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SPASTIC PARAPLEGIA IN MIDDLE AGEBy COLIN EDWARDS, M.R.C.P.

West End Hospital for Nervous Diseases

Before launching into this discussion one mustpause to define middle age. Obviously it is notthe age period which would have been indicated50 years ago, nor is it the actual middle of theaverage span of life. Its limits are set by con-vention and they are not clear-cut, but it does notbegin before 40 years of age and nowadays onecan hardly say that it ends before 65.

Paraplegia, with its serious restriction onmobility, is more dramatic and striking thanparalysis of the arms, and is apt to give its name todiseases which are more than paraplegic in theireffects. Hence a number of the conditions men-tioned will be essentially quadriplegic and more.

Spasticity, too, although a term which connotesessentially pyramidal involvement, with its clasp-knife type of muscular hypertonia, can occasionallybear superficial resemblances to extra pyramidalrigidity and so some extra pyrarpidal diseases willhave to be noted.

So much for the terms of reference.Consideration of a clinico-pathological state can

be approached with one's own idea of diseaseclassification as a background pattern. This willensure that one is comprehensive and is the safestmethod to follow if under pressure for time in anexamination. Viewing one's middle-aged spasticpatient as a problem in diagnosis, however, onewould inevitably tend to consider the diagnosis tosome extent in terms of probability, and the com-moner causes would come first to mind. That ishow I propose to discuss paraplegia now.As a final prefatory remark one must stress the

primary importance in neurology of history taking.The clinical signs of neurological disease are sospectacular that one can understand why studentsare unduly impressed by them-but in no branchof medicine is history taking more important, andit is certainly the major part of the task of diagnosisin our middle-aged paraplegic.

Disseminated sclerosis must rank as one of thecommonest causes of spastic paraplegia andalthough four-fifths of the cases begin beforemiddle age, it is some of these four-fifths, as wellas the cases beginning in the fifth and sixth de-cades, that make up many of the ranks of themiddle-aged spastics. The history will usuallypoint fairly definitely to the diagnosis. Any case

of early onset surviving into middle age will cer-tainly have had a remission and there may wellhave been subsequent exacerbations and re-missions. Transient visual disturbances-dim-ness due to a retrobulbar neuritis or diplopia dueto external ocular palsies-are common in theinitial attack and less so in exacerbations. Andsome patients are aware of their nystagmus whichmay often be transient also. Bladder disturbances-precipitancy or frequency-are also commonearly symptoms. Later comes retention andusually, last of all, incontinence.The motor symptoms of disseminated sclerosis,

however, are the commonest, and particularlythose involving the lower limbs. Heaviness orweakness of the legs after exertion is the mostusual and it is nearly always more marked on oneside. Where there is associated cerebellar dis-turbance and the disease has not begun until thefifth, sixth or early part of the seventh decade, onehas to consider the possibility of one of the cere-bellar degenerations of middle life-notably de-layed cortical cerebellar atrophy, and olivo-ponto-cerebellar atrophy, both of which show bilateralpyramidal involvement. In them, however, thecurve of development of the disease is continuousand progressive, nor are ocular manifestationscommon-except nystagmus.

Rarely Friedrich's ataxia may show a pre-dominance of lateral column degeneration over theposterior, and the legs may be spastic despiteabsence of tendon reflexes. The familial incidence,the foot and spinal deformities, and the lengthyhistory without remissions in spite of a varyingrate of deterioration should differentiate theseoccasional cases from disseminated sclerosis.Their early onset will serve to distinguish themfrom the cerebellar atrophies mentioned above.No laboratory confirmation of the diagnosis of

disseminated sclerosis is possible, but about halfof the cases on whose cerebrospinal fluid a sen-sitive Lange test is done show a curve of ' paretic 'shape or tending towards it. This is combined inabout one-quarter to one-third of all cases with aslight increase in globulin in the fluid and araised cell count. This combination goes a longway towards establishing the diagnosis.Of other paraplegias of inflammatory origin at

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this time of life those due to syphilis have per-haps been the commonest, although they arealready ceasing to be so. They most commonlymake their appearance late in the first half of life,and if they do appear for the first time in middlelife they will be seen in its early part and nottowards its end. Syphilis causes paraplegia mostcommonly by spinal meningo-vascular inflamma-tion, but also occasionally by setting up a par-enchymatous degeneration. The lesion inmeningo-vascilar cases is usually a meningo-mvelitis. The meningitis gives rise to pain of rootorigin. It occurs most commonly in the dorsalregion and it may occasionally irritate the anteriorroots too, causing muscular cramps or spasm.The meningitis spreads along the pial septa intothe cord and its progress and resolution producetract involvement. This process may take from afew days up to many months. Bladder dis-turbance is frequent and early. Spastic paralysisis often the result but quite frequently is notmarkedly bilateral. A bedside indication of thesyphilitic nature of the spinal lesion is the tendencyto patchy, cutaneous, sensory impairment, par-ticularly of pain sensation as shown by pin prick.So it is that the victim of syphilitic meningo-myelitis will sometimes show bedsores of sur-prising size in an area where tactile sensation isalmost normal. Where a severe transverse lesionof the cord supervenes suddenly in a case withother neurosyphilitic features (e.g., root pains, im-paired deep and pain sensibility and possiblypupillary changes and diminished tendon re-flexes) the cause is usually the thrombosing of aspinal artery due to endarteritis. More rare typesof syphilitic spastic paraplegia are those resultingfrom hypertrophic pachymeningitis, Erb's syphiliticspinal paralysis, gumma of the cord and syphiliticlateral and combined sclerosis.

Syphilitic hypertrophic pachymeningitis is com-monest in the lower cervical region. The greatdural thickening causes initially signs and symp-toms due to root compression-namely pain,paraesthesiae, muscular atrophy and impairedcutaneous sensation of nerve root origin. Ashypertrophy goes on the cord becomes compressedwith the production first of signs of pyramidalcompression (extensor plantar response and in-creased tendon reflexes) and later of actual slowlyincreasing spastic paraplegia and increasing sen-sory loss up to the level of the lesion.

Erb's syphilitic spinal paralysis has never re-ceived widespread acceptance, at least as a patho-logical entity. Clinically it shows a very slowlyincreasing spastic type of paraplegia with an onsetten to twelve years after the initial infection (i.e.,the period of parenchymatous degenerative neuro-syphilis). It may show remissions or even arrest.

It produces upgoing toes and increased tendon re-flexes but spasticity and paralysis do not becomemarked. Sensory disturbance is slight but thebladder may sometimes be involved, and there areoccasionally lightning pains. Argyll Robertsonpupils are occasionally found.

It is difficult clinically to separate Erb's syphiliticspinal paralysis from syphilitic lateral sclerosis,and indeed they may well be the same condition,but at times signs of lateral sclerosis with its spasticparesis are associated with those of posteriorcolumn involvement (loss of some, at least, of thetendon reflexes, ataxia, and loss of deep sensation).The condition is then named syphilitic combinedor postero-lateral sclerosis and is essentially aparenchymatous degeneration. With it may some-times be associated muscular atrophy due toanterior horn cell degeneration.Gumma of the cord is not common. It belongs

to the meningo-vascular group of spinal syphiliticdisorders and is often associated with some actualmeningitis (both lepto and pachymeningitis), andwith arteritis. It produces signs and symptoms ofan intramedullary tumour but the spasticity re-ported has been most usually unilateral withcontralateral sensory disturbance-the Brown-Sequard syndrome.

Finally, and rarely, the lower limbs may sharein the general rigidity of a Parkinsonian picture ofsyphilitic origin, due to a parenchymatous de-generation in the striatal area, the subthalamic andtegmental mesencephalic region. These rare casesusually show associated tabes dorsalis, generalparesis, or tabo-paresis.Whenever neurosyphilis is suspected as a cause

of spastic paraplegia cerebrospinal fluid analysiswith Wassermann tests, and also a blood Wasser-mann reaction, must always be done.

In meningo-vascular cases the fluid most oftenshows a high cell count, usually of 30 to 200,principally lymphocytic, although in gumma it maybe low, and in pachymeningitis it may be almostnormal.The cell count in spinal parenchymatous neuro-

syphilis is usually only slightly raised. TheWassermann reaction may be negative in the fluidin meningo-vascular cases but is positive in themajority. It is more frequently positive still inparenchymatous cases. It should be rememberedthat a negative blood Wassermann reaction inassociation with a positive Wassermann Reactionin the cerebrospinal fluid has been estimated tooccur in as many as 30 per cent. of cases of neuro-syphilis, and the test may be negative in bothblood and fluid in a small number (about io percent.) of undoubted cases. The protein is usuallyslightly increased in parenchymatous cases, moreso in meningovascular cases, whilst hypertrophic

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pachymeningitis gives rise to a steadily rising pro-tein culminating in a Froin's syndrome whenspinal block is established. A relative excess ofglobulin is commcon. In the occasional case ofrapid transverse myelomalacia due to spinal arterythrombosis, the cerebrospinal fluid may beentirely normal.

Subacute combined degeneration is a conditionwhich is still overlooked with surprising frequencyin its early stages. Its maximum incidence isround about the age of 50, but it may begin evenas early as the late twenties or as late as 70. Theprincipal early symptom is paraesthesiae in thefeet and legs and, to a lesser extent, in the hands.Sensations as of constricting bands round theknees or of girdles round the body are alsocommon. Weakness of the legs and generalfatiguability appear next and there may be ataxiaat an early stage. The signs and symptoms aresymmetrical and the onset insidious. Unlike dis-seminated sclerosis ocular and bladder symptomsare usually absent and it begins much later as arule than that disease. Early signs are limited toslight peripheral blunting of sensation whichspreads slowly up the limbs. There may be slightataxia and intention tremor, and there may besigns of pyramidal involvement. The blood countis seldom entirely normal, but very often it doesnot show a typical pernicious anaemia picture.Smoothness of the tongue is a common sign but isoften so slight as to be of less diagnostic value thanis commonly alleged. Achlorhydria is very nearlyconstant although some undoubted cases do showa slight response to histamine. Spastic paralysisis a late development in a majority of the cases,and nowadays there can be no excuse for its de-velopment. In the remainder, peripheral nerveand posterior column degeneration predominateover that in the lateral columns and a flaccidparalysis is the result. The plantar reflexes, how-ever, are extensor. Tabes may be simulated inthis second type, but serological tests and cerebro-spinal fluid analysis can exclude it.A subacute combined degeneration producing

spastic paraplegia occurs in pellagra, and usuallyin the advanced stages, although the neurologicalpicture is more commonly one of hypotonia andataxia. The typical skin lesions on exposed areasand the prominence of the accompanying mentalsymptoms and stomatitis should suffice to settlethe diagnosis. It is most likely to be missed incases of Fellagra sine pellagra and in countrieswhere the disease is not prevalent.Tumours of the spinal cord and canal are all

characterized by a steadily progressive historyand, with the occasional exception of a meningioma,they are accompanied by a rise in the cerebrospinalfluid protein. Indeed a marked rise in protein in

an otherwise normal fluid is virtually pathogno-monic of a space-filling spinal lesion. Usual butless constant features are motor weakness in thelower limbs which becomes spastic in type whenthe mass is above the conus medullaris, and sensoryimpairment which ends abruptly at a line trans-verse to the body axis. This sensory impairmentis frequently dissociated in type in intramedullarygrowths. Root pains at the level of the lesion arefrequent in extramedullary tumours, particularly ifthey appear posterior to the cord, and bladder dis-turbance comes relatively early in many intra-medullary growths but late in the extramedullaryones. Muscle atrophy at the segmental level of anintramedullary growth is not uncommon.These are some of the salient points to be re-

membered when one considers spinal cord com-pression, but it must be emphasized that there arevery many non-neoplastic causes of this. Therole of trauma is not likely to be overlooked wherespinal fracture or dislocation has occurred. Dis-location is sometimes only momentary and spon-taneouslv rectifies itself. This occurs principallyin the cervical region, and X-rays in such casesmay show no abnormality unless the spine beacutely flexed or extended for the purpose of thefilm-a procedure not without danger and sohardly justifiable. The cord compression in trau-matic cases is usually a momentary affair and re-sults in laceration which shows no recovery.Laminectomy is useless in such cases. There areat least two types of acute traumatic compressionswhich do call for surgery, however. The first iswhere only laminae are broken and the secondwhere evidence of a severe cord lesion (extensive inthe transverse sense) arises soon (i.e. within a fewdays), but not immediately, after a spinal injury.The reasons for removing fragmented laminae areobvious. The second group of cases includes anumber in which an intramedullary haemorrhageoccurs (haematomyelia) and some in which cordcompression is due to extradural haemorrhage(haematorrhachis). The cerebrospinal fluid maycontain blood if there be associated meningealhaemorrhage, but there is often a completelynormal fluid. It is worth remembering, too, thatthere may be no hint of a subarachnoid block eventhough a fairly extensive haemorrhage is present.Haemorrhage into the cord can occur followingvery slight trauma indeed such as sudden, rapidneck flexion, or it may be apparently spontaneous.It is more common before middle life, however.It occurs principally in males and usually wherespinal vascular abnormalitv is already present. Insuch cases of cord compression laminectomyshould be done. 'I he results of clot removal aresometimes most gratifying.

Late effects of trauma which may produce cord

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compression are thecal scarring, herniation of anintervertebral disc and arachnoiditis with cystformation (meningitis serosa circumscripta). Allthree conditions, if diagnosed early enough, can behelped considerably by surgery. The traumatichistory should put one on the alert although theremainder of the story is not usually distinguish-able from that of any slowly increasing space-occupying lesion. Thecal scarring virtually neveroccurs in the absence of easily recognizable pre-ceding bony injury. Because of their positionnear the intervertebral foramina, where they im-pinge on nerve roots, disc herniations are seldompainless, but when they cause cord lesions this isdue principally to interference with the cord bloodsupply, sometimes associated with arachnoiditis,and not to direct structural deformation of the corditself by the hernia. Cyst-forming arachnoiditisis seldom painful. It may be very slow in de-velopment and spastic spinal symptoms are moreprominent than the sensory ones. ft is a condition,of course, which may arise from many causes otherthan trauma-notably local spinal infections,general infections such as the specific fevers,syphilis, any acute meningitis, and secondary tospinal cord disease such as syringomyelia or dis-seminated sclerosis. The bulk of cases of spinalarachnoiditis, of course, are not characterized bycord compression, and many of the post-meningiticspastic states are due to a meningo-myelitis ratherthan to cord compression. In syphilis, hyper-trophic pachymeningitis, as already mentioned,may give rise to cord compression.

Other inflammatory causes of cord compressionwith spastic paraplegia are spinal caries and extra-dural abscess. This is most commonly tubercu-lous, but it may be due to one of the commonpyogenic organisms. In the latter group thepatient is usually acutely ill with septicaemia andthe diagnosis will probably prove obvious, but inthe tuberculous cases bony disease may not beapparent at a stage when cord symptoms are quitedefinite. The area of the spine near the cordlesion must be watched assiduously for signs ofthe inflammation which the patient's temperature,erythrocyte sedimentation rate and general con-dition will probably suggest. Tenderness of thespine is likely to be the first sign.

Frank Pott's disease of the spine need give riseto no difficulty, and although it is commonest inthe young it is also found in middle age and evenlate in life.

Rarely a hydatid cyst may form within thespinal canal and compress the cord, but this isalmost a curiosity even in countries where thedisease is common.Cord compression by acute meningeal ex-

tensions of Hodgkin's disease or acute leukaemic

tumours need offer no difficulty in diagnosis be-cause of signs of these diseases elsewhere. Bothconditions are much commoner before middleage and they will be very rare causes of spasticparaplegia in the middle aged.However it is neoplastic disease proper which is

by far the commonest cause of extradural cordcompression, and this is usually secondary car-cinoma invading bone. Primary growths areusually sarcomata.

In every case of spinal cord disease where adiagnostic lumbar puncture is done a manometrictest for the freedom of subarachnoid fluid flowmust be made, using jugular vein compression toraise the fluid pressure in the head. The absenceof. a block does not exclude a space-filling lesion,but if present it goes a long way towards estab-lishing such a diagnosis. Bedside examinationalone is often insufficient to localize the lesionwithin limits sufficiently narrow for a surgicalapproach. Myelography must then be used and atilting table with facilities for screening the re-cumbent patient are desirable. It is only byscreening that many partial blocks can be de-tected. The radio-opaque medium used can beintroduced by the lumbar route and allowed torun upwards or by the cisternal route and allowedto gravitate downwards. If the lumbar route isused care must be taken that substances such aslipiodol do not get up into the cranial cavity as theiodine may separate out and set up arachnoiditis byirritation. No more than 2 CC. of lipiodol isnecessary, and the stability of the preparation isvery important. Indeed it is desirable, as a rule,to try to avoid putting lipiodol into the theca unlessthere is a reasonable prospect of its subsequentremoval at operation.Another group of spastic paraplegics is that due

to acute myelitis other than syphilitic. These arealmost all sudden in onset. Those which are dueto direct extension from a vertebral abscess presentlittle difficulty in diagnosis. Many cases of acutetransverse myelitis, however, show no obviouscause. Their onset is rapid, even sometimes withthe speed of a stroke, and although they maycomplicate infectious illness such as smallpox ormeasles, and although some follow hard upon thegiving of a spinal anaesthetic, the aetiology of manyis remarkably obscure. The cell count in the fluidtends to be abnormally high and lymphocytic intype, and although virus infection has been blamedfor many of these cases this is an unproven sus-picion as yet.Most of these cases of acute myelitis occur

early in adult life but they are not rare in themiddle aged.

Sometimes the acute cord lesion is part of adisseminated encephalomyelitis which may com-

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plicate one of the exanthemata, may followvaccination, or may arise quite independently.Spastic paralysis is rare from such a cause, how-ever, most patients showing flaccidity during theacute state and, if they survive, recovery tends tobe well nigh complete.

These acute myelitides may be simulated bysudden cord compression due to vascular mishapssuch as haemorrhage into a vascular tumour, or asyringomyelic cavity, or by spontaneous haemato-myelia. Cerebrospinal fluid analysis will usuallyserve to distinguish these from the inflammatorycases where the cell count is almost always raisedand where subarachnoid block is uncommon.The preceding history, of course, often suppliesthe answer.

Syringomyelia perhaps merits a little specialconsideration. The disease will almost alwayshave declared itself, although sometimes very un-obtrusively, before middle age, usually first in thesensory field with dissociated loss over a hand orarm and extending on to the neck and thorax.Although most cases show signs of pyramidal tractinvolvement on one or both sides, only a fewdevelop spastic paraplegia, but this developmenthas occurred after the age of 40, either due to thesteady enlargement of the cavity in the cord or toits very occasional rapid distension by haemor-rhage. A spinal block may be set up and even atransverse cord softening. Syringomyelic casesshowing extensive cord tract involvement with a-complete or material degree of spinal block merit alaminectomy. Incision of the cavity wall in themid-posterior line with consequent relief ofpressure may lessen the upper motor neuroneparalysis considerably.

Perhaps next one should remember those de-generative cord diseases of quite unknown origin-the abiotrophies-which not infrequently causespastic paraplegia in the middle aged. The mostsinister is amyotrophic lateral sclerosis, painless,insidious and lethal. It is essentially a disease ofmiddle life. Muscular atrophy commonly be-ginning in the hand intrinsics is accompanied bymuscular fasciculation that is frequently wide-spread, with increased tendon reflexes (in contrastwith the syphilitic kind) and pyramidal involve-ment that sometimes produces very spastic legs.As a general rule the more spastic the case the lessis the atrophy and the slower the disease. Objec-tive sensory changes are absent except for oc-casional blunting of cutaneous sensibility roundthe periphery of limbs, due possibly to im-poverished circulation there. As in all the abio-trophies, cerebrospinal fluid analysis is normal.It is worth emphasizing, whilst talking of amyo-trophic lateral sclerosis, that muscular twitchingssometimes of a fibrillary or fascicular kind, often

occur in young, middle aged and elderly subjectsin the absence of any hint of muscular atrophy orof lateral sclerosis. They are provoked in some byfatigue and in others by smoking, but in manysubject no cause is apparent. The label ' myo-kymia ' has been given to certain varieties of these.One should never rush into a diagnosis of amyo-trophic lateral sclerosis merely because of thepresence of such twitchings. In doubtful casesthe electromyogram can give useful help in thedifferential diagnosis. Pure primary lateral sclerosiswithout atrophy of muscles (except ultimatelyfrom disuse) is an entity whose separate existenceis denied by many neurologists. It is contendedthat these are cases of amyotrophic lateral sclerosisbeginning in the pyramidal sphere and that ifwatched long enough amyotrophy will usuallyappear, or, if examined with sufficient care post-rnortem, typical anterior horn cell changes will berevealed. The surprising frequency, however,with which one sees such cases in the absence ofany vascular or syphilitic basis has raised my ownsuspicion that there does exist a primary abio-trophic lateral sclerosis, and one recent personalcase in a man of 6o with spastic paraplegia, noaccompaniments and a normal fluid, blood, gastricsecretion and vascular system, appears to havebecome statir after nearly three years.There is, of course, a progressive bilateral

pyramidal involvement without muscular atrophy,which is due largely to cerebral atheroma. Thedegree of paraplegia in these cases is usually mildand a pseudo-bulbar type of spastic dysarthriacommonly accompanies it. This speech impair-ment is due to bilateral pyramidal tract impairmentabove the level of the speech nerve nuclei. Cerebro-spinal fluid protein in such vascular cases is oftenslightly increased (e.g. to 6o to 8o mgm./Ioo cc.)in contradistinction to the two preceding types.Another abiotrophic type is heredo-familial

spastic paralysis which begins in the first half oflife (although often not until the third or evenfourth decade), but whose progress is usually re-markably slow, many of the victims living on toold age. It commences in the legs and it may beas much as 20 years before the arms are involved.There is no muscular atrophy and no sensorvchange but the degree of spasticity is often very-severe.Another ' pure' spastic paraplegia often per-

sisting into middle and old age from infancy isthat of cerebral diplegia (which includes Little'sdisease). Involvement of the upper limbs alsooccurs and some of the cases are associated withathetosis due to striatal damage. These cases showno deteriroration granted normal care, and con-siderable benefit from patient education is possible.The rigidity of striatal disease, whether of

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March I950 Book Reviews I77

Parkinsonian degeneration or encephalitis, canhardly be said to cause paraplegia, and never truespasticity.

Final consideration must be given to hysteria.Hysteria does not make its initial appearance inmiddle-aged subjects with a hitherto stable psycho-somatic history, and only the rash will diagnose itat this time of life if there is no trace of a previousneurotic diathesis. It is nQt uncommon, however,to see hysterical paraplegia in middle life. Thediagnosis is only difficult at the bedside in veryoccasional cases where plantar reflexes cannot beelicited and the characteristic non-anatomicalsensory loss of hysteria is absent. These are few,however, and the absence of an extensor plantarresponse in a severe spastic paralysis nearlyalways clinches the diagnosis. On the sensoryside it is always well to remember that the buttockand perianal skin areas are supplied through thelower sacral nerves from a cord level that is muchlower than that receiving sensation from the foot

and leg. Yet quite commonly the hysterical para-plegia which mimics a severe cord lesion willshow profound loss of pin-prick sensation in thelegs with normal buttock sensation. A carefullytaken history alone, however, usually takes onenearly all the way to the diagnosis in hystericalparaplegics.

It has not been possible in this article to do morethan outline a few of the salient diagnostic points inspastic paraplegia in middle life. To discusstreatment has been impossible. I would like toclose, however, with an important therapeuticgeneralization. Acute inflammation, haemorrhageor shock in the central nervous system as else-where in the body requires rest as the cornerstoneof treatment. Where C.N.S. function is impairedfrom any other cause, however, rest, except for thepurpose of recuperation from fatigue, is contra-indicated. This point is very important inparalysis in the young, but in middle life and afterit is vital.

BOOK REVIEWS

TUMOURS OF BONE

By CHARLES F. GESCHICKTER, M.D., and MURRAYM. COPELAND, M.D. 3rd Edition. Pp. xviii +8io, with 642 illustrations. London: J. B.Lippincott. 1949. 5 guineas.

This book is a unique work for reference in sofar as it tabulates the clinical, radiological, patho-logical and prognostic findings in a truly enormousnumber of cases of bone tumours. It is beautifullyproduced and almost over lavishly illustrated. Asin the previous editions each type of tumour isdealt with in all its aspects, illustrated by a summaryof case records, many hundreds in number, a chartof age incidence, a skeletal diagram of site in-cidence and numerous photographs of X-rays,macroscopic and microscopic specimens. In ad-dition, the authors make a detailed and persistenteffort to correlate the tumour picture with disorderof varying phases of bone development; at timescarried to illogical extremes, of which the followingstatement (p. iiI) is an example:-' The clinicalfeatures of primary chondrosarcoma reflect in partthe primitive histogenesis of this neoplasm. Thefrequency with which Negroes are affected (approxi-mately I 5 per cent.) is unusual among the osteo-genic sarcomas as a group, and suggests a lowerevolutionary form of osteogenesis for this tumour.'

The style is heavy and at times not lucid; repetitionsand summaries, however, do in most instancesclarify the authors' ideas. Certain sections shouldhave been omitted from this edition, in particularthe two introductory chapters by Dean Lewis andBloodgood. Their unassailable dicta that physicalexamination, roentgenographs, biopsies and bloodWassermann examinations are diagnostically helpfulare amply brought out in the later text and in anycase have long been universally appreciated. Thechapter on endocrinopathies is too short to serve anyuseful purpose. Table 76, listing the sites ofprimary carcinoma which have given rise to osseousmetastases, has not been altered since the firstedition in I93I and in our view underestimates therole of bronchial carcinoma. The table cites a totalof 334 cases of secondary bone carcinoma of whichonly 4 came from a primary in the bronchus incontrast to 134 from prostate, ioo from breast and22 from kidney. However, table 72 details thesites of metastases from bronchial carcinoma in3,2I2 autopsied cases. The numerous misprints,contradictions and repetitions lay this book open toeasy criticism, but they do not detract from the factthat it summarizes the findings in an impressivecollection of cases and in contrast to many textbooksproves really helpful to the reader searching a factualanswer to a concrete problem.

I.D.

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