold or 
 sexual excess. Possibly after concussion of spine. 
 
 Symptoms. — Slow onset of weakness and ataxia together. 
 Undue fatigue, unsteady gait. Romberg symptom. Dull pain in 
 back and legs, no lightning pains. Reflexes increased. Knee- 
 jerk high, ankle clonus present. Sexual power lost. Sphincters 
 less impaired than in tabes. Eye symptoms very rare. Tremor 
 of face and speech sometimes develops. 
 
 Differs from tabes in fact that the nerve-roots are not in- 
 volved. 
 
DISEASES OF THE NERVOUS SYSTEM. 41 
 
 Course. — Weakness increases slowly to paralysis. Rigidity 
 soon develops, and contractures. Death occurs from complica- 
 tions. 
 
 The Association Columns. 
 
 8. Antcro-Latcval Coliiiiin. — There is a large collection of 
 nerve-fibres forming a white column lying adjacent to the gray 
 matter of the cord, in front and inside of the pyramidal tract, and 
 inside of the direct cerebellar and antero-lateral ascending tracts, 
 extending as far forward as the anterior, nerve-roots. (See Fig. 
 1.) A portion lying next to the gray matter has been named the- 
 lateral liinitiJig layer. This column contains a few fibres, which 
 degenerate all the way upward to the medulla, and it is possible 
 that some sensory impulses are transmitted through it. (See Fig. 
 9. ) The major part of the fibres are, however, short, and serve 
 to connect the various segments of the cord with one another. 
 (See Fig. 8. ) In it pass the majority of the "association fibres" 
 of the cord, which harmonize the action of different parts. 
 
 g. Anterior Column. — This lies between the exit of the an- 
 terior nerve-roots and the anterior median column. It has the 
 same function as the antero-lateral column, and like it ends in the 
 formatio reticularis of the medulla. 
 
 There are very many polygonal cells scattered through the 
 gray matter in both horns and in the central gray which send out 
 to these columns an axis-cylinder process, which on entering the 
 column bifurcates, sending one branch down and the other up- 
 ward. These branches give off collaterals in their course, which 
 pass into the gray matter at various levels and terminate in brush- 
 like expansions. The original branches terminate in the same way 
 after having a longer or shorter course. Thus the majority of 
 the fibres in these columns are true association fibres. There are 
 a few such fibres also in the portion of the posterior columns 
 adjacent to the gray commissure. 
 
 Secondary Degenerations. 
 
 When the cord is divided by an injury or by transverse mye- 
 litis there results a defeneration in the various columns. 
 
4a DISEASES OF THE NERVOUS SYSTEM. 
 
 The anterior median and lateral pyramidal columns degen- 
 erate downward for their entire length. There is also a short 
 tract of degeneration downward in the lateral zone of the column 
 of Burdach. The anterior and antero-lateral columns degenerate 
 downward for a short distance. 
 
 The columns of Burdach and Goll and Gowers and the direct 
 cerebellar column degenerate upward through their entire length. 
 The columns of Lissauer, and the anterior and antero-lateral col- 
 umns degenerate upward for a short distance. 
 
 Such degenerations are due to the fact that the transverse 
 lesion cuts ojff the individual fibres from their nutrient cells, and 
 hence the distal end degenerates, the fibres nourished by cells 
 above the lesion degenerating downward and those by cells below 
 the lesion degenerating upward. 
 
 ]\Iyelitis. 
 
 This is an inflammation or softening of the spinal cord in- 
 volving an entire segment, both gray and white matter. 
 
 Pathology. — Cord looks normal, but feels soft at points ; or 
 may break in two and be soft enough to be fluid. On cutting it 
 the cut surface swells out as if semifluid ; the gray matter looks 
 red and capillary hemorrhages are seen ; the limit of white and 
 gray is indistinct. 
 
 Microscopically. — Large numbers of inflammatory corpuscles 
 everywhere. Nerve-cells and fibres swollen and degenerated, 
 granular and disappearing or atrophied. Neuroglia cells in- 
 creased. Deiter's spider cells present. Fatty and granular cells 
 ■everywhere as evidence of degeneration. Vessels are distended 
 with blood and ruptured ; walls ma}^ be infiltrated and thickened. 
 
 Secondary degenerations as already enumerated. 
 
 Etiology. — Males more than females. Soldiers, porters. 
 Age, ten to forty. Exposure to cold. Overexertion. Falls and 
 blows. Concussion of cord. Sexual excesses. Menstrual sup- 
 pression. After confinement. Injuries of the cord. Compres- 
 sion of the cord by disease of spinal bones or tumors. Secondary 
 to acute infectious diseases. Syphilis and chronic alcoholism, 
 
DISEASES OE IKE XER\'OUS SVSTEM. 43 
 
 often due to honiorrhao^e or to thrombosis in diseased vessels, 
 "spinal apoplexy." 
 
 Varieties. General. — Entire cord affected — ascending or de- 
 scending. 
 
 Disseiiiiitafed. — X'arious segments at different levels affected. 
 
 Traiisz'ersc. — One or two segments at one level aft'ected. 
 
 Syinptoms. — (i) Direct, due to destruction of cord tissue. 
 
 I. ^Nlotor. Paralysis, atrophy. R. D. Loss of tone in mus- 
 cles. 
 
 •^. Reflex. Loss of spinal reflexes. Paralysis of the 
 bladder and rectum, impotence 
 
 3. Sensory. Xumbness. Pain. Parjesthesia, ansethesia. 
 Hypersesthesia at upper level of lesion. Pain and tenderness of 
 back to heat. 
 
 4. A'asomotor and trophic. Lnperfect circulation. Skin 
 cold. Sweat profuse. Bedsores on buttocks, sacrum, and heels. 
 
 The distribution of the direct symptoms depends on the ex- 
 tent of the lesion. If general they are universal. If disseminated 
 they are scattered. If transverse they are limited to one level. 
 
 Diagnosis of level from situation of symptoms, motor or 
 sensory, see table, page 14. 
 
 Syiiipfoius. — (2) Indirect, due to cutting off' of impulses to 
 other parts. The cord transmits impulses to and from the brain. 
 In disseminated and transverse myelitis tracts are broken, (i) 
 Motor tracts to parts below, hence secondary lateral sclerosis 
 with its symptoms. (2) Sensory tracts from parts below, hence 
 secondary degenerations upward with their symptoms. 
 
 Secondary symptoms are : 
 
 1. Rigidity and increased reflexes, contractures, spasms of 
 legs, paralyzed muscles not atrophied, and no R. D. 
 
 2. Loss of bladder control without bladder paralysis, priap- 
 ism. 
 
 3. Imperfect sensation without incoordination. 
 
 4. Imperfect perception of pain ; hence bedsores from dirt, 
 bedsores over sacrum, glutei, heels, and ankles. 
 
 Examples : In general myelitis, direct symptoms throughout 
 bodv. 
 
44 DISEASES OF THE NERVOUS SYSTEM. 
 
 In disseminated myelitis, direct symptoms in irregular areas, 
 few indirect symptoms. 
 
 In transverse myelitis, direct symptoms very limited, in- 
 direct symptoms below the lesion. • 
 
 (a) Cervical transverse myelitis, direct symptoms in arms, 
 indirect in legs. 
 
 (b) Dorsal transvere myelitis, direct symptoms few, in trunk, 
 indirect in legs like lateral sclerosis, arms free. 
 
 (c) Lumbar transverse myelitis, direct symptoms in legs, 
 arms free, no indirect symptoms. 
 
 Course of General Myelitis and Disseminated Myelitis. — ■ 
 Aciite or subacute, onset in two weeks after a cold or great strain 
 or after typhus, typhoid, small-ppx, confinement, syphilis. Weak- 
 ness in limbs. Pains in back and limbs. Prostration. Then 
 paralysis. Pain and anaesthesia. Bladder and rectal symptoms. 
 Then patient is confined to bed and bedsores develop. Slow 
 course for a year to three years and occasionally gradual, im- 
 perfect recovery. Usually cystitis, bedsores, or 'pneumonia and 
 death. 
 
 Course of Transverse Myelitis. — Acute, onset after injury — 
 blow, fall, wound, dislocation of spine, or strain, causing hem- 
 orrhage in cord ; or from embolism of spinal arteries. 
 
 Chronic, onset after spinal caries with deformity and pres- 
 sure, or tumor in spinal canal or cord. Course depends on possi- 
 bility of removing the cause. 
 
 Diagnosis. — ]\Iyelitis z's. multiple neuritis, see page 11. 
 
 Myelitis vs. IMexixgitis. 
 
 Very rapid onset. Slower onset. 
 
 Fever moderate. Fever high. 
 
 Pain in back moderate, in limbs or Pain in back and body and limbs 
 
 body dull. very severe, increased by motion. 
 
 Hyperjesthesia slight in a band at Hyperesthesia of entire body and 
 
 upper level ol lesion. limbs very intense. 
 
 Anaesthesia below lesion. No anaesthesia. 
 
 No spasms or rigidity. Spasms of limbs and back with 
 
 rigidity of back appear early. 
 
 Paralysis total in some muscles Paralysis only apparent ; due to fear 
 
 with atrophy and R. D. of pain on motion, no atrophy. 
 
 Sphincters paralyzed. Sphincters not affected. 
 
 Bedsores and cvstitis. No bedsores or cystitis. 
 
DISEASES OF THE NERVOUS SVS'l'E.M. 45 
 
 ]Myelitis t's. Hysterical Parai'legia. 
 
 Anaestliesia below lesion includes Anaesthesia varies in level and geni- 
 
 genitals. tals never included. 
 
 If thighs are paralyzed and When legs are paralyzed reflexes 
 
 atrophied reflexes are lost. are exaggerated. 
 
 Usually some muscles atrophj' and Muscles rarely atrophy and R. D. 
 
 show R. D. never appears. 
 
 Sphincters usually involved. Sphincters rarely involved. 
 
 Diagnosis of level of lesion by distribution of anaesthesia, see 
 table, page 14. 
 
 Treatment of myelitis. 
 
 When onset is acute remove cause, and use counter-irritation, 
 ice-bag. or warm douche. Keep at perfect rest in prone position. 
 Give sedatives and ergot : in early stage give purgatives, calomel, 
 or salts. 
 
 ^^'hen case is chronic in onset or in cours'e : employ counter- 
 irritation. Cups, blisters, cautery, ether spray ; but not in cases 
 with tendency to bedsores. Use baths, douches, tepid and cold, 
 to spine. Keep up strength of patient by good diet, and regulate 
 digestion. Use massage to the limbs — hot baths for rigidity. Use 
 interrupted galvanic current to atrophied and paralyzed muscles. 
 
 Prevent cystitis by keeping catheters and parts clean and 
 aseptic. 
 
 Treat cystitis by washing out the bladder, as in surgery. 
 
 Prevent bedsores by careftil padding or water-bed, by spong- 
 ing with alcohol and alum-water, by frecj[uent change of position. 
 
 Treat bedsores by aseptic dressings, as in surgery. 
 
 For pain, apply heat or faradic brush to part. Give antipyrin, 
 antifebrin, phenacetine, morphine, salicin, salicylic acid. 
 
 For spasms, apply heat to spine, or hot bath to legs, or cups. 
 Give bromides. For rigidity, when beginning, pads and massage. 
 
 For incontinence of urine, pads of absorbent cotton, or wear 
 urinal. 
 
 Medicines in chronic myelitis : Iodide of potash, gr. x. to 
 XX., t.i.d. Xitrate of silver in pill with kaolin, gr. 1-4 t.i.d. in- 
 creased. Ergotin when congestion is suspected. Strychnine 
 when an increase of reflex activity is not present. Phosphorus 
 and arsenic as nerve tonics. Use ung. hydrarg. and KI in large 
 doses in syphilitic cases. 
 
46 
 
 DISEASES OF THE NERVOUS SYSTEM. 
 
 Hemorrhage into the Spinal Cord. 
 
 Hemorrhage into the spinal cord 
 or into the membranes is a rare oc- 
 currence, and is ahnost always due 
 to traumatism. The symptoms pro- 
 duced are those of sudden suspension 
 of all spinal functions at and below 
 the level of the hemorrhage. They 
 are therefore identical with those of 
 transverse myelitis, and the sudden 
 onset affords the only means of dis- 
 tinguishing the two diseases. Some- 
 times spontaneous hemorrhages in 
 the anterior horn cause symptoms of 
 anterior poliomyelitis. Sometimes 
 central hemorrhages cause symptoms 
 of syringomyelitis. 
 
 Tumors of the Spinal Cord. 
 
 Tumors rarely grow in the spinal 
 cord. They are usually secondary 
 to tumors elsewhere. All varieties 
 may occur. The symptoms produced 
 are those of transverse myelitis of 
 slow onset and characterized by ex- 
 treme pain at the level of the tumor 
 or in the sensory areas which corre- 
 spond to the segment in which the 
 tumor grows. The only relief is by 
 operation. The relation of the seg- 
 ments of the cord to the spinal col- 
 umn is shown in Fig. 11. 
 
 Brown-Sequard's Paralysis. 
 
 Hemorrhages in the cord, tumors 
 in or about the cord, and bony 
 growths or callus, the result of 
 injury, sometimes divide or com- 
 
 FiG. II. — Relations between the Segments 
 of the Spinal Cord and their Nerves and 
 the Bodies of the Vertebrae. (Gowers.) 
 
. DISEASES OF THE NERVOUS SYSTEM. 47 
 
 press one-half only of tlie cord. The symptoms resulting- 
 were first described by Brown-Sequard, and hence the condi- 
 tion has been named after him. This condition is as follows : 
 (i) on the side of the lesion there is paralysis with increased 
 reflexes, and sometimes a loss of muscular sense below the level 
 affected, and a marked hypersesthesia to touch and pain; (2) on 
 the side opposite to the lesion there is no paralysis, but there is 
 a loss of sensation of touch, temperature, and pain, and some- 
 times a development of bedsores below the level of the lesion ; 
 (3) at the level of the lesion there is a band about the body of 
 anaesthesia ,with another band of hyperaesthesia above it; the 
 band on the side of the lesion being a little higher than upon 
 the opposite side. 
 
THE BRAIN AND ITS DISEASES. 
 
 I. The Cortex of the Cerebral Hemispheres. 
 
 The cortex consists of gray matter spread out in a layer over 
 the cerebral hemispheres, 3mm. thick and about 200,000 sq. mm. 
 in extent ; its amount varying greatly in different persons ; its 
 development determining mental capacity. The development of 
 fissures throwing the cortex into folds enables this large extent 
 to be contained in the skull. 
 
 The Microscopic Appearance of the Cortex. — Cells arranged 
 in layers. 
 
 (1) Superficial or molecular layer J^- small cells. Much 
 neuroglia. 
 
 (2) Layer of small pyramids -^^ with many branches and 
 short process. 
 
 (3) Layer of large pyramids /q with few branches and 
 a long projection-fibre process. 
 
 (4) Layer of polymorphous cells fg- with many short 
 branches and a short process. 
 
 (5) ' Layer of fusiform cells /„ with short branches and 
 association-fibre process. 
 
 Fibres trasverse these layers, giving off collaterals, and 
 form an intricate network throughout the gray matter. There are 
 great variations in the structure of different regions. (See 
 "Quain's Anatomy," loth Ed., Vol. III. Starr's "Atlas of Nerve 
 Cells.") 
 
 The fibres arising from the cortex and constituting the white 
 matter beneath it are ( i ) association fibres passing to some other 
 part of the cortex; (2) commissural fibres passing to the cortex 
 of the opposite hemisphere; (3) projection fibres passing to the 
 basal ganglia, cerebral axis, or spinal cord. 
 
 Divisions of the Cortex into Lobes and Convolutions. — 
 
DISEASES OF THE NERVOUS SYSTEM. 
 
 49 
 
 Frontal lobe, 40 per cent. ; parietal lobe, 20 per cent. ; temporal 
 lobe, 20 per cent.; occipital lobe, 17 per cent.; Island of Reil, 3 
 per cent, of extent of cortex. 
 
 Landmarks on the Cortex. — Fissure of Sylvius, fissure of 
 Rolando, interparietal fissure, parieto-occipital sulcus, calcarine 
 fissure, callosomarginal fissure. 
 
 C<li.\ N lO-CCRIiURAL Toi'OCRAPII V. 
 
 To find the fissure of Rolando, lay down a line from the root 
 of the nose to the occipital protuberance over the top of the head 
 and take a point 0.557 of the distance back upon this line. This 
 
 df'sfan 
 
 Ccclp 
 pmu~ 
 
 Glahella 
 
 Fig. 12. 
 
 point will correspond to the upper end of the fissure. The fis- 
 sure makes an angle of 67° with the median line just measured. 
 Hence if two strips of metal, fixed to one another at this angle, 
 be placed on the head with their junction upon the upper end of 
 the fissure, when one strip is on the median line the other strip, 
 pointing forward and downward, must lie over the fissure of 
 
50 DISEASES OF THE NERVOUS SYSTEM. 
 
 Rolando. In its lower third the fissure becomes a little more ver- 
 tical than the strip. The fissure is about three and a half inches 
 long. 
 
 To find the fissure of Sylvius, la}^ down a base line from 
 the lower margin of the orbit to the auditory meatus. Lay down 
 a second line parallel to the base line from the external angular 
 process of the frontal bone backward one inch and a quarter, and 
 then measure upward one-quarter of an inch ; this gives point 
 one. Fnd the most prominent part of the parietal eminence and 
 from it draw a line downward perpendicular to the base line, and 
 on this take a point three-quarters of an inch below the eminence ; 
 this gives point two. Join these two points, and the line will lie 
 over the fissure of Sylvius. The anterior limb of the fissure will 
 be two inches behind the external angular process. The fissure 
 of Sylvius is about four inches long. 
 
 To find the parieto-occipital fissure, continue the line of the 
 fissure of Sylvius to the median line. At their junction lies this 
 fissure. Since all areas now open to surgical operation can be 
 located with a definite relation to these fissures, no further rules 
 are necessary. Since in opening the skull it is customary to make 
 a fenestra of at least an inch in diameter, and it is frequently 
 necessary to enlarge the opening much more, a procedure in no 
 way dangerous under aseptic conditions, there is no difficulty 
 in recognizing the fissures and convolutions exposed if the rules 
 are closely followed. Prior to the large incision of the scalp it is 
 well to mark certain points upon the skull by the sharp point of a 
 chisel, so that when the bone is laid bare surface landmarks may 
 still be kept in view. 
 
 Localization of Functions in the Cortex. 
 
 Proofs from comparative anatomy ; natural and experimental 
 atrophy ; process of development ; irritation and excision of cortex 
 with various results ; pathological lesions of limited extent with 
 secondary degenerations. 
 
 The functions of the cortex in general are : 
 
 (i) To receive impressions from the various sensory organs 
 as conscious perceptions. 
 
DISEASES OF THE NERVOUS SYSTEM. 51 
 
 (2) To associate these various simultaneous perceptions in- 
 to a mental image or concept. 
 
 (3) To retain these concepts as memories so that objects can 
 be recognized or recalled. 
 
 (4) To give expression to thought in action and in speech. 
 
 (5) To restrain the flow of thought and to inhibit or control 
 automatic and reflex acts. 
 
 It has been established that various powers of perception, 
 memory, and volition can be definitely assigned to various parts 
 of the brain; that each sense has its corresponding area in the 
 cortex, and each voluntary movement its point of departure from 
 the cortex. 
 
 It has been proven that perceptions leave behind them a phys- 
 ical trace inseparably connected with the area in which they 
 were originally received; that irritation of this area produces a 
 renewal in consciousness of the original perception as a memory, 
 which may be so vivid as to appear real, being then an hallucina- 
 tion ; that destruction of this area causes a loss of the power of re- 
 calling the previous perception or of recognizing it when repeated. 
 
 It has been proven that movements which are acquired by 
 practice, and are therefore the result of conscious effort, are al- 
 ways initiated from a definite area ; that this area is inseparably 
 related to movements ; since its irritation, b}- any cause, results in 
 the production of forcible movements of the nature of spasms, 
 and its destruction produces a loss of the power of movement or 
 paralysis of voluntary action. 
 
 It has been proven that the use of language involves both the 
 recollection of auditory and visual symbols and the initiation of 
 impulses of speech and writing, thus calling into play not only the 
 motor portion of the brain, destruction of which therefore causes 
 a loss of speech, but also the sensory portion of the brain, a lesion 
 of which will also cause aphasia. 
 
 There are certain areas upon the cortex of the brain, not 
 necessarily coextensive with either lobes or convolutions, whose 
 functions are accurately known. 
 
 These areas are: (i) The sensori-motor area. (2) The 
 visual area. (3) The auditory area. (4) The area of sensations 
 of smell and of taste. (5) The speech areas. 
 
52 
 
 DISEASES OF THE NERVOUS SYSTEM. 
 
 Fig. 13. — Diagram of the Fissures and Convolutions of the Convexity of the Left 
 Hemisphere of the Brain, with the areas presiding over various functions. The 
 speech areas are shown on this hemisphere. The motor area is more extensive on 
 the left than on the right hemisphere. 
 
 The Sensori-Motor Area. 
 
 The scnsori-inotor area includes the cortex of the anterior 
 and posterior central convolutions which border the fissure of Ro- 
 lando and the adjacent cortex in front and behind these convolu- 
 tions. Each hemisphere controls movement on the opposite side 
 of the body, but as the right hand is more generally used and is 
 better trained than the left, this area is larger on the left hemi- 
 sphere than on the right. 
 
 The cortex of the posterior part of the second frontal convo- 
 lution controls the movements of the eyes and head. Impulses 
 starting from this area produce conjugate movement of these 
 parts toward the opposite side. The eye district is. below, the 
 head district above. 
 
 The lower third of the anterior and posterior central convolu- 
 tions governs the movements of the face, tongue, larynx, and 
 pharynx. The eyebrows and cheeks are controlled by the upper 
 and forward part of this area ; the tongue and larynx by the lower 
 
DISEASES OF THE NERVOUS SYSTEM. 53 
 
 and forward part : the mouth, pliarynx, and platysnia by the hinder 
 part. 
 
 The middle third of the anterior and posterior central convo- 
 lutions governs the movements of the upper extremity ; the 
 shoulder motions being controlled in the anterior and upper part 
 of this area, the elbow motions in its middle part, and the h.and 
 and finger motions in its posterior and lower part. 
 
 The upper third of the anterior and posterior central convo- 
 lutions, including their junction in the paracentral lobule, con- 
 trols the motions of the lower extremity, the thigh, knee, foot,. 
 and toes being governed by various parts of this area from before 
 backward in the order named. 
 
 The parts susceptible of the finest and most delicate move- 
 ments, those directed by the most acute sensations, the lips, the 
 fingers, and the toes, lie furthest back in the motor area, in the 
 depth of the fissure of Rolando and in the posterior central con- 
 volution. Lesions in this convolution almost always cause some 
 loss of tactile sensation as well as paralysis, and hence this area 
 is thought to be the seat of tactile sensations as well of move- 
 ments, while some cases point to the localization of muscular sen- 
 sations in the area just behind that of motion. 
 
 The trunk or body motor centres lie between those of the leg 
 and arm. 
 
 There are no sharply defined sections of the motor area to be 
 assigned to special motions. Each motion, each part of a limb. 
 has a wide general representation over the cortex and a special 
 representation at a limited area. The areas of representation of 
 different limbs merge into one another ; thus, in the representa- 
 tion of the thumb we find that there is a focus, but that the thumb 
 is represented over a great deal of the upper limb region, and that 
 this representation diminishes in intensity gradually as we pass 
 from the focus upward. This explains the fact that the excision 
 of a small area does not totally paralyze the portion of the limb 
 represented chiefly on that area. The adjacent areas represent to 
 some extent that limb, and hence can govern it if need be. 
 
 The motor centres govern motor acts rather than special 
 muscles, each act involving a succession of movements of differ- 
 ent joints by various groups of muscles. 
 
54 DISEASES OF THE NERVOUS SYSTEM. 
 
 Cortical Spas)n and Paralysis. — Irritation in the motor area 
 produced by any kind of disease gives rise to localized spasms or 
 convulsions, called Jacksonian epilepsy. Destruction of the motor 
 area gives ries to paralysis. The point of beginning of the spasm 
 or the extent of paralysis depends on the part of the motor area 
 diseased. Hence, from the character of either of these symptoms 
 a conclusion can be reached as to the location of the disease. Cor- 
 tical spasm or paralysis usually begins in the face or in one limb 
 of one side and extends. The order of the progress also indicates 
 the location of the disease, e. g., from face to arm, then to leg; 
 or vice versa, e. g., spasm of shoulder, arm, and hand, vs. spasm 
 of fingers, arm, and shoulder : the disease is most intense in the 
 part first affected. Sensations of numbness precede the spasm. 
 A cortical spasm begins locally, and usually extends until one 
 side of the body is affected. It is usually followed by temporary 
 weakness. Consciousness is preserved. 
 
 Cortical paralysis is monoplegic in type vs. subcortical par- 
 alysis, which is hemiplegic in type. A slowly advancing paralysis 
 indicates a slowly extending destruction of tissue. Cortical par- 
 alysis is associated with increased reflexes, but there is no atrophy 
 and no change in electric reactions. Contractures develop late. 
 
 The Visua l Are a. 
 
 The area of sensations of sight is located in the occipital lobe 
 of the brain, including the cuneus on the median surface and the 
 occipital convolutions on the convexity. The cortex lying in the 
 calcarine fissure is the part primarily reached by the visual im- 
 pulses, but the parts named are also concerned in vision. Each 
 occipital lobe receives impressions from one-half of both eyes ; 
 hence a lesion in one lobe produces hemianopsia, a half-blindness 
 in both eyes, the blind field of vision being on the opposite side to 
 the lesion. This is termed homony mous hemianopsi a ; that is, 
 a blindness in the like-named halves of both visual fields. When 
 the right occipital lobe is affected, the patient cannot see anything 
 on the left side of the middle line as he looks forward. 
 
-V-w 
 
 
 
 
 z 
 
 
 V-tAi) 
 
 
DISEASES OF THE NERVOUS SYSTEM. 
 
 Fig. 14.— The \'isual Tract. The result of a lesion anywhere between the chiasm and 
 cuneus is to cause homonyrnous hemianopsia. III. Third nerve; S. N., substantia 
 nigra; R. N., red nucleus of tegmentum; L., lemniscus; T. G., fibres from optic 
 tract to corpora quadrigemina. 
 
 Irritation of the occipital lobe may cause hallucinations of 
 light or even of objects which are referred to the opposite visual 
 
56 DISEASES OF THE NERVOUS SYSTEM. 
 
 field. Destruction of the occipital lobe on the left side destroys 
 sight-memory pictures ; hence recognition of things seen may be 
 impossible, and reading power may be lost. 
 
 The Auditory Area. 
 
 The area of sensations of sound is located in the first and 
 second temporal convolutions of the brain. Each ear is connected 
 with both hemispheres ; hence deafness from a unilateral lesion is 
 only partial and is not generally noticed. But if both temporal 
 lobes are destroyed the patient becomes totally deaf. Irritation 
 of the temporal cortex may cause hallucinations of hearing. This 
 may be the first symptom of a convulsion whose origin is an irri- 
 tation in this part of the cortex. Destruction of the temporal cor- 
 tex on the left side causes word-deafness. (See speech areas.) 
 
 The Smell and Taste Area. 
 
 The area of sensations of smell and taste is located at the tig^ 
 ,of the temporal lobe on its under and inner surface, which rests 
 on the sphenoid bone. Each lobe is related to sensory organs on 
 both sides, and unilateral lesion does not often produce noticeable 
 symptoms. 
 
 The Speech Areas and Aphasl\. 
 
 The speech areas are of four kinds and in four locations. 
 They are limited to the left hemisphere in right-handed persons 
 and to the right hemisphere in left-handed persons. There is 
 the motor-speech area in the posterior part of the third frontal 
 convolution (Broca's convolution), in which the movements con- 
 cerned in the act of speaking are controlled. The use of language 
 and the power of talking are affected when this region is de- 
 stroyed. There is the andijory-jpccch area in the first and second 
 temporal convolutions, in which the memories of word-sounds 
 are stored up. The understanding of language and the power 
 of recollecting the names of objects are lost when this region is 
 destroyed. There is the visual-speech area in the ocdp^ital and 
 lower parietal region., in which th.e memories of printed words 
 

 iyl/t-^ 
 
 
 
DISEASES OF THE NERVOUS SYSTEM. 
 
 57 
 
 arc stored up. The untlerstanding of written language and the 
 power to read are lost when this region is destroyed. The pozver 
 of zcriting is a part of speech and is usually lost when the motor- 
 speech area is destroyed, but its exact location is not fully deter- 
 mined ; some cases pointing to the second frontal convolution, 
 others to the lower parietal convolution near the hand centre as its 
 probable cortical position. (See Fig. 15.) 
 
 It is accepted that every word in ordinary use has a complex 
 mental substratum, which may be termed the word-image, made 
 up of a number of memory pictures. The memory of the sound of 
 a word as spoken, the memory of the appearance of the word as 
 printed, the memory of the muscular movements needed to write 
 the word or to pronounce it, are known to be distinct from one 
 another and yet to be associated together. Loss of one of these 
 
 Hand 
 
 Touch 
 
 Hearing 
 
 Fig. 15. — Diagram to illustrate Aphasia. The cortical sensory and motor centres 
 are indicated by arrows. The secondary cortical centres of memories are indicated 
 by circles. I. Visual of Objects. II. Visual of Words. III. Tactile. IV. 
 Auditory. \'. Speech. \l. Writing. These are joined to each other by association 
 fibres which send impulses in both directions. Lesions of the association fibres 
 as well as lesions of the cortex cause aphasia. 
 
-"58 
 
 DISEASES OF THE NERVOUS SYSTEM. 
 
 memory-pictures, or disturbance in their. association, impairs the 
 integrity of the word-image, and produces such defects in its use 
 as are indicated by the names given to the respective varieties of 
 aphasia. A division of disturbances of speech has been made 
 into two great classes of sensory and motor aphasia — the first due 
 to defect in the receptive, and the second due to impairment of the 
 emissive functions of the brain. A further subdivision into sev- 
 eral varieties has been made. These are word-deafness, word- 
 blindness, agraphia, motor aphasia, and paraphasia. But, before 
 considering these defects, let us look at the physical basis of the 
 thought which lies back of the wor. Take the concept "bell" as 
 an example. 
 
 Fig. i6. 
 
 The concept of a bell is made up of separate memory-pictures 
 of its shape, size, color (visual-picture) ; weight (muscular-sense 
 picture) ; cold smooth surface (touch-picture) ; and sound (audi- 
 tory-picture). These various memories, received by different 
 senses and stored up in different parts of the cortex, are associated 
 together in a mental image of the object bell. 
 
DISEASES OF THE NERVOUS SYSTEM. 59 
 
 To this mental ima^c the word-image is added of the word 
 bell as heard, as printed, as spoken, as written, making up a eon- 
 geries of memory-pictures forming a "concept." Any one of 
 these memory-pictures may be lost by disease. If the memories 
 of the object are lost the symptom is called apraxia. If the memo- 
 ries of the word are lost the symptom is called aphasia. 
 
 To examine an aphasic thoroughly it is necessary to test — 
 
 1. The power to recognize objects seen, heard, felt, tasted, 
 or smelt, and their use. 
 
 This will determine whether the condition of apraxia is 
 present. 
 
 2. The power to recall the spoken name of objects seen, 
 heard, handled, tasted, or smelt. 
 
 3. The power to understand speech and musical tunes. 
 
 4. The power to call to mind objects named. 
 
 This will test the integrity of the auditory-speeech area and 
 of the association-tracts between other sensory areas and the 
 temporal convolutions. 
 
 5. The power to understand printed or written words. 
 
 6. The power to read aloud and to understand wdiat is read. 
 
 7. The power to recall objects whose names are seen. 
 
 8. The power to write spontaneously, and to write the names 
 of objects seen, heard, etc. 
 
 9. The power to copy and to write at dictation. 
 
 10. The power to read understandingly what has been 
 written. 
 
 These tests will determine the condition of the visual word- 
 memories in the angular gyrus, and of the connections between 
 this area and surrounding sensory and motor areas. 
 
 11. The power to speak voluntarily, and if it is lost, the char- 
 acter of its defects. 
 
 12. The power of repeating words after another. 
 
 This will test the mtegrity of Broca's centre and its associa- 
 tion-tracts. 
 
 I. Word-Dcafiicss. — If the memory of the sound of the word 
 is lost, the word cannot be called to mind and cannot be recognized 
 when heard. Show the patient a watch, and he is unable to name 
 
60 DISEASES OF THE NERVOUS SYSTEM. 
 
 it ; tell him it is a stone, a match, a watch, and notice whether he 
 dissents from the former and gives signs of satisfaction at the 
 last. If he does, he has only auditory amnesia, but not word- 
 deafness. If not, he is word-deaf, and is unable to understand 
 what is said to him. The lesion lies in the posterior half of the 
 first and second temporal convolution in the left hemisphere in 
 right-handed, in the right, in left-handed persons. This is one 
 variety of aphasia whose lesion is well known, though it rarely 
 occurs alone. 
 
 2. W ord-Blindncss. — If the memory of the appearance of 
 the word is lost, the visual image of it cannot be called to mind 
 or recognized, and then the patient will be unable to write spon- 
 taneously, for he cannot remember how the letter looks which he 
 wishes to write ; and he will be unable to read, because the shapes 
 of the letters and words seen arouse no recollection. As a matter 
 of fact, words are forgotten more easily than letters, and if a 
 patient is to relearn to read he must begin with letters and go on 
 to words. Figures are sometimes recalled when words are for- 
 gotten, and many a patient can do mathematical calculations on 
 paper who cannot read or write ordinary words. The reverse 
 may also be true, the patient being able to read and write, but 
 being unable to understand figures or calculate. Such patients 
 may also play cards or other games, if they are not physically 
 blind. It is not infrequently the case that persons who are thus 
 word-blind can write at dictation, or copy, and yet show no evi- 
 dence of understanding what has just been read or written. A 
 distinction must be made between those who can and cannot do 
 these things, though its pathological basis is still obscure. The 
 condition of visual amnesia with word-blindness is due to a lesion 
 
 • involving the inferior parietal convolutions and angular gyrus, 
 and is often associated with psychical blindness, but may occur 
 independently of it. Word-deafness and word-blindness fre- 
 cjuently occur together, and then the lesion is found involving 
 both the temporal and the angular convolutions. Some cases of 
 this condition have depended on a deep lesion in the temporc- 
 occipital region, breaking the association-tracts. 
 
 3. Motor Aphasia. — If the memory of the effort needed to 
 
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J - iXirwhk Bi^'V-rCu>i:tViAA 
 
 -f. ^6C, ^AJL^^ ^tC^^t^^WV, ^ ^^e^-<xA^ 
 
 
DISEASES OF THE NERVOUS SYSTEiM. 61 
 
 pronounce a word is lost, a true paralysis of active speech occurs, 
 though the muscles may not he weakened. This is the ordinary 
 form of motor aphasia, due to a lesion of Broca^s^entre. It is 
 to be noted that such a loss of speech involves a loss of the power 
 of repeating words after another, as well as of voluntary speech, 
 and is not accompanied by any inability to understand spoken or 
 written language. In the uneducated, as in children, the acts of 
 talking and writing are closely joined, as may be seen by watch- 
 ing the lips, which move in the act of writing. But among those 
 accustomed to write much these acts are independent, and it is 
 probable that many educated aphasics may be able to answer ques- 
 tions in writing when their efforts at speech fail. Reading aloud 
 will also be lost in motor aphasia, for here, too, the inability to 
 articulate hampers the patient. 
 
 4. Agraphia. — The independence of the effort-memory neces- 
 sary for writing, and connected with movements of the hand from 
 the effort-memories of speech, has been alluded to. When these 
 are lost alone the condition is known as agraphia. In such a 
 state the pen cannot be used. Copying, writing at dictation, and 
 voluntary writing are all lost. It has been noted already that 
 when a word cannot be called to mind, it of course cannot be writ- 
 ten. But words can often then be written at dictation, if the per- 
 son is one who writes much. Hence sensory agraphia and motor 
 agraphia must be distinguished ; the former being a part of word- 
 blindness, the latter not at all associated with inability to read. 
 The lesion of motor agraphia is unsettled, though a few facts point 
 to the posterior part of the second frontal convolution as the 
 probable seat of this function. It is not unlikely, however, that 
 the more exact localization of fine movements of the thumb and 
 fingers in the posterior central convolution by Horsley may be 
 followed by the discovery of the writing centre in this vicinity. 
 
 5. Paraphasia. — These forms of aphasia are due to a loss of 
 distinct memory-pictures. The several memory-pictures which 
 are united in the word-image may thus be reasonably regarded as 
 separate from one another in their location in the brain. But 
 since they are joined together to form the word-image, it follows 
 that the association-fibres joining the various areas are as neces- 
 sary to the use of even a single word as the various areas with 
 
62 
 
 DISEASES OF THE NERVOUS SYSTEM. 
 
 Fig. 17.- — The Association Fibres in the Centrum Ovale. A, Between adjacent con- 
 volutions; B, between frontal and occipital lobes; C, between frontal and temporal 
 lobes, the cingulum; D, between temporal and frontal lobes — lesion of this tract 
 causes paraphasia; E, between occipital and temporal lobes — lesion of this tract 
 causes word-blindness; C.N., caudate nucleus; O.T., optic thalamus. 
 
 their memories. It is really by association only that an object or 
 a word becomes a subject of thought or use. If these associations 
 are broken, the result is a defect of language characterized by 
 the misplacement of words, and the patient talks jargon. 
 
 •There are many forms of paraphasia as there are many asso- 
 ciation-tracts, and it is not yet possible to assign different cases to 
 their lesions. 
 
 It is evident that many differently located lesions will pro- 
 duce disturbances of speech. When the entire cortex is diseased 
 — as in paresis — aphasia also appears. 
 
 Defects in the appreciation and use of music are called amu-. 
 sia, and present the same varieties as aphasia. 
 
 T he Frontal Regio n. 
 
 There appears to be a certain relation between the frontal 
 lobes of the brain and the higher forms of intellectual activity, 
 the powers of fixing the attention and of reasoning and of self- 
 control. But disease here does not cause a loss of any one mental 
 faculty, and for the higher powers of the mind a general integrity 
 

 (f ir*nr~c^ •^ <2_-t.-T^ 
 
 1 
 
 l^'<J-4—1Si,o..,XXZ^ ; /lyt—O^-^J^-"-^^-'^-'^ 
 
6... /kM^ oue^ ^^^t^^ -1^ L.^^^Y^JL^-.^^^^:fl:^^ '^-^^ 
 
DISEASES OF THE NERVOUS SYSTEM. 63.: 
 
 of the entire brain, not of any one part, is necessary. When it is 
 considered that every concept is made up of numerous memory- 
 pictures joined together, each of which has a separate location in 
 the brain cortex, it becomes evident that to the process of thought 
 a healthy state of the entire cortex is necessary, and also of the 
 white matter beneath it, through which the associating fibres pass. 
 And it 'is therefore impossible for a single lesion anywhere to- 
 cause a loss of memory or of imagination or of judgment. Yet 
 for the co-ordination of facts into orderly series, for comparison, 
 and for analysis of knowledge gained through the senses, the 
 healthy state of the fontal lobes appears to be necessary. And 
 lesions in the frontal region, especially upon the left side, are quite 
 uniformly attended by mental dulness, apathy, lack of power of" 
 concentration, and imperfect self-control. 
 
 There are large areas of the cortex of the brain whose func- 
 tion is undetermined. These are much more extensive on the- 
 right hemisphere than on the left. There are no definite symptoms 
 produced, so far as we now know, by lesions in these areas ; but 
 the negative fact is certain, that lesions in them do not cause dis- 
 turbances of motion, of sensation, or of speech. 
 
 The cortex of the hemispheres upon the base of the brain 
 lying on the orbital plate, on the sphenoid and temporal bones, 
 and on the tentorium cerebelli, has as yet no assignable functions, 
 and lesions in these regions do not produce recognizable - 
 symptoms. 
 
 Symptoms of Cortical Disease. 
 
 In the study of cases of cortical disease, it is necessary at 
 the outset to distinguish general from local symptoms, for it is 
 the latter only which enable one to locate the lesion. General' 
 Symptoms are those which are common to various kinds of brain 
 disease in whatever region they are located. They are headache, 
 vertigo, digestive disturbances, general convulsions, optic neuritis, 
 with or without blindness, delirium, and coma. These are due- 
 either to an increase of the intracranial contents (as by the growth 
 of a tumor) and consequent presssure, or to some other interfer- 
 ence with the normal condition in the brain. They give no evi- 
 
64 DISEASES OF THE NERVOUS SYSTEM. 
 
 dence as to the exact region of the brain which is affected. They 
 merely indicate that the brain is diseased. 
 
 Local Symptoms, on the other hand, depend entirely for their 
 production upon the region of the cortex which is invaded. They 
 are disturbances of motion and of sensation of various kinds, and 
 of sensory perception ; disturbances of memory ; and loss of 
 speech. They may be divided into symptoms of irritation and 
 symptoms of destruction ; and it is not infrequently the case that 
 the former precede the latter in the course of a disease. An irri- 
 tative lesion produces symptoms due to an increased activity of 
 the area affected ; c. g., spasms, pain, tingling and numbness, 
 flashes of light, sounds, or hallucinations of smell and taste. A 
 destructive lesion produces symptoms due to a loss of function in 
 the area involved ; e. g., paralysis, anaesthesia, blindness, deafness, 
 loss of smell and taste, and of the use of language. Each of these 
 points to a different location of the disease, and is essential to its 
 localization. 
 
 II. Tracts Within the Brain. 
 The Association-Tracts. 
 
 The first system of fibres in the centrum ovale is the associa- 
 tion system. (See Fig. 17.) 
 
 It can be shown by careful dissection that each convolution 
 is joined to the two adjacent convolutions by fibres which pass 
 around the separating fissures. Also, that bundles of fibres exist 
 which pass from each convolution to the convolution next but one, 
 and so on. Hence, it may be stated that each convolution has a 
 possible connection with every other. Besides this association of 
 convolutions by small bundles of fibres, it is possible to find a 
 distinct set of association-tracts which pass between more or less 
 distant regions. One such tract passes from the frontal lobe, col- 
 lecting its bundles from all three convolutions, backward to the 
 occipital lobe. Another tract joins the occipital with the anterior 
 part of the temporal lobe. Another passes from the upper two 
 temporal convolutions forward to the third frontal convolution, 
 passing beneath the island of Reil. And a tract from the frontal 
 to the posterior temporal area may also be found. 
 
DISEASES OF THE NERVOUS SYSTEM. 65 
 
 The function of these association-fibres is to form the phys- 
 ical basis for the association of concrete memories and of psychi- 
 cal acts, and their integrity is necessary to thought. By studying 
 subjectively the association of ideas in the mind the importance 
 of their function is evident. \Mien they are destroved bv disease 
 various forms of paraphasia appear. 
 
 The Commissural Tracts. 
 
 The second system of fibres in the centrum ovale is the com- 
 missural system. This joins corresponding areas of the two hemi- 
 spheres with one another. The commissural fibres between .the 
 frontal, parietal, and occipital lobes of the two sides pass in the 
 corpus callosum. Those from the temporal lobes pass in the an- 
 terior commissure. The function of these fibres is to harmonize 
 the action of the two hemispheres. Simultaneous movements of 
 like nature can be made wath great facility with both upper ex- 
 tremities. Movements which are difficult when attempted with 
 the left hand alone become easy when associated with correspond- 
 ing movements of the right hand — as. for example, drawing a 
 circle, writing one's name. It is the commissural fibres joining 
 the motor convolutions only which can be thus tested. Failure 
 to perform easily corresponding bilateral motions in face, hands, 
 or feet would indicate some obstruction to conduction in them. 
 
 The Projectiox-Fibres. 
 
 The projection system includes those fibres which join a 
 definite area of the cortex with parts of the nervous system lying 
 below it, viz., some nervous mechanism in the basal ganglia, brain 
 axis, or spinal cord. Indirectly, through the medium of such 
 mechanisms, the external w^orld is projected upon the brain and 
 reaches consciousness, and voluntary impulses originating in the 
 brain are sent to the muscles. The fibres gather together within 
 the hemisphere at the upper level of the basal ganglia, and either 
 end in the optic thalamus or go on between these ganglia through 
 the internal capsule to the brain axis and spinal cord. 
 
 The majority of these fibres end in the optic thalamus, which 
 
66 DISEASES OF THE NERVOUS SYSTEM. 
 
 Fig. i8. — The Projection Tracts Joining the Cortex with Lower Nerve Centres. 
 Sagittal section showing the arrangement of tracts in the internal capsule. A, 
 Tract from the frontal lobe to the pons, thence to the cerebellar hemisphere of the 
 opposite side; B, motor tract from the central convolutions to the facial nucleus in 
 the pons and to the spinal cord; its decussation is indicated at K; C, sensory tract 
 from posterior columns of the cord, through the posterior part of the medulla, pons, 
 crus, and capsule to the parietal lobe; D, visual tract from the optic thalamus (O.T.) 
 to the occipital lobe; E, auditory tract from the internal geniculate body (to which 
 a tract passes from the VIII. nerve nucleus [J] to the temporal lobe; F, superior 
 cerebellar peduncle; G, middle cerebellar peduncle; H, inferior cerebellar peduncle; 
 CN, caudate nucleus; C.Q., corpora quadrigemina; \'t., fourth ventricle. The 
 numerals refer to the cranial nerves. 
 
 is thus connected with all parts of the cortex of the brain. Of 
 the function of these we know very little. Two large bundles, 
 however, are separable from the mass. 
 
 The Visual Tract. — One of these passes inward and forward 
 from the occipital lobe, and joins the pulvinar of the thalamus 
 and the external geniculate bodv. This is the visual tract. (Fig. 
 
 14.) 
 
 The optic nerves decussate partially at the chiasm, so that 
 
DISEASES OF THE NERVOUS SYSTEM. 67 
 
 each optic tract contains fibres from'both rctinse. Each tract passes 
 to the optic thalamus, external geniculate- body, and anterior cor- 
 pus quadrigeminum. Thence the fibres of the visual tract pass 
 out, to turn backward through the internal capsule and through 
 the centrum ovale to the cortex of the occipital lobe. A lesion 
 anywhere in this course causes homonymous hemianopsia. 
 
 The Auditory Tract. — A second bundle passes from the 
 temporal lobe upward to the thalamus, internal geniculate body, 
 and posterior corpus quadrigeminum, in which the auditory tract 
 from the acoustic nucleus ends. This conveys impulses of sound 
 from both ears to each temporal lobe, and is the auditory tract. 
 These are the only bundles of the thalamic radiations whose func- 
 tion is determined. (Fig. i8E.) 
 
 Some of the projection-fibres pass on through the internal cap- 
 sule without communicating with the basal ganglia, and of these 
 we know three distinct bundles. (Fig. i8 A.) 
 
 The first is collected from the three convolutions of the fron- 
 tal lobe, and passing between the caudate and lenticular nuclei in 
 the anterior division of the interal capsule, descends in it to the 
 base of the brain, and issuing in the inner third of the foot of the 
 crus cerebri, passes down to the pons, where it terminates in nu- 
 clei lying in the ventral half. The nuclei thus reached by these 
 fibres are also joined by other fibres from both hemispheres of the 
 cerebellum, which enter the pons at its lateral surfaces in the mid- 
 dle peduncles. Thus it is evident that a connection exists between 
 each frontal lobe and both cerebellar hemispheres, the crossed 
 connection being greater than the direct one. Of the function of 
 this tract we know nothing. 
 
 The Motor Tract. — The second bundle of the projection sys- 
 tem is the luotor tract. It comes from the posterior part of the 
 third frontal convolution, the two central convolutions, and from 
 the paracentral lobule, and passes out of the base through the 
 middle third of the crus cerebri. Its fibres collect at the middle 
 portion of the upper surface of the internal capsule, those from 
 the lower parts of the cortex passing straight inward, those from 
 the upper parts curving outward and downward to pass around 
 the side of the lateral ventricle. Thus within the centrum ovale, 
 
DISEASES OF THE NERVOUS SYSTEM. 
 
 Fig. 19. — The Motor Tract. S, Fissure of Sylvius; N.L., lenticular nucleus; O.T., 
 optic thalamus; N.C., caudate nucleus; C, crus; P, pons; M, medulla; O, olivary 
 body. The tracts for face, arm, and leg gather in the capsule and pass together to 
 the lower pons, where the face fibres cross to the opposite \'II. nerve nucleus, 
 while the others pass on to the lower medulla where they partially decussate, to 
 enter the lateral columns of the cord; the non-decussating fibres pass to the an- 
 terior median columns. The effect of a lesion situated at three points in the tract 
 is shown on the left side of the figure. 
 
 these fibres, if looked at from in front, appear like the sticks of 
 a fan, and like those sticks their relative position is altered in the 
 point of junction, where those passing inward from the lowest 
 part of the cortex lie in front of those which pass downward 
 from its upper part. Thus in the capsule the order from before 
 backward is, iirst, the fibres conveying speech impulses to the 
 pons and medulla ; second, the fibres conveying facial-motor im- 
 pulses to the pons; third, the fibres destined to the arm centres of 
 the cord ; fourth, the fibres transmitting impulses to the leg 
 centres in the cord. The fibres conveying impulses to the muscles 
 of the trunk lie between those to the arm and leg. (See Fig. 20.) 
 
DISEASES OF THE NERVOUS SYSrE>r. 69 
 
 From the anterior half of the posterior division of the capsule 
 this tract passes through the mi<ldlc third of each crus, through 
 the pons (where the division to the facial nucleus crosses to the 
 opposite side and ends), and thence by way of the pyramids of the 
 medulla to the crossed pyramidal and direct anterior median col- 
 umns of the spinal cord. It is evident, however, that the con- 
 centration of this tract is much greater in the capsule than in the 
 centrum ovale, where the individual fibres are scattered among 
 the other systems and occupy but a small area from before back- 
 ward. 
 
 Lesions beneath the third frontal convolution of the left side 
 produce motor aphasia. Lesions beneath the central convolutions 
 in the centrum ovale produce paralysis, which will vary according 
 to the position of the lesion. The nearer the lesion lies to the cor- 
 tex the more will the symptoms resemble those of cortical disease, 
 monoplegia being the rule. The nearer the lesion to the point of 
 junction at the capsule the more will the symptoms resemble those 
 of capsule lesion, hemiplegia being the rule. When the motor 
 tract is injured bv a lesion in the lower half of the pons, the result 
 is paralysis of the face on the side of the lesion and of the arm 
 and leg on the opposite side (alternating paralysis). 
 
 TJic Sensory Tracts. — The third set of fibres of the projec- 
 tion system include those which lie just posterior to the motor 
 tract, and which pass inward from the parietal convolutions. 
 These take a similar course to those of the motor tract, and fill 
 up to a considerable extent the space between it and the radiation 
 of the visual tract, toward the occipital lobe. The}' are mingled 
 with fibres which pass to the optic thalamus, but are separable from 
 them in foetal brains, and may be traced down through the capsule 
 to the tegmentum of the crus, where they divide into a portion 
 going to the lemniscus, and a portion going to the formatio reticu- 
 laris. The fibres can be traced through these tracts dowaiward to 
 the medulla and through the sensory decussation to the posterior 
 pyramids of the medulla in w'hich the posterior columns of the 
 spinal cord begin. See Figs. 21-24.) This set of fibres conveys 
 the sensations of touch, pain, temperature, and muscular sense, 
 and lesions in its course will cause disturbance of these sensations. 
 
70 
 
 DISEASES OF THE NERVOUS SYSTEM. 
 
 Fig. 20. — Horizontal Section through 
 the Brain. (After Strumpell.) NC, 
 nucleus caudatus; F, fornix; IC, 
 anterior half of internal capsule; OT , 
 optic thalamus; Fa, facial tract; M, 
 motor tract; S, sensory tract; O, 
 visual tract, in posterior half of in- 
 ternal capsule; IR, island of Reil; 
 NL nucleus lenticularis; EC, ex- 
 ternal capsule; V, lateral ventricle, 
 posterior cornu. 
 
 Lesions of the corpora quad 
 ness, and ophthalmoplegia. 
 
 Like lesions in the motor tract, 
 the rule obtains that the nearer 
 the cortex the more likely is the 
 lesion to cause an affection of a 
 single limb, while the nearer the 
 capsule the more likely is the 
 symptom produced to be liemi- 
 ansesthesia. A lesion in the 
 •lower half of the pons may pro- 
 duce alternating hemianaesthe- 
 sia, the face being anaesthetic on 
 the side of the lesion, nnd the 
 limbs on the opposite side. 
 
 From these facts it is evi- 
 dent that a lesion which lies in 
 the centrum ovale, at any point 
 posterior to the praecentral fis- 
 sure of the frontal lobe, may 
 produce recognizable symp- 
 toms, for it must affect either the 
 motor, or the sensory, or the 
 visual, or the auditory tracts, or 
 individual fibres of those tracts. 
 
 ■ in. The Basal Ganglia. 
 
 The symptoms produced by 
 lesions in the basal ganglia — 
 corpora striata and optic thala- 
 mus — are not to be distinguised 
 from those caused by lesions of 
 the projection-tracts which lie 
 near them in the internal capsule, 
 rigemina cause nystagmus, blind- 
 
 IV. The Cerebellum. 
 
 The cerebellum is the central organ of equilibriuuL It is 
 joined to the spinal cord by the direct cerebellar column, which 
 
TheMatarTmc/' 
 
 aieral pyramuLii 
 tract 
 
 r^ 
 
 
 
 Fiucajrt&f^uus 
 
 •sterOT-TTL body 
 
 fuuc^racvles 
 
 71UC curteai:-: 
 
 ■Xateml coliurtr. 
 
 • (^n, i/t£ firr-rf 
 
 Fl.;. -IX 
 The Motor Tract in the Cerebral Axis. 
 
 Fig. 22 
 
 The Tract of the Tactile Sense. 
 
Cen-M'u.'n > 
 
 rcuc-Cunea/us 
 Meckdia 
 
 Memory 
 decursatiJjn 
 
 ,Qii^ 
 
 LunuLbSCUs 
 
 Jted rvurleur 
 
 Cervbrt 
 
 TAele. 
 
 Fk;. 23 
 
 Fk;. 24 
 
 The Tract of Muscular Sense. 
 

DISEASES OF THE NERVOUS SYSTE^[.. 
 
 carries sensory impulses up to it through the inferior peduncle. 
 It is joined to the motor tract by the midd le peduncle, which con- 
 veys impulses to the pons and thence to the spinal cord, directing 
 balancing motions. It is joined to the cerebral hemispheres both 
 by the middle and superior peduncles, whose exact functiona are 
 unknown. 
 
 Lesions of the cerebellum, or of its peduncles, cause stagger- 
 ing g'ait. This differs from that in locomotor ataxia, for there is 
 no ataxia of the limbs when the patient lies down, giving support 
 to the body. When the middle peduncle is irritated the patient 
 staggers toward the lesion ; when it is destroyed he staggers away 
 from the lesion. Lesions of the cerebellum also produce vertigo. 
 
 \'. The Cerebral Axis. 
 
 The various long tracts which join the brain to the spinal cord 
 pass through the crus cerebri, pons, and medulla near to the 
 nuclei of origin of the cranial nerves. These tracts are shown in 
 Figs. 21-24. The cranial nerve nuclei were shown in Fig. 7. 
 
 Lesions of the cerebral axis, 
 ^^1?> such as small hemorrhages, 
 
 small areas of softening, or tu- 
 mors destroy these tracts and 
 also these nuclei. The tracts 
 as a rule decussate on, entering 
 the cord, hence a unilateral le- 
 sion of the cerebral axis causes 
 motor or sensory symptoms in 
 the extremities of the opposite 
 side The nuclei of the cranial 
 nerves send those nerves directly 
 outward without decussating; 
 hence, a unilateral lesion of the 
 cerebral axis causes motor or 
 sensory symptoms in the face 
 
 Fic. Jt. — The Motor Tract in Pons and ^i • i -r* .1 
 
 Medulla. Lesion at A causes hemi- ou the Same Side. From the 
 
 plegia of side opposite to lesion; le- f^nmhinpl-inrt of tViPQP tivn cf^tQ 
 
 sion at B causes alternating paraly- COmOinatlOn Ot tnCSC tU O SCt^ 
 
 sis; lesion at C causes paralysis of ^f cvmnl-nTTT; if IQ <^a>ivr fo rliacr 
 
 tongue on side of lesion and of ex- *-"^ S}. mpioms 11 IS eas\ tO Qiag- 
 
 tremities of opposite side; lesion at rin<^ripatp a Ip^inn of tViP rf^rp- 
 
 D causes paralysis of extremities of "OStlCaie d ICblOn Or me CerC- 
 
 opposite sides; lesion at E causes 'hral nvit; ^^pp Fio- •> ^ \ 
 
 paralysis of extremities of both sides. ^^^^ '^■^'^- V^^^ ^ ^&- "^-Z 
 
 "VE NUCLEUS. 
 
 yifnUOLEjs.O 
 
 Wj^lERlT. 
 
THE CEREBRAL DISEASES OF THE VASCULAR 
 
 ORIGIN. 
 
 Hemorrhage, E:\ibolism, Thrombosis, "Apoplexy." ■ 
 
 The most common cerebral diseases are those due to a rup- 
 ture of a vessel in the brain, cerebral hemorrhage, or to a stoppage 
 in a cerebral vessel, cerebral ciiibolisiii and cerebral tliroinbosis. 
 
 The cerebral circulation. See "Quain's Anatomy." 
 
 Pathology . — The condition which leads to such diseases is 
 chronic endarteritis : a chronic inflammatory process in the intima 
 and muscular coats of the vessels vith a production of new 
 cellular tissue which may (i) go on tmtil it obliterates the 
 lumen of the vessel, producing thrombosis; or (2) undergo cal- 
 careous degeneration, roughening the wall and inducing fibrin 
 deposits, which may occlude the vessel, producing thrombosis, 
 or be washed onward, producing embolism; or (3) undergo fatty 
 degeneration, thus eroding the intima and weakening the muscu- 
 lar coat, causing aneurisms (miliary or larger) which rupture, 
 producing cerebral hemorrhage. See Delafield and Prudden's 
 "Pathology." 
 
 Pathology of Cerebral Hemorrhage.- — The vessel ruptures. 
 The blood spreads out in the membranes, filling the fissures and 
 depressing the cortex, or if the hemorrhage is subcortical, tears 
 the surrounding brain. A clot forms, thin and flat on the cortex, 
 globular in the brain, which tears and compresses the brain- 
 tissue around it. This clot gradually shrinks and undergoes ab- 
 sorption, leaving a hsematin stain ; the disintegrated brain-tissue 
 undergoes fatty degeneration and absorption. There remains a 
 mass of softened tissue without or with a connective-tissue wall, 
 or finally a cyst, or a mass of sclerotic tissue or merely a scar. 
 The torn brain never reunites. From the point of laceration 
 degeneration begins, which e.xtends along the various tracts, e. g.. 
 
ly^ f 
 
DISEASES OF THE NERVOUS SYSTEM. 75 
 
 desccndins;- (legcneratiun in niutor tract through the cerebral axis 
 and spinal cord, or ascending degeneration in sensory tracts to the 
 cortex. When the presstire is removed the cortex may resume its 
 function or the uninjured tracts may resume their functions. 
 Hence partial recovery is the rule after cerebral hemorrhage. 
 
 Pafholoi^x of Cerebral Eiiibolisin or TJiroiiibosis. — The vessel 
 being occluded, the brain-tissue which is supplied with blood 
 through it is cut oft" from its nutrition. The first arrest of blood 
 supply is extensive, but when collateral circulation is established 
 the final area or region which softens may be small. In the cortex, 
 the collateral supply by anastomosing vessels is extensive. In the 
 basal ganglia and capsule it is very imperfect. Hence the perma- 
 nent effect of occlusion is more serious in the arteries entering the 
 base than in the small branches in the cortex. If large vessels in 
 the cortex, e. g., a main branch of a Sylvian artery, is plugged, 
 the area of softening may be extensive. A fatty degeneration and 
 a necrosis of brain-tissue follow the occlusion of the vessel. In 
 the softened tissue there are at first extravasations of venous blood 
 (red softening) ; later these are absorbed and the tissue in a stage 
 of fatty degeneration is yellow (yellow softening). If there is 
 simple necrosis without extravasation or fatty degeneration, the 
 brain has its natural color but is soft (white softening). The 
 softened tissue contracts, leaving a depression, or a cavity, or a 
 scar ; in some cases a cyst with smooth walls and serous contents. 
 
 The Sifiiafion of the Lesion . — Cerebral hemorrhage : in basal 
 ganglia involving the internal 'capsule in fiftv per cent., next in 
 frequency in centrum ovale, cortex, pons, and ventricles ; very 
 rarely in cerebellum. 
 
 Cerebral embolism, forty-nine per cent, left ; forty-one per 
 cent, right ; ten per cent, both hemispheres. Central ganglia and 
 capsule, sixty per cent. ; next in frequency cortex supplied by 
 middle cerebral artery, (i) motor area, (2) aphasic area, (3) 
 visual area. Least frequent pons and anterior or posterior cere- 
 bral arteries. 
 
 Cerebral thrombo sis is middle cerebral, basilar, vertebral, and 
 anterior and posterior cerebral vessels in order of frequency 
 named. 
 
 Et iology. — Thrombosis is common below age of forty-five ; 
 
76 DISEASES OF THE NERVOUS SYSTEM. 
 
 hemorrliag"e after forty-five ; age of maximum liability to hemor- 
 rhage, fifty to sixty. ]\Iales more liable than females to hemor- 
 rhage. Predisposing causes of endarteritis are gout, lithaemia,. 
 alcoholism, and syphilis ; associated diseases are nephritis, endo- 
 carditis, and emphysema. Anything which increases the heart £> cL^^-l^ co- 
 action may cause cerebral hemorrhage, e. g., fright, anger, exer- 
 tion, cold bath. Anything which weakens its action may cause 
 thrombosis. o-< ^^/^.r-cU^t^'^ ^^iU^^^Ly, f^-<-^ • 
 
 Syinptouis. — Preliminary : For months before the onset, ver- 
 tigo, insomnia, headache, inattention, and imperfect memory. 
 Temporary attacks of numbness in one-half of the body. 
 
 Sudden onset, "apoplexy," loss of consciousness. The result 
 depends on the size and rapidity of hemorrhage, or on the size of 
 the vessel occluded. 
 
 Paralysis of one-half of the body (hemiplegia), with coma 
 and convulsions, is the ordinary form. Face, red ; pulse, slow, 
 high tension, full ; respiration, deep, stertorous. Temperature 
 normal, but after some hours high, 102" to 104*^ F. Deviation of 
 eves and head may occur in large lesions ; the patient looks toward 
 the side of lesionr Pupils vary. Irlequality is most important 
 symptom, usually dilated on side of lesion. Hemiplegia, hemian- 
 sesthesia, and hemianopsia, at first. Reflexes suspended ; inhib- 
 ited by irritation for a short time, then exaggerated permanently.<rK/^^*^^<i 
 Rigidity of limbs when hemorrhage is large or into the ventricle ; 
 convulsion when hemorrhage is on cortex .or in ventricle. Urine 
 retained ; contains albumen and sugar, or may be passed involun- 
 tarih". \\-^ajujumJmx. l>\ti.<jULL* — -yu-a^ A^^^^SXc^ ^^ y-^i^ 
 
 Death may occur in one or two. days, in coma, with tempera- 
 ture of 108" Y. <J~^ '^ f^^ ^^ • 
 
 Usually there is a slow recovery of consciousness and perma- 
 nent paralysis, which gradually decreases during a year, and then 
 remams stationary. " ' 
 
 In lighter cases there may be no loss of consciousness, but 
 partial hemiplegia or arrest of any cortical function. 
 
 The permanent symptoms a week after the acute onset indi- 
 qate the situation of the lesion. The symptoms which remain at 
 the end of a month indicate its extent ; e. g., hemiplegia with hemi- 
 
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 4^' -^ .Y^-^-^ 
 
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 <_^ 63 -'jr-*' 
 
 
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 oj/^^ 
 
 ^AjI. 
 
 A.jC-4^~ ■ -^ <X 
 
 '/?Z^>u<--^Ti.,e-^i_-i? ^ .ai/tV'z ii-<x-C«.<Xy -^i^LLc^ iS!V ~3 /Zj2^^,^--«-<-*<^ 
 
 
 
 ^^^ Lc.^^L<^ ^^^ ~^^22Lc^. Z*^ 
 
 ^:i.«. <:*&<>' 
 
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 yU*--t^'^'i,<-«<^^--i^ _ 
 
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 (^Ui/Li.^.^'^^ ^UH^^-^oiy^ (f7^ ^ f<r^nK- ^ ^U^TQ^---'^-^ 
 
DISEASES OE 'rill-: XERVOUS SYSTEAL m 
 
 anaesthesia and hemianopsia at first: and permanent paralysis, 
 not total, in arm and leg- onl)-, without sensory affection finally. 
 In some cases there is a development after two months of con- 
 tractures in the paralyzed limhs. This indicates the existence of 
 descending degeneration in the motor tract. 
 
 Course. — After the acute onset, in which the patient is con- 
 fined to bed for two weeks to two months, depending on the 
 severity, the improvement begins ; the chief symptom being hemi- 
 plegia. The face is flat on the paralyzed side, and is slightly 
 drawn by the healthy muscles away from the paralyzed side so 
 that the mouth is crooked. The eye can be closed (vs. facial 
 palsy), and can be moved (vs. ophthalmoplegia). The tongue 
 deviates toward the paralyzed side. The finer motions of the 
 hand and arm are more permanently affected than elbow or shoul- 
 der motions ; and the upper extremity is carried in a flexed posi- 
 tion. The leg is stifif and extended, does not bend easily at the 
 knee, and the foot is dragged on its inner edge and swung around 
 in walking. The muscles of the trunk and respiration are very 
 rarely affected. The bladder and rectum may not be under full 
 control. There may be a diminution of sensation in the paralyzed 
 side, and possibly hemianopsia. Hemianaesthesia or hemianopsia 
 may. remain without hemiplegia. A total loss of all senses, smell, 
 taste, sight, hearing, and touch on one side only, occurs in hysteria 
 only. The tendon reflexes are usually much increased on the par- 
 alyzed side, and are somewhat increased on the other side as well. 
 The contractures which develop may cause pain, because the 
 limbs are rigid. Otherwise there is no pain. 
 
 Aphasia of some kind often accompanies right hemiplegia, 
 or may occur alone. (See page 56.) 
 
 Some mental symptoms are usually observed after an apo- 
 plexy, and ma}' be the only permanent symptoms. There may be 
 a lack of control of the emotions, so that the patient laughs or 
 cries with little cause; an irritability of temper; a lack of judg- 
 ment ; imperfect memory of recent events ; imperfect power of 
 concentrated attention ; general bewilderment, so that the patient 
 does not recognize his surroundings or friends ; mild delirium or 
 delusions ; or even dementia. These usually pass away gradually, 
 but sometimes remain. 
 
78 DISEASES OF THE NERVOUS SYSTEM. 
 
 The various symptoms, motor, sensory, aphasic, or mental,, 
 depend on the situation of the lesion, and enable a conclusion to 
 be arrived at regarding it. 
 
 In any case epileptiform attacks may develop, and continue 
 at long intervals after an apoplexy. 
 
 Diagnosis . Cerebral Heinon duLS'^. — In old persons with 
 atheromatous arteries and hypertrophied heart. Sudden onset of 
 coma during exertion or in excitement. Coma deepens ; tempera- 
 ture falls to 97° to 95'' F. in an hour; after three hours rises to 
 101° F. Gradual recovery of consciousness in three to five days, 
 with permanent symptoms of hemiplegia. 
 
 Cerebral Embolism. — At any age with heart disease, or after 
 childbirth. Sudden onset with no loss of consciousness or slight 
 condition of mental confusion, or rapid return of consciousness. 
 Temperature does not fall, but may rise to 102° F. Improve- 
 ment occurs within twenty-four hours to a marked degree, but 
 symptoms return in three or four days and are permanent, either 
 monoplegia, or hemiplegia, or aphasia. Jacksonian epilepsy may 
 develop after a few months. 
 
 Cerebral Thrombosis. — At any age, but chiefly in syphilitic 
 persons and in rnict^-'aged men. Premonitions usually occur. 
 Slower onset without coma, but dulness of mind. Consciousness 
 returns soon, if lost. Temperature does not fall ; may rise to 
 100" F. The paralysis resembles that in embolism. 
 
 The diagnosis between these three conditions is never posi- 
 tive. /XM^ttrVjAlc^ 0^ fi^. h\yrh<. (LLa-^iTiM^ i^iyc/u.^ u^ L TLc ta^^JL^ 
 
 Causes of co ma other than apoplexy : Syncope, epilepsy,, 
 uraemia, diabetes, alcoholism, opium poisoning, sunstroke, cerebral 
 injury. Apopletic coma is deep and patient cannot be aroused. 
 Face is congested, eyes turned to one side, pupils unequal, pa- 
 ralysis is unilateral, limbs may be rigid ; appearance indicates pre- 
 vious convulsions. Physical examination reveals absence of in- 
 jury and presence of predisposing disease, e. g., atheroma, en- 
 darteritis, cardiac disease, albuminuria, syphilitic scars. The 
 absence of diagnostic signs of other causes of coma confirms the 
 diagnosis of apoplexy. Reflex movements can be caused on non- 
 paralyzed side by producing pain. The tendon reflexes are often 
 

 
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 /^-AA-«. 
 
 hMjlJnJljU' 
 
 
 
 
 
 ■'-<'V_-^ 
 
 

 {YZ^J-X^^^,^ . JQ^^^^^L^^ ^=^-x.uu[-^ M^cjz>^.j^ U^ '^ .w^ 
 
 (f-^^tA. a,<;2.-cjH.vtA lA_<to <*M^uo-^\x.<..^.y\'2-^ fyA^^j-t.^ c^)-^..t-^ uiju^^j^ &ijHAjrJ^-ii. ' 
 
 I., , lAO I n „ ts ^ 'j 
 
 (aj i^-*^^ (tJU^-^K- 
 
DISEASES OE THE NERVOUS SYSTEM. 79 
 
 lost at the onset. The eremasteric rellex is always lost on the 
 paralyzed side. 
 
 Prognosi s depends on the depth of coma, on the condition of 
 pulse and respiration, on the constitution and age of the patient, 
 and on the number of previous attacks. 
 
 Treatment in stage of apoplexy : Rest ; quiet ; ice-bag to 
 head ; venesection in plethoric cases ; purgatives of a drastic na- (>iJt^ 
 ture ; stimulants if heart failure is present. 
 
 P\ir hemiplegia : Exercise ; massage ; faradism to the mus- 
 cles for purpose of exercise. 
 
 ^Medicines are of no use in either stage. 
 
 Cerebral Atrophy . 
 
 Cases of cerebral disease in children, either unilateral or bi- 
 lateral, present some peculiar features of three different types. 
 
 First, cases of hemiplegia with or without athetosis. 
 
 Secondly, cases of mental defects of various grades. 
 
 Thirdly, cases of sensory defect of different types. Epilepti- 
 form seizures of petit inal or of grand iiial type occur frequently 
 in patients who may be assigned to any one of these groups. 
 
 I. Infantile HciniplcQia . — The symptoms are the sudden de- 
 velopment of a unilateral paralysis after a series of convulsions 
 attended by high fever and its attendant discomforts, and a period 
 of unconsciousness of varying duration ; then a gradual improve- 
 ment in the paralysis after the active manifestations of the onset 
 have subsided ; and finally, a stationary condition, in which the 
 face is but slightly affected in its voluntary or automatic move- 
 ments ; the speech is usually regained, if it had been lost; the arm 
 is quite seriously paralyzed, the fingers being stiff and awkward, 
 and sometimes being in constant slow involuntary motion (athe- 
 tosis) ; the leg is held rather rigid, so that the child limps in 
 walking, and often develops a club-foot. There are, of course, 
 on the one hand, light cases in which the symptoms finally amount 
 merely to clumsiness in the fingers. There are, on the other hand, 
 severe cases in which a double hemipleg ia has occurred, both 
 halves of the body being equally affected, and in which both arms 
 are useless and both legs so stiff, so closely adducted, and so 
 
so DISEASES OF THE NERVOUS SYSTEM. 
 
 helpless, that walking is impossible ( diplegia) . The latter are 
 cases in which all the symptoms date from birth. In all cases 
 the paralyzed limbs are found to be affected in their growth and 
 development, so that they are smaller, colder, stiffer, and weaker 
 than the others ; the reflexes are exaggerated, but the electrical 
 reactions are not qualitatively changed, and the sensation is 
 normal. This condition remains through life as a permanent 
 defect, and although the division of contractured muscles or ten- 
 dons and the application of ingenious apparatus may correct de- 
 formities and make the paralyzed parts fairly useful, and although 
 the application of electricity to the muscles chiefly affected may 
 increase their nutrition and this prevent contracture which comes 
 from the unbalanced strain between the various muscles, yet any 
 great degree of improvement is impossible. In more than one- 
 half of these cases epileptic attacks are of frequent occurrence. 
 
 The cases which date from birth must be divided into those 
 in which there has been evidence of traumatism during labor, 
 and those in which there was none. In the former class it may 
 be stated confidently that cerebral hemorrhage, usually meningeal, 
 is the cause of the symptoms. In the latter class it is probable 
 that an intra-uterine encephalitis or some unknown cause has pre- 
 vented the foetal brain from developing. 
 
 The cases which have developed suddenly after birth are 
 cases in which the ordinary causes of hemiplegia in adults have 
 been acting, and must be traced either to encephalitis, hemor- 
 rhage, or embolism, or disease of the vessels. The degree of 
 spontaneous recovery in any case can be pretty well determined 
 by an examination at the end of the second year. A complete 
 cure never occurs. 
 
 The fits in organic epilepsy are likely to be more frequent 
 and severe than in idiopathic epilepsy ; as many as twenty con- 
 vulsions may occur daily for weeks at a time. These fits do not 
 destroy life, but render life a burden. When, however, they are 
 infrequent they may be benefited to some degree by the use of 
 bromides. 
 
 II. The second class of cases presents mental defects more 
 noticeable than physical symptoms. The child may be slow in 
 

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 Cij-*. 
 
 
DISEASES OE THE NERVO'US SYSTEM. «1 
 
 learning to talk, may soem unable to tix its attention upon any- 
 thing continuously, may be exceedingly active, in constant mo- 
 tion — the activity being, however, aimless ; may throw things 
 about, or tear things up, or put everything into its mouth ; may 
 be very difficult to manage because of its inability to retain and 
 combine impression.s with sufficient power to reason upon them ; 
 and mav, therefore, be incapable of appreciating the meaning of 
 punishment, if this be inflicted. Such children may have good 
 powers of perception, may recognize persons and objects, show 
 pleasure at bright colors, or music, or caresses; but fail to show 
 evidence of thought in the sense of reasoning power, judgment, 
 or self-control. Some patients constantly drule at the mouth, 
 cannot be taught cleanly habits, and are manifestly imbecile. 
 Other patients are quite bright in many directions, may even be 
 precocious, show talents in music, or drawing, or fondness for 
 mathematics, designing, languages ; yet are apparently unable to 
 appreciate moral ideas, cannot be taught to tell the truth, are 
 cruel and bad, will not control any of their impulses, and so are 
 the distress and despair of parents and teachers. It is those 
 mental qualities which are the product of the highest evolution 
 which have failed to develop in this class of cases. The final re- 
 sult is that they have to be taken care of all their lives, either at 
 home or by attendants, being incapable of supporting themselves 
 or directing their conduct. ^Nlany of them have epilepsy. Some 
 of them have hemiplegia. 
 
 III. The third class of cases is less common than the two 
 preceding, and is likely to escape observation unless carefully 
 investigated. The patients belonging to this class may be hemi- 
 plegic or may present no motor or mental defects, though they 
 may be the subjects of epilepsy. They do have defects of sensory 
 percepti on. Such defect may be in the form of hemianopsia or 
 of_deafne^a. It is probable that many cases of deafmutism belong 
 to this class, and in some persons, as in Laura Bridgeman, deaf- 
 ness, dumbness, and blindness coincide. 
 
 The pathological changes in the brain in these various cases 
 dififer widely, and are as follows, in the order of frequency : 
 
 Porencephalus, a localized atrophy or agenesis, leaving a 
 
82 DISEASES OF THE NERVOUS SYSTEM. 
 
 cavity in the cerebral hemisphere, which may be deep enoug-h to 
 open into the ventricle. 
 
 Sclerotic atrophy, an atrophic condition of the brain with an 
 increase of connective tissue and disappearance of the . nervous 
 elements ; affecting both hemispheres, or one only, or a part of 
 one only ; or limited to small areas in various parts. 
 
 Maldevelopment and apparent atrophic condition of the mi- 
 nute structures of the hemispheres, chiefly cortical, the cells re- 
 sembling those of a new-born child, but with no apparent gross 
 defects in the brain. 
 
 Atrophy, consequent upon the condition of softening pro- 
 duced by embolism or thrombosis, and limited in extent to certain 
 arterial districts of the brain. 
 
 M eningo-encephalitis, a condition shown by thickening and 
 adhesion between the pia and the brain, with destruction of the 
 cerebral cells and atrophy of the cortex. 
 
 Cysts lying on the brain and producing atrophy by pressure 
 or associated with atrophy due to the original lesion of which the 
 cyst remains as a trace. 
 
 Hemorrhage on or in the brain, as shown by the remains of 
 a clot, or by hgematin staining of a cyst, of the pia, or of the 
 sclerotic tissue. 
 
 Hydrocephalus with extreme dilation of the ventricles, so 
 that the brain tissue is reduced to a mere wall about the cavity. 
 
 These are the conditions found at death in cases presenting 
 the clinical features just studied. It is evident that they have this 
 in common, namely, a condition of atrophy of the brain. The 
 origin of this atrophy is not always clear. In some cases it is 
 clearly congenital and due to a maldevelopment of the embryo. 
 
 In other cases it is clearly traceable to injuries at birth s 
 In other cases it must be ascribed to affections of various kinds, 
 such as inflammations of the membranes or of the brain sub- 
 stance, or vascular lesions and their consequences, such as occur 
 in adults. But it is evident that the various processes of disease 
 have as a fairly uniform result a condition of atrophy with sclero- 
 sis of the brain, which may be termed sclerotic atrophy. The 
 
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DISEASES OF THE NERVOUS SYSTEM. 85J 
 
 difference in the clinical types is clue to the varying situation of 
 the lesion rather than to its varying nature. 
 
 For such conditions there can be no treatment. 
 
 Tumors of the Brain . 
 
 J\iricfics in order of fre(iuency : 
 
 Gil III ma : soft gelatinous, or hard cellular, situated on base 
 or in cortex, usually beginning in meninges. 
 
 Tubercular: hard masses, often multiple, especially frequent 
 in children, situated anywhere, sometimes primary, usually sec- 
 ondary. This is the variety in more than one-half the cases in 
 children. ^^ ^ i -^ - 
 
 Glioina: peculiar to the nervous system, cells and fibres like 
 the neuroglia, usually infiltratecp and without boundaries, but 
 single^ .usually vascular; hence symptoms vary and hemorrhage 
 occurs ; usually situated in the white substance. 
 
 Sarcoma of all varieties : fibro-, round-cell, spindle-cell, glio- 
 sarcoma, begin from connective tissue of membranes as a rule, 
 sometimes in the brain. Hard single tumors, of various sizes, 
 easily separable and well defined, situated on base, in meninges, 
 in cerebellum. ''-^*'— u^zs . 
 
 Carcinoma: rare, usually secondary. 
 
 Occasional variet ies ^■d.r^t fibromata, osteomata , psammomata, 
 cholesteatomata, angiomata . lipomata, ecchinococcus, and 
 cvsticercus.('' ew>t/<.^ut->-.^ ■^ ^1,^^—0.^ ^ 
 
 .j jieurisms of the base give rise to symptoms of tumor. 
 
 For Pathology of Tumcjrs, see Delafield and Prudden's '-Pathology." 
 
 Causes of Brain Tumor. — i. Predisposing: Sex: males twice 
 as freciuentlv affected as females. Age : children most liable, as 
 tubercular tumors are frequent. Young adults next. Old age ^..^-tA. * 
 is quite exempt, except from carcinoma. 
 
 2. Exciting. Injuries . Severe emotional shock. Unknown 
 in large majority. 
 
 Situation . — Cerebral cortex. twcnt\-five per cent. ; cerebel- 
 lum, twent}-five per cent. ; centrum ovale, fifteen per cent. ; basal 
 
84 DISEASES OF THE NERVOUS SYSTEM 
 
 ganglia, ten per cent. ; pons, ten per cent. ; crus and corpora quad- 
 rigemina, ten per cent. Others, five per cent. Qw.j!>m^") 
 
 Effects of Brain Tumor. — i. Direct effects . Irritation of 
 gray matter with nervous discharges, and destruction of brain- 
 tissue. (Uuuu-^-J^ « /a.4«.,-.^^t^^-tX--v -1 ^^....^.U^^ . 'Pvo-cC^t* iUrx:-JL 'i.^y^^.^^yi^Z^ 
 
 ^ 2. Indirect effect s. General pressure on entire brain. This 
 may be hmited by the falx or tentorium. It produces hydroceph- 
 akis by pressure on ventricle or veins of Galen. Vascular dis- 
 turbance by pressure on arteries and veins. Meningitis, localized 
 and not purulent, except in tubercular cases. Thinning of cra- 
 nial bones. 
 
 Effects of increased pressure are seen after death in flatten- 
 ing of the convolutions, anaemia and pallor of the brain, dry sticky 
 state of membranes, and distension of ventricles by serum. 
 
 S ymptoms of Brain Tumor. — I. General symptoms depend 
 on existence of a new growth independent of its position. cUm-./ 
 
 Head ache in nin ety^fiye^ per cent., constant or intermittent; 
 general or local ; dull and deep, increased by anything which de- 
 ranges the cerebral circulation. x Sometimes head is tender to 
 percussion at certain points ; may have evidence of pain even in 
 state of stupor ; it may be agonizing ; it may give feeling of band 
 about head ; it is often worse at night, causing insomnia, espe- 
 cially in gumma. 
 
 Mental disturbance, eighty- five j>er^ent. Dulness and 
 apathy, with imperfect attention and memory. Depression and 
 emotional state. Slow speech, gradual mental failure, childish- 
 ness,, and dementia ; fainting attacks, stupor, and coma in the last 
 stage. Occasionally delirium and active insanity. 
 
 Optic neuritis, eightv per cent Venous congestion. Swell- 
 ing of papilla, loss of disc outline ; radiating appearance about the 
 disc and hemorrhage ; then optic-nerve atrophy leaving white or 
 gray disc. In cases of subcortical tumor of small size it may be 
 absent. Sight may be affected ; visual field small and irregiilar, 
 or unimpaired for a time. 
 
 Vertig o or sense of giddiness, frequent in tumors in posterior 
 fossa. May occur in tumors anywhere on change of position. 
 May be due to paralysis of one or more ocular muscles. CUjujua.x« ejxJ2^ 
 
 

 
 <^>--r^r^.JLJL. ir\A^ 
 
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 lAAA^ 
 
 
DISEASES OF THE NERVOUS SYSTEM. H5 
 
 \'omiting. with or without nausea or relation to food. l''re- 
 quent in tumors in posterior fossa. ^ Ta^^^^ "^1^+^ 
 
 General convulsions of cpile])tic type. Petit iiial or t^rand 
 mal. 
 
 Xvstagmus. lateral oscillation of eyes. Frequent in disease 
 of corpora quadrig-eniina and cerebellum. ^^•-^■^ r-e.^^.^.^ ^i,*^ Ju,*.,,. 
 
 Loss of control over sphincters occurs, especially with tumors"- 
 in the frontal lobes. 
 
 Glycosuria and polyur ia, especially with tumors in the pos- 
 terior fossa. 
 
 Slow fiulse : 50 to 60. 
 
 II. Local symptoms dependent upon the position of the 
 tum or. 
 
 Frontal Lobes: Mental dulness. lack of control of emotions, 
 irritability, inattention, and childishness, dementia, loss of sense 
 of smell, <v!<^sl/a ^1 OvwCw^ -^ s-^f^^^^Mi^^ . 
 
 Left third frontal convolution. Motor aphasia. 
 
 Central Convolutions, and motor tra.d :. ^^lonospasm and 
 monoplegia when in or near cortex. Hemispasm and hemiplegia 
 when deep or in capsule. Sometimes slight ansethesia in para- 
 lyzed part. 
 
 Occipital Lobe and visual tract. Hemianopsia, noticed by 
 patient as unilateral blindness. Visual hallucinations and flashes 
 of light on one side. 
 
 T.eft Tei ijj )oral lirst and second coj Tyoliiiions^__ Sensory 
 aphasia: form, \yord-deafness. '?'yy^^(yiy^.j^..i,c^ • ■<!A.ctc:czt.^yvKU ^^vL—^ 
 
 Left Lozi^'er Parietal lobule and angular gyrus or in occipito- 
 temporal tract. Sensory aphasia: form, word-blindness. 
 
 Base of bra in. 
 
 Anterior fossa : Loss of smell. 
 
 Aliddle fossa : Hemianopsia, paralysis of ocular muscles. III., 
 IV., \^I. ; neuralgia of face and ansethesia, V. ; paralysis of III. 
 and opposite hemiplegia, neuroparalytic ophthalmia, nystagmus ; 
 bilateral spastic paralysis, deafness. 
 
 Posterior fossa : Paralysis of \'II., IX., X., XI., XII. ; vertigo 
 and aural symptoms ; cerebellar ataxia, tendency to one side ; 
 paralysis ^yidespread from medulla disease. 
 
 "u*. "^.^ (Uy<£^^K 
 
 
86 DISEASES OF THE NERVOUS SYSTEM. 
 
 Cerebellum : A'ertigo, vomiting, cerebellar ataxia when mid- 
 dle lobe is involved ; headache, frontal or occipital and severe ; 
 optic neuritis early. 
 
 Dia_!::;nosis. — Cerebral symptoms : g;eneral alone, or general 
 and local, point to the presence of a tumor. 
 
 Differentiation from chronic nephritis : By examination of 
 urine ; bv condition of heart, arteries, and blood-pressure ; by 
 appearance of optic disc and retina in many cases, hemorrhages 
 more frequent and white spots far from disc : by character of 
 headache, more severe in tumor ; by age of patient, young per- 
 son = tumor. 
 
 From hypermetropia with astigmatism and angemia, W2 th_ 
 me nstrual disorde r : By examination of eyes and relief by glasses ; 
 by cure of ansemia by diet. iron, and aloes : by slight degree of 
 headache and neuritis. 
 
 From hvsteria with migrain e : By study of the patient and 
 separation of real svmptoms : by condition of the optic disc. 
 
 From abcess : By history of trauma or of otitis media ; by 
 severity of early symptoms in abscess ; by fever in abscess ; by late 
 development of optic neuritis, rare in abscess. 
 
 To determine the location : Study carefully the local symp- 
 toms, "signal symptom."" c. g., numbness and twitching of 
 thumb. Study also the order of appearance of local symptoms : 
 thumb, hand, face. Compare the several local symptoms, paral- 
 ysis -j- aphasia, or -j- hemianopsia. 
 
 To determine the vai'iety : Estimate probable frequency of 
 various tumors at different ages. Look for history of syphilis, 
 tuberculosis, cancer, or sarcoma. Study rapidity of onset ; gli- 
 oma, tubercle, cancer are rapid. Study signs of irritation ; more 
 frequent in glioma and meningeal tumors. Study signs of varia- 
 tion in severity of symptoms ; more variation in glioma. Study 
 situation of the tumor ; basal tumors are often gumma, tubercle 
 sarcoma. Intracerebral tumors are often glioma, sarcoma. Pecul- 
 iar forms of hemiopia and earh- optic neuritis indicate sarcoma 
 of pituitary body or aneurism. 
 
 Course of the disease : Begins with general symptoms 
 usually. Sometimes begins with local spasm or a general con- 
 vulsion. (Gradual increase in severity and number of symptoms. 
 

 
 
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DISEASES OF THE NERVOUS SYSTEM. ^<T 
 
 Finally death in stupor or in general convulsion or suddenly, 
 from heart failure, or recovery under specific treatment. 
 
 Dura tion is from one to three years. 
 
 Prognosis, bad, excepting in gumma and when tunnjr can be 
 removed. 
 
 Treatment. — For gumma : Inunctions of mercury and KI to 
 three hundred grains daily. '^SvSLr^^y^t^^ ^^U^a^w^-w..^ ^ imJX^^'^^t^)) 
 
 S urgical treat ment : Removal is possible when diagnosis of 
 location is exact. There is danger of return. 
 
 For Cranio-Cerebral Topography, see page 40. 
 
 Abscess in the Braix. k uJL^-^^^^*^ ^ >a/-^l.^-c4,&. 
 
 Acute encephalitis with formation of pus results in an 
 abscess. (I )The abscess may extend rapidly, not being encapsulated, 
 and cause death izpr it may become encapsulated and develop 
 slowly, oif^Jbecome stationary and remain for years as a foreign 
 substance producing no symptoms, but finally enlarge or break. 
 (41 Occasionally multiple abscesses develop in the brain secondary to 
 ,-f pyaemia, producing cerebral symptoms in the course of that dis- 
 ease. There may be a secondary meningitis in either form. 
 
 Sitiiafwii . — Is usually in the temporo -sphenoid lobe or in the 
 frontal lobe or in the ^erebeUiuiL in the white matter. 
 
 Causes. — Chronic otitis media , forty per cent. Fracture of 
 cranial bones, thirty-five per cent. Chronic rhinitis , ten per cent. 
 Caries of anv cranial bone , ten per cent. Secondary to infectious 
 diseases, five per cent. 
 
 Sxniptoiiis.^After an injury or after otorrhcea or other cause 
 cerebral symptoms develop suddenly ; severe headachy vomiting, 
 mental distress and dulness, stupor, a chill, a high temperature 
 for a day or t\va^; leucocytosis, possibly convulsions ; rarely local 
 symptoms ; hemiplegia, hemianopsia, aphasia, cerebellar stagger- 
 ing. In a week the patient is very ill, with irregular tempera- 
 ture, sometimes with chills, sometimes no fever ; slow pulse ; in- 
 tense pain, delirium, stupor, and optic neuritis. If abscess ex- 
 tends death follows in two weeks, or suddenly from rupture. If 
 abscess discharges into ear or nose, or if it can be opened, symp- 
 toms subside. Rarel}' symptoms suliside spontaneously slowly, 
 
88 
 
 DISEASES OF THE NERVOUS SYSTEM. 
 
 the abscess becoming encapsulated and latent, and patient appar- 
 ently recovers, but is subject to headache and vertigo; and has 
 a relapse later. 
 
 Diagnosis. — 
 
 Abscess 
 
 Temperature.normal or not high. 
 Pulse slow. 
 Patient in stupor. 
 
 Spasms and rigidity rare. 
 Cranial nerves not involved. 
 Optic neuritis frequent. 
 
 Abscess 
 
 Temperature normal or not high. 
 
 Pulse slow. 
 
 Chill at onset not repeated. 
 
 Little sweating. 
 
 Head tender to percussion? 
 
 vs. Meningitis. 
 
 Temperature high without remission. 
 Pulse rapid. * 
 
 Patient irritable, all senses over- 
 acute. 
 Spasms and rigidity frequent. Ka->^-<--l-s -r 
 Cranial nerves involved early. -*- 'vi-^om^c^ >a Aju-- 
 Optic neuritis rare. i - i 
 
 z's. Thrombosis of Later.\l Sinus. 
 
 Temperature high with remissions. 
 Pulse rapid, weak. 
 :ir Chills frequently repeated. 
 Profuse sweating. 
 Pain over mastoid and jugular. 
 Thrombi in lungs. 
 
 Diagnosis of location is made parti v from the exciting cause 
 and partly from the local symptoms. 
 
 Prognosis fatal, unless abscess can be opened. 
 
 Treatment. — In the few cases in which the abscess can be 
 located, operation of trephining and drainage. 
 
 Cerebro-spinal Sclerosis. 
 
 Multiple or disseminated sclerosis is a rare disease affecting 
 the brain and spinal cord together. Small regions of sclerotic 
 tissue are found irregularly scattered through the entire nervous 
 system, without destruction of the axis cylinders of the nerve- 
 tracts. Its cause is unknown. 
 
 Symptoms. — Headache, vertigo, malaise, mental irritabilitv,. 
 inattention, imperfect memory, lack of self-control, and inability 
 to work. Later, tremor of hands increased by an effort to hold 
 them still, nystagmus, increased knee-jerk, stiff spastic gait, weak^ 
 ness, and finally general tremor on effort. Slow speech, each 
 

 
 . ^--«=l'''K,t-X7 
 
DISEASES OF THE NERVOUS SYSTE^r. 8^ 
 
 syllable separately eiiunciated without variation of tone. Optic 
 atrophy. Dementia and attacks of epilepsy and hemiple.c^ia may 
 finally occur. 
 
 Course is exceedingly irregular, symptoms may disappear for 
 months and then return. The disease is often mistaken for 
 hysteria. 
 
 Diaj^niosis is made by excluding all other organic diseases, 
 by nystagmus, tremor, and speech. 
 
 Treat inait. — Arsenic -gV gr. daily; solanin 14 gr. daily, 
 increased. 
 
 Syphilis of the Brain. 
 
 Syphilitic afifections of the nervous system may be produced 
 by: 
 
 1st. Syphilitic endarteritis. 
 
 2d. Direct action of the syphilitic poison upon the nervous 
 system. 
 
 3d. Syphilitic exudations in the meninges. 
 . 4th. Syphilitic deposits in the brain itself. 
 
 5th. Hereditary syphilis. 
 
 I St. Syphilitic endarteritis produces a progressive diminu- 
 tion in the calibre of the blood-vessels, resulting in a state of 
 anaemia, malnutrition of the brain supplied by the vessels afifected, 
 and leads to thrombosis followed by localized softening in the 
 area cut off from its blood supply. The symptoms of this condi- 
 tion are in the early stage those of malnutrition of the brain and 
 imperfect action in the regions afifected. The patients present at 
 first symptoms of neurasthenia , and later slight temporary sus- 
 pension of functions, such as temporary aphasia, numbness in one 
 limb or in one-half of the body, a condition of weakness not 
 amounting to paralysis in one limb or one-half of the body, 
 double vision, or vertigo. Stimulants to the heart relieve these 
 symptoms, but after a time if a thrombosis occurs the symptoms 
 of cerebral apoplexy suddenly appear. After such an apopletic 
 attack a partial recovery may ensue, but as a spot of softening 
 in the brain is usually left, a complete recovery is not to be ex- 
 Dected ; hence the fact that a syphilitic lesion which can be re- 
 
■yO DISEASES OF THE NERVOUS SYSTEM. 
 
 moved bv treatment is the cause of the apoplectic attack does not 
 warrant a more favorable prognosis in such cases. 
 
 2d. The toxic effects of syphilis on the nervous system are 
 manifested by general disturbances of function, which produce 
 the symptoms of neurasthenia of all the various types. As a rule, 
 in syphilitic neurasthenia the symptoms appear to be worse to- 
 ward evening and insoinaia. is more persistent than any other 
 symptom ; hence in general neurasthenia with insomnia any 
 syphilitic element must be looked for and treated before the 
 neurasthenia can be cured. Neurasthenia may occur in syphilitic 
 persons without any direct connection with the syphilis, which at 
 the time may be latent. A test of treatment is the only one en- 
 abling differential diagnosis to be made. 
 
 3d. Syphilitic exudations into the meninges of the brain and 
 syphilitic meningitis are exceedingly common as a sequel of syphi- 
 litic disease. From two to ten years after the infection gummy 
 -exudations may occur in any part of the brain, but are more fre- 
 quent upon the base of the brain and about the crus and pons. 
 The glue-like substance is deposited rapidly and extensively 
 through the meninges, producing pressure upon the subjacent 
 brain or upon the cranial nerves, and thus causing suspension of 
 function in the parts compressed. Occasionally the syphilitic ex- 
 udation takes the form of a hard tumor, which then produces the 
 regular symptoms of tumor of the brain. The symptoj iis of — 
 syphilitic gumma or syphilitic basilar meningitis are headache. "^ 
 worse at night, insomnia , mental irritability, vertigo, distressing 
 sensations in the head, occasional vomiting, and local symptoms 
 of paralysis of the c ranial nerv es, the third and sixth being the N^ 
 ■ones particularly affected. If the exudation is not upon the base, 
 •or occurs in the convexity or over the cerebellum, the local symp- 
 toms will be those of irritation or of arrest of function of the 
 particular portion of the brain affected. Thus spasms and paral- 
 ysis, paraesthesia and ansethesia, hemiopia, or any variety of 
 aphasia may be caused by the disease. The pressure upon the 
 vessels produced by syphilitic exudations adds to the complexity 
 of the symptoms. Convulsions are frequently observed in such 
 cases, both of a general and of a local tyP^- Increased thirst and 
 hunger and polyuria are often found. The course of the case 
 

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 X. 
 
 
DISEASES 01' Till'". XKRVOUS SYSTEM. 91 
 
 IS more rapid in its onset than that of brain tumor, but resembles 
 it in all other respects and may be associated with optic neuritis. 
 The symptoms sul)si(le rapidlx' under inunctions of mercury and 
 large doses of iodide of potash, and hence prognosis is good in 
 the majority of cases, though relapses are frequent. 
 
 4th. Syphilitic deposits in the brain itself may be of the 
 nature of small dessimated spots, producing chronic indurative 
 or sclerotic processes of small regions of softening. The symp- 
 toms of this afifection are identical with those of general paresis, 
 and can only be distinguished from paresis by the result of treat- 
 ment. 
 
 5th. Hereditar}' syphilis occasionally produces the symptoms 
 of cerebral atrophy or the symptoms of multiple cerebro-spinal 
 sclerosis in children, and in either of these conditions this fact 
 must be kept in mind, and if other signs of hereditary syphilis are 
 discovered this element must be considered in the treatment. 
 
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FUNCTIONAL NERVOUS DISEASES. 
 Neurasthenia. 
 
 Nervous prostration, nerve tire, nervous irritable weakness 
 is a functional disease of the entire nervous system, brain, spinal 
 cord, spinal and sympathetic nerves, dependent upon malnutri- 
 tion, characterized by nervous weakness and irritability. 
 
 A balance between expenditure of energy and nutrition must 
 be preserved. 
 
 Brain overwork or anxiety ; 
 
 Spinal cord overwork by long marches or sexual overaction. 
 
 Nerve overwork by various occupations in which a single act 
 is repeated ; 
 
 Vasomotor work in maintaining vascular tone and nutritive 
 processes, all require a sound basis and rest at periods. 
 
 When balance between store and expenditure of energy is. 
 broken, exhaustion results. Then nature enforces rest by fatigue^ 
 by sleep. One may disregard nature, but if so one must pay the 
 penalty. 
 
 Causes. — I. Excessive expenditure of nerve energy. 
 
 Primary neurasthenia more common than secondary. 
 
 Influences favoring its production : 
 
 1. Bad hereditary influences. Weak nervous system. 
 
 2. Feebleness in childhood, with poor nervous system. 
 
 3. W^rong methods of training and education. 
 
 4. The struggle for existence. Kant's rule, eight hours 
 
 for work, eight hours for diversion, eight hours for 
 sleep. 
 
 5. Anxiety, worry, mental depression, fear. 
 
 6. Mental or physical overwork. 
 
 7. Sexual excesses. 
 
 II. Deficient supply of nervous energy. 
 Secondary neurasthenia. 
 
DISEASES OF 'J"HE NERVOUS SYSTEM. 93 
 
 inrtuences favoring its production : 
 
 1. Weakening diseases of all kinds of organic nature. 
 
 2. Indigestion and dyspe]->sia, with auto-infection by 
 
 products. 
 
 3. Gout, rheumatism, uric-acid diathesis. 
 
 4. Infectious diseases, typhoid, grippe, malaria. 
 
 5. Alcoholism or abuse of drugs. 
 
 Result of the action of these causes is to produce malnutri- 
 tion of the nervous system and state of irritable weakness. 
 
 1. The power of continuous activity is impaired; weakness 
 results ; hence, mental work is imperfect ; attention flags ; mem- 
 ory fails ; ambition ceases ; physical activity is imperfect ; exer- 
 cise tires one ; lassitude ; vegetative functions are impaired. Di- 
 gestion is poor ; constipation occurs ; vascular tone is impaired ; 
 heart feeble. Balance must be maintained between blood supply 
 and functional activity. When this is impaired work is impossi- 
 ble. Secretions are changed in amount and character, e. g., urine. 
 
 2. The power of mental and physical control is impaired and 
 irritability results ; inhibition may be partly automatic and partly 
 conscious ; it must be conscious and voluntary to prevent morbid 
 fear and apprehension ; influence of fear is to inhibit all nervous 
 acts — e. g., walking on ice, oral examination, stage fright ; this 
 control is weakened, and hence irritability results. 
 
 Symptoms of Neurasthenia. — 
 
 1. Cerebral: Headache — dull, occipital, frontal; sensitiveness 
 of scalp ; vertigo ; insomnia ; cerebral sensations — fulness, band, 
 pulsation. 
 
 2. Mental : Apprehension — morbid fears, of places, people, 
 solitude, etc. ; inattention and forgetfulness ; incapacity for work ; 
 idiosyncracies become prominent ; irritability of temper ensues ; 
 anxiety and exhaustion ; imperfect respiration and rapid pulse. 
 
 3. Spinal : Pain, especially in nape of neck and sacrum ; 
 irritation ; hypersensitiveness ; sensitiveness about ribs and inter- 
 costal nerves ; weakness, legs give out ; sexual irritation, erections, 
 impaired power ; emissions ; bladder irritability, frequent mic- 
 turition. 
 
 4. Vasomotor : Flushes, cold extremities ; undue sweating : 
 
94 DISEASES OF THE NERVOUS SYSTEM. 
 
 transient blueness or oedema; tache ccrchrale of Trousseau; 
 tachycardia ; palpitation. 
 
 5. Gastro-intcstinal : Indigestion and dyspepsia, especially 
 acid stomach ; imperfect liver action ; constipation ; pseudomem- 
 branous colitis ; distension of abdomen with gas. 
 
 6. Sensory and motor symptoms : Indefinite pains and par?es- 
 thesia ; joint affections; apparent paralysis — no change in electric 
 activity ; vision imperfect ; asthenopia ; visual field may be re- 
 tracted. Other senses rarely affected ; tinnitus. 
 
 Diagnosis made by the existence of a cause ; the absence of 
 objective signs of organic disease; the temperairr^nt of the 
 patient; the variability of symptoms; the dispropott'on between 
 complaint and actual power. 
 
 Treatment. — Absolute necessity of establishing ncrve-energ}' 
 by restoring balance between store and expendirure. Hence 
 supply nutritive elements to nervous system by p-opcr food,, 
 properly digested; by increasing circulatory power; by exercise; 
 by hydrotherapy; by massage; and diminish exper.fl.'ture of 
 nervous energy by rest, if necessary absolute, and by diveision. 
 
 Direct treatment may be by tonics of all kinds ; by sedativcs,^ 
 if patient is extremely nervous; by electricity; £alvan>.s,n. Treat 
 symptoms only when absolutely necessary. C-jmbat the desir*: of 
 these patients for drugs, and their depcud-nce on stimujrmts and 
 opiates. 
 
 Hysteria. 
 
 A functional disturbance of the nervous system characterized' 
 by mental and moral perversion, lack of self-conrtol, and dis- 
 orders of any or all the bodily functions. 
 
 Women, between fifteen and twenty-five years, or at an}- age.. 
 
 Men, at an}- age, and even children, may be affected. 
 
 Causes. — Hereditary inHuence very marked ; malnutrition 
 of the nervous system from anaemia ; indigestion ; from bad 
 habits of life; emotional excitement; fear, anxiety, jealousy; 
 tendenc}- to imitation }ielded to ; epidemics of hysteria ; uterine 
 and ovarian irritation is a rare cause. Traumatism, especially 
 accidents attended bv great fear. Several causes mav concur. 
 
S6 DISEASES OF THE NERVOUS SYSTEM. 
 
 tional strain ; scream, convulsion, opisthotonus, facial expression, 
 series of short attacks, fit of crying, passes water, cataleptic 
 rigidity, hysteroepilepsy. 
 
 The character of the symptoms varies greatly. The symp- 
 toms appear and disappear suddenly. 
 
 The course of the disease : Chronic condition with periods of 
 intensity ; cure, sudden and marvellous ; great variation in symp- 
 toms ; very rarely death in convulsion or from suicide. 
 
 Diagnosis is never made from a single symptom, but from 
 a study of the general condition. 
 
 Treatment. — Mental change and moral education; h3'dro- 
 therapy ; the rest cure ; mental therapeutics ; tonics, strychnine, 
 iron, and quinine. 
 
 Symptomatic remedies : 
 
 Sedatives for the nervous state, bromides, valerian, laven- 
 der, asafoetida. Opium is to be avoided, for habit is easily 
 formed. 
 
 For convulsion, prevent injury, don't use chloroform, use 
 cold water, hold patient, stop respiration, don't press ovaries, 
 give emetic. 
 
 For faints, irritation over heart by ice, internally spirits 
 ammonia, or lavender. 
 
 For spasms, hot or cold applications, cautery. 
 
 For paralysis, electricity, especially faradism. 
 
 For pain, hypodermics of water after one of morphine, local 
 applications of sedatives. 
 
 Epilepsy. 
 
 Epilepsy is a functional neurosis characterized by sudden 
 transient loss of consciousness with spasmodic actions of the 
 muscles. 
 
 There are three varieties. 
 
 (i) Petit nialj in which the loss of consciousness is very 
 brief and the spasm slight or absent. 
 
 (2) Grand mal, in which there is a coma, a general convul- 
 sion, with biting of the tongue, frothing at the mouth, some- 
 

 <s6<_-^. 
 
 
DISEASES OF THE NERVOUS SVSTE^r. 97 
 
 times involuntary micturition, and a general weakness and a 
 deep sleep following the coma. 
 
 (3) Psychicp.l attacks in which a sudden mental aberration 
 occurs with acts of violence, or odd actions lasting several 
 hours or even days. In all the varieties the patient is uncon- 
 scious during the attack, no matter what he does, has after- 
 ward no memory of what occurred in the attack, and is often un- 
 aware that he has had any attack at all. 
 
 Etiology. — It is more common in males than in females. It 
 is a disease of early life, but no age is exempt. Many cases 
 can be traced to some injury or organic disease of the brain in 
 infancy or childhood. Any organic brain disease may cause 
 epilepsy in adult life. It is a frequent ,«equal of injuries of the 
 head or brain. It is also of toxic origin : chronic alcoholism, 
 lead poisoning, tobacco poisoning, syphilis, or any of the in- 
 fectious diseases may be followed by epilepsy. In nervous chil- 
 dren intestinal toxaemia may cause it. Peripheral irritation long 
 continued in a very nervous person may cause it ; e. g., foreign 
 lx)dies in the nose or ear, irritation of teething, adenoids in the 
 throat, phimosis, painful scars. In the majority of cases no 
 cause can be found. In the aged arterial sclerosis and multiple 
 areas of cerebral softening are a cause. 
 
 Theory of the Disease. — The nerve cells store up energy 
 which is liberated in any act of mind or will in a moderate de- 
 gree and is accompanied by sensations or muscular acts. In 
 epilepsy it is supposed that this energy is suddenly liberated with- 
 out moderation and hence sensations are forced upon conscious- 
 ness (the aura) and muscles are thrown into violent action 
 ( the convulsion ) . All expenditure of nerve energy is followed 
 by exhaustion until the supply is renewed. Hence the coma, 
 sleep and weakness following the attack. The reason why nerve 
 cells in some persons are ready to discharge their energy- spon- 
 taneously or on slight provocation is unknown. Any mental or 
 physical strain is capable of setting off the explosion. ^lany 
 poisons in the blood are also capable of doing so. The reason 
 bromide and other sedatives check the disease is because they 
 reduce the tendency to the sudden discharge. 
 
98 DISEASES OF THE NERVOUS SYSTEM. 
 
 Symptoms. — The attack is often preceded by some sen- 
 sation, a numbness, gastric sensation, a vertigo, a flash of hght, 
 a sound, a fixed idea. This is called an aura. It is an indi- 
 cation of the organ of the body or of its corresponding region 
 of the brain in which the irritation begins. The convulsion 
 may be general or localized in one part, of the latter it indicates 
 some irritation in the motor area of the brain. Thus many 
 tumors begin with a local spasm or a general fit. The attack is 
 followed by a sleep which is evidence of exhaustion of the brain. 
 Every possible variation in the severity of attack from a petit 
 mal of an instant's duration to a grand mal of many hours has 
 been observed. When a series of grand mal attacks occur the 
 condition is termed status epilepticus. This is the only danger- 
 ous form, as death rarely occurs in an attack. The pupils oi 
 epileptics are always dilated and though they contract again 
 dilate in light. The memory becomes poor as the disease goes 
 on. Judgment is impaired. A final state of dementia is ob- 
 served in many cases. 
 
 Prognosis. — Recoveries are rare. The disease is chronic, 
 but the intervals between attacks may be lengthened by treat- 
 ment. ^^Ooo^U-b^ ^ i :AJbtT>-et— > t» 7 y^"^ o_>j^v,r2c^ 
 
 Treatment. — A simple diet from which meat is almost ex- 
 cluded. Suflicient amount of bromide of potassium and sodium 
 and ammonium combined to hold attacks in check, given on 
 rising and at bed time well diluted. Other remedies are tincture 
 of simulo, one teaspoonful ; antipyrin, 15 grains; solanum 
 carolinense, 20 drops ; chloral, 10 grains ; Belladonna, Digitalis. 
 Heart tonics may be combined vAt^ all these remedies. Bromide 
 acne is to be treated bv^arsenic and hot baths. When bromide 
 causes delirium, as it may. it is to be avoided, 
 
 L. f',.'^o{aM<x*«^ coA^U---^ ^' Chore \. 
 
 Qiorea, or St. Mtus Dance, is a functional neurosis char- 
 acterized by sudden quick twitching of the muscles. 
 
 . Etiology. — It follows rheumatism in 30 per cent, of the 
 cases. It is preceded or attended by endocarditis and valvu- 
 lar disease in 25 per cent, of the eases. It follows mental shocks 
 

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DISEASES OF THE NERVOUS SYSTEM. «9 
 
 in 40 per cent, of the cases. It is often attended by anaemia. 
 It occurs in the spring time after the house confinement of 
 winter. It is more common among the poorly nourished. It 
 is a disease of childhood, but adults occasionally are affected. 
 
 Symptoms. — The twitching may be unilateral or bilateral. 
 It may aflfect the face chiefly, or this may escape. It leads to 
 grimaces and diflficulty of talking. It may be so intense as to 
 necessitate care in bed. Usually it is of slight degree. It may 
 cause apparent ataxia and weakness in the muscles affected, but 
 is not followed by paralysis. Heart murmurs are found in many 
 cases, sometimes anaemic and transient, often organic. Anaemia 
 is often present. The child is often very irritable and fretful. 
 The course of the case is slow, from three to six months. Re- 
 lapses are very frequent. 
 
 Prognosis is good for recovery, but bad for recurrence. 
 
 Treatment. — Arsenic gradually increased to point of tol- 
 erance ; antipyrin or §xalgin in moderate dose according to age. 
 
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