J. Neurol. Neurosurg. Psychiat., · J. Neurol. Neurosurg. Psychiat., 1956, 19, 109. ASTUDYOF 25 CASES OF COMPRESSION OF THE CAUDA EQUINA BY PROLAPSED INTERVERTEBRAL DISCS BY W. BRYAN

J. Neurol. Neurosurg. Psychiat., 1956, 19, 109.

A STUDY OF 25 CASES OF COMPRESSION OF THECAUDA EQUINA BY PROLAPSED INTERVERTEBRAL DISCS

BY

W. BRYAN JENNETTFrom the Depar-tment of Neurological Surgerv, Radeitie' Itnfirmary, Ox1forl

Most cases of sciatica due to intervertebral disclesions are in fact partial cauda equina lesions.Commonly they are unilateral and there is muscularweakness, wasting, reflex abnormalities, and sensoryimpairment referable to compression of one ormore roots. These defects are rarely disabling inthemselves and are of importance chiefly in diag-nosis and localization. In some cases the weaknessmay amount to complete paralysis of the anteriortibial group of muscles and a drop foot results. Ina smaller number there are profound bilateralsigns: total distal paralysis of the lower limbs,sensory loss in the whole sacral distribution, andsphincter paralysis. This is one type of lumbar disclesion which does not respond to conservativetreatment, and it is the only type which may con-stitute a threat to life. It is remarkable that it hasnot figured more prominently in the vast literaturewhich has accumulated since Mixter and Barr(1934) "discovered" the intervertebral disc lesion22 years ago.The largest number reported together is eight,

described by Ver Brugghen (1945) with one fatalbut unverified case. There are other isolated casesin the literature of which I have collected 34 withverified lesions and with sufficient data to makesome useful comparisons with the present series.(Dandy, 1929 and 1942; Eyre-Brook, 1952;French and Payne, 1944; Kaplan and Umansky,1951 ; Kennedy, Hyde, and Kaufman, 1948;Nicaud, 1947; O'Connell, 1944; Rouques, David,and Pautrat, 1948 ; Schneider, 1949). This paperreports a further 25 verified cases, which weretreated in the Radcliffe Infirmary and associatedhospitals in Oxford between 1937 and 1955, duringwhich time about 1,000 cases of lumbar disc lesionwere verified at operation. Although the incidenceis thus about 2% in the surgical material (similarto that found by Ver Brugghen), the actual incidenceof cauda equina paralysis in all lumbar disc lesionsis clearly not so high because almost all cases ofcauda equina compression are operated on, whereasonly a small proportion of cases of sciatic pain

presumed to be due to disc lesions are dealt withsurgically and so verified.

Paralysis of the cauda equina may be the firstsignificant manifestation of a lumbar disc lesion,although more commonly it is a sudden complica-tion of an attack of " ordinary " sciatica, either aninitial attack or one of a series of recurrent attacks.Two types of lesion have been encountered. Inthe first there is a massive protrusion of the discwhich takes up all the available room in the vertebralcanal and behaves much like a large extrathecaltumour. In other cases the disc protrusion issmaller, by no means large enough to fill thevertebral canal or crush the cauda equina and oftenof the type seen in cases of uncomplicated sciatica,but it is associated with a well demarcated band ofdense adhesions within the theca which stranglethe roots of the cauda equina.

Case 1.-A. H., a man, aged 56 (R.I. 7352/40), 20years before admission had an attack of backache andleft-sided sciatica for two weeks. In the 18 months beforeadmission he had three or four attacks of right-sidedsciatica with backache, and four months before admissionan attack proceeded to bilateral sciatica. The morningafter this he woke with complete double sphincterparalysis and the right leg useless and numb. He haddeveloped decubitus ulcers on one buttock and bothheels two to three weeks before admission.On arrival he was toxic, pyrexial, and hiccoughing,

the blood urea being 140 mg./100 ml. He could notmove the right leg against gravity whilst paralysis wascomplete below the knee ; there was distal weaknessand wasting in the left leg. Sensory loss was asym-metrical, involving the saddle area and on the right L.4and L.5 dermatomes as well. The ankle jerks wereabsent and he had retention of urine (with infection) anda patulous anal sphincter. The C.S.F. protein was 600mg./100 ml. and the fluid was xanthochromic; myelo-graphy showed a block at L.2-3 interspace.The patient died of uraemia a fortnight after admission

without having been operated on, and at necropsy asmall disc protrusion was found compressing the rightthird lumbar root. This lesion appeared to be too smallto have accounted for the paralysis, but on opening thetheca there was found to be a dense and sharply de-

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marcated band of arachnoid adhesions exactly oppositethe disc protrusion. This band was lightly adherent tothe inner aspect of the dura, but the roots of the caudaequina were firmly embedded in it and could only beisolated by sharp dissection. Above and below this bandthe leptomeninx appeared to be normal.

This type of lesion, which is less common than themassive prolapse, is also seen in association withdisc lesions in other parts of the vertebral canal, forexample, in the cervical region where some authorsregard it as important in the myelopathy associatedwith cervical spondylosis. Pathologically, it maybe thought of as a " friction arachnoiditis ", and,although a chronic process, paralytic symptomsmay develop just as suddenly as when a massiveprotrusion is present (Stookey, 1927). The primarypathological process, the protrusion of the disc intothe vertebral canal, must be similar to that inordinary sciatica but differing in some cases in sizeand in some in the tendency for adhesions todevelop around the nerve roots within the theca.This study was undertaken to see whether anyreason could be found for some cases behaving inthis serious manner, whether any steps could betaken to prevent it, and what the results of treatmentwere. It will be seen that the first two objectiveshave succeeded only to a very limited extent. It willalso be seen that the term " compression " is usedas a convenient description of the syndrome,although not all the cases were subject to actualcompression by a massive protrusion.

Analysis of CasesFifteen of the patients were men, 10 were women,

The youngest was 20 years old, the eldest 72, andthe remainder about equally distributed betweenthe fourth, fifth, and sixth decades. Compressionof the cauda equina thus occurs rather later than theuncomplicated sciatic pain which usually leads apatient to seek advice for a disc lesion.

In 14 cases there was a history of repeated attacksof backache and sciatica for many years. Therewas nothing very unusual about these attacks,although in two cases the sciatic pain had beenbilateral and in two others it had alternated betweenthe two sides. In most cases the final attack beganjust as the previous ones had done, although itusually developed into the most painful attack yetexperienced. In one case the paralysis occurredfour years after an operation for a disc protrusionat the same level.

In 11 cases the cauda equina symptoms occurredin the first attack. In one case there had beencontinuous back pain and sciatica for 12 monthsbefore the onset of cauda equina paralysis, butusually it was a much shorter period, the shortest

being three weeks. In two patients in this group thelesion was related to pregnancy and the puerperium:in one, back pain and sciatica began in the fourthmonth of pregnancy and were followed a monthlater by symptoms of cauda equina compression;in the other, back pain and sciatica began in thethird week of the puerperium and were followedtwo months later by compression symptoms.O'Connell (1944) described four cases in thepuerperium.

In 12 cases the onset o>f compression was sudden;in the remainder it was rapid, complete paralysisdeveloping over a few days. In these latter casesthe march of events simulated inflammatory lesionssuch as epidural abscess or even a rapidly growingtumour.When the onset is sudden, it might be expected

that it would be attributed to some sudden move-ment, strain, or other injury but that was so in onlythree cases, whilst in four other cases, by contrast,the paralysis came on whilst the patient was restingin bed. Of the former three cases one developedsphincter paralysis during a game of cricket,another gave a violent cough whilst in bed withsciatica and was immediately aware of numbnessand paralysis of both legs and had sphincter paraly-sis, whilst the third patient had a profound caudaequina paralysis immediately after manipulation ofthe back for long-standing sciatica.

Case 2.-J. B., a woman aged 33 (R.I. 16687), had anattack of right-sided sciatica at the age of 16 years. Itpersisted in greater or less degree for three years, andshe was then completely free from symptoms for 14years until 10 months before admission when, followinga mild back strain, there was a gradual recurrence ofpain in the back and down the posterior aspect of bothlower limbs. Despite various forms of physiotherapy,the pain persisted and after eight months she was bed-ridden with it. Three weeks before admission, the lumbarspine was manipulated under general anaesthesia. Onrecovering from the anaesthetic, she was free from pain,but complained of numbness and weakness of the legs,and was unable to empty the bladder.On examination there was gross distal paralysis of

both lower limbs, affecting all the muscles supplied bythe lowest lumbar and all the sacral nerve roots. Theknee jerks were present, the ankle jerks absent, as alsowere the plantar responses. There was deep sensory lossalong the lateral border of the feet, on the posterioraspects of the legs and thighs, over the buttocks andperineum, that is, the areas supplied by the fifth lumbarand all the sacral roots. There was retention of urine andincontinence of faeces, with loss of the anal reflex. Thecerebrospinal fluid contained 200 mg. protein/l00 ml.

There seemed to be clear evidence of compression ofthe cauda equina and at operation a large protrusion ofthe lumbo-sacral disc was removed.

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Recovery was slow. Improvement in motor power andsphincter control continued for three years, but whenlast seen nine years after operation, the patient still hada slightly waddling gait and also sensory loss. Thevesical sphincter had improved to the point where bytaking care she could avoid incontinence, but there was

still occasional rectal incontinence.

SymptomatologyPain.-As noted above practically all these

patients had pain of greater or less degree before theonset of paralysis, and in character and distributionit resembled that of the common lumbar disc lesion.It is significant, however, that 14 patients hadbilateral sciatic pain in the paralytic attack, althoughit was usually much more severe on one side thanthe other. It is also interesting that four patientsexperienced sudden and dramatic relief of painwith the onset of paralysis. I have known this tooccur in many cases of sciatica with the onset of a

drop foot and it must mean that severe compressionhas abolished pain conduction as completely as

that of the motor impulses.Two patients had very little pain, and the diag-

nosis in such cases may be very difficult. One ofthese patients awoke one morning with a profoundcauda equina paralysis and only on subsequentquestioning would he admit to having had, forthree weeks before the onset of paralysis, slightdiscomfort in the back and in the right sciaticdistribution. A disc protrusion was found atL.5-S. 1. The other case was very unusual in havinghad little pain and no demonstrable sensory loss.

Case 3.-E. F., a man aged 52 (R.I. 82610/47), was

referred because of the discovery of a high proteincontent in the C.S.F. in the course of investigation forretention of urine.The story was that 10 years previously he had suddenly

developed incontinence during a game of cricket. Thiscleared up, except for stress incontinence, within a fewdays. Eight months before admission he developedchronic retention with overflow and a month later anattack of acute retention led to emergency admission toanother hospital. A suprapubic cystostomy was doneand he returned to work as a gardener. At a subsequentadmission to see if any cause could be found for thesphincter paralysis, a lumbar puncture revealed a greatexcess of protein in the cerebrospinal fluid and he was

accordingly referred for a neurosurgical opinion.This patient denied having had sciatic pain at any

time, but he had had mild lumbago five years previouslywhich had neither incapacitated him nor led to his seekingmedical advice. His bowels moved normally with noincontinence, and sexual functions were normal.On examination, the patient was a healthy looking

man. He had learned to manage the suprapubic cysto-stomy so that it was only a minor inconvenience. Move-ments of the lumbar spine were normal, and there was

no demonstrable weakness of the lower limbs. Thereflexes were normal except that the left ankle jerk andthe left cremasteric reflex were absent. There was nodemonstrable sensory defect. Radiographs of thevertebral column were normal. Lumbar puncture inthe fourth lumbar space revealed a manometric block,and the cerebrospinal fluid contained 520 mg. protein/100ml. Myelography demonstrated an obstruction oppositethe second lumbar disc. At operation a small calcifiedprotrusion of the second lumbar disc was found. It wasobviously too small to cause compression of the thecaand its contents, but on opening the theca a dense bandof fibrous thickening of the arachnoid was found. It wasso thick and opaque that the roots of the cauda equinacould not be seen through it, although above and belowthis lesion the leptomeninx looked normal.

Five years after operation he reported no significantchange, but said that he had had some back pain andright-sided sciatica at times, but it was in no waydisabling.

Paralysis of Muscles.-In 11 cases there wasprofound paralysis. This usually involved theanterior tibial and peroneal groups and the calfmuscles, although in some cases one group wasaffected more than another and the legs wereinvolved asymmetrically. The functional effect wasprofound paralysis of the legs and feet, and if anincomplete lesion it was usually a unilateral orbilateral foot-drop. In six cases there was nosignificant motor paralysis, in which cases thedisturbance was limited to sensory and sphinctericfunctions.The ankle jerks were absent on both sides in 16

cases, on one side in six ; in a single case bothwere present although they were previously knownto have been absent.

Sensation.-In all but one case (Case 3 above)there was objective sensory loss, characteristicallyin the whole sacral distribution and involving allmodalities. When the sensory defect was so com-plete and extensive, the patients were often aware ofnumbness, but in some cases they did not seem tohave noticed it until their attention was called to it.In 11 cases the sensory loss was less complete andwas often asymmetrical, that is, there was completeloss in the whole sacral distribution on one sidebut in the other side the loss was limited to theperianal and perineal region. In five cases the losswas confined to a small area around the anus and inthe perineum. Such cases emphasize the importanceof a complete sensory examination, as it mayprovide the only objective evidence of a neurogeniccause for sphincter paralysis.

Sphincters.-Some degree of paralysis of the analand vesical sphincters occurred in all but two of the25 cases. In 14 it was complete with retention of

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urine and a patulous anal sphincter leading usuallyto faecal incontinence. In the rest there was some-thing short of this, for example, intermittentretention, loss of vesical and urethral sensation, or

constipation with defective anal sensation. Complete(double) sphincter paralysis was always accom-panied by profound bilateral sensory loss in thesaddle area, often in the whole sacral distribution.In some of these cases there was a remarkableescape of motor power, that is, the patient hadcomplete sphincter paralysis, extensive sensory loss,absent ankle jerks, and yet no muscular paralysis.We have encountered only one case of significantsphincter paralysis due to a disc lesion in which thesensory and motor defects were strictly unilateral,whilst in Case 3 (above) the paralysed bladder wasaccompanied by neither motor nor sensory deficit.That sphincter paralysis is so common a feature inthis series is understandable because it is usuallythis complication which leads to their admission tohospital: although the preceding pain may havebeen the most severe yet experienced, the patientand his doctor are familiar with it, and defects insensation and motor power may not be very obtru-sive when the patient is already in bed. But everyoneappreciates the gravity and inconvenience ofsphincter paralysis and there is usually no delay inseeking admission to hospital once it occurs. And itis often this symptom alone which demands opera-tion, that is, the pain has often cleared up and thesensory and motor deficits are not enough in them-selves to warrant operation.

InvestigationsPlain Radiographs.-As in other cases of inter-

vertebral disc lesions, radiographs were of valuechiefly in excluding other causes of cauda equinacompression, such as intraspinal tumour. In sevencases there was some narrowing of the appropriatedisc space, and in six others there were localarthritic changes, but in none were the radiologicalfeatures regarded as diagnostic.Lumbar Puncture.-As the majority of these

lesions occur in the fourth and fifth lumbar discs,lumbar puncture at the usual site (third or fourthinterspace) will often be above the lesion. Even so,in each of the 21 patients from whom fluid wasobtained there was an increase in the proteincontent. This varied from 55 to 590 mg.l/00ml.,with more than 100 mg. in 15 cases. In threepatients specimens were obtained from both aboveand below the lesion, and a manometric block wasdemonstrated between the two sites of puncture.In two of these the fluid was xanthochromic bothabove and below the lesion, the protein content

being 500 mg. in both specimens in one case and590 mg. below and 100 mg. above in the other.In the third case the values were 70 mg. above and90 mg. below. It was not possible to correlate thevariations in the protein content of the fluid witheither of the two types of lesion encountered atoperation. It might have been supposed, forinstance, that the cases in which there was fibrousthickening of the arachnoid would have shownhigher protein contents in the fluid whether fromabove or below the lesion, but that was not con-stantly so: indeed both the highest and the lowestprotein contents were found in cases with markedarachnoid thickening.

In all cases in which the puncture was donebelow the lesion, a partial or complete manometricblock was found. In two cases repeated effortsfailed to obtain any fluid, a common experiencewith other expanding lesions of the cauda equina.Myelography.-This was done in 18 cases, in 16

of which there was a complete obstruction to thepassage of the opaque medium. In most there wasan irregular margin at the site of the obstruction,suggesting an extrathecal lesion, but in two casesthere was a smooth, rounded margin as is commonlyseen with intrathecal neoplasms. The opaque sub-stance was in each case introduced into the lumbartheca, either above or below the lesion, and thuseither the upper or lower margin of the lesion wasdemonstrated.

Findings at OperationWith the exception of Case 1, all patients were

operated on. The site of the lesions is indicated inTable I.

TABLE 1

SITE OF LESION

Lumbar Disc Cases in Series Reported Cases

1 - I2 I (+ case 1) 53 3 114 10 1 15 12 6

26* 34

* In two cases lesions were found at both fourth and fifth spaces.

It will be noted that 22 of the 26 lesions occurredat the common sites associated with uncomplicatedsciatica. In the two cases with double lesions itwas the two lower spaces that were affected.

In 17 cases there was a massive loose fragmentlargely filling the vertebral canal, behaving muchas an extrathecal tumour. In the remainder theprotrusion although large was no larger than isoften seen in cases of ordinary sciatica, but in each

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of these the theca was opened and focal thickeningof the arachnoid was found. In these cases thechanges in the arachnoid seemed to be of moreimportance than the size of the disc lesion. It isinteresting that the patients with arachnoid changeshad on the whole no longer histories than thosewithout such changes, and that in three of them,without any massive disc protrusion, the onset ofthe cauda equina syndrome was sudden.

These arachnoid changes may also account forpersistence of a myelographic obstruction after theprotruded disc material has been removed. This isnot surprising, as it is unlikely that removal of anextrathecal mass would have any immediate effecton structural changes within the theca. That aclinical problem exists, however, is demonstratedby the following case.Case 4.-B.C., a woman aged 27 (R.I. 186976/54), had

suffered from six attacks of back pain each of a week'sduration since a trivial back strain six years previously.Three weeks before admission bilateral sciatica super-vened in one of her attacks. A fortnight later she awoketo find weakness and numbness of the legs and she hadretention of urine.On examination there was a profound flaccid weakness

of both legs, but the paralysis was not quite complete,that is, there were feeble movements of the toes andankles. The ankle jerks were absent and there wassensory loss below L.5. Puncture at the L.4-5 interspacerevealed no manometric block and the C.S.F. proteinwas 65 mg./100 ml. Myelography (from below) showeda complete block at L.3-4, however.At operation a moderate-sized lesion was removed

from the L.3-4 level extrathecally. There was no imme-diate improvement but in fact some deterioration inmotor power. She was screened again the day afteroperation and the opaque medium was found to beimmobile. Subsequently a cisternal injection was madebut this too was completely held up at the site of theoriginal lesion. It was decided to re-explore lest a frag-ment of disc had been missed and this was done 14 daysafter the first operation. No disc material was seen sothe theca was opened and the arachnoid was foundadherent to it. There was no subarachnoid space, onlya little loculated C.S.F., and the roots were adherent tothe arachnoid. No attempt was made to separate theroots. Progress from that time was very slow.Although persistence of a myelographic abnor-

mality after operation may thus be due to arachnoidadhesions, the possibility of there being two lesionsmust be remembered. In one case in the presentseries, a persistent defect led to re-exploration withthe discovery of a second lesion at the space belowthat originally explored.

Post-operative Course and Long-term Follow-upIn addition to Case 1, who died unoperated, one

patient died nine days after operation from un-

associated pathology, though operation doubtlessinitiated her final collapse (Case 5). All the re-maining patients have been followed up since theirdischarge from hospital, some for as long as 14years. Only four of them have made completerecoveries as regards muscular power, sensation, andsphincter control.

It is widely known that recovery from cauda equinalesions is slow but it is doubtful if it is realizedjust how unsatisfactory it can be. In general themotor recovery is better than the sensory and allthe surviving patients are walking again. Once thecompressing lesion has been removed motorrecovery occurs slowly by regeneration, as in aperipheral nerve damaged in continuity. AsO'Connell (1950) has pointed out, the sensorylesion in these cases is proximal to the posterior rootganglion and if it is severe enough to cause degenera-tion there can be no improvement. That somesensory recovery occurs is due to the fact that atthe outset the lesion is not complete and somepartially damaged roots ultimately recover. Sphinc-ter paralysis is often the most serious aspect of theproblem for obvious reasons, and a patient maybecome fully ambulant, free of pain, and in no wayinconvenienced by sensory loss, yet still not haveadequate control of the sphincters. It may be threeor four years before the end state in regard tosphincter control is reached, and the patient willneed a good deal of encouragement and reassuranceduring this time, in addition to careful observationof the urine to ensure that chronic infection doesnot do irreparable damage.Of the few who still had back pain or sciatic pain

at the time of operation, all were relieved imme-diately, and there has been no recurrence of painexcept in Case 3 in which there was profoundarachnoid thickening. In general, the patients witharachnoid changes recovered more slowly and lesscompletely than those in whom there was a massivecompressing lesion without arachnoid changes.

Paralysis of the limb muscles may persist for twoto three months after operation before there is anysign of recovery, and improvement once startedcontinues only very slowly. It is difficult to assessthe rate of progress but it appears that the greatestimprovement occurs in the first two years afteroperation, although several patients have professedcontinuing improvement after as along as five years.Some of this protracted improvement is probablydue to the patient learning to make better use ofpermanently weakened muscles, as occurs in othercases of static paralysis. Of the seven patients whohave left hospital having had significant paralysisbefore operation only two have made complete

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motor recoveries. All the remainder are fullyambulant, however, most of them with only a slightlimp. The ankle jerks were still absent at the mostrecent examination in 11 cases, while in two othersthey returned at the second and third yearrespectively.

Sensation usually recovers more slowly and lesscompletely than motor power, and it was possibleto demonstrate some impairment in the pre-operative distribution in 11 cases up to nine yearslater. The loss is commonly less profound andextensive, however, and usually causes no incon-venience. None of the patients is known to havedeveloped trophic changes.Of the 14 patients who had total paralysis of the

bladder and bowel before operation and have lefthospital, only two have regained full control andsensation (Table II). Seven acquired full control of

TABLE ILDEGREE OF RECOVERY IN 14 CASES IN THIS SERIES

WITH COMPLETE DOUBLE SPHINCTER PARALYSIS

Case Compression- S Length ofNo._ operatn Bladder Bowel Function Follow-upIntervaol (yr.)

1 I month F F - 133 3) weeks F F - 22/125 2 weeks G F Impotent 47 3 months F G Normal 59 I week P G - 5

11 2 weeks VG VG Normal 512 3 days G G - 514 3 weeks VG F - 915 2 months G G Normal 1316 2 weeks G P - 417 2 weeks G NM -23 2 weeks G G -I20 1 week VG VG 14/1225 7 months - __ _ Nil

VG perfect.G = perfect control, no incontinence, but imperfect sensation.F= occasional incontinence, not requiring permanent pre-

cautions.P = requires appliance.NM= no mention.

TABLE I IIPOST-OPERATIVE COURSE (CASES IN THIS SERIES ANDFROM LITERATURE WITH SUFFICIENT INFORMATION)

Degreero Perfect Perfect ccasional RequiringRecovery Pefc Control Incotn- Appliance

MotorPresent series .. 8 3 2 2 (=15)Literature .. 8 8 9 3 28)Total .. .. 16 11 11 5 (=43)°,' (oftotal) .. 37 26 26 12

BladderPresent series .. 6 6 4 1 (= 17)Literature I.11 5 - I (=17)Total . .. 17 I I 4 2 (=34)% (of total) .. 50 32 12 6

the bladder and are never incontinent but they havedefective vesical and urethral sensation and severalare occasionally incontinent of faeces. The rest haveoccasional incontinence but in only two is this

so frequent that an appliance has to be worn.All but one have been followed for a year, and ninefor over four years.

In general the bowel recovered less well than thebladder and there are only five patients who are notoccasionally incontinent of faeces. In two of thesethe bowel has recovered more completely than thebladder.Of the 14 males we have precise information

about sexual activity in only four. One is impotentand three say they are normal. It is interesting tonote that in two of these recovery of the bladderand bowel had been incomplete and there is somecontinuing defect in sensation in the lower sacralsegments.

DiscussionOur experience accords fairly closely with the 34

other recorded cases which we have analysed. Inthese there was a striking preponderance of males atand past middle life. Two cases followed a majorspinal injury without fracture, the diagnosis beingmade, in the presence of normal manometry, bymyelography (Schneider, 1949). One case (Dandy,1929) followed therapeutic manipulation for bilateralsciatica, a massive prolapse at L.3-4 being foundsubsequently. Three other cases (Ver Brugghen,1945) of sudden onset were related to a violentsneeze or cough, whilst a fourth patient (Tolosa andEctors, 1953) related the onset of the cauda equinasyndrome to stooping down to pick something offthe floor during an attack of sciatica. Two-thirds ofthe patients had long histories of recurrent backacheand sciatica and over half of them had bilateralsciatica in the compressing attack. Profoundparalysis occurred in all but three, whilst the anklejerks were absent on both sides in 25 cases, on oneside in six and were present in two cases. Sensoryloss in the saddle area was found in 24 of the 28cases in which a sensory examination was recorded.Complete sphincter paralysis is mentioned in 22cases. A high protein content in the spinal fluidfrom below the level of the lesion is frequentlyfound but there is no record of high values fromabove the lesion.

Myelography was done in 22 cases and in all ofthem a gross lesion was demonstrated but thedifficulty of differentiation between a disc lesionand a neoplasm seems to have been considerable.French and Payne (1944) say that on the basis ofthe myelogram five of their eight cases were operatedon with the diagnosis of tumour.The site of the lesion in these 34 recorded cases is

shown in Table I. It will be seen that half were inthe upper lumbar region as opposed to the common

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fourth and fifth lumbar discs, lesions which areresponsible for the vast majority of uncomplicatedcases of sciatica. Arachnoiditis was reported inthree of one series of five cases operated ontransdurally (Tolosa and Ectors, 1953).

It is difficult to assess the post-operative coursein many of these cases because of insufficient data.It appears, however, that only four of the 34 madecomplete recoveries-an even smaller proportionthan that in this series. (The results, reduced tostandards as nearly as possible comparable to thisseries are set out in Table III, which shows that only11 were followed for more than six months.) Inregard to sphincter recovery, there are two featuresworthy of note. One is that in most cases there isno mention of the bowel, which we found to recoverless well than the bladder. The other is that thenumber of " very good " recoveries of the vesicalsphincter is probably too high, this designationhaving been awarded (by us) for such comments inthe papers as " can control urine " or " bladderworking again". Our experience in following upthese patients for long periods is that they oftenminimise the shortcomings of the sphincters, sopleased are they to have them working at all. Morethan once there is a note in our records to say" bladder (or rectum) normal" and a later note bya more searching observer mentions significantdefects present ever since the operation.

In the literature on spinal arachnoiditis there islittle suggestion of a relationship with prolapsed discuntil French (1946) reported 13 cases of localizedlumbar arachnoiditis explored by operation inwhich a disc lesion was found in eight, whilst theremaining cases were early ones in which he thoughtit possible that a small disc lesion might have beenmissed. The general symptomatology of these caseswas similar to those reported in our series but manywere less severely disabled. The C.S.F. proteinswere much lower than in our series whilst therecoveries seem to have been much less satisfactorywith regard to relief of pain.

Several other points emerge from a considerationof our cases and those recorded in the literature.Compression of the cauda equina by intervertebraldisc lesions is quite unpredictable although the possi-bility is slightly greater in patients of middle ageand over. Bilateral symptoms and signs commonlyprecede serious compression and indicate itsimminence. There is evidence too that a suddenmovement may precipitate a compression lesion,and although we cannot avoid many such movementswhich occur in the course of daily life, to employsudden or violent movement (for example, manipu-lation of the spine) as a therapeutic procedure seems

to be risky. We are aware of the fact that thereported cases make up a very small proportion ofthe vast number of patients who have had manipu-lations for back pain and sciatica, but that thiscomplication can occur and that it is quite un-predictable, makes us feel that manipulation shouldnot be undertaken without due thought and know-ledge of the risks. Eyre-Brook (1952) refers to acase and warns against manipulation. The questionhas obvious medico-legal importance.

Diagnosis is usually not difficult. The con-siderable elevation of the spinal fluid proteincontent may lead to the suspicion of a neoplasm,but the presence of a myelographic obstructionwould indicate an exploration in either case. Itshould be mentioned that myelography is importantin revealing the site of the lesion, as in five of thesecases, and in half of those reported in the literature,the lesion was above the fourth and fifth discs, theones usually explored in cases of sciatica. Myelo-graphy is also of value in indicating the presence oftwo lesions, one of which might not have beensuspected from the clinical evidence.One condition with which compression may be

confused is the diabetic myelopathy described byGarland and Taverner (1953). The five patientsdescribed in their paper all had sciatic pain, muscleweakness, and absent tendon reflexes; four hadraised protein in the C.S.F. None had any sensoryloss, a useful but not reliable differentiating feature(see Case 3 of the present series), but in three casesthere was at some time an extensor plantar responsewhich would have ruled out a cauda equina com-pression. This problem of the possible relationbetween diabetes and cauda equina paralysis arosein one of our cases.Case 5.-M.S., awoman aged 72 years (R.L 198778/54),

a moderately severe and poorly controlled diabetic of12 years standing, had had an attack of left-sided sciaticasix years before admission. Three weeks previously shehad a recurrence followed after a week by gradual weak-ness of the left foot, then by numbness of the whole leg and aweek before coming here she developed urinary retention.

She was still in severe pain with very limited spinalmovement and straight leg raising diminished to 40° oneach side. There was an almost total palsy of the leftfoot with sensory loss in the entire sacral distribution onthe left and in the lower sacral segments on the right aswell. The protein content of the spinal fluid was 120 mg./'100 ml. and there was a complete block at L.4-5 on themyelogram. The blood pressure was 220/110 mm. Hgand the blood sugar 290 mg.At operation a large loose fragment was found

completely extruded from the disc space and severalsmaller ones still in the space. She was relieved of painbut there was no other striking change in her neurologicalstate in the nine days during which she survived. She

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went gradually downhill, finally developing diabeticcoma. At necropsy there were bilateral hypernephromatareplacing most of the renal tissue, the blood vessels werein good condition, but the bladder was severely inflamed;there was no evidence of ascending urinary infection.When operating for cauda equina paralysis some

modifications of the technique used for uncompli-cated cases of sciatica may be necessary. A moreliberal exposure must be made, if necessary a fullbilateral laminectomy, in order to see the lesion andavoid too vigorous retraction of the theca. If toapproach the lesion extrathecally entails too muchretraction (and in many of these cases the spinalcanal is tightly filled) there must be no hesitation inopening the theca. The roots are then separatedand the anterior theca over the bulge incised. Assoon as the massive fragment, which is usuallyfound in these very tight cases, is removed there isplenty of room and the exenteration of the discspace may be completed by the ordinary extrathecalapproach. There is no need to close the incision inthe anterior theca but that in the posterior is closedin the usual manner.That operation for uncomplicated sciatica may

not guarantee against a subsequent compressivelesion developing is shown by the following case.Case 6.-C. N., a man aged 61 (R.I. 22631/42), first

attended in 1942 when he was 57. He had had bilateralsciatica and paraesthesiae in the sacral distribution on andoff for 10 years. At operation a moderate protrusionwas removed from L.4-5 on the right. He made acomplete recovery and remained well until 1946.He returned then with the complaint that since

" ricking his back " eight months previously he hadsuffered a gradual onset of backache and bilateralsciatica (worse on the right). Symptoms had beenprogressively worsening in the last four months and hehad been in bed for two months, during which time hehad noticed progressive weakness of the legs. Incon-tinence of faeces and hesitancy and difficulty withmicturition had come on two weeks before admission.

There was marked bilateral palsy with wasting, in-cluding the buttocks, bilateral sensory loss in S.3, 4, and5, and absent ankle jerks. Lumbar puncture at L.2-3showed no block and the protein was 120 mg./100 ml.At operation the dura was opened and matted bluish-

red roots were found stretched over a massive protrusionjust to the right of the centre at L.4-5 (the site of theprevious lesion) ; there was a massive free fragment.He left hospital six months after operation with littlemotor improvement but able to void in the sittingposition. Within a year he could walk 40 yards withoutsticks, and a year later, according to a letter from him,was indulging in gardening and fishing.

This is the only instance that we know of in whichserious compression has occurred after an operationfor an intervertebral disc lesion. It is, however, an

argument for a radical operation, if an operation isto be done at all, for all lesions no matter howsimple. Removal of only the protrusion causingvisible compression of a root is not sufficient andshould be followed by vigorous exenteration of theinterior. In operating for ordinary uncomplicatedsciatica we have found on many occasions largeloose fragments of annulus fibrosus in the interiorwhich might well have been extruded subsequentlyhad they not been removed at the time.

In these cases we found no evidence that the degreeof recovery was related to the time interval betweenthe onset ofcompression and the operation (see TableII). Nevertheless there is everything to be said foroperation as soon as possible after the onset of para-lysis. Indeed an emergency operation in a rapidlyprogressive case might prevent complete paralysis.That is to say that a patient who has pain, incipientweakness, and sensory loss might be spared sphincterparalysis if operated on in time. It might also bethat the chances of arachnoid adhesions developingare lessened the sooner the compression is relieved.

SummaryTwenty-five cases of cauda equina compression

due to a verified prolapsed intervertebral disc aredescribed, including two fatal cases. The.sympto-matology, clinical details, and results of lumbarpuncture and myelography are discussed, togetherwith the operative findings and follow-up afterleaving hospital.

Thirty-two further cases culled from the literature,including one fatal but unverified case, are reviewed.The incompleteness of recovery in most cases

and the possibility of a fatal issue are stressed.Attention is drawn to the risk of precipitating thisserious complication by manipulating uncomplicatedcases of sciatica believed to be due to prolapsedintervertebral disc.

I wish to thank Mr. J. B. Pennybacker for his constanthelp and encouragement in the preparation of this paper.All the cases reported were under his care.

REFERENCESDandy, W. E. (1929). Arch. Surg. (Chicago), 19, 66).--(1942). J. Amer. med. Ass., 119, 474.Eyre-Brook, A. L. (1952). Brit. J. Surg., 39, 289.French, J. D. (1946). Surgery, 20, 718.

, and Payne, J. T. (1944). Ann. Surg., 120, 73.Garland, H., and Taverner, D. (1953). Brit. nmed. J., 1, 1405.Kaplan, A., and Umansky, A. L. (1951). Amer. J. Surg., 81, 262.Kennedy, F., Hyde, B., and Kaufman, S. (1948). J. nerv. ment.

Dis., 108, 32.Mixter, W. J., and Barr, J. S. (1934). New Engl. J. Med., 211, 210.Nicaud, P. (1947). Sem. H6p. Paris, 23, 2065.O'Connell, J. E. A. (1944). Surg. Gynec. Obstet., 79, 374.--(1950). Ann. royv. Coll. Surg. EngI., 6, 403.Rouques, L., David, M., and Pautrat, J. (1948). Bull. Soc. me;d.

H6p. Paris, 64, 18.Schneider, R. C. (1949). J. Bone Jt Surg., 31A, 566.Stookey, B. (1927). Arch. Neurol. Psychiat. (Chicago), 17, 151.Tolosa, E., and Ectors, L. (1953). Acta neurol. psychiat. belg., 53,

431.Ver Brugghen, A. (1945). Surg. Gynec. Obstet., 81, 269.

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J. Neurol. Neurosurg. Psychiat., · J. Neurol. Neurosurg. Psychiat., 1956, 19, 109. ASTUDYOF 25 CASES OF COMPRESSION OF THE CAUDA EQUINA BY PROLAPSED INTERVERTEBRAL DISCS BY W. BRYAN