No. 3424.

APRIL 13, 1889.

ABSTRACT OF

The Gulstonian LecturesON

SECONDARY DEGENERATIONS OF THESPINAL CORD.

Delivered at the Royal College of Physicians,March, 1889,

BY HOWARD H. TOOTH, M.D., F.R.C.P.,ASSISTANT PHYSICIAN TO THE NATIONAL HOSPITAL FOR THE PARALYSED

AND EPILEPTIC.

LECTURE I.

AFTER a brief preliminary reference to the terms of thebequest and the development of our knowledge of thecentral nervous system, the lecturer proceeded to a shortsummary of the features of Wallerian degeneration in cutnerves, pointing out the primary loss of transparency whichoccurs with the cleavage of the myeline, and which ismarked by a diminution of irritability of the nerve to allstimuli. Under the microscope the white substance is seento split into short cylinders, later on completely liquefyingand appearing as droplets within the sheath. At the sametime the nerve corpuscles increase in size and number, andthe axis cylinder undergoes changes pari pu.ssm.. Ulti-mately the degenerated materials of the white substanceand axis cylinder mingle and gradually become absorbed,leaving only the primitive sheath with its proliferatednuclei. Regeneration occurs by the appearance of primitivefibrils in the old sheaths; at first small, they graduallyenlarge and acquire a myeline investment. The fibres inthe cord differ from those of peripheral nerves in possessingno definite primitive sheath or nerve corpuscles, the placeof these structures being taken by the neuroglia. Thecauses of secondary degeneration are (1) destruction oftrophic centres in the brain or medulla, (2) interruption inthe continuity of fibres, and (3) destructive lesion of theposterior nerve roots, severing the nerve fibres from theposterior root ganglia. Besides the secondary degeneration I’proper, there is a traumatic degeneration, which is essen-

tially inflammatory, extending for about one centimetreabove and below the lesion, and affecting the wholediameter of the cord, but being more particularly markedin the course of the fibres of the ascending and descendingtracts above and below respectively. There is considerableinfiltration of leucocytes, and both the axis cylinders andthe large cells of the grey matter are swollen and granular.Numerous laeunse occur filled with "vitreous masses "

(Homen), and also material referred to broken-down myelineand altered portions of axis cylinders. After experimentallesions, also, collections of purulent matter are found,but not in cases free from septic contamination, which, how-ever, exhibit marked proliferation of endothelium in the peri-vascular lymphatics and great thickening of the neuroglia.(Specimens were prepared by hardening in bichromate ofammonia or potash, having been examined both before andafter by the naked eye. Sections were stained by picro-carmine, cochineal, and by the special methods of Weigert,Pal, and Upson, after cutting in celloidin.) The changes .have been observed in the living animal with the nakedtye five days after the occurrence of the lesion, but after(leitth they are obscured by the loss of translucency in thehealthy tissue. After hardening in the bichromate thedegenerated parts appear yellow on a brown ground, thechange being well marked on the sixth day after injury.By the third day (Homen) the changes are only visible in Ithe tracts above the lesion, appearing below on the fifth.At first the axis cylinders are swollen, and stain verydeeply with carmine or acid fuchsin, refusing other dyes. i

Only the peripheral portion of the myeline remains, which which has a strong affinity for the acid fuchsin stain and also also for the Weigert htematoxylin, and has been called the the erythrophile substain." CASE 1. rr-tarre of Spine, 1vith Compression of Cord j

betlceen the ,5’i.ctle and Seventh Cervical Roots.-The anterior iand lateral regions were chiefly affected, but many normal tNo. 3424.

nerve fibres existed in all parts. The cord was obtained onthe eleventh day. In the neighbourhood of the lesion wereswollen axis cylinders, with a narrow ring of myeline stainingwith haematoxylin. These differ from the fibres in true

secondary degeneration by their large size and affinity forcarmine and aniline dyps, being less readily coloured bvfuchsin. Sections above the fourth cervical and below thethird dorsal exhibit only the features of a perfectly normalcord. It appears, therefore, that the changes are slowerin man than in the monkey. The early chemical changesapparent to the naked eye appear to occur simultaneouslythroughout the length of the fibre, but the actual histologicalchanges pass along the nerve fibre at varying rate. T.-i thesecond week the axis cylinder and myeline are completelyfused into a granular mass, having a rather larger diameterthan the original fibre, and staining nearly black with theWeigert haematoxylin. In two months the myeline isabsorbed, and the degenerated fibres refuse the hsematoxylin ;so that the degenerated area stands out colourless, or nearly

so, against the rest of the section.CASE 2. Sarcoma compressing and destroying the Cordbeloiv the Sixth Dorsal Root, causing death after tu:omonths.-There were granular changes, with fusion of theaxis cylinder and myeline, followed by absorption, the paleascending tracts being rendered conspicuous by Weigert’shfpmatoxylin method, very little increase of nuclei or ofneuroglia being seen. In other cases of five and six weeks’standing, though degenerative changes are obvious by themicroscope the constant colouring with hsematoxylin is notshown, owing to the myeline being still unabsorbed. Afterfour months the appearances differ but little from thosealready described, the absorption of myeline is more com-plete, and the degenerated region therefore refuses thehaematoxylin more completely and appears lighter. Sclerosisproceeds at different rates in different tracts, the ascendingones taking precedence. The posterior median columnomes first, then the crossed pyramidal tract, afterwards thelirect cerebellar, followed by the direct pyramidal. Afterfive months there is distinct thickening of the neuroglia,he fibre spaces being now filled with homogeneous instead)f granular material, and, although these are smaller,;here is as yet no obvious contraction of the degeneratedtrea.

CASE 3. S’ofteraing qf the Posterior and 1?Tiddle Thirds ofthe Right Internal Capsule, attended by Paralysis oj’theLeft Side of the Body, and later by Paralysis and Ric2ditz/Of both A rms and Legs, with Hemianaesthesia and Analgesia ,:fitfal after f2e 1nonths.-Post mortem, there was profounddegeneration of the anterior median column or directpyramidal, and of the crossed pyramidal tract; the lattermost marked. Weigert’s hpematoxylin still stained theremains of nerve fibres, showing that the myeline was notyet completely absorbed. The neuroglia was much increased,as were also the nuclei, especially around the vessels. Somedegenerated fibres were almost obliterated, while, on theother hand, many natural fibres were scattered through the

degenerated area.CASE 4. Pott’s Disease, with Corrapression of Cord in theMid-dorsal Region>’ fatal after six 1nonths-The ascendmgtracts, posterior median column, and direct cerebellar tractwere deeply degenerated, the former consisting principallyof dense connective tissue, though an occasional mass ofmyeline was seen faintly stained. There was still noobvious contraction of the sclerosed tissue. The process of

degeneration is progressive, and is probably complete forall fibres in three months. Afterwards the diseased areabecomes less conspicuous after hardening by the bichromates,and is found to consist only of connective tissue, whichcontracts and remains finally as a scar marking the site ofthe lesion.Secondary spinal degeneration differs from the Wallerian

degeneration of nerves principally in the absence of all active echanges referable to the nerve corpuscles in the latter. Inthe cord, nerve fibres, severed from their trophic centre,simply die or undergo a change analogous to necrosis, theirresidue being removed by absorption and replaced by pro-liferation of the neuroglia. This process is of a languidnature, very different from inflammation, and inflammatoryluclei are conspicuous by their absence. Moreover, the truesecondary degeneration is a very different matter to thetraumatic change in the neighbourhood of the lesion, where,f anywhere, inflammation may be supposed to exist. Onthe other hand, in Wallerian degeneration of nerves, though

p

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the breaking up and removal of the axis cylinder andmyeline may be of an analogous necrotic nature, theenlargement and proliferation of the corpuscles of the primi-tive sheath are evidence of life and activity, and the occur-rence of regeneration by the appearance of new fibrils withinthe sheath is an entirely additional feature.The question of regeneration of fibres in the cord has

been the subject of much controversy. Experiments on thelower animals point to the possibility of some amount ofrepair in them as we descend the scale, and also to itsgreater activity in young animals. In man, however, thereis little evidence of this power, with the exception of a caseunder the care of Dr. Gowers and Mr. Horsley, in whichcomplete recovery took place after removal of a tumourwhich, by indenting and pressing on the cord, had producedparalysis with increased reflexes in the lower extremities.

LECTURE II.

Commencing with a brief reference to early observationson degenerating tracts in the cord, and a short account ofsome of its grosser histological features, together with asketch of the more obvious changes observed in the upperpart of the central nervous system consequent on destructivelesions in the cortical motor area, the lecturer illustratedthese by citing Case 3, in which a lesion of the middle andposterior parts of the right internal capsule was followedby complete degeneration of the longitudinal fibres of theupper and middle portions of the right pons, none beingaffected in the fillet. At the commencement of the pyramidsthere was great diminution in the area of the degeneratedtract, referred to the constant giving off of fibres to theadjoining nuclei of grey matter. At the decussation thedegenerated fibres could be traced to the opposite lateraltract, interlacing with healthy fibres ; whilst, when decus-sation was complete, the affected strands were groupedtogether just external to the posterior horn, exhibiting insection a roughly triangular outline with the apex towardsthe centre, and having one side parallel to the grey matter,the base being parallel to the periphery of the lateralcolumn, but not quite reaching it in the upper part of thecord. In dogs and monkeys the section was more nearlycircular, and the results of experiments indicated thatcertain parts of the tract conveyed fibres from correspondingparts of the brain.Case 5, being one of complete transverse crushing of th{

cord between the eighth cervical and first dorsal roots,exhibited extensive traumatic degeneration of all fibres,except those in immediate contact with the central gre)matter, for a distance of one inch below the injury. Opposit{the second dorsal root the crossed pyramidal tract had itsgreatest development, diminishing thence downwards. Thitract has been stated to end at the level of the seconclumbar root, but degenerated fibres can be found as low athe fourth lumbar, or even lower. The crossed pyramidatract does not reach the edge of the section above, as th<direct cerebellar tract intervenes, but it extends to thEsurface in the dorsal region, commencing between the sixtland eight dorsal roots. Retaining its shape and positioiclose to the posterior horn in the upper part of the cord, ivleaves this lower down, and comes to be represented onlby a small patch at the periphery of the lateral columnThough the degenerated fibres have not been definiteltraced into ganglion cells, and maintain a position in tlusection as remote as possible from the anterior roots, yet, amot careful examination has failed to detect any degeneration in these roots, it is highly probable that the fibres of thitract form connexions with the ganglion cells of the grematter. On physiological grounds it is certain that they djnot cross, at least as a whole. The direct pyramidal tracconsists of fibres, which on leaving the pyramid do nocross, but run down in the anterior median column on the sam,side. In its fullest development it extends the entire lengtlof the anterior fissure. The area of degeneration may exten(to the anterior roots along the outer edge of the sectionand any lessening in size also occurs in this regionSecondary degeneration of this fasciculus is always asscciated with that of the crossed pyramidal tract, and hanever been observed alone. Pitres has shown that it isometimes affected in cortical lesions of the brain, and thasometimes both sides are degenerated with a unilateralesion. Bouchard stated that the tract did not reac’beyond the mid-dorsal region, but in Case 3 it was distincto the eleventh dorsal root, and in another case could b

recognised by the naked eye as low as the second lumbar.It is almost certain that the fibres cross in the cord, pro-bably in the anterior commissure, as in cases of its degenera-tion no paralysis occurs on the same side. It appears to.contain motor fibres, distributed, according to Gowers,principally to the upper extremity, but may possiblycontain many commissural fibres.

Recrossedfibres.-Pitres cites ten out of forty cases of hem i-plegia from unilateral lesion, in which degeneration of thepyramidal tract of the same as well as of the opposite sidewas found. In some it was of equal intensity on both sides;in others it was less on the same side. In six the directpyramidal tract on the same side was affected, and in threethere was degeneration on both sides. The pyramid of theopposite side was quite unaffected. Clinically also thereare indications of degeneration on the same as well as onthe opposite side to the lesion. Pitres considers that fibresfrom the pyramid of the medulla may pass into the crossedpyramidal tract, the direct pyramidal tract, and the

pyramidal tracts of the same side. Charcot suggests therecrossing of fibres from the crossed pyramidal tract throughthe anterior commissure, but there is at present noanatomical evidence of this. Sherrington states that therecrossed tract does not appear till about the third cervicalroot; the degenerated fibres are few, and extend but a shortdistance down the cord. In monkeys examined by thelecturer after experimental interference by Messrs. Horsleyand Spencer, there was obvious degeneration of the crossedpyramidal tract and very scanty degeneration in the corre-sponding tract of the same side as the lesion. Homen also,after semisection of the cervical region in dogs, founddistinct degenerating fibres in the opposite lateral tract,commencing 1 cm. below the lesion, and traceable as fadown as that on the injured side. There was at the sametime degeneration of the anterior pyramidal tract. Descend-ing lesions are also exhibited by scattered fibres in theantero-lateral and anterior root zone in Case 5 andMonkey 7. In this mixed zone degenerated fibres can bedetected as low as the eighth dorsal root, and in the anteriorroot zone to the sacral region. For a short way below thelesion, changed fibres are found in the periphery of theopposite lateral column in a position respected by theascending fibres of the direct cerebellar tract in the sectionabove the lesion.

Postero-lateral descending degeneration, &deg;‘ comma-shapedtract," occupying the centre of the column with a roundedhead and thin curved tail extending almost to the

periphery, is rarely absent. In Case 5 it was well markedand traceable by the microscope below the mid-dorsal region.In another similar case it was traceable to the sixth dorsalroot. It was found on the same side after semisection in

. monkeys, and is best marked after lesions high up in thecord. The fibres are most probably commissural.

Fibres de,generating 1lpwards.-Immediately above thelesion (1 to 2 cm.) traumatic degeneration affects most of thesection, sparing, however, the lateral limiting layer around

, the grey matter, and influencing most deeply the posteriorparts and periphery of the section. The postero-lateralcolumn shows normal fibres at the second root above, and

, the area degenerated rapidly decreases upwards until at thefifth root it assumes its normal dimensions. This is due tothe number of unaffected fibres entering at the posterior

, roots and the numerous commissural strands, this columabeing a principal conductor of the posterior root fibres. The

; postero-median column exhibits only a narrow strip of. degeneration along the whole length of the posterior fissure,; receding backwards so as essentially to form a small. triangle only, at the extreme posterior extremity, when the. lesion is low down. This diminution is due to fibres passingJ in from the postero-lateral tract. In tabes dorsalis theJ postero-lateral columns are affected below and the postero-

median only above. Some fibres traverse the entire lengthL of the column to the medulla. There is probably no cross-L ing, and the fibres appear to terminate in ganglion cells of, the posterior vesicular column, arranged in groups in. the upper region of the cord, whilst others end in the grey- matter which projects backwards into the posterior columnin the lower part of the medulla : the postero-median9 column here being called the processus gracilis, with theb nucleus gracilis; and the postero-lateral column, the pro-1 cessus cuneatus, with the nucleus cuneatus. When the1 degeneration is extensive, the altered fibres occupy a posi-t tion both inside and behind the nucleus gracilis; when solelys of posterior root fibres, on the inside only.

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Pesult of division of posterior roots.-A monkey, in whichall the posterior roots of the cauda equina on the right sidewere divided, exhibited loss of common and pain sensation,also probably of muscular sense, and absence of the knee-jerk on that side. Examination of the cord discloseddegeneration only at the top of the posterior horn, oppositethe fifth lumbar vertebra. Ascending, the degenera-tion gradually spreads inwards, reaching its maximumat the first lumbar, where it involves the entire posteriorregion except the unaffected entering fibres at the extremetip of the posterior horn and a small triangle at the posteriorextremity of the median fissure, which is composed of firmnerve fibres extending the whole length of the column.The posterior median column is most deeply affected oppo-site the eleventh dorsal nerve, the area of degenerationdiminishing upwards above this to a small patch againstthe posterior septum rather below its middle. The de-

generated fibres entering between the third and fifthlumbar inclusive appear to pass up in the grey matter ofthe posterior horn to join the ganglia in the posteriorvesicular column, some passing forwards to join nerve cellsin the anterior horn. In a second monkey, in which theposterior roots of the last dorsal and upper three lumbarnerves were divided, corresponding changes could be reco-gnised, there being especially a great dearth of fibresin the grey matter of the posterior horn, the central andlateral regions, and the vesicular column, and even a

diminution in the anterior horns of the injured side.There was apparently no change in the ganglion cells.In both experiments the posterior columns were aloneaffected, the direct cerebellar and the antero-lateral tractsescaping entirely. In man, there is no reason to believethat degeneration commencing in the peripheral nerves canextend past the root ganglion to the cord. When, however,lesion of the roots has occurred, secondary degenerationhas followed the same path indicated by experiment. Ina case of locomotor ataxy affecting only the cervical andupper dorsal region reported by Dejerine, there was mostintense degeneration of the posterior roots of the affectedregion, with sclerosis chiefly of the postero-lateral columnbelow and of the postero-median above--sparing, however,the small triangular fasciculus at the extreme end of themedian fissure. Lange also records a case in which all thesigns of locomotor ataxia were produced by a tumourpressing on the posterior roots of the cauda equina, attendedwith ascending degeneration to the dorsal region. Most ofthe lower posterior root fibres pass into the postero-lateralcolumn, whence they enter the posterior horn and join theganglion cells in the posterior vesicular column andanterior horn, or pass into the pustero-median column, andare conveyed to the nucleus gracilis of the medulla, thefunction of these last being principally visceral. There is acrossing of the fibres in the grey matter of the cord.

LECTURE III.

The direct cerebellar tract is most constantly degeneratedafter the posterior median column. It is situated in theperiphery of the lateral column, extending forwards fromthe region of the posterior bone to about the middle of thearc of the lateral column. Schultze cites a case of fractureof the ninth dorsal vertebra, causing compression of thecord opposite the tenth pair, in which was an area ofdegeneration extending round the periphery of the sectionfrom the posterior to the anterior roots, and continued upto the cervical region. In a case described by Gowers thecrush was situated opposite the eleventh dorsal, and thoughthe antero-lateral tract was affected, the direct cerebellartract was not degenerated at all. From these two cases itmay be inferred that the lowest point of origin of the fibresof the direct cerebellar tract is between the ninth andeleventh dorsal roots, though it is probably usually higherup. Kahler and Pick quote twenty-seven cases of trans-verse lesion, in all of which the posterior column wasaffected, and in those above the ninth dorsal the direct cere-bellar tract as well, this tract not being degenerated whenthe lesion was below that point. In a case of compressionirom a tumour at the sixth, seventh, and eighth dorsalB’ertebrae, sections at the first dorsal showed the directcerebellar tract to be plainly degenerated. There are alsomany normal large fibres and a few small, only those of theformer kind being degenerated, unless the others have been<,completely absorbed. The large amount of tissue inter-vening between the fibres is evidence that many have so

disappeared. From these facts it is obvious that new fibresare entering, principally of the large variety. Anteriorly,the great majority of fibres in the antero-lateral tract aredegenerated, both large and small. The sign of directcerebellar tract degeneration diminishes upwards, till at thelevel of the fifth cervical it is quite distinct and gatheredinto a small patch against the top of the posterior horn,where, however, it contains many normal fibres. At thesecond cervical only one or two isolated fibres mark thedegeneration in this tract; at the same time the antero-lateral tract remains highly degenerated. The direct cere-bellar tract, then, if degenerated secondarily to lesions ofthe lower dorsal region, is small, and tends to disappearbefore reaching the medulla. If the lesion is high up inthe cord the distribution is different. In Case 5, in whichthe injury occurred between the eighth cervical and firstdorsal, the whole of the antero-lateral region is affectedimmediately above the lesion, with the exception of a fewfibres immediately adjacent to the grey matter. Ascendingroot by root, the area involved diminishes, and there is atendency to separation into an antero-lateral and directcerebellar tract by the invasion of a mass of normal fibres,the two, however, being closely associated again in the lowerpart of the medulla.There is anatomical evidence of the origin of the direct

cerebellar tract in the posterior vesicular column of Clarkeextending from the eighth dorsal to the second lumbar, andappearing again above in the upper cervical region andmedulla, which is admitted by most to be in connexion withthe posterior roots. There is ample proof that its fibres donot come from the posterior roots of the lower extremities.Dr. Gaskell has given the most convincing reasons for

regarding the posterior vesicular column as intimately con-nected with the visceral system, the nerve fibres of whichare of the very finest calibre, corresponding to those passingto and from the vesicular column. An examination of thenormal cord in monkeys shows these fine fibres to pre-ponderate in the direct cerebellar tract just external tothe posterior roots in the lumbar and lower dorsal region,becoming fewer in proportion to large ones up to theseventh cervical, whence they are practically absent up tothe level of the first. In a monkey in which the posteriorroots of the sixth, seventh, and eighth cervical and firstdorsal nerves were divided, there was anaesthesia of the left bupper extremity, and the animal was killed on the twenty-eighth day.At the level of the first dorsal there is a slip of degenera-

tion in the postero-external column close to the posteriorhorn. A root higher there is extensive degeneration of theposterior region, with the exception of a small wedge at theextremity of the posterior septum, and complete andabsolute degeneration of that part of the direct cerebellartract lying next the posterior horn (the part which consistsof large fibres only). This is continued up the whole of thecervical region to the medulla in the restiform body. Fromthis it appears, then, that the fibres of the posterior cervicalroots, and probably of the upper dorsal, enter largely intothe formation of the direct cerebellar tract. In cases wherethe roots of the lower cord were divided, the fact wasemphasised that this tract was not affected, showing thedifference in composition of this tract in the upperas compared with the lower region of the cord. Thefine fibres in the periphery of the lateral tract in thelower dorsal region cannot be ascending ones, or they woulddegenerate upwards. At the level of the seventh or eighthdorsal the fibres of the crossed pyramidal tract come to thesurface and take the position of the direct cerebellar tract.This descending tract contains vast numbers of fine fibres.It is highly probable, then, that these are the fibres seen inthe peripheral part of the lateral column in the lower dorsalregion, and it is extremely likely that they enter into com-munication with the cells of the grey matter, probably ofthe posterior vesicular column, and that they are the fibreswhich have been seen crossing the lateral column. Therecan be little doubt that many of the fine fibres in connexionwith the posterior vesicular column do ascend, either in theposterior median column or in the antero-lateral ascendingtract. This tract occupies the anterior part of the lateralcolumn or "mixed zone" between the anterior root zone anddirect cerebellar tract, with which in places it is continuous.It forms a wedge-shaped area, with its base at the peripheryand its apex towards the grey matter, or sometimes deflectedso as to insinuate itself between the crossed pyramidaland direct cerebellar tracts. The antero-lateral tract

722

exhibits degenerated fibres in all transverse lesions of thecord, even when too low down to affect the direct cerebellartract, pointing to the origin of its fibres in or below thelumbar region. The absence of degeneration after sectionof the posterior roots shows that some of the fibres arederived from them, and if further proof of its existence as atract distinct from the direct cerebellar is required, it maybe said that Bechterow has described it developing at aperiod distinct from other parts of the cord. The antero-lateral region contains many line fibres like the crossedpyramidal tract and posterior median column, more par-ticularly in the lower parts of the cord, though they are

I

still numerous in the cervical region. Their diminutionhere may be due to the absence of any true posteriorvesicular column. It is therefore suggested that the antero-lateral fibres arise solely from the grey matter; its fine fibres,which are very numerous below, are centripetal from theposterior vesicular column, the large fibres being in con-nexion with groups in the anterior horns.In a case of locomotor ataxy with sclerosis of the antero-

lateral and posterior regions, contributed by Drs. Iladdenand Sherrington, the area of tine fibres in and about theposterior horn (Lissaner’s tract) was profoundly degenerated,as were also those of the posterior vesicular column, whilst,though no degeneration of the ganglion cells here was

visible, there seemed to be a diminution in number of thelarger variety. The degenerated fibres in the lateralcolumn, though diffused at first in the mid-dorsal, are con-centrated into the antero-lateral tract in the cervical region,and can be traced up to the medulla. This seems toconhrmthe idea that the antero-lateral tract fibres are derived fromthe posterior vesicular column. It is. possible that theprimary lesion may be in the fine fibres (Lissauer’s tract),and that there may be degeneration of the post-vesicularcolumn, leading to a conesponding degeneration in theantero-lateral tract.As to the termination of these two ascending tracts. The

direct cerebellar tract maintains its position close in frontof the posterior horn, where it expands above into thetubercle of Rolando ; a little higher it lies in front of theascending root of the fifth nerve, which later passes forwardbetween this tract and the substantia gelatinosa, just beforethe direct cerebellar tract enters the restiform body. Thedegeneration may be traced up to the point where the tractlies between the roots of origin of the eighth nerve; here thefibres take an oblique direction to pass to the cerebellum,and are very difficult to follow, but experiments on animalsindicate the termination of this tract in the superiorvermiform process of the cerebellum. The antero-lateraltract, <1S seen in monkeys after experimental lesions of thecord, is distinct from the direct cerebellar at the level of thefirst cervical root ; higher up, however, the two approach Ione another, and at the level of the commencement of theolive appear as one long tract along the lateral periphery ofthe section. At the point where the direct cerebellar tractpasses behind the ascending root of the fifth, the two areagain separated by normal fibres. Above this some fibresmay be ttaced near the periphery of the medulla in the anglebetween the olive and the surface as far as the point of exitof the seventh and eighth nerves. Loewenthal performeda transverse section of the cord, the result being degenera-tion of both direct cerebellar and antero-lateral tracts. Hetraced the latter, under the name of the " ventral cerebellarfibres," through the pons into the superior peduncle of thecerebellum. It is possible, then, that the fine fibres of thetract end in the nucleus lateralis, and that the large fibresgain the cerebellum by way of the superior peduncle.

Visceral nerve fibres, medullated and of the finest calibre,form the white ram us communicans constituting the visceralbranch of every typical spinal nerve. These fine fibres,afferent and efferent, appear in the posterior and anteriorroots respectively, and are connected accordingly with theganglion of the root or the adjacent visceral ganglia, inwhich they lose their medullary sheatn. The conception ofthe nerves and roots of a typical spinal segment would be :1. A posterior root, with a ganglion having a fixed position,the root being made up of large fibres (somatic) and smallfibres (splanchnic), at&iuml;erent in direction. 2. An anteriorroot, consisting of large and small fibres not in connexionwith any ganglion, and a number of small fibres which arein connexion with ganglia; but the ganglia are remote and Iof no fixed position.

In the cervical region the upper roots of the spinalaccessory and the lower roots of the vagus contain all the

visceral fibres arising from that part of the cord. They passto the ganglion of the vagus trunk, where many of themlose their medulla. In the sacral region these fibres appearas the nervi erigentes, so that there are three principal out-flows of visceral nerves, representing the cervical splanchnics,the abdominal splanchnics, and the pelvic splanchnics. Inthe cord the fine fibres either occur in bundles by them-selves or mixed with the large fibres, and terminate in theganglia of the grey matter. Efferent visceral fibres occurplentifully in the anterior pyramids of the medulla, thepyramidal tracts above in the pons, and the crossed pyra-midal tracts all the way down the cord. Afferent fibresascend in the mixed zone of the antero-lateral tract, in thebolder zone between the posterior horn and point of emer-gence of the posterior roots, in the posterior median column)and especially in the wedge-shaped area at the extremeposterior end of the posterior septum.

ABSTRACT OF

The Lumleian LecturesON

ENTERIC FEVER,Delivered at the Royal College of Physicians,

April, 1889,BY JOHN HARLEY, M.D,

PHYSICIAN TO ST. THOMAS’S HOSPITAL.

LECTURE I.

THE disease which I have selected for consideration inthe lectures which I have the honour to deliver to this

College is one of vast interest and importance, for it knowsno local bounds, flourishes equally well in the crowded cityand in the open country, and lays low alike the strong andthe weak, the rich and the poor. History deplores that.which should give encouragement to the advocates of peace,for whenever a nation selects her hardiest and healthiest

sons, and sends them ever so well provided upon a militaryexpedition, many more succumb to disease than are de-

stroyed by the enemy. Indeed, some patient and politiccommanders have been satisfied to entrust the disorganisa-tion and destruction of an army solely to the sure andunrelenting hand of disease.

In considering this subject, I propose first of all to searchfor its origin, then to trace its association and relationshipwith other diseases in further illustration of its origin, andlastly to call attention to the treatment of the disease, thematerials serving for this purpose being the cases whichhave come under my care in St. Thomas’s Hospital duringthe last ten years and those whose histories are given in theMedical Reports of the War of the Rebellion of the UnitedStates of America. In considering the etiology of enteric.fever, I shall not confine my inquiries to a narrow field, butshall be prepared to find a variety of influences accidentallycombining to produce the same result&mdash;the developmentof enteric inflammation. We are all assured that filthyair and filthy food or drink are producers of entericfever, and inferentially we may go a step further andconcede that filth generated within will also produce it.Science, however, is not satisfied with generalities, but seeksto know the immediate cause, to isolate the simple factors,and then to ascertain how these can set up a specific morbidaction; but the more the view is narrowed the greaterdo the difficulties become. Granted, for example, thatwater which lias filtered through cesspools a little higherup the valley is the cause of an outbreak of enteric fever inthe village below, what particular constituent of this fluidis it that produces the disease? Is it a chemical compound,or is it an organised body? If it be the former, it exists insuch tenuity that the chemist fails to detect its presence;if it be the latter, it is a microscopic dot.Micro-organisms exist in the clear lrmpid sewage filtrate

which causes enteric fever, and they also abound in thestools of patients suffering from this disease. But what ofthese ? Within the last few years the influence of micro-

organisms in the production of disease has engaged the