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THE DIAGNOSIS OF DISEASES 
 OF THE CORD, 
 
 LOCATION OF LESIONS, 
 
 t B Y,U 
 
 .Dr. Grasset, ■ 
 
 CLINICAL PROFESSOR AT THE UNIVERSITY OF MONTPELLIER, ASSOCIATE 
 
 OF THE NATIONAL ACADEMY OF MEDICINE, 
 
 LAUREATE OP THE INSTITUTE. 
 
 TRANSLATED BY 
 
 & 
 
 Jeanne CrSous. M.D., 
 
 DEMONSTRATOR' OF NERVOUS DISEA5ES AND ELECTRO-THBRAPBUTICS 
 IN THE UNIVERSITY OF MICHIGAN. 
 
 GEORGE WAHR, 
 
 PUBLISHER, 
 
 ANN ARBOR, MICHIGAN. 
 
 43 
 
Copyright, 1901, 
 By GEORGE WAHR. 
 
THE DIAGNOSIS 
 
 OF 
 
 DISEASES OF THE CORD. 
 
 INTRODUCTION. 
 
 Given a patient in whom a disease of the cord 
 has been recognized, how can the exact location of 
 the medullary change be determined clinically ? 
 
 What system or systems of the cord are exclu- 
 sively or principally attacked ? 
 
 At what level of the spinal axis is the lesion lo-> 
 cated ? 
 
 I wish to sum up here the elements of the answer 
 the present neuro-pathology permits to this ques- 
 tion, which is an interesting one to practitioners 
 generally. ^ 
 
 For if this chapter of clinical geography of the 
 cord, founded by the chiefs of the French neuro- 
 pathological school, Duchenne, of Boulogne, Vul- 
 pian and Charcot, seemed at the beginning a chapter 
 of pure science, today it has been so enlarged, con- 
 firmed and made so exact that it is now absolutely 
 practical, accessible and useful to all. 
 
 In the first place the necessary indications for 
 surgical intervention were found here. This field 
 increases every day in proportion as the operations 
 become less dangerous and their technique is per- 
 fected. 
 
 Further, the different conditions called classic- 
 ally diseases of the cord are anatomico-clinical syn- 
 dromes characterized by the fixity of their symp- 
 
4 Introduction. 
 
 toms and the fixity of the location of the correspond- 
 ing lesion. Whence it results that the diagnosis of 
 this location of the lesion constitutes the complete 
 diagnosis of this syndrome. 
 
 Thus to recognize progressive muscular atrophy 
 or tabes, it is sufficient to recognize that the lesion, 
 in the patient examined, is located in the anterior 
 horns of the grey substance or in the posterior bun- 
 dles. 
 
 Then, without denying the importance of ana- 
 tomical and nosological diagnoses which when pos- 
 sible should complete the physiological, it may be 
 said that the physiological diagnosis of the location 
 of the lesion is absolutely of primary necessity for 
 all physicians today. 
 
 The natural division of this little book is into 
 two chapters, ist. In the first chapter we will study 
 the semeiology of the systems of the cord, that is to 
 say, the signs by which is recognized the location 
 of the medullary change in such or such system of 
 this organ (anterior horns, posterior horns, poster- 
 ior columns, etc). 2nd. In the second chapter we 
 will seek to make a diagnosis of the location of the 
 lesions. 
 
 The study of the clinical anatomy of the cord 
 ought to be the appointed prelude and indispensable 
 basis for pathology. For it is useless to refer to the 
 ordinary anatomical description. Anatomical anatomy 
 is useful to the clinician ; it is the foundation. But 
 physiological anatomy is still more necessary. A 
 symptom is a function pathologically deviated. Then 
 it is necessary to have a basis of functional or physio- 
 logical groupings of organs to make a work useful in 
 practical medicine. 
 
 This study which requires too much to be made 
 here, will be the object of a special publication. 
 
I. THE DIAGNOSIS OF DISEASE OF THE 
 MEDULLARY SYSTEM. 
 
 We will study successively in this chapter the 
 eight following syndromes : 
 
 i. The syndrome of the posterior columns: sen- 
 sory troubles and ataxia ; 
 
 2. The syndrome of the antero-lateral columns : 
 pareto-spasmodic state, contractures and intentional 
 tremor. 
 
 3. The associated syndrome of the posterior and 
 lateral columns: ataxo-spasmodic state; 
 
 4. The syndrome of the anterior horns : muscu- 
 lar atrophy ; 
 
 5. The associated syndrome of the anterior 
 horns and the lateral columns: spastic muscular 
 atrophy ; 
 
 6. The syndrome of the centro-posterior grey 
 substance : dissociation of sensation, called syringo- 
 myelic (and vaso-motor troubles) ; 
 
 7. The associated syndrome of the anterior 
 horns and of the centro-posterior grey substance 
 (syndrome of the whole grey substance) : muscular 
 atrophy, dissociation of sensation, called syringo- 
 myelic, and vaso-motor troubles ; 
 
 8. The syndrome of the lateral half of the cord : 
 hemiparaplegia crossed. 
 
 For each syndrome we will study successively: 
 1st. The group of cases in which the lesion is lim- 
 ited to this system (lesions and symptoms) ; 2nd. 
 Those in which the lesion attacks this system without 
 being exclusively limited to it (lesions and symp- 
 toms) ;'3rd. The synthesis of the syndrome (clinical 
 description, pathological physiology and differential 
 diagnosis). 
 
 5 
 
6 The Diagnosis of 
 
 1. The Syndrome of the Posterior Columns: 
 Sensory Troubles and Ataxia. 
 
 A. There is only one group of cases in which the 
 lesion is systematically limited to the posterior col- 
 umns -.tabes or progressive locomotor ataxia. 
 
 Let us sum up the lesions and. symptoms. 
 
 I. Although a gelatinous degeneration of the 
 posterior columns of the cord was anatomically 
 noted by Hutin in 1827, it may be said that the path- 
 ological anatomy of tabes began with Bourdon and 
 Luys (i860) a short time after the masterly clinical 
 description of Duchenne (1858). 
 
 In the first period a primary systematic sclerosis 
 of the posterior columns in their entirety was 
 claimed; in the second period (Charcot and Pierret, 
 1 871) more was determined: The principal, initial 
 "lesson was localized in the external part of the pos- 
 terior columns (posterior root zones). 
 
 Finally in the third period, the lesion of the pos- 
 terior roots appeared most constant (Leyden and 
 Vulpian) ; then the starting point of the lesion was 
 placed in the ganglions (P. Marie, 1892) and tabes 
 was made a disease of the sensory protoneurone 
 (Brissaud 1895, deMassary 1 1896). 
 
 In fact, the lesions of tabes, in the beginning is 
 localized in the external bundle of Charcot and Pi- 
 erret; then in the more advanced stage it includes 
 the zone of the entrance of the posterior roots of 
 Philippe, that is the zone of Lissauer and the cornu- 
 root zone of Marie. Finally in a case of long dura- 
 
 "Massary (de). Le tabes dors, degener. du protoneur. 
 centrip. Th. Paris, 1896. — Voir aussi pour ce paragraphe: 
 Philippe. Le tabes dorsalis. Paris, 1897; et Gerest. Les 
 affections nerveuses systematiques et la theorie des neur- 
 ones. Paris, 1898. 
 
Diseases of the Cord. 7 
 
 tion the column of Goll is invaded, especially in the 
 upper portion of the cord. The principal and con- 
 stant lesion is in the exogenous fibres, root fibres, cyl- 
 inder axis prolongations of the ganglions. The en- 
 dogenous fibres often found intact (Marie, Strum- 
 pell), have also been found involved (Philippe) ; 
 the descending fibres at first (triangle of Gombault 
 and Philippe, oval center of Flechsig, postero-inter- 
 nal band, comma tract of Schultze), the ascending 
 fibres later (the cornucommisural zone dying last of 
 the posterior columns). But all these endogenous 
 fibres will be attacked only in the second stage con- 
 secutive to the lesion of the exogenous root fibres. 
 
 In the grey substance the lesion of the cells of 
 the vesicular column of Clarke is doubtful or incon- 
 stant ; the alteration of the nerve fibres of this same 
 region (the collaterals given off by the posterior 
 root fibres) is on the contrary very frequent. 
 
 The lesion of the posterior root is very frequent 
 but not constant. In the ganglions the cells as a 
 rule are intact. 2 
 
 Let us omit all extra-medullary lesions (nerves, 
 bulb), which are of no interest here. 
 
 Brissaud's conception then that tabes is a lesion 
 of the sensory protoneurone may be admitted. Only, 
 if we do not wish to admit a dynamic or un- 
 recognized lesion of the ganglion in many cases, it 
 is necessary to say that the primary, essential loca- 
 tion of the lesion in tabes is the intra-medullary part 
 of the sensory protoneurone, that part of the pos- 
 terior column which we know contains the cylinder 
 axis prolongations of the spinal ganglions. 
 
 If with Brissaud we compare the neurone to a 
 tree, the sensory protoneurone is attacked in its 
 
 2 Voir sur ce point important: Gerest. hoc. cit., p. 235. 
 
8 The Diagnosis of 
 
 branches. We shall see that in spasmodic tabes the 
 same way the disease in the pyramidal bundle is in 
 the intra-medullary portion of the cylinder axis pro- 
 longations of the cortical motor protoneurone. Both 
 ataxic tabes and the spasmodic are diseases of the 
 intra-medullary prolongations of the extra-medul- 
 lary neurone. (The spinal ganglion for posterior 
 tabes, the cerebral cortex for lateral tabes). 
 
 Anatomically this change in the posterior root 
 fibres in tabes involves the myeline especially, and 
 degenerations at first descending and then ascend- 
 ing in the endogenous fibres follow this primary 
 process. 
 
 The topography alone of the lesions is what in- 
 terests us here, as we shall write a chapter on medul- 
 lary geography alone. 
 
 2. We ought now to put together from this loca- 
 tion of the lesion the important and essential symp- 
 toms of tabes, at least those which are clearly of 
 medullary origin. They may be said to have been 
 nearly all described by Duchenne 8 in his historical 
 memoir of 1858 and by Charcot* in his "Lecons de 
 la Salpetriere." 
 
 They may be grouped under the following 
 heads: lightning-like pains, visceral crises (gastric, 
 etc.), girdle sensation, anaesthesias and paraesthe- 
 sias, plantar anaesthesia in patches, tingling in the 
 forearm, retarded and false localization, abnormal 
 painful persistence of the sensations excited, dissocia- 
 tion (persistence of thermal sensibility), diminution 
 or abolition of the muscular sense, abolition of the 
 patellar tendon reflex (Westphal), of the Achilles 
 
 "Duchenne. De l'ataxie locom. progr. Arch, gkn de 
 mid. 1858-1859. 
 
 'Charcot. CEuv. compl., t. I, Lee. II, III et IV; t. II. 
 Leg. II et IV. 
 
Diseases of the Cord. 9 
 
 tendon reflex (Babinski), 6 diminution or abolition of 
 muscular tonicity, hypotonicity (Frenkel), 6 involun- 
 tary movements in repose (ataxia of tonicity), 7 pare- 
 sis or paralysis of the sphincters (vesical troubles), 
 motor incoordination, influence of closing the eyes on 
 the upright position and on the gait (Romberg), 
 trophic troubles, arthropathies, osteopathies, ecchy- 
 moses, perforating ulcer. 
 
 B. In a series of diseases we find the posterior 
 columns involved, the lesion not being exclusively 
 limited to this system. We will rapidly review 
 them: General paralysis, disseminated sclerosis, 
 Friedreich's disease, syringo-myelia, spinal menin- 
 gitis. 
 
 1. The relation between tabes and general paral- 
 ysis has been much discussed since Baillarger, 8 that 
 is to say the question of posterior spinal lesions in 
 general paralysis. 9 
 
 First it must be admitted that tabes and general 
 paralysis are two distinct diseases in order that the 
 discussion take place. 
 
 In one group of cases, tabes and general paraly- 
 sis are frequently, according to some (Ballet and 
 Renaud) rarely, according to others (Joffroy and 
 Rabaud) superimposed in the same subject. These 
 cases from this point of view belong to our preced- 
 
 °Babinski. Soc. med. des. hop., 21 oct. 1898. 
 
 "Frenkel. Ueb. Muskel-Schlaffheit (Hypotonie) b. d. 
 tabes dors. Neurol. Centralbl. 1896, t. XV, p. 355. 
 
 'Voir nos leg. sur les mouvem. involont. au repos, chez 
 les tabet. Ataxie du tonus, in Le?. de Clin. med. 2 e serie, 
 1896, p. 271. 
 
 "Baillarger. De la paral. gener. dans ses rapp. avec l'at. 
 locom. Ann. med. psychol. 1862, t. VII. 
 
 "Voir pour tout ce paragraphe: Rabaud. Contr. a l'et. 
 des lesions, spin, poster, dans, la paral gener. Th. Paris, 
 1898. 
 
io The Diagnosis of 
 
 ing paragraph "A." For tabes is always the same 
 symptomatically and anatomically, whether associ- 
 ated or not with another disease, as general paraly- 
 sis. . 
 
 Then there is another group (which is especially 
 interesting here) in which general paralysis (a sin- 
 gle disease) has symptoms and lesions of a posterior 
 medullary location. 
 
 The lesions in this case closely resemble those of 
 tabes, in a section of cord examined by an expert 
 observer. They differ only in the discontinuity, 
 diffusion and irregularity of the sclerosed zones, the 
 relative or absolute integrity of the posterior roots, 
 and Lissauer's zones, the frequency or constancy of 
 cellular lesions of the grey substance. (Rebaud). 
 
 For the symptoms, we find also from the clinical 
 tables such as for a long time have been diagnostic 
 of tabes. But the appearance of cerebral symptoms 
 disturbs the picture. Thus the tendon reflexes then 
 become exaggerated and the special motor troubles 
 of the general paralytic replace the true ataxia with 
 Romberg's symptom. 
 
 2. Disseminated sclerosis has for a long time been 
 considered as a disease principally if not exclusively 
 motor because of Charcot's 10 masterly description. 
 But the patches of sclerosis may be located also in 
 the posterior columns ; and may simulate to a certain 
 point that of locomotor ataxia; Romberg's sign, 
 motor incoordination, lightning pains, hypaesthe- 
 sias, and even urinary troubles (Erb Oppenheim). 
 
 The same observation, adds Raymond, 11 "was re- 
 ported to ,me by one of our present internes of a 
 patient who died during the service of M. Gaucher 
 
 '"Charcot. CEuv. cotnpl., t. V, Lee. VI, VII et VIII. 
 "Raymond. Leg. sur les mal. du syst. nerv. 1897, t. II 
 P- 550. 
 
Diseases of the Cord. 1 1 
 
 at the hospital of Saint Antoine. During his life 
 this patient had presented, independently of a gen- 
 eral spasmodic stiffness, severe pains in the ex- 
 tremities, both upper and lower, imputable to 
 patches of sclerosis in the posterior columns and the 
 corresponding roots." 
 
 3. According to the latest works the principal 
 lesion in Friedreich's disease (Hereditary Ataxia) is 
 in the posterior columns, but especially in the col- 
 umn of Goll and also in the column of Gower and 
 the direct cerebellar tracts and their origin in the 
 grey substance (the cells of Clarke's column). 
 
 Among the symptoms corresponding to this le- 
 sion note: on one hand, an ataxia which is related 
 rather to the cerebellar ataxia than to that of tabes 
 in that it is accompanied by staggering and is only 
 slightly modified by closure of the eyes (the tabeto- 
 cerebellar gait of Charcot) , spontaneous movements 
 (ataxia of tonus) and abolition of the tendon re- 
 flexes, on the other hand there is usually absence of 
 sensory affections (anaesthesias) and of lightning 
 pains. 
 
 4. In syringo-myelia the lesion does not gener- 
 ally affect the posterior columns. But in certain 
 cases these columns may participate in the lesions 
 and these cases pertain here. 
 
 Raymond 12 has collected quite a large number of 
 observations on syringo-myelia in which the anaes- 
 thesia was complete instead of dissociated. In these 
 cases the lesion involves the posterior columns. 
 
 Such are the cases of Joffroy and Achard, Ho- 
 men, Oppenheim, and Schuppel. 
 
 In a word, Schlesinger, who has made the best 
 
 "Raymond. Leg. sur les mal. du syst. nerv. 1897, 2 e 
 serie, p. 510. 
 
1 2 The Diagnosis of 
 
 study of the participation of the posterior columns 
 in syringo-myelia has shown that in these columns 
 three regions were especially invaded by the glioma- 
 tosis i. e. ist. The part contiguous to the posterior 
 grey commissure; 2nd. The portions of the column 
 of Goll adjacent to the posterior median fissure; 
 3rd. The zone between the columns of Goll and 
 Burdach. 
 
 5. Chronic spinal meningitis and more especially 
 leptomeningitis (the inflammation of the pia-mater) 
 are associated with lesions of the posterior columns. 
 This is the condition in the cases of tabes with con- 
 comitant meningitis (Vulpian, Dejerine). 
 
 6. In ergotism Tuczek 13 described (A) clinically, 
 "paresthesias, such as tinglings, numbness, light- 
 ning pains, girdle pains, diminution of sensation to 
 pain, lack of equilibrium when the eyes are closed," 
 ataxia and finally abolition of the knee jerks; (B) 
 anatomically, lesions of Burdach's columns, Goll's 
 being intact. In a word, symptomatically and ana- 
 tomically tabes. 14 
 
 7. Equally well Tuczek studied the medullary 
 lesions of pellagra: 15 the posterior columns are at- 
 tacked in the column of Goll with integrity of the 
 column of Burdach, the symptoms depending upon 
 this lesion are nearly none: knee jerk is more often 
 exaggerated than abolished, no anaesthesia, no true 
 ataxia except at times in the upper extremities. 
 
 In the same part of the posterior cord medullary 
 
 "Voir P. Marie in Traite de med. de Charcot Bouchard, 
 1894, t. VI, p. 314- 
 
 "Rapprocher notre note sur les "Dangers du seigle er- 
 gote dans l'ataxie locotn. progress." Progres medical, 17 
 mars 1884. 
 
 "Voir P. Marie in Traite de med. 1894, t. VI, p. 319. 
 
Diseases of the Cord. 13 
 
 lesions have been described in lepra. 10 But these 
 lesions seem secondary and it is impossible to at- 
 tribute to them a special symptomatology in the 
 midst of the clinical picture of this disease. 
 
 C. With the aid of these various proofs we can 
 now make the synthesis and the pathological physi- 
 ology of the syndrome of the posterior columns. 
 
 The symptoms given may be grouped under two 
 heads : Sensory troubles and ataxia. 
 
 The sensory troubles are : Lightning-like pains, 
 paraesthesias, anaesthesias, (especially of the mus- 
 cular sense) and abolition of the tendon reflexes. 
 
 All these symptoms are explained by a lesion of 
 the root fibres of the posterior columns ( intra- 
 medullary prolongations of the ganglionic sensory 
 protoneurone) or of the first neurones of the relays 
 (ascending prolongations of the neurones of the 
 posterior horns). 
 
 The mechanism of ataxia from a lesion of the 
 posterior column has been and still is much dis- 
 cussed. 
 
 Walking, all movements, even the most simple 
 in appearance, and the maintaining of the body in 
 whatever position, are really complex acts. Immo- 
 bility itself is active. It is the cord itself which pre- 
 sides over the coordination of the muscular con- 
 tractions and relaxations necessary to obtain and 
 maintain each position. Tonus is a part of this gen- 
 eral function; it is concerned in the maintenance of 
 immobility in one position and one attitude. 
 
 This medullary influence is a reflex one. The 
 centripetal excitation of this reflex comes from the 
 skin, the joints, and especially the muscles. This 
 excitation penetrates the cord by the posterior roots 
 
 "Voir Jeanselme et Marie. Sur les les. des cord, pos- 
 ter, dans la moelle des lepreux. Revue neurol. 1898, p. 751. 
 
14 The Diagnosis of 
 
 and the root fibres of the posterior columns. It can 
 be comprehended easily how an alteration of these 
 columns seriously interferes with this reflex; 
 whence we have general hypotonia, sphincter trou- 
 bles, loss of tendon reflexes, and ataxia (of movement 
 and of tonus). , 
 
 Some centripetal impressions useful in this me- 
 dullary function of regulation come also by the 
 senses and particularly by sight. 
 
 In the normal state these sensorial excitations 
 are secondary and accessory and can at a given mo- 
 ment fail without much interference with equil- 
 ibrium and the coordination of movements. When, 
 on the contrary, in consequence of a lesion of the 
 posterior columns the excitations normally the chief 
 ones (muscle) fail, the sensorial excitations become 
 important ; the patients then use their eyes as crutches 
 (Althaus), and their sudden closure causes an in- 
 creased disturbance in coordination, Romberg's sign. 
 That is not saying that the ataxic watches or is 
 obliged to watch his feet, but he uses his eyes to 
 take from around him marks -and fulcrums to make 
 up for the reflex automatism of his cord. He walks 
 with his brain in place of with his cord. And when 
 this help fails he loses his equilibrium by a kind of 
 sudden vertigo which is Romberg's sign. 
 
 From this it is seen that contrary to the classical 
 opinion it is not necessary to consider Romberg's 
 sign as the consequence of the loss or diminution of 
 the muscular sense. I believe I have demon- 
 strated 17 that there is no parallelism nor necessary 
 
 "Du vert, des atax. (signe de Romberg) in Leg. de clin. 
 med. 1896, 2e serie, p. 312. — Rapprocher cette definition du 
 vertige: "la conscience du trouble de l'equilibre du corps", 
 (Frank K. Hallock, Journ. of nerv. and ment. diseases 
 1898, p. 175, Anal, in Gaz. hebdorn. 1899, p. 82.) 
 
Diseases of the Cot d. 1 5 
 
 responsibility between Romberg's sign and the state 
 of the muscular sense and that in certain cases of 
 tabes it can be clearly shown that Romberg's sign is 
 present when it is impossible to make out the least 
 diminution of muscular sense by the most delicate 
 tests. 
 
 The excitations from the muscles (as all the 
 others), once in the cord divide: some provoke me- 
 dullary reflexes, others go to the higher centers 
 where they produce impressions of muscular sense. 
 The first may be alone involved in the lesion of 
 tabes and then incoordination and Romberg's sign 
 are found, but in the same patient the second may 
 ascend to the brain and the muscular sense per- 
 sist. 
 
 It is in this way that cutaneous reflexes' can be 
 abolished when the tactile sensibility remains intact. 
 
 In other words, in the intra-medullary conduc- 
 tion the reflex paths may be suppressed without the 
 direct paths to the brain being interrupted and then 
 ataxia and Romberg's sign are present without neces- 
 sarily a disappearance of the muscular sense. 
 
 This is so true that the tabetic deprived of his 
 medullary automatic gait continues to walk by his 
 brain. And as in the cord certain fibres can take 
 the place of others 18 the tabetic can reeducate his 
 cord with his brain. 
 
 This explains the success of Frenkel's method in 
 tabes. 19 
 
 "Dans mon Rapport au Congres de Moscou, j'ai cite un 
 fait de Erb et de Schultze dans lequel rataxie a gueri sans 
 que "la lesion des cordons posterieurs ait gueri ; il y avait 
 done eu suppleance, formation de nouvelles voies physiol- 
 ogiques dans la moelle. 
 
 "Voir le Rapport, cite ci-dessus, sur le traitement du 
 tabes in Leg. de clin. med. 1898, 3 e serie, p. 634. 
 
1 6 The Diagnosis of 
 
 Then, and in conclusion, incoordination and 
 Romberg's sign prove only a change in the posterior 
 root tracts' which go to the medullary reflex centers 
 of coordination and tonus. The muscular sense is 
 affected in its turn when the lesion, more extensive, 
 involves also the posterior sensory tracts which go 
 to the higher cerebral centers. 
 
 D. For each syndrome studied by us the dif- 
 ferential diagnosis consists in indicating the symp- 
 toms by which the medullary origin of this syn- 
 drome is recognized. That is to say, the symptoms 
 which differentiate it from more or less analogous 
 syndromes of cerebral (or rather intracranial), peri- 
 pheral (neuritic) or neurosic origin. 
 
 i. Lesions of the cerebral cortex may cause sen- 
 sory troubles ahd a kind of ataxia, which here is 
 really related to the loss -of the muscular sense. 20 
 This syndrome differs from that of the posterior 
 columns in being strictly hemiplegic, accompanied 
 by other plainly cerebral symptoms (as the "stroke" 
 and hemiplegia) and not accompanied by symptoms 
 plainly medullary spinal (as lightning-like pains, 
 sphincter troubles and abolition of tendon reflexes). 
 
 By the same class of differential symptoms may 
 be distinguished lesions of the opto-striate bodies 
 and the internal capsule which also can produce by 
 anaesthesia and post-hemiplegic chorea, a form of 
 ataxia. 21 
 
 The cerebellar syndrome resembles the posterior 
 cord syndrome in many points. But the gait of the 
 little brain is intoxicated, a zig-zag, reeling, stagger- 
 ing one with only a little or no Romberg's sign, no 
 
 20 Voir Anesth. d'orig. cortic in Revue de mid. et de Mr. 
 1880, n° 2 ; a la suite du travail de Tripier. 
 
 zl Voir notre travail sur une variete non decrite de 
 phenom. posthemipl. (forme hemiatax.) in Progres mid., 
 13 nov. 1880. 
 
Diseases of the Cord. 1 7 
 
 lightning-like pains, no sphincter troubles ; and on the 
 contrary, from the cephalic lesion there are vomit- 
 ing and other symptoms from the intracranial vicin- 
 ity. 
 
 2. Peripheral lesions can produce pains (more 
 or less lightning-like) anaesthesia, abolition of ten- 
 don reflexes, but not ataxia with the Romberg sign, 
 and no sphincter troubles. 
 
 3. For the neuroses, chorea can be easily distin- 
 guished since the abnormal movements take place in 
 repose and have a wide range (movements in repose 
 being rare and not extensive in a lesion of the pos- 
 terior columns). 
 
 Hysteria, is more difficult of recognition because 
 it can simulate tabes and more often still is associ- 
 ated with it. The distribution of the anaesthesias, 
 the sphincter troubles and the various symptoms of 
 the neurosis (stigmata, attacks) generally permit 
 the diagnosis. 
 
 2. The Syndrome of the Antero-Lateral Col- 
 umns : Paretospasmodic State, Contrac- 
 tures and Intention Tremor. 22 
 
 A. The constituent clinical elements of this syn- 
 drome are : 
 
 1. Contractures, permanent, variable (sleep, re- 
 pbse, chloroform, Esmarch bandage) or latent (re- 
 vealing themselves in voluntary movements) : it is 
 the type of the manifestation of a lesion or the ab- 
 sence of the pyramidal bundles. 
 
 22 Voir nos leg. sur les contractures et la portion spinale 
 du faisceau pyram. (le syndr. paretospasm. et le cordon 
 lateral), in Nouveau Montpeltier mid. 1899, Janvier a mars; 
 et une Note sur les contractures et la portion spinale du 
 faisceau pyram. in Revue neurol. 1899, p. 122. 
 
1 8 The Diagnosis of 
 
 2. With the least intensity and less limitation 
 of the lesion there is paresis with exaggeration of 
 the tendon reflexes (patellar tendon reflex, tendon 
 Achilles studied by Babinski), clonic phenomena 
 (clonus or epileptoid tremor of the foot, knee 
 clonus) the phenomena of the toes (Babinski), ex- 
 tension of the toes on excitation of the sole of the 
 foot. 23 
 
 3. When the lesion of the antero-lateral columns 
 leaves some fibres intact in the midst of the sclero- 
 sis, an intentional tremor, typical of disseminated 
 sclerosis, absent in repose, develops on action and is 
 increased by a repetition of the act. 
 
 B. This system is exclusively attacked and in 
 consequence the syndrome is pure in three diseases : 
 late contractures of hemiplegics, spasmodic tabes, 
 (ataxic paraplegia), and Little's disease. 
 
 1. Described by Suavages among paralytic con- 
 tractures, late contracture of hemiplegics is sepa- 
 rated from the early contractures by Todd (1856) 
 and joined by Charcot and Bouchard (1866) to the 
 descending degeneration of the pyramidal bundle 
 already described by Cruveilhier above the pyramids 
 and by Turck ( 1851) below. Next comes Brissaud's 
 masterly study (1880). 
 
 It may be said that for all neurologists (we shall 
 discuss in a paragraph of the pathological physi- 
 ology the opposed opinion of van Gehuchten) the 
 late permanent contracture of hemiplegics with ex- 
 
 Z3 Nous rapprochons tous ces elements dans le meme 
 groupe symptomatique, malgre les publications de Maurice 
 de Fleury (1884) et de van Gehucten (1897). — Pour rous 
 ces phenomenes, voir : Sternberg. Die Sehnenrefl. u ihre 
 Bedeut 1 d. Pathol, d. Nervensystems, ^Leipzig, 1893 ; et 
 Garnault. Contrib. a l'et. de quelques reft, dans l'hemipl. 
 de cause organ. Th. Paris 1898. 
 
Diseases of the Cord. 19 
 
 aggeration of the tendon reflexes is the syndrome of 
 a lesion of the pyramidal fibres, consecutive to one 
 of a cerebral center. 
 
 2. Spasmodic tabes has been more discussed. 
 
 Erb and Charcot described the syndrome in 1875 
 under the name of spastic spinal 'paralysis and of 
 spasmodic tabes dorsalis and attributed it to a lat- 
 eral sclerosis by reasoning from analogy only. 
 
 The first autopsies weakened this view. 24 Ley- 
 den from the beginning, Raymond from 1885 and 
 till today 1898, deny this anatomo-clinical syn- 
 drome. This is also P. Marie's opinion (1892), 
 who uses the word only for the infantile forms (Lit- 
 tle's disease) . I believe on the contrary with Brissaud 
 (1895) that spasmodic tabes exists in the adult with 
 a lateral sclerosis as the anatomical substratum. To 
 constitute an anatomo-clinical syndrome such as this 
 it is necessary that there.be; clinically always the 
 same symptom picture, anatomically a lesion of a con- 
 stant location. 
 
 But aside from this constant lesion there may be 
 other lesions, variable and clinically latent, without 
 suppressing or altering the clearness of the type. 
 
 Thus Jean Charcot showed that Aran-Duchenne's 
 progressive muscular atrophy exists without an 
 amyotrophic lateral sclerosis even when the lesion 
 is not strictly limited to the anterior horns of the 
 grey substance. In order that the case become an 
 amyotrophic lateral sclerosis it is necessary that the 
 lateral lesion should be so important that it does not 
 remain latent. 
 
 In the same way we may include in spasmodic 
 tabes some cases of lateral sclerosis in which the le- 
 
 "Pitres a publie la premiere autopsie d'un tabes spas- 
 modique de Charcot: c'etait une sclerose en plaques. 
 
20 The Diagnosis of 
 
 sion extends slightly to some cellular groups, but 
 without amyotrophy, or to the tracts of Goll and to 
 the cerebellar tracts without symptoms, or compli- 
 cated by absolutely distinct lesions in the brain, for 
 instance. 
 
 Applying these principles to the criticism of the 
 facts published during the last years we will retain 
 a great number of observations rejected by Ray- 
 mond- 5 and will say with Brissaud "By one of those 
 revivals always necesssary it is now proved to us 
 that a primary sclerosis of the lateral columns is not 
 a myth. It really exists, and it is necessary to go 
 back to it to find the cause and to conceive the path- 
 ogeny of a great number of cases of spasmodic 
 tabes dorsalis." And as I have already remarked 
 elsewhere, the same year ( 1898) where, in his third 
 volume of clinics, Raymond said that the lateral 
 theory of spasmodic tabes "has been completely de- 
 stroyed," his interne Lorrain, under him, supported 
 a thesis on family spasmodic paraplegia, which 
 proves that the destruction of this theory is not com- 
 plete. Then there is a second group of very clear cases 
 in which there are clinically a pareto-spasmodic 
 state and contractures, and anatomically lateral 
 sclerosis. 
 
 3. Without retaining the more or less limited 
 etymological sense of the word I reserve by the ex- 
 ample of Brissaud and of van Gehuchten the name 
 
 2S Tels sont notamment les faits de Strumpell (1879), 
 Stoffela (1878), Morgan (1881), Aufrecht (1880), Min- 
 kowski (1884), Jubineau (1883), Westphal (1884).— Voir 
 aussi la these de notre interne d'alors, Guibert (Montpellier 
 1892), les travaux de Jegorow (1891) et de Shule (1894), 
 !ijs memoires de Strumpell echelonnes de 1880 a 1894, les 
 faits cites par Brissaud (1895), celui de Dejerine et Sottas 
 (1896) et la Th. de Lorrain (Contrib. a l'etude de la parapl. 
 spasm, familiale 1898). 
 
jp is eases of the Cord. 2 1 
 
 of Little's disease for cases of spasmodic rigidity, 
 observed in children born prematurely, without in- 
 itial cerebral phenomena, and anatomically due to 
 the absence of the development (at the time of 
 birth) of the spinal portion of the pyramidal tracts. 
 I eliminate thus from the group not only infantile 
 spasmodic hemiplegias but all infantile cerebral di- 
 plegias. 26 
 
 In these cases, thus defined, we find the clinical 
 syndrome described above, and anatomically, not a 
 lesion, but an absence of the pyramidal tracts. 
 
 C. Besides these three diseases the whole history 
 of which is made up of the anatomo-clinical syn- 
 drome studied, we find this same syndrome (with 
 others) in a certain number of other diseases. 
 
 Such is first disseminated sclerosis : In this dis- 
 ease the change in the antero-lateral columns is 
 shown, 1st, by the characteristic tremor, an inten- 
 tion tremor, originating in action and exaggerated 
 by the repetition of an act; 2nd, by the pareto- 
 spasmodic phenomena which after the tremor con- 
 stitute the most frequent and most characteristic 
 symptoms of disseminated sclerosis. 
 
 When a diffuse myelitis or a compression of the 
 cord changes, either directly or indirectly, by second- 
 ary descending degeneration the pyramidal fibres, 
 we find also the syndrome we are studying. We dis- 
 cuss further along (in chapter 2) the cases of flac- 
 cid paraplegia in compression of the cord or in 
 transverse myelitis. 
 
 M C'est le seul moyen de ne pas faire un groupe flou sans 
 caracteristique clinique ou anatomique, et de repondre aux 
 objections de Raymond, qui arrive a cette conclusion decour- 
 ageante: "Les faits demontrent qu'a l'heure actuelle il'nous 
 est impossible d'etablir.un rapport fixe entre le mode_ de 
 groupement et de localisation de ces symptomes et les lesions 
 constitutes a. l'autopsie." 
 
22 The Diagnosis of 
 
 Certain symptoms of general paralysis (exag- 
 geration of the tendon reflexes, tremor) are also de- 
 pendent upon a change in this medullary system. 
 
 D. After all has been said and after what I have 
 developed elsewhere, I believe it necesssary to keep 
 the law I promulgated in 1877 and 1878 after Char- 
 cot and Strauss (1875) and to say, despite the op- 
 position of certain authors, notably Raymond, that 
 the permanent contractures of the pareto-spasmodic 
 condition of medullary origin are in constant rela- 
 tion to a lesion of the spinal part of the pyramidal 
 fibres. 
 
 But the pathological physiology of the syndrome 
 remains obscure. 
 
 1. With Charcot, Vulpian and Brissaud 27 (1875 
 1880) it is necessary to think the permanent con- 
 tracture due to a permanent muscular hyperactivity 
 by an exaggeration of tonus. But, to explain the 
 exaggeration of tonus, these authors admit that 
 there must be a lesion of the pyramidal fibres, act- 
 ing as strychnia, by exciting the root cells (center 
 of tonus). 
 
 To the second part of their theory we may ob- 
 ject: (A). Sclerosis of the pyramidal fibres should 
 not have a special action on the cells ; posterior scle- 
 rosis should have the same result; this clinically is 
 not so; (B). We cannot comprehend the perma- 
 nence of an exciting action exercised by a sclerosis 
 without inflammatory activity; (C). In Little's dis- 
 ease one cannot comprehend that the absence of the 
 pyramidal fibres excites the cells as a sclerosis of the 
 same bundle. 
 
 It remains, then, to find how a lesion of, or the 
 
 "Je ne dis rien des theories de Folin et Hitzig qui sont 
 refutees partout. 
 
Diseases of the Cord. 23 
 
 absence of the pyramidal fibres produces this exag- 
 geration of tonus shown by contracture. 
 
 2. Since Adamkiewicz (1881) it has been ad- 
 mitted that tonus is submitted to a higher regulating 
 action formed by two antagonistic actions : The one 
 inhibitory, which passes by the lateral columns, the 
 other exciting, which the same author makes pass 
 by the posterior columns. 
 
 From this notion the theory of Anton (1890) 
 and of Pierre Marie (1892) follows. 
 
 The anterior root cell, the center of reflex tonus 
 is a machine under pressure; an inhibitory action 
 exercised by the higher centers normally arrives by 
 the pyramidal fibres; when the pyramidal bundles 
 are altered, destroyed or absent the inhibition is sup- 
 pressed, the center free to excitation overacts ; hence 
 we have hypertonus and permanent contracture. 
 
 Here we have an advance in this theory over the 
 preceding. But it is open to a serious objection 
 (van Gehuchten) : This theory does not explain 
 that the symptomatology may be different when the 
 lesion affects the cerebral portion or the spinal por- 
 tion of this same pyramidal bundle, that in the first 
 case there is paralysis, in the second contracture, 
 that after a cerebral lesion the contracture appears 
 only when the lesion descending has become sub- 
 pontal and spinal. 
 
 This prime objection can be made by all the 
 authors (Jackson, Bastian, Freund, Raymond) who 
 locate in the brain (cortex) the origin of the inhibi- 
 tory action transmitted by the pyramidal tracts to 
 the anterior root cells. 
 
 3. Van Gehuchten 28 (1896, 1898) mentioned a 
 
 28 J'ai essaye de montrer ailleurs que la theorie de Mya 
 et Levi (1896), adoptee par Gerest (1898), ne resout pas 
 
 non plus la question. 
 
24 The Diagnosis of 
 
 new element useful in the elucidation of this ques- 
 tion. The inhibitory action of tonus comes from the 
 higher centers, passes indeed by the pyramidal fibres 
 but the exciting action passes by the indirect ponto- 
 cerebello-spinal paths. Whence the pyramidal bun- 
 dle is differently constituted in its cerebral and 
 spinal portions : The lesion of the cerebral portion 
 causes total paralysis ; that of the spinal portion, in- 
 volving only" the inhibitory paths of tonus, brings 
 about contracture. This explains very well the flac- 
 cid paralysis at the beginning of a cerebral lesion 
 and the contracture of Little's disease or of lateral 
 sclerosis at the onset, and here is the advance over 
 preceding theories— but this does not explain the 
 late contracture of the hemiplegic, it does not ex- 
 plain how the cerebral paralysis, flaccid at the be- 
 ginning, becomes spastic when the lesion extends 
 below and becomes sub-pontal. 
 
 Van Gehuchten understands the objection and 
 responding to it admits that the late contracture 
 of the hemiplegic is entirely different from the 
 medullary contracture at the onset and from spas- 
 modic contracture ; in the hemiplegic the exaggeration 
 of the tendon reflexes is related to the pathogeny of 
 spasmodic contracture, but the permanent contract- 
 ure which is thus separated from the exaggeration 
 of the tendon comes simply from the fact that the 
 extensors are generally more paralyzed than the 
 flexors and so these less opposed by their antago- 
 nists contract. 
 
 Gerest very justly discussed this special theory of 
 the contracture of hemiplegics: (A). In the ex- 
 tended cerebral softening there is not this unequal 
 distribution of paralyses and yet contracture de- 
 velops; (B). It is not understood why the contract- 
 ure develops only late in hemiplegics; (C). In cer- 
 
Diseases of the Cord. 25 
 
 tain cases (neuritis for example) the paralysis can 
 be very unequally distributed and yet contracture of 
 the least paralyzed does not follow. 
 
 I add that it seems to me absolutely anti-clinical 
 to separate the contracture of hemiplegics from ex- 
 aggeration of tendon reflexes and from spasmodic 
 contractures. 
 
 The pareto-spasmodic syndrome is always the 
 same in its symptomatic expression and always cor- 
 responds to the same location of the lesion whether 
 it is cerebral or spinal ; a single thing distinguishes 
 one from the other, that is the date of the appearance 
 of the contracture; simply because contracture 
 belongs solely to spinal and because the cerebral be- 
 comes spinal late, while the spinal is spinal from the 
 onset. To dissociate the contractures of hemiple- 
 gics and the exaggeration of their tendon reflexes 
 seems to me equally artificial and refuted by the 
 clinic. 
 
 Among all the arguments given by van Gehuch- 
 ten to oppose the contracture of hemiplegia to 
 spasmodic contracture a single one is impressive: 
 in the spasmodic form tonus is diminished. I might 
 be contented to reply that this seems paradoxical 
 with all the theories of contractures and in conse- 
 quence with Babinski we must simply describe it as 
 "singular." But we can reply more peremptorily. 
 In a recent work on the question Marinesco (1898) 
 concludes : "Even admitting that Babinski's con- 
 clusions have a general value this relaxation ordi- 
 narily exists in the non-paralyzed muscles, not in 
 the contracted muscles, 
 
 "The result is that in no way should we conclude 
 from Babinski's studies, as van Gehuchten has done, 
 that the contracted muscles of the hemiplegic are 
 found relaxed." 
 
26 
 
 The Diagnosis of 
 
 Then the second part of van Gehuchten's theory 
 is not acceptable. 
 
 But, with only the first part of his ideas, we 
 cannot respond to the objection formulated against 
 all the theories which place the regulating center of 
 tonus in the cerebral cortex. Then, we have not yet, 
 despite all our accumulated efforts, a satisfactory 
 theory of the relation between contracture and the 
 pyramidal tracts. 
 
 A Q Cerebral cortex 
 
 aa- 
 b- 
 
 O Cerebellum 
 C 
 
 D OSpinal cord 
 
 Fig. .. 
 
 4. The failure of all these theories to refute the 
 last objections is due to the fact that all place the 
 crigin of the inhibitory or controlling action exer- 
 cised on tonus in the cerebral cortex. To remove 
 all difficulties it is necessary and sufficient to place 
 the higher center of the regulation, of tonus not in 
 the cerebral cortex, but lower in the pons. 
 
 Let us admit for a moment this hypothesis. Be- 
 low in A (Fig. 1) is the cortical center of voluntary 
 movements, which acts on the tonus when we wish 
 to modify this reflex; in B (in the pons) is the cen- 
 ter which rules automatic tonus. From this center 
 
Diseases of the Cord. 27 
 
 B (as from center A) direct fibres (by the pyra- 
 midal tract) go toward D (spinal center of reflex 
 tonus) which carry inhibitory impulses, and in- 
 direct fibres (by the cerebellum C) which carry ex- 
 citing actions. 
 
 When the lesion is located at a (cerebral por- 
 tion of the pyramidal tract) there is motor paraly- 
 sis; the orders given by A cannot reach D either by 
 the direct or indirect fibres. But the tonus is not 
 affected since its automatic center B remains in nor- 
 mal connection with D by the two classes of. fibres, 
 inhibitory and exciting. Then, no contractures. 
 
 When the lesion is located at b, that is to say 
 the spinal portion of the pyramidal tract is attacked . 
 at the onset or finally, the tonus is no longer intact 
 since B the automatic center of tonus no longer com- 
 municates with D by the inhibitory paths B D and- 
 still communicates with it by the exciting paths BCD. 
 
 It is indeed understood that the symptomatology 
 differs according as to whether the lesion initially 
 takes place above or below aa and that it also 
 changes when the lesion initially above a finally in- 
 vades the region below aa. 
 
 Here then is an hypothesis which answers all the 
 objections ; it consists simply in placing in the pons 
 (B) and not in the cortex (A) the automatic regu- 
 lating center of tonus. 
 
 This hypothesis is not unreasonable physiologic- 
 ally. 
 
 The cerebral cortex has certainly an action on 
 the reflexes and on the tonus : the proof lies in the 
 fact that we can modify voluntarily the attitude of 
 our body, can act voluntarily on what Barthez calls 
 the force of the fixed position, can to a certain limit 
 control the sphincters. 
 
 But there is another thing : the complex reflexes 
 as tonus have an automatic regulating center and it 
 
28 , The Diagnosis of 
 
 is from this center that the inhibitory and exciting 
 actions we are studying arise. 
 
 This automatic center is entirely distinct from 
 the voluntary center (cortical) as it is distinct from 
 the lower simple reflex center (spinal). 
 
 We maintain some attitudes, even complex ones, 
 entirely without voluntary action and higher con- 
 sciousness. 
 
 It is this automatic center that I locate in the 
 pons. The physiologists have made some experi- 
 ments which seem to establish this point. 
 
 Vulpian says, "It is the pons which presides over 
 the normal attitude of animals." He shows a very 
 young rabbit and a pigeon from which all portions 
 of the encephalon anterior to the pons have been re- 
 moved, and which hold themselves in the normal 
 attitude, raising themselves if they are put on the 
 back or on the side. A fowl thus operated upon can 
 hold itself on one foot or hide its head under its 
 wing. More recently Goltz has shown a frog with- 
 out a brain doing "acrobatic exercises; if it is put 
 on a plank which gradually inclines it climbs and 
 passes over from one side to the other without fall- 
 ing." Two dogs, from which Goltz had extirpated 
 the greater part of the cerebral hemispheres "were 
 essentially reflex machines eating and drinking." 
 Hedon who reported some experiments, concludes, 2 * 
 "that animals deprived of the brain preserve besides 
 organic functions which remain intact, various fac- 
 ulties which may be classified under the titles of 
 equilibration, of coordination of movements and of 
 emotional expression." 
 
 These various experiments show that the regu- 
 lating center of the attitude is neither in the cord nor 
 
 '•"•Hedon. Precis, de physiol. 2« edit. 1899, P- SH- 
 
Diseases of the Cord 29 
 
 the brain. For if, in the frog above cited, the mu- 
 tilation is extended and a part of the bulb is re- 
 moved the tendency toward the normal attitude im- 
 mediately is rendered impossible. Hence the center 
 of attitude is. located in the pons or at least in the 
 mesencephalon. 
 
 But some say (Brissaud) that the contractures 
 as in strychnia poisoning, only exaggerate and im- 
 mobilize the attitude. We can say then that from 
 this pontal (or mesencephalic) center a double regu- 
 lating action on tonus arises, an inhibitory by the 
 pyramidal fibres, and an exciting by the ponto-cere- 
 bellar fibres. 
 
 Then the contracture of spinal origin is allied to 
 an alteration or absence of the pyramidal fibres, this 
 alteration determining the contracture by the sup- 
 pression of the inhibitory action on tonus which 
 arises from the pons and goes to the root-cells by 
 the pyramidal fibres. 
 
 E. The differential diagnosis needs to be made 
 only from neuroses and cerebral lesions. 
 
 For the neuroses, paralysis agitans with a 
 tremor (in repose) has entirely different characters 
 from that of disseminated sclerosis ; hysteria has its 
 stigmata and its other peculiar symptoms and often 
 has contractures, but mobile, fleeting ones, usually 
 without exaggeration of the tendon reflexes and 
 without clonic phenomena. 
 
 When the contractures are of cerebral origin, 
 they are early if from a local lesion, or accompanied 
 by other symptoms either of a tumor or of an acute 
 or subacute encephalitis. 
 
 Tetanus or strychnia poisoning and intoxica- 
 tions with contractures all have a special clinical 
 history which easily distinguishes them from af- 
 fections of the medullary lateral system we are 
 studying. 
 
30 The diagnosis of 
 
 3. The Associated Syndrome of the Posterior 
 and Lateral Columns: Ataxo-spasmodic 
 State. 
 
 I called attention (after others) to this anatomo- 
 clinical syndrome in 1886 80 and the very title of my 
 work shows I did not wish to confound this that I 
 called "combined tabes" with what has been called 
 "combined or associated sclerosis" of the cord. This 
 latter term, purely an anatomical one, is applied to 
 a great number of separate cases forming hence a 
 confused group. 
 
 In proportion as the histological technique has 
 been perfected more and more accessory lesions have 
 been discovered by the side of the principal lesion 
 and then studying the combined sclerosis we con- 
 clude, as P. Marie, that they are a diffuse group 
 having jio separate existence. 
 
 I believe that it is good, on the contrary, to re- 
 serve the name of combined tabes for the single 
 complex anatomo-clinical syndrome formed by the 
 superposition in the same subject, not of two lesions, 
 but of two well defined anatomo-clinical syn- 
 dromes: ataxic tabes with its posteripr sclerosis, 
 and spasmodic tabes with its lateral sclerosis; that 
 is to say ataxo-spasmodic tabes with postero-lateral 
 sclerosis. Thus defined, the group is very clear, 
 well characterized, as all the anatomo-clinical syn- 
 dromes, at the time bv a fixed location of the lesion. 
 
 This is admitted by Brissaud who finds "detest- 
 
 ""Tabes combine (ataxo-spasmodique) ou sclerose pos- 
 terolater. de la moelle. Arch .de newrol. 1886, t. XI, p. 156 
 et 380; t. XII, p. 27. — Voir aussi Tarbouriech. Contrib. a 
 l'etude du tabes combine. Th. de Montpellier 1888, n° 83, 
 et Guibert. Et. clin. de la scler. primit. des cord, later de la 
 moelle. Th. de Montpellier, 1892, n° 23. 
 
Diseases of the Cord. 3 r 
 
 able" the word combined tabes but admits what he 
 calls "ataxo-spasmodic paraplegia" if not as a special 
 at least as a "definite nosographical variety." 
 
 We do not ask more. 
 
 Combined tabes is the disease which is exclu- 
 sively manifested by this anatomo-clinical syndrome. 
 
 Besides this other diseases may also have. this 
 syndrome, but in the midst of others. I would cite 
 without insisting upon them, disseminated sclerosis, 
 general paralysis, diffuse myelitis and also medullary 
 arteriosclerosis on which P. Marie has insisted with 
 reason. 
 
 There is nothing to say of the pathological physi- 
 ology contained in the two preceding paragraphs nor 
 of the differential diagnosis of which we have also 
 analyzed the constituent elements. 
 
 4. The Syndrome of the Anterior Horns : Mus- 
 cular Atrophy." 
 
 A. In two important groups of cases the lesions 
 are systematized exclusively to the anterior horn 
 cells : progressive muscular atrophy (type of Aran- 
 Duchenne) acute spinal, atrophic paralysis (infan- 
 tile and adult). We add to these certain cases of 
 experimental myelitis. 
 
 1. Clinically discovered by Duchenne (1849) 
 and by Aran (1851) progressive muscular atrophy, 
 had its pathological anatomy fixed by all the French 
 school from Cruveilhier (1853) to Haven, Charcot 
 and Vulpian. 
 
 Then from this classification, initially too large, 
 there have been successively removed the progres- 
 
 "Voir nQS leg. sur trois cas d'atr. muscul. L'atr. muscuL 
 est le syndr. du neurone moteur central (bulbomedull.) in- 
 ferieur, in Leg. de clin. med. 1898, 3e serie. p. 793. 
 
32 The Diagnosis of 
 
 sive myopathies, neuritis, amyotrophic lateral scler- 
 osis, syringo-myelia and P. Marie has finished by 
 writing, "The progressive muscular atrophy of Du- 
 chenne of Boulogne 32 does not belong there." 
 
 This was an exaggeration. 
 
 As we have said above a propos of lateral sclero- 
 sis you can retain in a given classification some 
 cases whose lesion is not strictly limited to a system 
 provided that the lesion outside of the system is ac- 
 cessory, of little importance, and above all clinically 
 silent. 
 
 On this principle, we find the thesis of Jean 
 Charcot, 33 observations of Strumpell, Oppenheim, 
 Dejerine, Darkchewitsch and a personal experience 
 (plus one more recent of Raymond) 34 which es- 
 tablish histologically the existence of this syndrome 
 and its lesion. Hoffman 35 equally has shown that in 
 the hereditary amyotrophies a certain part should 
 be classed as the Aran-Duchenne type. 
 
 Here then is the first group of cases the exist- 
 ence of which remains indisputable,- characterized, 
 clinically, by the muscular atrophy, anatomically, by 
 a lesion of the anterior horns of the grey substance. 
 
 2. It was still Duchenne who fixed the clinical 
 
 82 Pierre Marie. Existe-t-il une atr. muse, progr. Aran- 
 Duchenne? Revue neural. 1897, t. V, p. 686. 
 
 m Jean Charcot. Contrib. a l'et. de l'atr. muse, progr., 
 type Aran-Duchenne. Th. Paris 1895. — Voir aussi Tzedep- 
 ogolu. Th. Montpellier 1892. 
 
 "Raymond. Clin, des mal. du syst. nerv. 1897, 2« serie, 
 p. 449. — Voir aussi Targowla. Un Job moderne, atr. muse, 
 du type Aran-Duchenne chez un chemineau. Nouv. Inconog. 
 de la Salpetr. 1897, t. X, p. 415. 
 
 3B Hoffman. Ueb. d. progress, spin. Muskelatr. in Kin- 
 desalter aus. famil. Basis. Deutsches Zeitschr. f. Nervenh. 
 1893, t. Ill, p. 427 et Weit Beitr. z. Lehre von d. heredit! 
 progr. spin. Muskelatr. im Kindesalter. Ibid. 1897, t. X p' 
 292. (Trav. de la clin. d'Erb et du labor. <T Arnold). 
 
Diseases of the Cord. 33 
 
 description of infantile spinal atrophic paralysis,™ 
 already seen by Underwood (1774), Heine (1840), 
 Rilliet and Barthez (1851) : after an acute period of 
 generalized paralysis the disease is localized in some 
 muscular groups and is manifested exclusively by 
 an atrophy. 
 
 Vulpian and Prevost (1866) were the first to 
 localize the lesion in the anterior horns of the grey 
 substance. A localization confirmed by Lockhart, 
 Clarke (1867), Charcot and Joffroy (1870). 
 
 Duchenne had already seen that the same dis- 
 ease may develop in the adolescent and the adult, 
 and all the later works have confirmed the existence 
 of an acute spinal paralysis of the adult, clinically 
 and anatomically identical with that of the infant. 
 
 3. Experimentally 31 with old cultures of the 
 streptococci of erysipelas Rogers (1891) was "able 
 to reproduce in six animals a system myelitis 
 characterized from an anatomical point of view by 
 a degeneration of the anterior horn cells ; from the 
 symptomatic point of view by an ensemble of phe- 
 nomena comparable to progressive muscular at- 
 rophy." 
 
 Some analogous results have been obtained by 
 Gilbert and Lion (1891) with the coli-bacillus, 
 Bourges (1893) with the erysipelococcus, Thoinot 
 and Masselin (1894) with the coli-bacillus and the 
 staphylococcus. 
 
 B. But it does not seem necessary to dwell on 
 the diseases which attack the anterior horns without 
 being exclusively localized there: it suffices to say 
 
 3 °Voir les theses de Duchenne fils, Montpellier, 1864, 
 n° 8 ; et Laborde, Paris 1864, n° 163. 
 
 "Voir notre Rapport au Congres de Bordeaux sur les 
 Myel. infect., in Leg. de clin. med. 1898, 3 e serie, p. 540. 
 3 
 
34 The Diagnosis of 
 
 that when the anterior horns are thus attacked, clin- 
 ically there will be muscular atrophy. 
 
 This is what happens notably in certain compli- 
 cated cases of tabes, in certain syringo-myelias, in 
 certain old hemiplegias with descending degenera- 
 tions, in certain abnormal cases of disseminated 
 sclerosis, in pachymeningitis. 
 
 C. The synthesis of the syndrome of the anterior 
 horns is all made since it is reduced to amyotrophy, 
 and the pathological physiology does not require 
 discussion : it is the expression of a trophic action 
 exercised on the muscle by the cell bodies of the 
 central inferior motor neurone. 
 
 D. Differential diagnosis. It is necessary first 
 to eliminate the neurosic origin of amyotrophy 
 when it is met. 
 
 Since Babinski's memoir 88 the facts concerning 
 hysterical muscular atrophy have been multiplied 
 but in these cases (very rare, moreover), there are 
 no fibrillary twitchings, no reaction of degeneration, 
 and there are other symptoms of hysteria. 
 
 The truly diagnostic difficulty consists in distin- 
 guishing spinal amyotrophies from neuritic amyo- 
 trophies, and from myopathic amyotrophies. (The 
 brain by itself does not cause muscular atrophy). 
 
 In neuritic amyotrophies the distribution of the 
 atrophy is that of one or more nerves, the paresis or 
 paralysis is more marked, there are pains (spon- 
 taneous and on pressure of the nerve trunks), the 
 tendon reflexes are diminished or lost, the etiology 
 is a special one and retrocession frequent. 
 
 In myopathies there are no fibrillary twitchings, 
 tendinous retractions are frequent, no reaction of 
 
 ""Babinski. De l'atr. muscul. dans les paral. hyster. Arch, 
 de neurol. 1886. Voir Gilles de la Tourette. Traite din! 
 et therap. de l'hyst. 1895, t. II, p. 503. 
 
Diseases of the Cord. 35 
 
 degeneration, begins more frequently at the extrem- 
 ity of a limb, often there is a family history of the 
 same. 
 
 5. The Associated Syndrome of the Lateral 
 Column and the Anterior Horns: Spastic 
 Muscular Atrophy. 
 
 From 1865 Charcot observed a sclerosis of the 
 lateral tracts in amyotrophy and with Joffroy 
 (1869- 1 879), described amyotrophic lateral sclerosis 
 (Charcot's disease) which is thus clinically defined: 
 "a progressive paresis of certain muscles, at times 
 followed by atrophy and more often by contractures 
 of these muscles or by phenomena analogous to mis 
 contracture" as the rigidity, more or less difficult 
 to overcome, the tremor in certain cases; then we 
 should add the exaggeration of the tendon reflexes 
 and the clonic phenomena. 
 
 Anatomically there is in the cord (let us not con- 
 cern ourselves here with the medulla nor with the 
 brain) a lesion of the anterior horns as in progres- 
 sive muscular atrophy and an alteration of the pyr- 
 amidal fibres as in descending degenerations. P. 
 Marie 39 and Brissaud have shown that there is also 
 a lesion of the mass of the. antero-lateral fibres and 
 especially of the short fibres called the fibres of the 
 cells of the cord, which put the various segments of 
 the cord in relation with each other. This lesion of 
 the intramedullary relay neurones plays perhaps a 
 considerable role, if not an exclusive one (Brissaud, 
 Gerest) in the production of amyotrophic lateral 
 sclerosis. This completes, without disturbing, the 
 
 m Pierre Marie. Leg. citees, 1892 et Soc. med. des hop. 
 1893, dec. 
 
36 The Diagnosis of 
 
 first notion of the anatomo-clinical syndrome we 
 are studying, the pyramidal lesion remaining more- 
 over "much the more salient" (Marie). 
 
 A single case constitutes a real exception in this 
 group ; it is that of Senator ( 1894) : a clinical pic- 
 ture of amyotrophic lateral sclerosis and no lateral 
 sclerosis on autopsy. But this observation remains 
 isolated and is incomplete since the brain was not 
 examined. 
 
 If amyotrophic lateral sclerosis manifests itself 
 exclusively by this anatomo-clinical syndrome this 
 same syndrome may also be found, more or less as 
 an episode in other maladies as diffuse myelitis, dis- 
 seminated sclerosis, 40 etc. 
 
 There is nothing to say of the pathological 
 physiology and the differential diagnosis which has 
 not been said in paragraphs 2 and 4. 
 
 6 . The Syndrome of the Centro-posterior Grey 
 Substance: Dissociation of Sensation 
 called Syringo-myelic (and Vaso-motor 
 Troubles). 
 
 A and B. This syndrome has been studied in 
 syringo-myelia, where perhaps it is found most fre- 
 quently. 
 
 But it is certainly also found in other cases and 
 the expression syringo-myelic, for this dissociation 
 of sensibilities preserves an error if taken literally. 
 
 Named by Ollivier of Angers ( 1827) syringo- 
 myelia is an anatomical condition (known since 
 1688) characterized by the presence in the cord of 
 abnormal cavities. We say there is a hydro-myelia 
 
 "Voir notamment le fait recent de Brauer. Neurot. 
 Centralbl. 1898, p. 638. et Revue neurol. 18^1), p. 22. 
 
Diseases of the Cord. 37 
 
 (the analogue of hydrocephalus) when there is a 
 dilation of the central canal. 
 
 Developing Grimm's ideas ( 1869) Simon 
 (1874), and Leyden (1876) Roth 41 in a series ot 
 works since 1882 and Dejerine 42 in 1889 have at- 
 tributed syringo-myelia exclusively to a medullary 
 gliosis and have considered the two expressions as 
 synonyms. But giving the ideas of Hallopeau 
 (1870) in detail and of Charcot and Joffroy ,(1869) 
 Joffroy and Achard 43 and others have shown that 
 syringo-myelic cavities can have a myelitic origin 
 also, and Souza Martins 44 has shown that it may 
 equally be observed in lepra. On the other hand, 
 medullary gliomatosis may evolve without produc- 
 ing cavities. The synonymousness then of the two 
 must be refused and the word syringo-myelia must 
 keep its original anatomical meaning. 45 
 
 The principal symptom of syringo-myelia is the 
 following, dissociation of sensation, analgesia and 
 thermo-ansesthesia with preservation of tactile sen- 
 sation. Kahler 46 and Schultze 47 first diagnosticated 
 a syringo-myelia by this symptom. The thing be- 
 came classic. 
 
 With Roth and Dejerine this syndrome has been 
 
 "Roth. Arch, de neurol. 1887-89, n°s 42 e t suiv. 
 
 "Dejerine. Soc. mid. des hop., 22 fevr. 1889. 
 
 "Joffroy et Achard. De la myel. cavitaire. Arch, de 
 physiol. 1887. 
 
 "Souza Martins. Un caso de syringom. depend, della 
 labra. Anal, in Revue neurol. 1894, p. 307. 
 
 "Brissaud, qui a bien etudie la dissociation "syring- 
 omyelique" dans la pachymeningite cervicale hypertrophique 
 (Leg. sur les mal. nerv. 1895, p. 196) et cite les cas avec 
 autopsie de Joffroy, de Pierret et de Koeler, les considere 
 comme des exemples de gliomatose consecutive, sedondaire. 
 
 "Kahler. Prag. med. WochenschriH, 1882 et 1888. 
 
 "Schultze. Virch. arch. 1882, et Zeitschr. f. klin. Med., 
 t. XIII. 
 
38 The Diagnosis of 
 
 completely limited to this lesion and the qualifica- 
 tion "syringo-myelic has been given to this disso- 
 ciation of sensation. 
 
 Thus this symptom ha's become an absolute sign 
 of syringo-myelia superior even to the anatomical 
 facts. Thus Dejerine insisted to Joffroy that he 
 had observed a true syringo-myelia (although it was 
 at the autopsy) unique because the patient had not 
 presented the dissociation called syringo-myelic. 
 
 I believe that I was one of the first* 8 to protest 
 (1889) against this view which reversed all that is 
 known of the semeiology of the nervous system. 
 All the symptoms known are in relation with the lo- 
 cation of the change; only this would have ex- 
 pressed not the location but the anatomical nature 
 of the change. This would be improbable. 
 
 To support my protest I have collected two 
 orders of proofs which I will recall; adding to them 
 the documents prepared since then, which have sin- 
 gularly confirmed and rendered definite the thesis 
 under discussion. 
 
 1. Syringo-myelia can exist without the syn- 
 drome of dissociation. 
 
 I have cited a. personal experience observed with 
 my colleague Carrieu. Since, out of 66 cases with 
 clinical and autopsy observations, referred to in 
 Anna and Baumler's thesis (1887) I found 55 in 
 which there was neither the entire syndrome nor 
 any of the constituent elements of the syndrome 
 (and this is also in gliomatosis and lacunar my- 
 elitis). 
 
 Since then proofs of this first proposition have 
 
 "Voir nos leg.' sur le Syndr. bulbomedull. constitue par 
 la thermanesth., . l'analg. et les troub. sudor, ou vasomot. 
 (subst. grise lateroposter.), in Mont pettier med. aout 1889 
 et Leg. de clin. med. 1891, i^e sene, p. 186. 
 
Diseases of the Cord. , 39 
 
 accumulated. First there is the observation of Jof- 
 froy and Achard 40 on syringo-myelia demonstrated 
 on autopsy and having produced total anaesthesia 
 without any dissociation. 
 
 Then Rosenblath 60 published two cases of syr- 
 ingo-myelia (with autopsy) without sensory 
 troubles or at least without dissociation; Preobra- 
 jensky, 61 a case of syringo-myelia, not gliomatous: 
 total anaesthesia without dissociation. Dimitroff 02 
 began an important. work on syringo-myelia with an 
 observation of his own without sensory troubles. 
 Dejerine and Thomas 58 have observed a recent case 
 without sensory troubles. 
 
 In the great monograph of Schlesinger 54 (1895) 
 may be found a number of details on abnormal types 
 of syringo-myelia and finally Raymond 55 has many 
 times insisted on the clinical polymorphism of this 
 
 m Joffroy et Achard. Un cas de mal de Morvan avet 
 aut. Arch, de med. experim. 1890, p. 540. 
 
 ""Rosenblath. Z. Casuist, d. Syringom. etc. D. Arch. 
 f. klin. Med. 1893, t. LI, p. 210 {Revue neurol. 1894, p. 11). 
 Trav. de la clin. med. de Leipsig. 
 
 "Preobrajenski. Mem. med. 1894. (Revue neurol. 1895, 
 P- 75). 
 
 " 2 Stephan Dimitroff. Ueb Syringom. (Trav. de la din. 
 rned. du prof. Eichhorst a Zurich), Arch. f. Psych. 1896, 
 t. XXVIII, p. 582 et 1897, t. XXIX, p. 299: fait suite au 
 travail d'Anna Baiimler, et analyse 297.observ. (jusqu'en 
 octobre 1891). 
 
 "'Dejerine et Thomas. Un cas de syringom. type scapu- 
 lohumer. avec integr. de la sensibil., suivi d'aut. (integr. de 
 la subst. grise mediane). Soc. de biol., 10 juillet 1867, (Re- 
 vue neurol. 1898. p. 153. 
 
 "Schlesinger. Die Syringomyelic (trav. de la 3« clin. 
 med. et de l'lnstitut d'anat.- et de physiol. des centr. nerv. 
 a l'Univers. de Vienne). Leipsig et Vienne 1895. (526 in- 
 dicat. bibliogr. classees par ordre alphabet d'auteur). 
 
 ""Raymond. Clin, des mal. du syst. nerv. 1896, t. I, p. 
 315 et 327, et 1897, t. II, p. 580 et 516. 
 
40 The Diagnosis of 
 
 disease. This last author insists especially on the fre- 
 quency of the total anaesthesia (non-dissociated) 
 m syringo-myelia and cites the findings of Miura 
 (1889), Rumpf (1889), Hochhaus (1891), Homen 
 (1894), Oppenheim (1893), Schuppel. He cites 
 also some reports of syringo-myelia in the form of 
 disseminated sclerosis (Brutton, Rosenblath) then 
 reports a form of spasmodic tabes : Strumpell 
 (1880), Kahler (1882), Reisinger and Marchan& 
 (1884), Schlesinger (obs-7), Raymond (1893). 
 
 The demonstration of our first proposition is then 
 well established : syringo-myelia can exist without 
 the syndrome of dissociation. 
 
 2. The dissociation syndrome can exist without 
 syringo-myelia. 
 
 Morvan described (1883), under the name of 
 analgesic panaritia, paresis of the upper extremities, 
 a disease which bears his name and in which one 
 often finds the dissociation syndrome. Gombault 
 and Reboul ( 1889) made an autopsy on one of the 
 patients of Morvan with dissociation. They found 
 a neuritis, a myelitis, but no medullary lacuna. 
 
 In 1889 I declared the principle, although 
 unique, and expressed the conviction that "Similar 
 cases existed and would multiply themselves when 
 attention was directed to this point." This has been 
 largely realized. 
 
 First Charcot 56 found syringo-myelic dissocia- 
 tion in hysteria, in lepra (Leloir, Babinski, Thi- 
 bierge) and in compression of the cord 57 or of 
 nerves (Critzman). Minor 58 described it in many 
 
 ""Charcot. Lee. du mardi 1889, p. 517. 
 
 "Charcot. Un cas de pseudosyringom. in Sem. mid. 
 1891, p. 193. 
 
 ""Minor. De l'hematom. centr. Soc. de neurol. et de 
 psych, de Moscou, 17 dec. 1893 et Rech. clin. et anat. sur 
 
Diseases of the Cord. 41 
 
 cases of traumatic haemato-myelia. 59 Freund 60 
 carefully studying sensory troubles in disseminated 
 sclerosis, described "syringo-myelic" dissociation in 
 ten observations of this disease (with peculiar char- 
 acter of less duration than in true syringo-myelia). 
 
 In 1892 apropos of a personal case at Brissaud, 
 Jean Charcot 61 studying "the dissociations called 
 syringo-myelic in compressions and section of nerve 
 trunks," recalls the fact that diverse dissociations 
 are found in diseases of the skin, 62 (psoriasis, ec- 
 zema) and again finds true dissociation in a series 
 of cases of section or compression of nerves (Letie- 
 vant, Weir Mitchell, Richet, Chaput, Blum).. 
 
 More recently Cavazzani and Manca 63 have 
 found this same dissociation after a traumatic sec- 
 tion of the radial nerve. And the same year ( 1895) 
 Brissaud 64 was able to say; "The clinic has in- 
 structed us on the pretended pathognomonic value 
 of syringo-myelic dissociation." 
 
 This dissociation of sensibility no longer per- 
 tains to' a single disease." And he cites a case of 
 Brown-Sequard with dissociation cured by anti- 
 
 les aff. traumat. de la moelle suivies d'hematom. centr. et de 
 format, cavitair.es centr. Congres de Moscou 1897 {Revue 
 neurol. 1894, p. 212 et 1897, p. 549). 
 
 S0 Voir Verchere. De la paresie analges. a panaris, des 
 extrem. super. De la paresoanalg. des extrem super, ou 
 raal de Morvan. Revue des sc. med. 1891, t. XXXVIII, p. 
 
 324. 
 
 ""Freund (de Breslau). Ueb. d. Vork. von Sensibili- 
 tatsstor bei. mult. Herdskler (trav. de la clin. du prof. 
 Westphal). Arch. f. Psych. 1891, t. XXII, p. 317 et 588. 
 
 "Jean Charcot. C. R. de la Soc. de Biol. 1892. p. 941. 
 
 ""Rendu. Les anesth. spont. Th. d'agreg. Paris, 1875. 
 
 m Cavazzani et Manca. Alteraz. della sensibil. termice 
 e tattile in seg. a les. del nervo rad. Rif. med. 1895, n° 57 
 (Revue neurol. 1895, p. 534). 
 
 "Brissaud. Leg. sur les mal. nerv. 1895. 
 
42 The Diagnosis of 
 
 syphilitic treatment and in consequence without 
 syringomyelia. 
 
 In 1896 Max Laehr 63 reported a series of facts 
 of "syringo-myelic" dissociation in some cases of 
 the Brown-Sequard syndrome without syringo- 
 myelia, especially those of Muller (1871), of Char- 
 cot and of Gombault (1873) Gowers (traumatic 
 hemorrhage) Beevor (syphilitic tumor), Steel and 
 Williamson (1893). 
 
 The same year Schlesinger 66 published a case 
 (and calls attention to three other personal cases) 
 of intramedullary tumor (without syringo-myelia) 
 with dissociation. 
 
 Hariot and Henri Meunier 67 observed an analo- 
 gous syphilitic gumma. There is also a case of dis- 
 sociation by syphilitic meningo-myelitis which Pia- 
 ott and Cestan 68 published, while David Edsall** 
 studied the dissociation of sensibility of a syringo- 
 myelic type in Pott's disease, and which James Hen- 
 
 b Max Laehr. Ueb Storr. d. Schmerz-Temperatur. Emp- 
 find. in F. von Erkank. d. Riickenm. (Klin. St. mit besond. 
 Berucksicht. d. Syringom.) Trav. de la clin. du prof. Jolly. 
 Arch. f. Psych. 1896, t. XXVIII, p. 773. 
 
 ""Schlesinger. Tumeur medull. (Gliosarc de la reg. 
 cervic.) Club med. Vien., 22 Janvier 1896. (Revue neural. 
 
 1896, p. 441). 
 
 "Hanot et Henri Meunier. Gomme syphilit. double de 
 la moelle epiniere ayant determ. un syndr. de Brown-Seq. 
 bilat. avec dissociat. syringomyel. Nouv. Inconogr. de la 
 Salpet. 1896, p. 49 (meme cas commun. par Henri Meunier 
 au Congres de 1'A. F. A. S. a Carthage 1896.) 
 
 m Piatot et Cestan. Syndr. de Brown-Seq. avec dis- 
 sociat. syringom. d'orig. syphilit. Ann. de dermatol. 1897, p. 
 713 et Revue neurol. 1897, p. 645. 
 
 "David Edsall. Soc. neurol. de Philadelphie, 20 dec. 
 
 1897. The lourn. of nerv. a. ment. Dis. 1898, p. 257 et Re- 
 vue neurol. 1898, p. 742. 
 
Diseases of the Cord. 43 
 
 drie Lloyd 70 demonstrated in traumatism of the 
 cord. 
 
 In a work inspired by Marinesco, Vines 71 shows 
 "that syringo-myelic dissociation is not a rare symp- 
 tom in various cases of chronic myelitis." Dejenne 
 and Thomas 72 have observed dissociation in a case of 
 hypertrophic gummatous pachymeningitis. • 
 
 And Raymond 73 recently has written : "It is not 
 very long ago that dissociated anaesthesia was 
 thought to pertain properly to syringo-myelia. A 
 sort of pathognomonic signification was attributed 
 to it. Today it is recognized that this variety of 
 anaesthesia is observed in very diverse pathological 
 circumstances. It seems natural this should be so. 
 
 If a gliomatous tumor or any other neoplasm 
 can produce these symptoms by interrupting the 
 conductors of sensibility it is easily conceived that 
 the lesion may be of any nature, a hemorrhage, 
 focus of softening, or an islet of sclerosis, 74 the 
 
 . "James Hendrie Lloyd. Traumat. aff. of the cerv. reg. 
 of the Spin. cord, simulat. Syringom. The Journ. of nerv. 
 a. ment. dis. 1894, p. 343 {Revue neurol. 1894, p. 450) : his- 
 toire clinique de deux cas. — A Study of the los. in a case of 
 trauma. Brain. 1898 (Revue neurol. 1898, p. 613) : autop- 
 sie de l'un des deux faits precedents. 
 
 ^Vines. Despe dissociationen. Romania medicala, 1898 
 p. 122 Anal, par Marinesco in Revue neurol. 1898, p. 850. 
 
 "Dejerine et Thomas. Un cas d'hemiparapl. avec an- 
 esth. croisee. Syndr. de Brown-Seq. suivi d'aut. Arch, de 
 physiol. 1898, p. 594. 
 
 "Raymond. Clin, des mal. du syst. nerv. 1897, t. II, 
 P. 549- 
 
 "Cest la pensee qu'ont egalement enoncee Hanot et 
 Meunier, dans leur travail deja cite de 1896: "...Quoi de 
 plus naturel, des lors, qu'une pareille lesion, equivalant 
 physiologiquement a une lacune syringomyelique ait deter- 
 mine la dissociation des sensibilites, telle qu'on le recontre 
 dans les cas de gliomatose medullaire?" 
 
44 The Diagnosis of 
 
 symptoms will be the same in all cases as facts 
 prove." 
 
 We can then affirm as demonstrated today the 
 proposition which we supported in 1889 on a single 
 disputable case : the syndrome dissociation can exist 
 ■without syringo-myelia. 
 
 C. From all that precedes it results that the ana- 
 tomical unity of the dissociation syndrome is not 
 made by the presence of medullary gliomas, nor by 
 the presence of medullary cavities nor by the pres- 
 ence of a single constant medullary lesion, but that 
 for this syndrome as for all other medullary symp- 
 toms, the unity is only made by the unity of the lo- 
 cation of the lesion. It is necessary then to seek 
 now what the unique and constant location of the 
 lesion is corresponding to this dissociation syn- 
 drome. We shall thus come to the pathological 
 physiology of this syndrome. 
 
 In the medullary sensory system it is not a lesion 
 of the posterior columns which gives rise to our syn- 
 drome. For in the syndrome of the posterior col- 
 umns (which we have already studied above) there 
 is total anaesthesia or if there is dissociation it 
 is tactile anaesthesia and especially muscular which 
 dominates with persistence and often exaggeration 
 of the sensation of pain and temperature. This is 
 then an inverse dissociation and in a manner comple- 
 mentary to the dissociation called syringo-myelic. 
 Further, in many observations with very distinct 
 "syringo-myelic" dissociation, the integrity of the 
 posterior columns is noted and in observations of 
 syringo-myelia with total anaesthesia there has been 
 noted on the contrary a participation of the posterior 
 columns in the lesion. 
 
 In every case of syringo-myelic dissociation the 
 alteration is in the posterior horns of the grey mat- 
 ter. 
 
Diseases of the Cord. 45 
 
 We have indeed cited some cases in which the 
 dissociation appeared to respond to a lesion of the 
 peripheral nerves. But then it is permissible to 
 suppose that the neuritic lesion has extended to the 
 medullary centers as in Marinesco's 75 case. It may 
 also be said that "There are. distinct points on the 
 skin for tactile and thermal sensibility." 76 But for 
 our study it is sufficient to say that when the so- 
 called syringo-myelic dissociation is due to a medul- 
 lary lesion, the change is in the posterior horns of 
 the grey matter. 
 
 This is the clinical conclusion which is the same 
 as in 1889. 77 Physiologically the question has ad- 
 vanced less. 
 
 Moreover, I can cite only the celebrated experi- 
 ment of Schiff which has not been repeated : he 
 made a complete section, except the posterior col- 
 umns of the dorsal cord of a rabbit. The animal 
 preserved touch sensation very distinctly and com- 
 pletely lost sensations of heat and pain. 
 
 In 1894 Holzinger 78 undertook the following 
 experiment in the clinical laboratory of Bechterew 
 of St. Petersburg. He cut the dorsal cord of dogs ( at 
 
 "Marinesco. Les polynevr. en rapport avec la th. des 
 neur. Soc. de. Biol., 30 nov. 1895. Voir aussi Presse med. 
 28 dec. 1895 et Rapport au Congres de Moscou sur l'histo- 
 pathol. de la cell, nerv., aout 1897 (Revue neurol. 1896, p. 
 54 et 70; 1897, p. 523) : "Par consequent, conclue-t-il, il 
 n'existe pas de nevrites sans reaction des cellules des nerfs 
 atteints." 
 
 70 Hedon. Precis, de physiol. 1896. Voir dans ce livre 
 (p. 474) les fig. de Goldscheider. 
 
 ""En un mot, on peut dire que l'alteration des comes 
 posterieures a pour traduction symptomatique le syndrome 
 sur lequel je me suis longuement etendu." Leg. de clin. 
 med., ire serie, p. 243. 
 
 "Bechterew. Die sens. Bahnen in Riickenm. Neurol. 
 Centralbl. 1894, p. 647. 
 
46 The Diagnosis of 
 
 the level of the 3rd and 4th pairs of nerves) and 
 noted : 1st. For sensation to pain (A) hypaes- 
 thesia, transitory (some days) bilateral on section 
 of the lateral half of the cord; (B) nothing, on si- 
 multaneous section of the posterior columns, of the 
 grey matter and of the anterior columns, and of the 
 anterior part of the lateral columns with a part of 
 the anterior horns; (C) analgesia of all the body 
 below level of lesion by the section of the two lateral 
 columns or by section of the posterior half of the 
 cord ; only in this latter case the section must be 
 a little before (anterior to) the pyramidal tracts; 
 2nd. For tactile and muscular sensations, anaes- 
 thesia when the posterior columns are destroyed 
 (and then also ataxia). Some analogous results con- 
 firmative of the same conclusions appear to have been 
 obtained by Miinzer and Wiener. 7 " 
 
 From these physiological and especially these 
 clinical reports the probable path in the cord of the 
 fibres conducting pain and temperature 80 may be 
 deduced. 
 
 All conducting fibres enter by the posterior root 
 and penetrate the posterior horns of the same side 
 at once: whence we have thermic and pain anaes- 
 thesia in certain cases of a lesion limited to the pos- 
 terior horns; analgesia of the same side as the le- 
 sion. 81 In these cases the analgesia and thermo- 
 
 '"Munzer et Wiener. Sur la destr. isol6e de la subst. 
 grise medull. Arch. f. experim. Pathol, u. Pharmak., t. 
 XXXV, p. 113. et Revue neurol. 1895, p. 586. 
 
 "Voir notamment sur ce point le travail deja cite de 
 Max Laehr (1896) et celui de Schlesinger. Localisat. d. 
 Schmerz u. Temperatursinnsbahnen in Ruckenm. Wien. 
 physiol. Club 26 mars, Neurol. Centralbl. 1895, p. 751. 
 
 "Tel est le cas presente (avec autopsie) par Dejerine et 
 Sottas a la Societe de Biologie le 23 juillet 1892 (p. 716 des 
 C. R. ) . 
 
Diseases of the Cord. 47 
 
 anaesthesia are segmental, each segment of the limb 
 having its special medullary center. 82 
 
 Then these conducting fibres pass to the opposite 
 side (by a commissure) : whence we have crossed 
 analgesia when the lesion is above the level of the 
 center of the region affected (the case in Brown- 
 Sequard syndrome). This intra-crossing does not 
 seem to take place at the same height for the dif- 
 ferent fibres, thermic and algesic of the same re- 
 gion ; for. in a lesion limited to the posterior horns, 
 the two peripheral zones of anaesthesia are not 
 necessarily superimposed. After their intra-cross- 
 ing these conducting fibres pass into the grey mat- 
 ter and very probably pass at once into the sensory 
 bundles of the anterior lateral columns (notably into 
 Gower's bundle) . 
 
 As to tactile and muscular impressions, they are 
 not obliged to pass by the relay neurone (posterior 
 horn) of their region. When this neurone is de- 
 stroyed they continue either by the relay neurones 
 of a higher level or by the posterior white substance 
 alone and thus reach the brain ; whence we have the 
 so-called syringo-myelic dissociation of sensation in a 
 part of a limb of the same side as the lesion when the 
 lesion is located in the corresponding region of the 
 posterior horn. 
 
 Above this relay neurone thermic and pain im- 
 pressions continue by the grey substance and the 
 lateral columns, while tactile impressions follow" 
 another path (posterior columns). From this one 
 can understand that a lesion limited to this level can 
 produce so-called syringo-myelic dissociation of the 
 opposite side as compared with the lesion if located 
 
 82 Voir nos Leg. sur les Sympt. medull. a distrib. segment, 
 publiees par mon chef de clin. le D r Gibert dans le Nouveau 
 Montp. medical (1899). 
 
48 The Diagnosis of 
 
 at one point, and inverse or complementary (tabe- 
 tic) dissociation, 83 if seated at another point. 
 
 Then, to resume, from pathological physiology 
 it is perceived that the dissociation called syringo- 
 myelic is not exactly the syndrome of the posterior 
 horns,** but often the syndrome of the second sen- 
 sory neurone, (the first neurone of the relay), the 
 cellular bodies of which are in the posterior horns, 
 and ivhose cylinder axis prolongations are in the 
 lateral column and especially Gowe/s bundle of the 
 opposite side; that is to say, that the dissociation is 
 on the same side as the lesion when this attacks the 
 cellular bodies of this neurone and that the dissocia- 
 tion is on the side opposite the lesion when this in- 
 volves the prolongations of this same neurone. 85 
 
 D. To make the differential diagnosis of this 
 syndrome it is sufficient, as soon as the dissociation 
 is established, to discuss its origin ; hysterical, neu- 
 ritic, or medullary. 
 
 In hysteria the distribution may be segmental; 
 but there are other symptoms which permit a diag- 
 nosis of the neurosis. It becomes more difficult 
 when there is a hystero-organic association. Sug- 
 
 M La dissociation inverse ou complementaire est constit- 
 ute par l'anasthesie tactile et mu:culaire avec conservation et 
 souvent exaltation de la sensibilite a la temperature et a la 
 douleur. 
 
 "Pour Marinesco (Soc. med. des hop. 6 mars 1896), la 
 dissociation syringomyelique est due a l'interruption du con- 
 tact utile entre les collaterales et certains neurones de la 
 corne posterieure; ce phenomene d'addition et de renforce- 
 ment n'ayant plus lieu quand la corne posterieure est de- 
 truite. 
 
 85 Au moment de mettre sous presse, nous recevons un 
 travail de van Gehucten sur "la dissociation syringom- 
 yelique de la sensibilite dans les compressions et les rrau- 
 matismes de la moelle epiniere, et son explication physiol- 
 ogique." (Sem. med. 1899, n° 15, p. 113). 
 
Diseases of the Cord. 49 
 
 gestion here seems to be the only absolute means of 
 resolving the question. 
 
 As to the peripheral origin I believe this rare 
 without medullary involvement. On the other hand 
 the dissociation is then always distributed according 
 to the nerve territories and not in segments ; and there 
 are all the other ordinary symptoms of neuritis. 
 
 E. It is now time to consider that sudorific and 
 vaso-motor disturbances make a part of the syn- 
 drome of the posterior horns. 
 
 I will devote to them only an appendix to the 
 general chapter as their physiological and semei- 
 ological history are not complete. 
 
 In a patient whom I studied in 1889 there were 
 more exaggerated sweats and hyper-thermia on the 
 same side as the thermo-anaesthesia and the anal- 
 gesia. I have collected 29 cases, borrowed from 
 various authors, 86 in which there was with the dis- 
 sociation of sensibility on one part, sudorific or vaso- 
 motor troubles on the other. 
 
 From this frequent association of the two classes 
 of phenomena we have already inferred that prob- 
 ably the lesions corresponding to the symptoms have 
 the same location or both locations are near. 
 
 The physiologists do not appear to know any- 
 thing of this location of the meduTlary vaso-motor 
 center (or of the great sympathetic). 
 
 Some make the anterior columns intervene 
 (Brown-Sequard, Schiff) Or the column of Clarke 
 (Jacubowitz, Gaskell), but without proving their 
 convictions. 87 
 
 86 Strumpell, Furstner et Zacher, Glaser, Remak, 
 Schultze: Will, Gull, Lockart-Clarke, et Hughlings- 
 Jackson, Westphal, Krauss, Oppenheim, Freund, Roth, 
 Morvan, Proust, Dejerine, Rumpf, Moutard-Martin. 
 
 "Voir les art. Vasomoteurs de Nuel et Sympathique de 
 Francois Franck in Diet, encyclop. des sc. med. 
 4 
 
5© . The Diagnosis of 
 
 . The hesitation of the physiologists is still greater 
 for the localization of the medullary center of the 
 sudorific nerves. 88 
 
 In the clinic, Bouverat showed hyperidrosis in 
 various cord diseases, but without saying anything 
 as to the location of the lesion. In 1882 Pierret 8 * 
 established much more, and by applying the an- 
 atomo-clinical method to the study of the vaso- 
 motor troubles of tabes he places the lesion in the 
 intermedio-lateral tract of Clarke. 
 
 This is' where we were in my lessons in 1889. 
 
 A little later the observations of the Saltpetriere 
 on syringo-myelic dissociation in hysteria appeared, 
 and most remarkable the patient in whom Charcot 
 demonstrated this neurosic dissociation was studied' 
 by Gilles de la Tourette 90 .from the point of view of 
 the trophic, vase-motor and oedematous troubles. 
 Among these hysterics who "simulate syringo-my- 
 elic dissociation we find swollen, oedematous, cold, 
 cyanosed hands which singularly resemble the "suc- 
 culent hand," which Marinesco describes as in the 
 true syringo-myelics. 
 
 Again hysteria has not so gross a physiology 
 and associates in its manifestations, symptoms 
 which often belong to organic lesions : so-called 
 syringo-myelic dissociation and trophic and vaso- 
 motor troubles. 
 
 In 1897 Marinesco 91 took up the question of 
 
 "Voir Francois Franck, art. Sueur in Diet, encycl. des 
 sc. med. 
 
 ""Pierret. Acad, des sc. 1882, et Putnam. Th. de Paris, 
 1882. 
 
 - ""Gilles de la Tourette et Dutil. Contrib. a l'et. des 
 tr. troph. dans i'hyst. Atr. muse, et ced. Nouv. Iconogr r de 
 la Salpetr. 1889, p. 251. 
 
 "Marinesco. De la main succulente. Nvuv. Iconogr. de 
 la Sdlpetr. 1897, p. 84 et 202. 
 
Diseases of-', the Cord. 5 1 \ 
 
 vaso-motor troubles in syringomyelia apropos to 1 
 this oedematous hand which with P. Marie he called ■ 
 the "succulent" hand. 
 
 He recalled first many cases which had never 
 been collected ; then he added more , recent cases,: . 
 those of Massius (1890), Hoffman, Colemann and 
 O'Carroll (1893), Dayot and Reijnes (Louazelle 
 1890), with four personal observations. (Clinic of 
 P. Marie and of Raymond) . 
 
 He declares Pierret's opinion as to the location 
 of the medullary center of the vaso-motor nerves 
 not admissible, and accepts rather that of Remak 92 
 according, to which this center is in the posterior 
 grey horns ; each segment of the cord containing its 
 sensory and vaso-motor centers for the correspond- 
 ing limb. 
 
 In fact, certain anatomists 93 admit today that the 
 motor influence leaves the cord by the posterior 
 roots and goes from there by the rami communi- 
 cantes to the sympathetic ganglions. 
 
 It is permissible to think that these fibres which 
 come from the posterior roots of the cord, arise in 
 the posterior horns of the grey substance or in 
 neighboring parts (Lenhossek and Cajal make them 
 come from the base o'f the anterior horns "also from 
 wjthin and near the canal as well as from outside)." 
 ' Despite the obscurity which still persists on this 
 question I believe we may conclude clinically that 
 the dissociation of sensation callled syringb-myelic 
 is' the syndrome of the posterior horns of the cord 
 and that the vaso-motor and sudorific troubles 
 
 "Remak.. Berl. klin. Wochenschr.. 1889, ng 3 (cit. Mari- 
 neScd). 
 
 ""Voir Van Gehuchten. Anat. du syst. nerv. de l'hom., 
 2e r edit. 1897; p. 895, et Poirier. Traite d'anat'hum. 1884, 
 t. TO, p. 215. ; - :• . - ■■ • 
 
5? The Diagnosis of 
 
 (when they are of medullary origin) are the syn- 
 drome of the posterior and central grey matter 
 (base of the anterior horns). 
 
 7. The Associated Syndrome of the Anterior 
 Horns and of the Centro-posterior Grey 
 Matter (the Syndrome of the entire Grey 
 Matter): Muscular Atrophy, Dissocia- 
 tion of Sensation called Syringo-myelic 
 and Yaso-motor Troubles. 
 
 This syndrome, the anatomo-clinical and patho- 
 logical physiology of which is explicitly contained 
 in paragraphs 4 and 6, is especially found in two 
 classes of cases : syringo-myelias with amyotrophies 
 and amyotrophies with vaso-motor troubles. 
 
 1. Syringo-myelia shows itself by amyotrophy 
 and dissociation of sensation at a time when the 
 lesion involves simultaneously the anterior and pos- 
 terior portions of the grey matter : in these cases the 
 amyotrophy has the characters which we have as- 
 signed to amyotrophies of medullary origin. 
 
 Marinesco has insisted on the frequency of the. 
 preacher's hand in these cases as described by Char- 
 cot and Joffroy in hypertrophic cervical pachymen- 
 ingitis and characterized by the predominance of 
 atrophy in the regions of the ulnar and median 
 nerves; further in these same patients the muscular 
 atrophy (of the Aran-Duchenne type) always has a 
 very segmental distribution. 94 
 
 2. In amyotrophies there is often noted hyper- 
 thermia, the violet or livid hand (Vulpian). I have 
 noted hyperthermia, and local sweats. Frommann, 
 
 "Voir le fait d'amyotr, en «rant recem. publie par Crocq 
 (Journ. de neurol. de Bruxelles 1899). 
 
Diseases of the Cord. 53 
 
 Friedreich, Wunder, Leich, Leyden have also de- 
 scribed exaggerated sweats in certain amyotrophic 
 cases. 95 
 
 It seems useless to insist further on this point. 
 
 8. The Syndrome of the Lateral Half of the 
 Cord: Crossed Hemiparaplegia. 
 
 A. In 1849, Brown-Sequard 98 described the 
 symptoms observed after a lesion of the half of 
 the cord: there is a crossed hemiparaplegia or 
 Brown-Sequard syndrome, characterized by motor 
 paralysis and hyperaesthesia of the same side as the 
 lesion, and anaesthesia of the opposite side. 
 
 More exactly we find: 1st. On the side corres- 
 ponding to the lesion a motor paralysis, normal or 
 exaggeration of the various sensations, a zone of 
 anaesthesia in the upper portion of the part near the 
 lesion and often a zone of hyperaesthesia above, hy- 
 perthermia and paralysis of the sympathetic, ar- 
 thropathies, muscular atrophy; 2nd. On the side 
 opposite the lesion there is preservation of voluntary 
 movement and of the muscular sense, anaesthesia 
 in all forms, sometimes a zone of hyperaesthesia 
 above the level of the lesion (the crossed sensory 
 troubles rising not quite so high as those on the side 
 of the lesion). 
 
 All authors have confirmed this clinical descrip- 
 tion. It has been completed by showing that often 
 
 "Voir notre Trait? des mal. du syst., nerv. 4 e ed (en col- 
 lab, avec Rauzier), 1894, t. I, p. 610. 
 
 '"Les divers travaux de Brown-Sequard sur l'anesthesie 
 spinale croisee sont echelonnes depuis sa these en 1846 
 jusqu'en 1894. Les memoires les plus impbrtants sont ceux 
 de 1849 a la Societi de Biologie, de 1863 dans le Journal de 
 la physiologie, de 1868 et 1894 dans les Archives de physi- 
 ologie. 
 
; 54 T-he Diagnosis of 
 
 the anaesthesia is dissociated (of the syringo-myelic 
 type) ; the same had been noted in certain observa- 
 tions collected at first by Brown-Sequard, especially 
 those of Vigues. Sometimes there is only thermo- 
 anaesthesia. 
 
 This unilateral dissociation is habitually crossed 
 in relation to the lesions. More rarely it is direct, 
 especially in the case of Dejerine and Sotttas. 97 In 
 this latter case, the motor paralysis which is always 
 direct (as in the classic cases) is on the same side 
 as the anaesthesia ; then we do not have the Brown- 
 Sequard syndrome proper. However, these are 
 cases which we ought not to overlook when study- 
 ing the syndrome of the lateral half of the cord. We 
 will take them up again apropos to the pathological 
 physiology. 
 
 The Brown-Sequard syndrome is clear and com- 
 plete (as we shall describe it) when the lesion is 
 -exactly limited to the lateral half of the cord. We 
 observe it in an attenuated and incomplete form 
 when the lesion, more extended is more marked in 
 one half than in the other. In this case the motor 
 paralysis and anaesthesia are bilateral; only the 
 paralysis is more marked on the side of the lesion 
 and the anaesthesia (complete or dissociated) is 
 •more marked on the side opposite to the lesion. 
 
 Complete or incomplete, the Brown-Sequard 
 syndrome is always a very good sign of the medul- 
 lary location of the lesion. Outside of the cord two 
 different lesions are necessary to produce this. 
 
 B. tThe diseases capable of producing the 
 Brown-Sequard syndrome' (complete or incomplete) 
 are numerous. Any medullary lesion will produce 
 
 "Dejerine et Sottas, Soc. de Biol., 23 juillet 1892. Obs. 
 deja citee. 
 
Diseases of the Cord. 55 
 
 it with the single condition that it inyolve exclu- 
 sively a half of the cord or only one half of the cord 
 more than the other. 
 
 .We will note: traumatic lesions (fracture, lux- 
 ation, hemorrhages, bullet wounds), vertebral ar- 
 thritis, spinal meningitis, hemorrhagic foci, diffuse 
 myelitis, syringo-myelia, tumors, various syphilitic 
 localizations, 98 (syphilomas, - myelitis, gummatous 
 meningitis), etc. 
 
 C. The pathological physiology of this symp- 
 tom still remains difficult and is much discussed 
 despite the works. which it has provoked for a half 
 century. 
 
 It concerns us to study in extent only crossed 
 anaesthesia. For, for the direct paralysis no one 
 disputes the pathogeny which is very simple, the 
 lesion involving the medullary motor fibres which 
 have already crossed at the pyramids. 
 
 To explain the crossed anaesthesia, Brown-Se- 
 quard, in his first works, admitted that the medul- 
 lary sensory fihres cross in the cord at every level of 
 the cord from their, entrance into the cord by the 
 posterior roots. This explains the crossed anaes- 
 thesia; the hyperesthesia above the level of the le- 
 sion is due to irritation of the surrounding part, as 
 is also the hyp'eraesthesia of the same -side as the 
 lesion; the direct-zone of anaesthesia at the levehof 
 the lesion is due to a change in the nerves at their 
 entrance into the cord :before their crossing. 
 
 Physiologically" Brown-Sequard shows anaes- 
 
 "Voir Lamy. La meningomyel. syphil. Paris. 1893.— 
 Sottas. Contrib. a l'etude. anat., clin. des paral. spin, 
 "syphil. Paris 1894! — Gilles de la, Tourette. " Formes clirt 
 et trait, des myel. L syphil. Les Actualites medic. • 1899: , 
 
 "Voir pour tout ce paragr. . Dbjerine et Thomas! .;Un 
 cas d'hemiparapl. avec ariesth. .croisee'. • Syjidr„de-:Bfowri- 
 Sequard suivi d'aut. Arch, de physiot. 1888, p. 594. 
 
56 The Diagnosis of 
 
 thesia of the hinder limbs after a double hemi-sec- 
 tion, one in the dorsal region, and the other in the 
 cervical region or after a longitudinal section sepa- 
 rating into two lateral halves the lumbar enlarge- 
 ment of the cord, (Galien's experiment, remade by 
 Fodera 100 1823). The same experiment in the cervi- 
 cal region produced complete anaesthesia of both 
 anterior limbs with preservation of sensation in the 
 hinder limbs. 
 
 To this theory the physiologists have made and 
 still make numerous objections and Vulpian 101 who 
 was one of the first adversaries of Brown-Sequard's 
 ideas, admitted that the hyperaesthesia (in a uni- 
 lateral lesion of the cord) above and below the level 
 of the lesion is produced by the local excitation and 
 that the crossed anaesthesia is due to a depression 
 correlative to the excitability of the analogous parts 
 of the cord ; the physiological balancing of the two 
 halves of the cord. 
 
 These are some of the arguments of the adver- 
 saries to the theory of the intra-medullary intra- 
 crossing of the sensory tracts. 102 
 
 1. Among animals after unilateral section of the 
 cord, if hyperaesthesia is the rule (Fodera, Vul- 
 pian) crossed anaesthesia is on the contrary "a phe- 
 nomenon of very variable intensity in different ani- 
 mals and is not generally absolute." 
 
 2. Unilateral section has moreover less influ- 
 ence on the hinder limbs the further it is from the 
 lumbar cord. (Vulpian). 
 
 3. Tn the experiment of Van Deen (unilateral 
 
 ""Fodera (1823) et Schops (1827) avaient entrevu le 
 syndrome de Brown-Sequard. 
 
 '"Vulpian. Art. Moehe epin. (Physiol.) in Diet, en- 
 cycl. des sc. med. 1874, 2« serie, t. VIII. 
 
 1K Voir l'art. cite de Dejerine et Thomas. 
 
Diseases of the Cord. 57 
 
 section toward the posterior portion of the-dorsal cord 
 and a complementary unilateral section in the cervical 
 region) both hinder limbs retained sensation even 
 if one unilateral section extended over the median 
 line (dog, Vulpian; rabbit, Schiff). 
 
 4. The longitudinal section of the lumbar en- 
 largement in the median line produces only a simple 
 diminution of sensation (Ore). 
 
 5. More recently S. Mott 103 reached analogous 
 conclusions for the monkey : painful and thermic sen- 
 sations can be conducted by both sides of the cord, 
 but touch sensations and those of pressure are prin- 
 cipally conducted by the same side; there will be a 
 considerable retardation in the transmission of the 
 impressions received by the paralyzed side and some 
 errors in localization. In resume, in the monkey an- 
 aesthesia is principally direct. 
 
 6. Gotch and Horsley 104 have made researches 
 as to the electric modifications which are produced 
 in the various bundles of the dorsal cord when elec- 
 tric excitation is applied to the sciatic nerve or to the 
 posterior roots of the lumbar plexus. In a way they 
 measure by the intensitv of this electric modification 
 the quantity of nerve energy which passes into these 
 bundles of the cord when the nerve in question is 
 excited. 
 
 In the cat and monkey, the current in the cord is 
 principally unilateral and of the same side in the 
 proportion of 80 per cent and principally by the pos- 
 terior column. 10 •" , 
 
 10S Mott. Res. of hemis. of the spin. Cord in Monkeys, 
 Philos. Transact. 1891, Cit. Dejeririe et Thomas.— Voir 
 aussi la discussion de ces exper. par Marinesco in Sent, 
 med. 1806, p. 263. 
 
 1m Gotch et Horsley. On the mammalian nerv. syst, its 
 Funct. and their Localis. determ. by an electr. Meth. Phil- 
 osoph. Transact. 1891. Cit. Dejerine et Thomas. 
 
5 8 The Diagnosis of 
 
 Many months after the hemi-section of the cord 
 the -electric modification above the hemi-section is 
 .three times less strong than if the excitation is applied 
 to the opposite side. 
 
 In resume Dejerine .and Thomas grouping the 
 facts of experimental physiology 108 conclude that 
 the intra-crossing of the sensory tracts is not com- 
 plete in the cord; undoubtedly a partial intra-cross- 
 ing occurs; that in certain animals the intra-crossed 
 fibres are more numerous than the direct; in other 
 animals (the monkey and the cat) the contrary is a 
 -fact. 
 
 Impressed by all these arguments Brown-Se- 
 quard 107 himself toward the close of his life aban- 
 doned his first theory. He recalls that a puncture of 
 -the posterior cord of one side can produce the syn- 
 drome; that after first a unilateral section in the 
 cervical cord with consecutive hemianaesthesia, if a 
 second dorsal unilateral section were made hyper- 
 -aesthesia replaces the hemianaesthesia and vice 
 'versa; that hemianaesthesia consecutive to a uni- 
 lateral section of the cord may disappear after z 
 ■stretching of the sciatic nerve on the side of the 
 ■anaesthesia. And then according to him the anaes- 
 thesia in his syndrome becomes a matter of inhi- 
 bition and the hyperesthesia a matter of over-ac- 
 tivity. 
 
 105 I1 seriat utile d'etablir que, chez ces animaux, l'excitar 
 tion electrique est comparable, pour les voies de conduction 
 intramedullaire, a l'excitation venue des organes sensitifs 
 peripheriques. 
 
 ""Voir aussi Bottazzi: Sur Themis, de la moelle epin. 
 "Riv. sperifti. di fren. 1896, t. XXI etRevue neurol, 1896J p. 
 •372. 
 
 . 107 Brown-SEQUARD. Rem. a propos. des rech. du Dr Mott 
 sur les effets de la sect, d'uhe moitie later, de la moelle epin. 
 Arch, de physiol. 1894. 
 
Diseases, of ~the -Cord. 59 
 
 This opinion so plainly settled has separated the 
 clinicians from the. physiologists. And, so Bris- 
 saud 108 has continued to defend and to represent in 
 a scheme the intra-medullary dissociation of the sen- 
 sory tracts, Raymond 100 appeared disposed to take 
 up Brown-Sequard's last opinion, and Dejerine and 
 Thomas, recognizing that it is formulated in "very 
 .vague terms" are tempted however "to take into 
 .consideration the last opinion of Brown-Sequard, 
 already moreover sustained by Vulpian." And they 
 ;add "Whatever it is, it is impossible to put Brown- 
 Sequard's theory on a solid basis, especially when 
 theories 110 are preferred to facts." 311 
 ., It seems to me that the question can be presented 
 _in a less discouraging manner. Without lessening the 
 .value of the conclusions accumulated by experi- 
 mental physiology it may be remarked that all these 
 .experiments establish a single thing: the mode of 
 jntra-medullary transmission of sensory impressions 
 in animals. — 
 
 But in man things may. take place differently: 
 
 I08 Brissaud. HemiparapV spin avec hemianesth. croisee, 
 "syndr. de Brown-Sequard in Leg. sur les mal, nerv. 1895, 
 p. 246, (leg du 15 dec: i893)>-Le double syndr. de Brown- 
 Sequard. dans :1a syph. spin Progris med. 1897 n°s 29 et -51. 
 Voir aussi Londe. Double syndrt de Brown-Sequard- dans 
 Je mal de Eptt. Revue neurol. 1898, p. 356. .. . ,. 
 
 ""Raymond. .' Synd. de Brown Sequard d'orig. probabl. 
 'syringomyel: (Leg.du 28 juin 1895) in Cljn.-desinal. du 
 syst. nerv'. 1896,.' If. I, p. &i 5 et suf-iin cas d'hemis, -trauma! 
 •de la moelle- ( syndr ._de Brown-Sequard). .Leg. dn.20 nov. 
 1896 in Clin, des mal. du syst. nerv. 1898, t. Ill, p. '508. 
 
 "°Le schema qui est un moyen indispensable d'enseigrie- 
 ment ne me parait pas si dangersux tant qu'il reste ce qu'il 
 'devrait ttfujours '-etre:^un resume et urie expression' syn- 
 thetjque, toujour> revisabjes, des'f aits observes. ^ ■: 
 ,.-. lw Voir aussi- les idees de Dejerine dans la these (Paris 
 i.899) de Zbng sur les voies centrales de la sensibilite 
 generate. 
 
60 The Diagnosis of 
 
 the specialization of functions in the nervous system 
 is always increasing in proportion as you go up the 
 animal scale. If this principle, which I believe indis- 
 putable, is admitted, it must be recognized that the 
 anatomo-clinical method is the only one which can 
 decide whether one should or should not apply the 
 conclusions of experimental physiology to man. 
 
 That is to say that the clinical facts if they are 
 pretty numerous and well observed, have their value 
 by the side of and in the face of physiological facts. 
 
 To 24 observations collected by Brown-Sequard 
 in his memoir of 1863 a great many new facts have 
 been added, many of which are recent and with 
 autopsy and all establish the reality of Brown-Se- 
 quard's syndrome ; that is to say prove that in a uni- 
 lateral lesion of the cord there is a direct motor 
 paralysis and crossed anaesthesia. 
 
 Then in conclusion, it seems to me irrefutable 
 that things take place from this point of view dif- 
 ferently in man and animals. 
 
 If Brown- Sequard's syndrome is admitted as a 
 clinical law (and this appears certain) the intra- 
 medullary crossing of the sensory fibres in man 
 must be admitted. We come back then to Brown- 
 Sequard's first theory which alone explains or at 
 least expresses the clinical fact. 
 
 Anaesthesia is direct in a limited region where 
 the sensory fibres are injured at their entrance into 
 the co.rd before their intra-crossing; it is, on the 
 contrary, crossed in the more extended region where 
 the sensory fibres are injured in their intra-crossing. 
 Hyperaesthesia develops by irritation of the neigh- 
 boring parts in limited regions where the sensory 
 fibres pass into the cord on the side of the lesion. 
 
 By combining this with what has already been 
 said in the pathological physiology of the dissocia- 
 
Diseases of the Cord. 6l 
 
 tion called syringo-myelic, it can be understood how 
 crossed dissociation occurs in certain Brown-Se- 
 quard cases. 
 
 D. The differential diagnosis is short. The 
 Brown-Sequard syndrome complete or incomplete is- 
 in a word characteristic and corresponds always to 
 the medullary site of the lesion. 
 
 A single case should be distinguished, that of a 
 double lesion. The syndrome is pathognomonic of 
 a medullary origin only when the direct paralysis 
 and crossed anaesthesia can be explained by a single 
 lesion. . • 
 
 If there is a double lesion (extra-medullary, 
 root, or neuritic) the distribution of the affection 
 will generally follow the nerve territories instead ot 
 being segmental; further the two lesions will gen- 
 erally have appeared at different times and each 
 one will have its peculiar independent symptoma- 
 tology. 
 
II. DIAGNOSIS OF THE HEIGHT OF THE 
 LOCATION OF MEDILLARY LESIONS. 
 
 1. General Principles as to Diagnosis of the 
 Height of Lesions. 
 
 In the preceding chapter, studying the semeiology 
 of the various systems of the cord we have en- 
 deavored to make the diagnosis of the breadth of 
 the location of the medullary lesion. 
 
 It remains now to indicate the elements of a 
 diagnosis as to the height of the lesion. 
 
 . Being given a lesion of the cord, the following 
 elements useful in making this diagnosis may be 
 derived : 
 
 i st. The external signs of the initial lesion : frac- 
 ture, luxation, deviation, gibbosity. To give to these 
 signs (when one finds them) their full semeiologicai 
 value as to the medullary location, it is necessary to 
 call attention to the correspondence between the 
 spinous processes (the part most accessible to clin- 
 ical exploration) and the vertebral bodies and in 
 consequence to the roots of the various spinal 
 nerves. 
 
 Here are the indications given by Chipault 112 on 
 the relation of the spinal processes to the origin of 
 the spinal roots : "In the adult, in the cervical re- 
 gion add one to the number of a determined process 
 to give the number of the root which rises at this 
 
 u2 Chipault. Sur les rapp. des apoph. epin. avec la 
 moelle, les rac. medull. et les men. Th. de Paris 1894 — Cit. 
 Raymond. Clin, des mal. du syst. nerv. 1896, t. I, p. 275 
 62 
 
Diseases of the Cord* 63 
 
 level ; in the upper dorsal region, add two; from the 
 6th to the nth dorsal process add three; in the 
 lower part from the nth and the subjacent inter- 
 spinous space they correspond to the last three pairs . 
 of lumbar nerves, the 12th dorsal process and the . 
 subjacent space correspond to the sacral pairs.." 11 * 
 
 2. -The motor paralysis and anaesthesia fur- 
 nish valuable information by their distribution and 
 especially. by their upper limit. 
 
 When the lesion affects an entire section of the / 
 cord the. paralysis and anaesthesia involve the part 
 below the lesion particularly, but if the lesion is par- 
 tial only the region whose innervation depends on 
 the zone destroyed is affected. 
 
 3rd. A more disputable and today still more dis- 
 cussed question is that of the semeiological value of 
 the state of the reflexes. 
 
 At first sight the matter appeared very, simple 
 to the clinicians who applied the classic formula of 
 the physiologists : the reflex power of the cord is 
 increased in the parts separated from the higher 
 centers by a section of the cord ; the brain normally 
 exercises an inhibitory action over the reflex power 
 of the cord ; when a section or a lesion hinders the 
 passage of this inhibitory action, the reflexes are ex- 
 aggerated below the section or the lesion. On the 
 other hand, when the lesion involves a zone of the 
 cord the reflexes which have their center exactly in 
 this zone will naturally be. lost. 
 
 From. this arises this clinical rule, which was of 
 
 U3 On trouvera a la, page 657 du Traite d'anat. hum. de. 
 Testut. 3 e edit. 1897; V. II, uri tableau coiilplet des' "origihes 
 spinales des nerfs rachidiens rapportees aux apophyses epin- 
 euses." 
 
64 The Diagnosis of 
 
 great assistance in the diagnosis of the height of the 
 medullary lesion : when a lesion affects a section of 
 the cord the reflexes whose centers are below the 
 lesion are exaggerated, and the reflexes whose cen- 
 ters are at the level of the lesion are lost. This is 
 the classic law -applied in transverse myelitis and in 
 compression of the cord. 
 
 But there are facts which seem to weaken this 
 law. In 1890 Bastian 114 published four cases in 
 which the cervical or dorsal cord was entirely de- 
 stroyed and where the reflexes were abolished, the 
 bladder and rectum alone remaining intact.' From 
 this the attention was directed to the flaccid para- 
 plegia of certain cases of transverse myelitis and of 
 certain compressions of the cord and other cases 
 have been published, first by Bowlby, Rooth, 
 Babinski 115 and ourselves. 116 Vulpian 117 had 
 mentioned the disappearance of the reflexes in cer- 
 tain cases of transverse myelitis where the lesion 
 was deep, and Kadner (1876), Weiss (1878), Kah- 
 ler and Pick (1880), Schwartz (1882), Thorburn 118 
 (1887-1888) have published analogous cases. 
 
 More recently the observations of Jackson 
 (1892), Bruns (1893), Gehrardt (1894), Hitzig 
 (1894), Egger (1895), Hoche (1896), Habel 
 (1896), and the important memoirs of van Ge- 
 
 1u Bastian. Brit. med. Journ.. 1890, p. 480. Anal, in 
 Rev. des sc. med., t. XXXVI, p. 520 — Premiers trav. du 
 meme sur ce sujet en 1882 et 1886. 
 
 115 Babinski. Parapl. flasque par compress, de la moelle. 
 Arch, de mid. experim. 1891, p. 228. 
 
 1I6 Mal de Pott et parapl. flasque anesthes. (leg. de 1893) 
 in Leg. de elm. mid. 1896, 2« serie, p. 372. 
 
 I17 Cit. Brissaud. 
 
 " 8 Cit. Van Gehuchten. 
 
Diseases of the Cord. 65 
 
 huchten, 111 * Marinesco 120 and Brissaud 121 have ap- 
 peared. 
 
 From all these documents it must be concluded 
 that the ancient classic law of the reflexes is no 
 longer true, and that in a certain number of cases 
 there is an abolition of reflexes whose medullary 
 centers are below the level of the lesion. It is less • 
 easy when the theory of these facts is attempted. 
 
 Bastian has taken the opposite- of the classic the- 
 ory : in the normal state the action of the higher 
 centers is necessary to the medullary reflex; when 
 this dynamogenic action is suppressed by a section 
 or complete lesion all the reflexes below are abol- 
 ished; the reflexes are preserved or exaggerated 
 only if the transverse destruction of the cord is par- 
 tial. This theory explains .very well the new facts of 
 flaccid paraplegia, but fails by taking no account of 
 spastic paraplegia; though these cases (as in the 
 observations of physiologists in animals) exist and 
 perhaps are in the majority. To meet Marinesco's 
 opinion Brissaud has shown that there are cases of 
 transverse and complete lesion, verified by autopsy, 
 with, preservation or exaggeration of reflexes. Such 
 cases are those of Gehrardt, Senator and those 
 which Brissaud communicated to the Congress at 
 Angers. . Then, the theory of Bastian is also as im- 
 
 11!, Van* Gehuchten. Le mecan. des raouv. refl. Un cas 
 de compress, de la moelle dors, avec abolit. des refl. Journ 
 de neurol. 1897, p. 262, 282, 302 et 322; et Etat des refl. et 
 anat. pathol. de la moelle lombo-sacree dans les cas de parapl. 
 Basque dus a une les. de la moelle cervico-dors. Ibid. 5 
 juin. 1898. 
 
 ""MarinesCo. Sur les parapl. flasques par compression 
 de la moelle. Sem. med. 1898, p. 150. 
 
 121 Brissaud. La parapl. flaccide par compress. Revue 
 neurol. 1898, p. 350; et Congres d' Angers, aout 1898; (Ibid 
 P. S89). 
 
66 The Diagnosis of 
 
 possible to sustain as the old classic theory : both are 
 too exclusive and neither explains all the facts. 
 
 Van Gehuchten's theory is derived from Bastian's 
 only the Louvain professor adds the notion of a 
 double cortico-spinal path maintaining the medul- 
 lary tonus by the action of higher centers : a direct 
 inhibitory path, an indirect (by the medulla) excit- 
 ing : a lesion of the pyramidal fibres exaggerates the 
 reflexes ; a complete lesion of the cord suppresses all 
 the reflexes. This theory is liable to the same ob- 
 jections as Bastian's. 
 
 A definite theory does not appear to have been 
 found. However, Brissaud showed in a great many 
 observations of cases of flaccid paraplegia an altera- 
 tion of the nerves or of the medullary cells below 
 the lesion, that is at the level of the paralysis. 
 
 If this view were accepted, the old classic theory 
 might persist. 
 
 When the lesion is cervico-dorsal the reflexes of 
 the lumbar region will be exaggerated so long as 
 there is no secondary lesion of the nerves or lumbar 
 cells. When this secondary lesion exists the re- 
 flexes having their centers in this region will natu- 
 rally be abolished. 
 
 This is what I expressed theoretically in 1893 
 when I said, 122 "The gibbosity occupying the cer- 
 vical or dorsal region, the paraplegia will be dorso- 
 lumbar in its aspect;" and by its secondary lesion, 
 adds Brissaud. 
 
 _ Pierret 123 accepted this view and declared "That 
 the lack of secondary contracture could be attributed 
 to a peripheral neuritis." 
 
 ™\jt<i. citee sur le mal de Pott et la parapl. flasque anesth. 
 p. 394- 
 
 ""Pierret. Congres d'Angers, aout 1898, p. 583. Revue 
 neurol. 1898, p. 583. 
 
Diseases of the Cord. 67 
 
 Whatever these disputable theories may be let us 
 remember that the reflexes are not -always exag- 
 gerated nor preserved below the lesion. Then, when 
 they are exaggerated, this can be used in the diagno- 
 sis of the height of the medullary lesion ; but when 
 they' are lost they cannot always be utilized in this 
 direction. 
 
 4. These things said, we will study successively 
 the semeiology of the conus medullaris, sacral, lum- 
 bar, dorsal, brachial and cervical cords. 
 
 The syndromes may be divided into two groups : 
 the syndromes of the root distribution and syn- 
 dromes of the metameric or segmental distribu- 
 tion. 124 
 
 It is known that for the same part of the cord the 
 distribution of symptoms is not identical and the 
 twd orders of symptoms are not superimposed. The 
 root distribution is observed when the medullary le- 
 sion involves the zones. of entrance of the roots, and 
 the segmental when the lesion affects the centers 
 themselves of the cord. Moreover, physiological 
 segmentalization can be naturally observed only in 
 the lumbar cord and above. From this it results 
 that we will have only a single syndrome (radiculo- 
 segmental) for the conus and sacral cord while for 
 the portipns above we will separately describe the 
 root and segmental syndrome. 
 
 1M "Segmentaire" veut dire ici symptome se distribuant 
 "par segment de membre." 
 
68 The Diagnosis of 
 
 2. The Root-Segmental Syndrome of; the 
 (.'omis Medullaris. 125 
 
 The anatomists 126 limit the terminal conus to the s 
 level between the last sacral and the first coccygeal 
 pair. 
 
 The clinicians include the last two (Raymond) 
 or three (Muller) sacral pairs. 
 
 In favor of this last limitation Muller has given 
 arguments derived from the histological structure: 
 the anterior roots there become scarce and the pyra- 
 midal tracts disappear. 
 
 Let us then adopt this definition of the conus: 
 the most inferior portion of the cord 127 from which 
 arise the last three sacral pairs (3rd, 4th and 5th) 
 and the coccygeal nerves. 
 
 To philosophically retain the distribution of the 
 nerves of the conus it is necessary to place man on 
 four feet; then the sensory region of these nerves is 
 the most posterior surface of the body ( sacrum, coc- 
 cyx, anus and perinaeum), as to the motor distri- 
 
 1ZB Voir nos leg. sur les paral. nucleaires des nerfs sacres in 
 Leg. de clin. mid. 1898, 3 e serie, p. 249; Dufour. Contrib. 
 a l'etude des nerfs de la queue de cheval et du cone terminal. 
 Th. d Paris 1896; Raymond. Sur les les. de la queue de 
 cheval ( 14 et 21 dec. 1894) et hematomyelie du cone terminal 
 (24 mai 1895) in Leg. sur- les mal du syst. nerv. 1896. t. I, 
 p. 252 a 314 ; Muller. Untersuch. iib d. Anat. u Pathol, d. 
 untersten Riickenmarksabsch. (Clin. med. du prof. Strum- 
 pell a Erlangen) D. Zeitschr. f. Nervenh., t. XIV, p. 1, (22 
 dec. 1898). Bonne bibliogr. p. 88 et Schmeas interessants, 
 pi. I et Ii. 
 
 ^Charpy in Traite d'anat. hum. de Poirier. 
 
 I2 'On pourrait rattacher au cone medullaire le filum ter- 
 minal. Mais si, pour l'anatomiste, ce filum represente une 
 moelle coccygienne ou caudale, plus ou moins rudimentaire, 
 on peut dire qu'il n'existe pas pour le^clinicien; a ce niveau 
 il n'y a plus pour lui que la, queue de cheval. 
 
Diseases of the Cord. 
 
 69 
 
 bution, it is to the muscles also of the analogous re- 
 gions. 
 
 This settled or accepted, the following (accord- 
 ing to Miiller) are the motor functions and the sen- 
 sory region of this segment of the cord which is 
 situated at the level qf the second lumbar vertebra : 
 
 Conus Medullaris. 
 
 as 
 
 > ». 8, 
 
 w 
 
 at ta n 
 
 ■5.3 3 
 g-» - 
 
 S' » 
 
 * 
 
 3 s> 
 
 
 .2. 
 
 » ft 
 g » 2, 
 
 SB 
 
 IS' 
 o*o 
 c E. 
 
 S3" 
 
 su CI 
 < 
 
 
 13 
 
 en 
 
 c o 
 
 " •a 
 
 s 
 3 
 
 w 
 
 a 
 
 'B. 
 
 S 5' 
 1-1 2 o 
 
 3- -a 
 
 a 
 a. 
 
 
70 The Diagnosis of 
 
 From this table the syndrome of the conus can 
 be deduced : 128 It is essentially made up of troubles 
 of micturition and of defecation (obstinate constipa- 
 tion or relaxation on the part of the bowels; reten- 
 tion or incontinence of urine), absence of erection 
 and anaesthesia of the penis, »rethra, scrotum, peri- 
 naeum, anus, coccyx and of the sacrum. This 
 picture is more or less complete according to the 
 case. 
 
 The morbid causes which can determine this 
 syndrome are : Traumatism (a blow in this location, 
 a shot producing a fracture, a hemorrhage) , tumors 
 (Raymond names lipomas, myomas, sarcomas, gli- 
 omas, cavernous lymphangiomas, medullary can- 
 cers), syphilis, tuberculosis, meningeal hemorr- 
 hages, etc. (Duwour). 
 
 As to the differential diagnosis that must be 
 made from lesions of the cauda equina. This will be 
 best considered after the study of the syndrome of 
 the sacral cord. 
 
 3. The Boot- Segmental Syndrome of the 
 Sacral Cord. 11 * 
 
 The sacral cord as to location has nothing to do 
 with the sacrum. It corresponds to the first lumbar 
 vertebra and gives rise to the first sacral and the 
 last lumbar pairs. Following is its motor and sen- 
 sory distribution according to Muller : 130 
 
 •"Raymond cite les faits de Lachmann (1882), Kirchoff 
 (1884), et Oppenheim (1889), Lubovitch (1894, Revue neu- 
 rol, 189s, p. 20) et Peterson (1895, Revue neural, 1895, p. 
 412) ont conteste qu'une lesion limitee au seul cone ait pu 
 determiner la paralysie complete de la vessie et du rectum. 
 
 m Voir les travaux deja cites pour le syndrome du cone 
 medullaire. 
 
 m0 Sano (Journ. de neurol. 1897, p. 277) place le centre 
 des muscles du pied et des muscles de la jambe dans une 
 
Diseases of the Cord. 
 Sacral Cord. 
 
 7i 
 
 to 
 
 
 "8 
 
 P 
 
 re so 
 
 S.!tt- g =| 
 
 re re 5* m " to 
 
 2 ™ 5'°. -2. 
 
 2 .- KTw ST 
 S _j, c ; w "> 
 
 3 "i »-t o 
 358=. 
 
 "J^. re re ST 
 
 8? H 
 S S. 
 
 """go » 
 
 r* r* .— X V 
 
 crtr-S" — 
 re n> ^ ^ 
 
 "1 S rt r+ 
 
 n> 2 re S, 
 
 5-g-s: 
 
 2" o *^* 
 
 Bs-a 
 » s 
 
 01 Q- 
 
 re 
 TO 
 
 .01 
 
 3 
 
 T)50 
 ^ o 
 
 s&g.a 
 
 S.n s O. 
 
 3 3"?! 
 
 a re _ 
 • En ^ 
 
 ►d 
 o 
 
 PS" 
 
 on? 
 
 » 
 
 J>M O » fi 
 
 g irs i 
 
 re ^ U." - o. 
 
 13 P 03 rt- — 
 
 to 3 re re 
 
 ' Os — 3 us 
 cSSB 
 
 
 73 
 
 o **> 
 
 3r 
 re . 
 
 B" 
 
 colonne de la 4 e saeree aje S e lombaire; le centre des fes- 
 siers, de la 2<* saeree a la S e lombaire ; celui du quadriceps 
 femoral, de la 4 e a la 2& lombaire ; celui des muscles abdom- 
 inaux, de la i re lombaire et au-dessus...Ces resultats ont ete 
 discutes a la Soc. beige de neurol. — Yan Gehuchten et de 
 Buck {Revue neurol. 1898, p. 510) cbncluent de leurs re- 
 cherches: "l*> les noyaux d'innervation des muscles de la 
 jambe et du pied occupent la partie posterieure des comes 
 anterieures de la moelle et s'etendent depuis la partie super- 
 
7 2 The Diagnosis of 
 
 To synthetize this table, placing man, as for the 
 conus on four feet and putting the lower limb in its 
 primitive position (turned outward at an angle of 
 90 degrees from the positive position) the internal 
 surface and the large toe forward, we find the sacral 
 cord presides over the sensibility of the posterior 
 and external surfaces of the lower limbs corre- 
 sponding to a long posterior surface of this lower 
 limb (including the sole of the feet) ; the muscles 
 (rotation outward, flexor of leg and extension of 
 foot) are also those of the posterior surface. 
 
 Following are the various partial paralyses, the 
 superposition of which constitutes the total motor 
 syndrome of the sacral cord: pes valgus, (long pe- 
 roneus), pes varus (short peroneus), impossibility 
 of flexing the foot on adduction (anterior tibial 
 group), impossibility of flexing the foot on abduc- 
 tion (long extensor of the toes), foot drop, steppage 
 (whole of the external popliteus), equilibrium in 
 walking 131 but not static coordination ; impossibility 
 of extending the foot, of flexing and turning the 
 toes laterally (internal popliteus), impossibility of 
 flexing the leg on the*thigh (semi-tendinous, semi- 
 membranous, biceps) ; abduction of the thigh im- 
 
 ieure du 5 e segment lombaire j usque vers l'extremite inferi- 
 eure du 4 e segment sacre; 2° il existe deux grands noyaux 
 denervation de ce segment du membre inferieur; tin pre- 
 mier noyau tres grand, comportant probablement plusieurs 
 subdivisions, s'etend de l'extremite superieure du s« segment 
 lombaire jusqu'a la partie inferieure du 3* segment sacrd; 
 und second noyau, egalement assez volumineux, surtout vers 
 son milieu, mais semblant unique, commence, en arriere du 
 premier, a partir du 2 e segment sacre et s'etend jusque vers 
 l'extremite inferieure du 4 e segment sacre." 
 
 ""Voir mes le?. sur un cas de pseudo-tabes post-infectieux 
 (par. symetr. posterysipel. du tibial anter.), in Le?. de Gin. 
 med. 1896; 2« serie, p. 245. 
 
Diseases of the Cord. 73 
 
 possible, rotation difficult, difficulty in climbing 
 .stairs (glutei). 
 
 For the sensibility the anaesthesia includes: in 
 front, the upper part of the foot and the external 
 part of the leg ; behind, all, except the internal part 
 •of the leg and the lower half of the thigh 
 
 To make the sensory syndrome of the sacral cord 
 ■complete it is necessary to add to this distribution 
 the anaesthesia of the conus medullaris, the topo- 
 graphy of which we described above. 
 
 The pains, when they exist, will be in the domain 
 of the sciatic. 
 
 But, to appreciate the semeiological value of a 
 pain from the point of its location it must be re- 
 called that it is there a phenomenon of excitation and 
 not of destruction, and that in consequence the seat 
 of a pain often indicates a point near the diseased 
 region rather than the altered part itself. 
 
 To complete the syndrome it is necessary to 
 know the reflexes which have their centers below or 
 .at the level of the sacral'cord. 
 
 We already know that in the conus are the ano- 
 vesical and genital reflexes. In lesions of the sacral 
 •cord these reflexes will often be exaggerated (re- 
 tention and priapism) at other times' diminished or 
 abolished (incontinence, impotence). 
 
 In the sacral cord are the plantar and tendon 
 Achilles reflexes. 
 
 The plantar reflex is a cutaneous reflex which 
 we studied above apropos to its qualitative altera- 
 tion described by Babinski. In the normal state it 
 responds, according to Babinski, 132 by a general 
 flexion of the thigh on the pelvis, Of the leg on the 
 -thigh, and of the toes on the metatarsals. Bris- 
 
 182 Babinski. £oc. de biol. 22 fevr. 1896, Cit. Ganault. 
 
74 The Diagnosis of 
 
 saud 133 studied the slightest manifestations of this 
 reflex and demonstrated them in the isolated con- 
 traction of the adductors (adduction of the point of 
 the foot) and especially in the isolated contraction of 
 the tensor of the fascia lata. 
 
 Ganault 13 * confirmed Brissaud's conclusions and 
 added for other cases the contraction of some special 
 foot muscles. 
 
 The center of this plantar reflex is in the sacral 
 cord : center of the 2nd and 3rd sacral roots when it 
 acts only by movements limited to the toes, 5th lum- 
 bar segment when there is contraction of the tensor 
 of the fascia lata, the whole of the sacral cord when 
 plantar excitation causes all the reflex flexion of the 
 lower limb. 
 
 This is the first reflex which will be abolished in 
 destructive lesions of the sacral cord. 
 
 The reflex of the tendon Achilles has its center 
 in the first sacral segment (Gowers). 135 It also will 
 be abolished in destructive lesions of the sacral cord. 
 
 With the whole of these considerations of the 
 nervous troubles, the anaesthesia and the state of the 
 reflexes we have an entire syndrome of the sacral 
 cord. 
 
 The differential diagnosis of this syndrome of 
 the sacral cord is to distinguish it from that of the 
 cauda equina. It is at times difficult, at least when 
 it affects the lower portion of the cauda equina 
 which corresponds to the sacrum ; for in its upper 
 part it includes the lumbar and sacral roots together, 
 and the diagnosis must be made rather from the 
 
 133 BrisSaud. Le refl. du fascia lata. Gaz. hebdom. 1896, 
 P- 253- 
 
 "'Ganault. Contr. a l'etude de quelques refl. dans 
 l'hemipl. de cause organ. 1898, p. 86. 
 
 ""Gowers. Cit. Sternberg. * 
 
Diseases of the Cord. 75 
 
 syndrome of the lumbar cord. But in its lower part 
 the cauda equina includes only the sacral roots, 
 wherefore its alteration will give the same symptom- 
 atology as the alteration of the centers of these 
 roots. For the sacral nerves it is a question (which 
 occurs for all nerves) of differential diagnosis be- 
 tween nuclear and root paralyses (or neuritic) ; for 
 the root lesions are intra-spinal neuritic lesions. 
 
 Nothing proves better the difficulty of this diag- 
 nosis than the case in which Erb 186 claimed a lesion 
 of the cauda equina, and at autopsy seven years later 
 Schultze 137 established a lesion of the cord. Bech- 
 terew 138 also thinks "That it is impossible to know 
 whether a lesion involves the cord or the roots to 
 which the medullary segment gives rise." 
 
 I however believe this diagnosis possible, at least 
 in certain cases. 189 
 
 Nothing can be deduced from the anaesthesias, 
 paralyses or amyotrophies. They are the same for 
 the nerves whatever may be the height of the lesion. 
 The reaction of degeneration, the symmetry of the 
 affection, the cause, the onset and evolution of the 
 disease can do nothing to make the diagnosis clearer. 
 
 On the contrary, I believe the consideration of 
 the following four orders of symptoms are useful: 
 
 1. The objective and often external signs which 
 indicate the location and height of the lesion : spon- 
 
 1m Erb.. Ueb. Spinallahm (poliomyel. anter. acuta) bei 
 Erwachs. u» tib. verw. spin. Erkrank. Arch. f. Psych. 187.5, 
 t. V, p. 758!. Ofis; VI. 
 
 '"Schultze. Z. different. Diagn. d. Verletz. d. Cauda eq. 
 und d. Lendenanschw. D. Zeitschr. f. Nervenh. 1894, t. V, 
 P- 147. 
 
 188 Bechterew. Cit. Dufour, loc. tit., p. 62. 
 
 130 Voir mes leg. citees sur les paral. nucleaires des nerfs 
 sacres, p. 269. 
 
76 The Diagnosis of 
 
 taneous or provoked pains, 110 gibbosity, displace- 
 ment. These signs, often very useful, are not of ab- 
 solute value. An intra-spinal post-traumatic hemor- 
 rhage may not show and especially remain at the 
 very place of the traumatism. Dufour has indeed re- 
 marked that the dura mater in the cauda equina pro- 
 tects the lumbar roots more than the sacral roots. 141 
 
 2. The dissociation of certain reflexes when it 
 exists: I speak of the abolition of certain reflexes 
 and the exaggeration of others below. 142 
 
 3. The syndrome of Brown-Sequard when it 
 exists (which is very frequent) anaesthesia more 
 marked on one side, paralysis more marked on the 
 other, proving a medullary origin. 
 
 4. The dissociation called syringo-myelic, when 
 found, is a good sign of medullary origin despite 
 -the cases which we have cited above and in which 
 the said dissociation would have been produced by 
 a neuritis. 
 
 4. The Boot Syndrome of the Lumbar Cord. 
 
 The lumbar cord which corresponds to the first 
 four lumbar roots is at the level of the bodies of the 
 10th, nth and 12th dorsal vertebrae. Following, 
 still according to Muller, are its sensory and motor 
 regions : 
 
 1M Les douleurs sont plus frequentes dans les lesions de la 
 queue de cheval que dans lesions de la moelle sacree. 
 
 " l Le sac dur,al se termine au niveau de la 2£ vertebre 
 sacree et a partir de ce point les racines sacrees (portion 
 inferieure de la queue de cheval) sont plus exposees, nofam- 
 ment aux hemorragies extra-durales, qui ne pouvant pas 
 filtrer a travers le duremere se collecteraient plus bas dans 
 le canal sacre. 
 
 lu Nous retrouverons mieux ce signe a propos de la moelle 
 lombaire. 
 
Diseases of the Cotd. 
 
 77 
 
 Lumbar Cord. 
 
 li 
 
 S * 
 
 re 2 w 
 
 b g =r 
 
 H.re"i3 
 go co. 
 
 c c ST" 
 fi 2 
 
 0) 
 
 ft. 
 
 2 ft 
 
 w 
 p 
 
 C 2. 
 n c 
 
 P re 
 n 
 
 S" 
 
 CD 
 C 
 
 w 
 
 ~6> 
 
 ft- 
 
 8 § 
 e ft 
 
 U™ 
 
 
 r 
 
 o 
 
 Si 
 
 ft) 
 
 25 > 
 
 P S 
 
 p 1 Kg 
 
 p 
 
 BT3 
 
 O o-t 
 
 1 ^p 
 0.„ B 
 
 *• ft 
 
 £. — b' 
 
 S^ 2. 
 
 *^ re ^- 
 op"-. _. 
 ■ " g. p 
 
 5'^ s 
 
 <» g 
 
 "I p 
 
 s 
 
 a. 
 
 o re 
 
 J* " 
 
 re "■ P- 
 
 £? p w 
 -. ^ — . 
 
 !" "■ re 
 
 ° 3 
 
 "■ 2. 
 
 B*cr. 
 
 re r> 
 
 - El 
 "2 'Si 
 
 > 
 
 B 
 
 B 
 
 p - O T3 
 
 g 
 O 
 B 
 
 en 
 
 iw* 
 
 5" 
 
 o 
 
 re 
 
 -j 
 
 T> 
 P 
 
 P 
 
 C 
 
 a. 
 o 
 
 On placing man, as for the sacral cord, on four 
 feet and the lower limbs in the primitive position, 
 we see that the lumbar cord presides over the sensi- 
 bility of the internal and anterior surfaces, that is to 
 say of the anterior segment of the lower limb and 
 
78 The Diagnosis of 
 
 over the mobility of the same regions (adductors, 
 rotators within, extensors of the leg). 
 
 To sum up the distribution of these three seg- 
 ments of the cord, we see that man being in the po- 
 sition given above, the three segments of the cord 
 which are the one in front of the other (the conus 
 behind, the sacral cord in the middle, the lumbar 
 cord in front) respectively innervate three segments 
 placed also one before the other: the conus inner- 
 vates the caudal segments (or its location), the sacral 
 cord innervates the postero-external part of the 
 lower extremity, and the lumbar cord innervates the 
 antero-internal part of the lower extremity. 
 
 These synthetic views should aid in fixing in the 
 memory this sensori-motor distribution of the three 
 first (lower) segments of the cord. 
 
 In every case from the above table it should be 
 easy to deduce the syndrome produced by an entire 
 section of the lumbar cord. 
 
 In a word, there is complete paraplegia with an- 
 aesthesia up to the lower part of the abdomen, 
 sphincter troubles and often bedsores on the sacrum, 
 amyotrophy when present is limited to the muscles 
 which the table gives as directly innervated by the 
 lumbar cord. The muscles depending upon the 
 sacral cord are paralyzed because their communi- 
 cation with the brain is interrupted, but they escape 
 atrophy because their medullary center is not 
 changed. When there is pain it is generally at the 
 limits of the lesion; above under the form of ileo- 
 lumbar neuralgia, below under the form of crural or 
 sacral neuralgias. 
 
 As to the reflexes we must always distinguish 
 between those whose center is below the lesion and 
 those whose center is at the level of the lesion. 
 
 In the first group we have the sphincter reflexes, 
 
Diseases of the Cord. 79 
 
 the tonus of the muscles innervated by the sacral 
 cord, the plantar reflex and the tendon Achilles re- 
 flex. When (which is most frequent) the reflexes 
 are exaggerated there is a spastic paraplegia (at 
 least in the sacral region), that is to say the contrac- 
 tures produce pes .equinus; there is clonus and re- 
 tention of urine and faeces. 
 
 Of the reflexes having their center in the lum- 
 bar cord itself the patellar tendon is the principal 
 one. The roots of the lumbar plexus make up the 
 arc. 143 The roots, the integrity of which seems 
 necessary for the maintenance of the patellar reflex, 
 are in the rabbit (Tschiriev) the 6th lumbar, in the 
 dog (Westphal) 5th, 6th, 7th lumbar, in man (Gow- 
 ers) 2nd, 3rd and 4th lumbar. So that the center 
 of this reflex is in the lumbar cord. Then, the abo- 
 lition of the patellar tendon should make a part of 
 the syndrome of the lumbar cord. 
 
 As, in another place, we have seen that with a 
 lesion in this location the reflex of the tendon Achil- 
 les may be exaggerated, we would have this strange 
 dissociation an example of which we have pub- 
 lished, 14 * on one part abolition of the patellar tendon 
 reflex, 145 and on the other in the same limb clonus. 
 
 Another reflex (a skin reflex) also has its. center 
 
 "'Voir Sternberg. D. Sehnenrefl. u. ihre Bedeut f. d. 
 Pathol, d. Nervensyst. 1893, p. 34. 
 
 1M Lec. de clin. med. 1898, 3 e serie, p. 252. 
 
 "°On pourrait parler ici du reflexe contralateral des ad- 
 ducteurs de P. Marie. Ce reflexe (voir la Th. citee de 
 Ganault, p. 56) es provoque par la percussion du tendon 
 rotulien et peut persister alors que le reflexe rotulien ordin- 
 aire est abol'i, mais la condition pathogenique intra-medul- 
 laire de ce phenomene n'est pas encore assez nettment 
 etablie pour que nous nous y etendions ici. II en est de 
 meme du reflexe rotulien paradoxal, c'est-a-dire des sujets 
 chez lesquels la percussion du tendon rotulien fait flechir la 
 jambe au lieu de la soulever. 
 
So The Diagnosis of 
 
 in the lumbar cord, the cremasteric. 146 The quick 
 elevation of the testicle is produced by friction or 
 brusque pressure on the skin of the supero-mternal 
 part of the thigh or better at the level of. the ring of 
 the third adductor. In the female there would be 
 an analogous reflex from the groin, a contraction of 
 the most inferior fibres of the abdominal wall. The 
 center of this reflex is in the lumbar cord (ist and 
 2nd segments). 
 
 Then the patellar and cremasteric reflexes will be 
 abolished in lesions of the lumbar cord and this 
 abolition is contrasted with the maintenance or even 
 exaggeration of the tendon Achilles and plantar 
 reflexes. " 
 
 The differential diagnosis is easier than for the 
 sacral cord for lesions of the cauda equina cannot 
 produce complete paraplegia with sphincter troubles. 
 The question will arise only when the syndrome of 
 the lumbar cord is reduced and incomplete. 
 
 On the same principle given above for the 
 sacral cord we may base the following: the object- 
 ive and external signs will indicate the height of 
 the lesion in the spinal column, the dissociatidn of 
 the reflexes (very important), the Brown-Sequard 
 syndrome (if it were only indicated) and the so- 
 called syringo-myelic dissociation of sensibilities. 
 
 5. The Segmental Syndrome of the Lumbo- 
 sacral Cord. 
 
 All we have said in paragraphs 2, 3 and 4. is 
 based on the distribution of the spinal roots. It is 
 therefore the root semeiology. These are the root 
 syndromes of the lumbosacral cord. By the side of 
 
 ""Voir Ganault. Th. citee, p. 3. 
 
Diseases of the Cord. 81 
 
 these it is necessary to look at also the segmental 
 syndromes of the lumbosacral cord. 
 
 The characteristic symptom is that it is seg- 
 mental: there is often here a complete or dissociated 
 anaesthesia; it does not correspond then either to a 
 nerve or root distribution, but to a segment of a 
 limb; its upper limit is a circular line perpendicular 
 to the axis of the limb.. 
 
 When this segmental anaesthesia is limited to the 
 foot, it may be confounded with a nerve or root an- 
 aesthesia (sacral plexus) ; when it extends over all 
 the lower extremity it may be confounded with an 
 anaesthesia from all the lumbo-sacral plexus. But 
 when it involves, for example, all the lower part of 
 the limbs and is limited above by a circular line at 
 the lower third of the thigh, neither the nerve nor 
 root distribution can be invoked, the segmental dis- 
 tribution must be admitted. 
 
 Debove and Pafmentier 147 have observed some 
 cases of syringo-myelia in which thefmo-analgesia 
 or thermo-anaesthesia were thus disposed as stock- 
 ings. . ' ! 
 
 Chipault 148 has described anaesthesia from 
 Pott's disease in the shape of boots, in that of long 
 stockings (up to the middle of the thigh) in that of 
 drawers (up to the umbilicus), and a hyperaesthesia 
 up to the middle of the thigh in a medullary disturb- 
 ance. 
 
 . Thus, although the segmentalization may be less 
 distinct and less frequent in the lower limbs than in 
 
 "'Debove, in Leg: du mardi de Charcot, t. II, p. 506.. — 
 Parmentier. Nouv. Iconogr. de la Salpetr. 1890, p. 219. 
 Cit. de BrisSaud, in Le?. citee's sur les mal, nerv., p. 220. 
 
 ""Chipault. La topogr. de l'anesth, pottique. Revue neu- 
 ral. 1896, p. 293, et Quelques types clin. nouv. de les. radicul. 
 et medull. Presse med. 1896, p. 85. 
 
82 The Diagnosis of 
 
 the upper, the clinician must admit it. The seg- 
 mental syndromes are recognized by their segmental 
 distribution: the seat of the lesion is in these cases 
 in a section of the lumbo-sacral cord as much higher 
 as the segment of the limb attacked is itself higher. 
 
 6. The Boot Syndrome of the Dorsal Cord. 
 
 The dorsal cord, which extends from the 2nd to 
 the 9th dorsal vertebrae, corresponds to the origin 
 of the dorsal pairs of nerves from the 2nd to the 
 1 2th. 
 
 Each of these nerves innervates, from a sensory 
 point of view, a band of the trunk. The upper band 
 (2nd dorsal) extends from the upper part of the in- 
 ternal surface of the arms. From the 3rd to the 4th 
 dorsal nerves the zones are above the breast, which 
 is included in the zone of the 5th ; from this to the 
 navel is included in the zone of the ioth. 1 * 9 The 
 zone of the 12th is confined to the upper zone of the 
 lumbar cord. 150 
 
 These zones, horizontal to the upper part of the 
 trunk, become more and more oblique from above 
 downward and from behind forward in proportion 
 as you descend. 
 
 Each zone is innervated principally by the cor- 
 responding pair of nerves and accessorily by the 
 pairs immediately above and below (Sherrington). 
 It results,»that when a root is cut, the anaesthesia is 
 not complete in the corresponding region and that 
 in a given anaesthesia it is necessary to look for the 
 
 ""Un fait de Mackintosh (The Brit. med. Journ. 1898, 
 p. 478. Revue neurol. 1898, p. 203) montre que la zone sen- 
 sitive de la dixieme racine dorsale n'atteint pas l'ombilic. 
 
 ""Voir la distribution d'apres i'horburn in Marinesco, 
 Sem. med. 1896, p. 259. (.iravaux de Sherrington. Hors- 
 ley....). 
 
Diseases of the Cord. 83 
 
 lesion four inches above the line of anaesthesia 
 (Horsley). 
 
 For the motor distribution see the following 
 table according to Testut : 
 
 
 Intercostal 
 
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 en 
 
 
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 Cf, 
 
 
 
 
 
 
 
 
 
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 From the anatomo-physiological facts the syn- 
 drome of the dorsal cord may be easily deduced : 
 Paralysis and anaesthesia, in a complete lesion of the 
 
84 The Diagnosis of 
 
 cord, in the whole region, motor and sensory, lo- 
 cated below the lesion. Beside the bedsores, which 
 are as in the lumbo-sacral cord, there are other im- 
 portant trophic' disturbances : there may be a herpes 
 of the trunk, which then outlines the distribution of 
 the roots. 
 
 For the reflexes we will have loss and more often 
 exaggeration of all those having centers below the 
 dorsal cord (the patellar tendon and cremasteric are 
 included). As to the reflexes having their center in 
 the dorsal cord and which will be lost in the total 
 destruction of the latter, the clinician recognizes 
 only the abdominal. 161 
 
 The abdominal wall retracts if the skin of the 
 belly is lightly stroked (cutaneous reflex), or when 
 this wall is percussed [tendon (?) reflex]. As 
 studied by Roseribach, Bodon, Parisot, Ostankoff, 
 Dinkier, Pitres, etc., this reflex pertains to the re- 
 gion of the 9th (upper reflex), 10th, nth, and 12th 
 (middle and lower reflexes) pairs of intercostal 
 nerves. 
 
 We will make the differential diagnosis after the 
 following paragraph: 
 
 7. The Segmental Syndrome of the Dorsal 
 Cord. 
 
 The study of medullary segmentalization has 
 been made mostly from the clinical history of zonas 
 of the trunk (Brissaud). 162 
 
 Many authors 153 have already remarked clinic- 
 ally that thoracic zona is horizontal and often 
 crosses the intercostal paths instead of being super- 
 
 161 Ganault. Th. citee. 1898, p. 102. 
 
 "TJrissaud. Le zona du tronc et sa topogr. Bull, mid 
 1896, p. 27 et 87. 
 
 153 Brissaud cite: Baerensprung, Balmanno Squire " 
 Leroux, Head. 
 
Diseases of the Cord. ■ 85 
 
 imposed upon them. Some have concluded from 
 this that zona is not of nervous origin, others that 
 the thoracic nerves have one course, "sensibly hor- 
 izontal." Both opinions are impossible to support. 
 Brissaud was the first to analyze and give a theory 
 of the fact. 
 
 There are thoracic zonas of two nervous orig- 
 ins: Those of neuritic or ganglionic origin follow 
 the course of the nerves, the others of medullary 
 . origin are horizontal. At • the upper part of the 
 thorax they are over the nerves, which are also 
 horizontal. But in proportion as they descend the 
 nerves become more and more oblique from above 
 downward and from behind forward, and the zonas 
 remain horizontal, crossing the nerves at more and 
 more of an angle. 
 
 These horizontal zonas of the trunk represent 
 very well the form of the zones of the distribution 
 of the various segments of the dorsal cord. The 
 neuralgias and the bands of anaesthesia, of hypaes- 
 thesia or hyperesthesia, which present the same 
 distribution, must be added here. Thus Achard 154 
 has described a band of dissociated anaesthesia, the 
 topography of which was exactly that of an abdom- 
 inal zona. 
 
 With these various symptoms the complete seg- 
 mental syndrome of each segment of the dorsal* 
 cord is established. 
 
 8. The Root Syndrome of the Brachial Cord. 
 
 The brachial cord, which extends from the 4th 
 cervical to the 2nd dorsal vertebra, corresponds 
 to the origins of the 5th, 6th, 7th and 8th pairs of 
 cervical and of the 1st pair of dorsal nerves. 
 
 Following is the table of the sensori-motor dis- 
 
 . 154 Achard. Syringom. avec amyotr. du type Aran-Du- 
 , chenne et anesth. dissociee en bande zosteroide siir le tronc. 
 Gas. hebdqm, 1896, p. 361 et Revue neurol. -1896, p. 377. 
 
86 
 
 The Diagnosis of 
 
 tribution borrowed. from Testut, who has described 
 it according to Thane (for motility) and Thorn- 
 burn (for sensibility) : 155 
 
 Brachial Cord. 
 
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 ""Voir aussi Allen Starr. Brain 1894, p. 481, Revue 
 neuroL 1894, p. 570. v , , 
 
 1M Pour simplifier, je supprime, dans le tableau de Testut, 
 les muscles a cote desquels il y a un point d'interrogation. 
 
Diseases of the Cord. 87 
 
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88 The Diagnosis oj 
 
 The sensory root distribution of the various por- 
 tions of the brachial cord may be easily derived by 
 placing the subject on all fours, the upper extrem- 
 ity turned at an angle of 90 (in the primitive posi- 
 tion), the thumb in advance. The sensibility is then 
 seen to be distributed in three parallel bands (each 
 occupying the entire length of the extremity), the 
 posterior innervated by the 1st dorsal and 8th cer- 
 vical, the middle by the 7th, and a part of the 6th 
 cervical, the anterior by a part of the 6th and the 
 5th cervical. 
 
 Then, as for the lower extremity and the trunk, 
 the zones of root distribution sucdeed each other 
 in the same order and manner as the spinal pairs 
 themselves. 
 
 For the motor distribution, it may be recalled 
 that the lower pair (1st dorsal) correspond to the 
 median and ulnar, the upper pairs (5th, 6th and 7th 
 cervical) to the circumflex and radial. Marinesco 
 has defined the position of these nuclei of origin in 
 a recent work. 157 He shows notably that each nerve 
 has a principal nucleus and some accessory nuclei, 
 and that each nerve derives its origin from many 
 medullary segments. "Thus the ulnar and median, 
 the principal source of which is constituted by the 
 eight cervical segment, still receive fibres from the 
 7th cervical and more from the 1st dorsal." 
 
 The reflexes which have their centers in this por- 
 tion of the cord are the cutaneous and tendon re- 
 flexes of the upper extremity, the tendon reflex of 
 the biceps having the highest medullary center ( 5th 
 cervical) . 
 
 In the same region is also the cilio-spinal center, 
 
 15T Makinesco. Contr. a l'etude des localisat. des noyaux 
 moteurs, dans la moelle epin. Revue neurol. 1898. p. 463. 
 
Diseases of the Cord. 89 
 
 the presence of which is important in the semeiology 
 of this region. The exciting oculo-pupillary fibres 
 leave the cord by the 8th cervical and especially the 
 1st dorsal, and reach by the rami communicantes the 
 inferior cervical sympathetic ganglion. 
 
 The experiments of Claude Bernard and Mad- 
 ame Dejerine-Klumpke (1885) show that when 
 in an animal a section or laceration of the roots of 
 the brachial plexus is made, pupillary phenomena 
 are seen to follow whenever the rami communi- 
 cantes of the first dorsal pair are injured, and only 
 then. 
 
 There are also some confirmatory clinical facts. 
 Raymond 158 cites those of Prevost, Pfeiffer, Heub- 
 ner, Bruns, Monter, Muller, and particularly Sands 
 and Seguin (1873). In the last case there was 
 traumatic paralysis of the brachial plexus without 
 oculo-pupillary symptoms. To stop the violent pains 
 Seguin cut the lower roots of the plexus, and my- 
 osis appeared. Oppenheim was able to excite the 
 first dorsal pairs in a man whose spine he had tre- 
 phined. Excitation of the first dorsal pair alone 
 determined a considerable mydriasis, which was 
 maintained for some seconds.. 
 
 Clinically, if the mydriasis indicates excitation 
 of this cilio-spinal center (the lower part of the 
 
 "'Raymond. Paral." radicul. du plexus brach. (7 dec. 
 
 1894) ; paral. radieul. sensit. du plex. brach. (22. mars 1895) ;. 
 
 un cas de paral. radicul. du plex. brach. dr. (24 avril 1896). 
 
 Leg. sur Us mal. du syst. nerv. 1896, t. I, p. 217 et 239; 
 
 -1897, t. II, p. 379- 
 
go The Diagnosis of 
 
 braehial cord), a destructive lesion of this same re- 
 gion of the cord would bring about myosis, narrow- 
 ing of the palpebral fissure and retraction of the 
 ocular globe. 
 
 From all this the description of the root syn- 
 drome of the brachial cord easily results : Pains, 
 •paralysis, anaesthesias, amyotrophies, vaso motor 
 troubles and reflexes are distributed according to the 
 anatomo-physiological table which we give. 
 
 The syndrome may moreover be total or partial. 
 In the latter group there are many varieties, but two 
 principal types may be easily distinguished : the su- 
 perior and inferior types. 
 
 In the superior type (Erb, Duchenne), the del- 
 toids, biceps, brachialis anticus and supinator 
 longus (Erb) are involved, and often also the supra 
 and sub-spinous muscles, the clavicular bundle of 
 the pectoralis major, the supinator brevis (Du- 
 chenne). It is a paralysis, partial or complete, of 
 the 5th and 6th cervical pairs. 
 
 In the inferior type (Klumpke) the muscles of 
 the median and ulnar are attacked : paralysis of the 
 1st dorsal pair. 
 
 The oculo-pupillary troubles serve only to estab- 
 lish the height of the lesion. They also permit one 
 to say whether the lesion is, in certain cases, in the 
 brachial plexus or in its roots. For the troubles do 
 not appear when the same nerves (8th cervical and 
 1st dorsal) are affected below the emergence of the 
 rami by the great sympathetic. This is then a potent 
 element in differential diagnosis. 
 
Diseases of the C'ord. 91 
 
 9. The Segmental Syndrome of the Brachial 
 Cord. 
 
 Brissaud derived the theory of medullary seg- 
 mentation from the segmental anaesthesias of the 
 limbs in syringo-myelia and from the segmental 
 zonas of the limbs. 
 
 For the syringo-myelia 150 he cites a case of Gil- 
 les de la Tourette and Zaguelmann (1889), and one 
 of' Parmentier (1890) of thermo-ansesthesia as 
 gloves (long ones up to the elbow), then a case of 
 Debove and one of Souques (1891) of dissociated 
 anaesthesia as sleeves. He analyses the cases and 
 shows that especially for the gloves, a part of three 
 nerves, ulnar, median and radial, are necessary. 
 
 It is not the root distribution which we know 
 to be in longitudinal bands parallel to the- axis of the 
 limb. It is the segmental distribution correspond- 
 ing to the medullary segmentation. 
 
 For the sonas 1 " it is also seen that the eruptiou 
 presents a segmental distribution. Such are the 
 cases of Head and Mankopf. 
 
 Brissaud next notices that it is the same in many 
 cutaneous diseases. "Thus the case of sebaceous 
 ichthyosis of Biefel has the transverse zones of syr- 
 ingo-myelia. On the arms in particular, two large 
 cylindrical bracelets surround the middle portion of 
 , the humeral region." In a recent work on the rela- 
 tion of chronic eczema to anaesthesia of the skin, 
 Stonkovenkoff and Nikolski have noted the exist- 
 ence of anaesthesias in symmetrical patches and per- 
 
 im Brissaud. Leg. sur les mal. nerv. 1895, p. 215. 
 
 100 Brissaud. Sur la distritmt. metamer. du zona des- 
 membr. Presse med. 11 Janvier 1896 et Revue neurol 1896, 
 p. 710. 
 
•92 The Diagnosis oj 
 
 pendicular to the axis of the limbs in subjects hys- 
 terical or not hysterical. 
 
 Finally, scleroderma™ which may be distrib- 
 uted according to the track of a nerve or present a 
 root topography, may also have a segmental distrib- 
 ution. 
 
 For the motor nerves, Joseph Collins 162 has al- 
 ready established that "the cell groups which give 
 origin to the brachial plexus are three in number, 
 and extend from the upper part of the 4th cervical 
 pair to the lower part of the 1st dorsal. The cells 
 of the upper part of this area supply the muscles of 
 the shoulder and arm. The cells of the lower part 
 supply the forearm and hand. 
 
 The nuclei of the flexors are external and at a 
 lower level than those of the extensors. The cells 
 which give rise to the nerves which innervate the 
 extensors are situated nearer the median line than 
 those which innervate the flexors. 168 
 
 The same year from a case of muscular atrophy 
 with autopsy, Graham M. Hammond 164 concludes 
 also that one cellular group of the cord gives rise 
 to the muscular nerves of the forearm and another 
 group to those of the hand. 
 
 More recently, I myself 165 described a segmental 
 
 161 Brissaud. Pathogenie du processus scleroderm. Presse 
 mid. 1897, p. 285 {Revue neurol. 1897, p. 365) et Drouin. 
 Quelques cas de sclerod. local, a distrib. metamer. Th. Paris 
 1898. 
 
 102 Joseph Collins. The New-York med. Journ. 1894, 
 p. 40 et 98. Revue neurol. 1894, p. 105. 
 
 16B 0n peut rapprocher ces donnees de celles que Marin- 
 esco a irivoquees pour expliquer la frequence de la "main de 
 predicateur" dans la syringomyelic 
 
 jm Groeme M. Hammond. The New-York med. Journ. 
 1894, p. 1. Revue neurol. 1894, p. 116. 
 
 ""Congres des neurolog. de Marseille, avril 1899. Voir 
 aussi. nos leg. sur les Sympt. segmentates de la moelle que 
 le D r Gibert va publier dans le Nouveau Montpellier mid- 
 
Diseases of the Cord. 93. 
 
 tremor (hand and wrist) In a case of sclerosis in 
 patches. 
 
 The segmental syndrome of the brachial cord 
 is then thus characterized by sensory, trophic or mo- 
 tor symptoms having for their common character 
 the involvement of a segment of the limb limited by 
 a circular hne perpendicular to the axis of the limb 
 (line of amputation or of disarticulation). 
 
 10. The Syndrome of the Cervical €ord. 
 
 We include under the name cervical cord only 
 the portion of the cord which corresponds to the 
 first 3 vertical vertebras and gives rise to the first 
 4 cervical pairs. 
 
 From the sensory point of view this medullary 
 segment innervates the neck and the occipital re- 
 gion, above the region (already described) of the 
 brachial and dorsal cords and limited by the region 
 of the trigeminal. Its line of demarcation from the 
 latter region 166 follows the inferior border- of the 
 lower jaw and the posterior border of its upright 
 branch, passes in front of the ear and goes straight 
 up to the top of the head to join the same line of 
 the opposite side. In this sensory region of the 
 cervical plexus the posterior nart is innervated by 
 the posterior branches (sub-bcciptales) of the first 
 2 cervical nerves, and the anterior part by the an- 
 terior branches of the first 4 cervical nerves. 
 
 Here is the table (after Testut) of the motor 
 distribution of the first 4 "cervical pairs : 1UT 
 
 ical et le fait d'amyotrophie en gant que vient de publier le 
 D r Crocq (Journ. de neurol.). 
 
 ""Voir la fig. 48s de la p. 576 du t. II du Traite d'anat d. 
 Testut, 3e edit. 1897. 
 
 '"'Mayet. Traite de diagn. med. et de semeiol. 1898, t. I r 
 536. 
 
,94 The Diagnosis of 
 
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 "2. o S o> 3, B >a 
 
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 2. «.-"> ^--, S 
 
 CD en c CD <d . 
 
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 c c c >2 
 
Diseases of the Cord. 95 
 
 In resume, for the sensibility, on putting the 
 subject on four feet, the head hanging (the neck 
 and occiput in front), the cervical plexus gives two 
 bands, one anterior (the occipital region and the 
 neck), the other posterior (the ear and anterior 
 part of the neck). 
 
 The topography of the anaesthesias in lesions of 
 this cord are naturally deduced from , that. The 
 pains are: 1st, painful torticollis, pains at the neck' 
 and at the occiput as a collar; 2nd, the length of 
 the phrenic (from the base of the chest or in the 
 shoulder with painful points at the level of the costal 
 insertions of the diaphragm — 7th to 10th rib — to 
 the neck in front of the anterior scalenus, behind to 
 the limit of the spinous processes of the 3rd and 4th 
 cervical). 
 
 For motility, the cervical cord presides : 1st. 
 over the various movements of the head on the 
 trunk (flexion, rotation, extension) ; 2nd, over the 
 movements of the diaphragm (phrenic). The symp- 
 toms of excitation or of paralysis of the first mus- 
 cular group are easily foreseen: Convulsions (tics) 
 or paralysis of rotation, of flexion or of extension 
 of the he'ad. As to the diaphragm, Duchenne has 
 established the symptoms of its .paralysis. 
 
 In inspiration the epigastrium and hypochondriac 
 regions are depressed instead of dilated, at ' the 
 same time that the thorax increases in volume, and 
 inversely during expiration. If there is simply a 
 paresis, the phenomenon appears only in deep or 
 agitated respirations ; if the paralysis is unilateral, it 
 appears only on one side. At the same time respira- 
 tion is more frequent, especially on the least effort 
 to walk or speak or on the least excitement. All the 
 extraordinary muscles of inspiration become active 
 then, the face is flushed and the patient suffocates. 
 
96 The Diagnosis. 
 
 The voice is feeble and the slightest utterance puts 
 him out of breath. Expectoration is difficult or im- 
 possible. Defecation requires great efforts and is 
 accomplished with much difficulty. 
 
 The differential diagnosis of this cervical syn- 
 drome should be made from the brachial or dorsal 
 syndrome and from the bulbar syndrome. 
 
 The first will be made by the presence of symp- 
 toms which from the beginning pertain exclusively 
 to the cervical cord and which we have described. 
 
 The second will be made by the absence of truly 
 bulbar symptoms such as ocular paralyses, paralyses 
 of the lips, tongue, deglutition, ansestheiias of the 
 trigeminal, etc. 
 
TABLE OF CONTENTS. 
 
 Introduction, .... 3 
 
 I. The Diagnosis of Disease of the Medul- 
 lary System, ... 5 
 
 1. The syndrome of the posterior columns: 
 
 sensory and ataxic disturbances, . 6 
 
 2. The syndrome of the antero-lateral col- 
 
 umns : pareto-spasmodic state, con- 
 tractures and intention tremor, . 17 
 
 3. The associated syndrome of the poste- 
 
 rior and lateral columns: ataxo-spas- 
 mddic state, . . 30 
 
 4. The syndrome of the anterior horns: 
 
 muscular atrophy, . . . 31 
 
 5: The associated syndrome of the lateral 
 coiumns and the anterior horns: spas- 
 tic muscular atrophy, . 35 
 
 6. The syndrome of the centro posterior 
 
 grey substance-; syringo-myelic disso- 
 ciation of sensibility (and vaso-motor 
 troubles), . 36 
 
 7. The associated syndrome of the anterior 
 
 horn and of the centro-posterior grey 
 substance (syndrome of the whole grey 
 substance): muscular atrophy,- syringo- 
 myelic dissociation of sensibility and 
 vaso-motor troubles, . 52 
 
 8. The syndrome of the lateral half of the 
 
 cord: crossed hemiparaplegia, . 53 
 
ii Table of Contents. 
 
 II. The Diagnosis of the Height of the 
 
 Medullary Lesion, . . 62 
 
 1. General principles of the diagnosis of 
 
 the height of lesions, 62 
 
 2. The root-segmental syndrome of the 
 
 conus medullaris, ... 68 
 
 3. The root-segmental syndrome of the 
 
 sacral cord, . . . .70 
 
 4. The root-segmental. syndrome of the 
 
 lumbar cord, . 76 
 
 5. The segmental syndrome of the lumbo- 
 
 sacral cord, .... 80 
 
 6. The root syndrome of the dorsal cord, 82 
 
 7. The segmental syndrome of the dorsal 
 
 cord, ..... 84 
 
 8. The root syndrome of the brachial cord, 85 
 
 9. The segmental syndrome of the brachial 
 
 cord, . . . .91 
 
 10. The syndrome of the cervical cord, 93 
 
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