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but in only one has it persisted. Presumably this is dueto their age (50-72, with a mean of 61 years).The " surgical " group is pleasing to deal with. It is

now our routine practice to defibrillate in the operating-theatre immediately after mitral valvotomy before thepatient has recovered from the anxsthetic. We have alsoused the same procedure in one patient with idiopathicfibrillation who required prostatectomy. For other remed-iable conditions-following thyroidectomy, pericardiec-tomy, or repair of an atrial septal defect-we usually waita week or two, then if sinus rhythm has not occurredspontaneously D.c. defibrillation is attempted. Whether

attempts to convert patients in group 5 above will provejustifiable remains to be seen. It is the only group ofwhich we have some doubt.

Contraindications to Atrial DefibrillationContraindications are few and probably the only dan-

gerous one, at least theoretically, is tight mitral stenosisawaiting valvotomy. The increased efficiency of theheart which results from sinus rhythm might well causepulmonary oedema in these patients. The proper time fordefibrillating these would be after valvotomy, in the

theatre, while the patient is still under the anxsthetic.Also unsuitable for conversion is the elderly patientknown to have a poor prognosis from some accompanyingdisease. The various conditions listed under group 2above obviously constitute contraindications until approp-riate treatment of the cause of the fibrillation has been

. shown to be ineffective in abolishing the arrhythmia.Summary

Of a hundred patients in whom atrial defibrillation wasattempted by means of a condenser discharge, eighty-fourwere converted to sinus rhythm. Of these forty-four sub-sequently reverted to atrial fibrillation, leaving a success-rate of 40%.

It is essential to position the direct-current shock in thecardiac cycle by means of an electronic synchroniser. Theoptimum position for the impulse seems to be at or nearthe nadir of the s wave of the electrocardiogram.

Anticoagulant therapy is not used routinely but onlyfor those patients with recent onset of fibrillation, a his-tory of embolism, mitral stenosis, or large hearts.

Anaesthesia of very short duration, using intravenousmethohexitone, is preferred because defibrillation with-out general anxsthesia is too unpleasant.

There was no evidence that any serious cardiac damageresulted. No burns were sustained.

In two patients, embolism-one cerebral and one pul-monary-may have resulted from treatment, but bothoccurred 2 days after conversion to sinus rhythm. Bothrecovered rapidly and completely.

Three patients in the series died, but no death wasdirectly related to treatment.The major indications for attempting conversion to

sinus rhythm are atrial fibrillation threatening life by vir-tue of an uncontrollable ventricular rate or because of

embolism, and atrial fibrillation perisisting after the under-lying cause has been treated.

It is too early to know whether a worth while propor-tion of patients will maintain sinus rhythm. Inevitablysome will revert to atrial fibrillation. For this reasonmaintenance therapy with digitalis is advised. Not onlyis there no convincing evidence that quinidine preventsreversion to atrial fibrillation, but the drug is dangerouswhen used for that purpose.

It is a pleasure to acknowledge our colleagues who have helped us

with this work, and in particular Mr. M. P. Curwen, who advisedon the trial of quinidine, Dr. A. W. Grogono, Dr. P. Taggart, andDr. 1. Weinbren, Mr. L. D. Kitchen, and Miss Joan Goulding, oursenior cardiographer, who has given many hours of unstinted helpoften at very inconvenient times.

REFERENCES

Aber, C. P. (1962) Thorax, 17, 274.Askey, J. M. (1962) Amer. J. Cardiol. 9, 491.Burchell, H. B. (1964) Lancet, i, 775.Cookson, H. (1930) Quart. J. Med. 23, 309.Garvin, C. F. (1941) Amer. Heart J. 21, 713.Goldman, M. J. (1960) Progr. cardiovasc. Dis. 2, 465.Graettinger, J. S., Carleton, R. A., Muenster, J. J. (1963) J. clin. Invest.

42, 938.Graham, G. K., Taylor, J. A., Ellis, L. B., Greenberg, D. J., Robbins,

S. L. (1951) Arch. intern. Med. 88, 532.Grogono, A. W. (1963) Lancet, ii, 1039.Hansen, W. R., McClendon, R. L., Kinsman, J. M. (1952) Amer. Heart J.

44, 499.Hanson, H. H., Rutledge, D. I. (1949) New Engl. J. Med. 240, 947.Killip, T. (1963) J. Amer. med. Ass. 186, 1.Kitchen, L. D. (1963) Lancet, ii, 1310.Kory, R. C., Meneely, G. R. (1951) J. clin. Invest. 30, 653.Lammerant, J., Veall, N., De Visscher, M. (1961) Nuclear Medicine, 1, 353.Lewis, T. (1922) Amer. J. med. Sci. 163, 781.Lown, B., Amarasingham, R., Neuman, J. (1962) J. Amer. med. Ass. 182, 548.

— (1963) Personal communication.Oram, S., Davies, J. P. H., Weinbren, I., Taggart, P. (1963) Lancet, ii, 159.Phillips, E., Levine, S. A. (1949) Amer. J. Med. 7, 478.Sokolow, M. (1939) Amer. Heart J. 18, 494.Trever, R. W. (1963) Ann. intern. Med. 59, 732.Wade, O. D., Bishop, J. M. (1962) Cardiac Output and Regional Blood

Flow. Oxford.Wetherbee, D. G., Brown, M. G., Holzman, D. (1952) Amer. J. med. Sci.

223, 667.

BURNED EPILEPTICSD. O. MAISELS

M.B. Edin., F.R.C.S.E.SENIOR REGISTRAR

B. V. M. CORPSM.B. St. And., F.R.C.S.E.

REGISTRAR

LIVERPOOL REGIONAL BURNS AND PLASTIC UNIT, WHISTON HOSPITAL,PRESCOT, LANCS

"

Lord, Have mercy on my son, for he is an epileptic and hesuffers terribly; for often he falls into the fire ..."-MATTt-tsw,xvn, 15 (Revised Standard Version).A COMMITTEE under the chairmanship of Lord Cohen

(Central Health Services Council 1956) estimated that theincidence of epilepsy in the general population was at

least 4 per 1000, and others have put the figure somewhathigher (Lancet 1961); this indicates that there must be inthe region of a quarter of a million epileptics in this

country. The problem of the burned epileptic, therefore,presents a great challenge, not only to those called uponto treat the burns of these unfortunate people but, in thefield of preventive medicine, also to the family doctor,public-health authorities, and the patients’ families.

Since March, 1962, when a new regional burns unitwas opened at Whiston Hospital, we have carried out aprospective study of all epileptics admitted. We herereport some of our findings in the patients admitted upto December, 1963, and discuss their implications.

FindingsIncidence

During the period under review, there were 351 admissionsto the unit for recent burns, of which 34 (i.e., 10%) were thedirect result of an epileptic fit. 1 epileptic patient was burnedtwice during this period, and 2 epileptics were readmitted forlate reconstructive surgery. Thus 35 epileptics were availablefor study.

During the same period a number of patients were admittedwith burns which resulted from " blackouts " due to under-lying conditions other than epilepsy. Many of these patientswere severely burned, and because most were elderly and thecommonest causes of the " blackouts " were hypertensionand/or degenerative cerebrovascular or cardiovascular disease,the mortality in this group was particularly high.

Fig. 1 shows the age and sex distribution of all the cases

admitted, and distinguishes the industrial from the domestic

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burns. The proportion of children is relatively low becausethe majority who get burned in this region are admitted to theAlder Hey Children’s Hospital. The 2 schoolboys whose burnswere classified as industrial were involved in an explosion ina school laboratory.There were no industrial cases among the epileptics, and in

fig. 2 we have set out the epileptic admissions against the totalnumber of domestic admissions.

Figs. 3 and 4 distinguish the burns from the scalds; in ourcases the burns tend to be deeper and are therefore a moreserious problem. Among the epileptics, burns are relativelymore common.

Admissions of males and females in the domestic categorywere about equal. Yet of the females, epileptics constituted17O (21 of 122), while for the males this figure was only 11 %(13 of 115). Thus, the epileptic females outnumbered themales in the proportion of approximately 3/2.Previous BurnsNo fewer than 16 of our epileptics had been burned pre-

viously as theresult of an

epileptic fit.The number of

times varied from once to " frequently ", and 1 patient had beenadmitted to Whiston Hospital alone on four previous occasions.Aura

Symptoms of warning of an impending epileptic fit may bedivided into prodromata and auras (Lennox and Lennox 1960).Prodromata precede the seizure by hours or days, auras byseconds or minutes. On this basis, only 6 of the 35 epilepticpatients had auras, and another 3 had prodromata. This groupof patients will be discussed later.FireguardsWe consider that all fires in an epileptic’s home should be

guarded. The optimum guard is the nursery type, and itshould be fixed to the wall, but a smaller guard, if firmly fixedcan be adequate. On this basis, the fireguards in our ep!ieptics’homes were as follows:

JJ

In 3 cases the patient was actually tending the fire when thefit occurred.

Medication

Epileptics are notorious for their inconsistency in takinganticonvulsive drugs. 8 of our

patients admitted that they hadneglected to take their drugs forvarying periods before admis-

sion ; and, while we have no

accurate information on this

point, it was our impression thatmost of the epileptics had fewerfits while in hospital where theirmedication was more regular.

IntelligenceAn attempt was made to assess

the intelligence of the epilepticpatients. This was done after

observing the patients duringtheir period in hospital and inconsultation with the nurses,who have much closer contact

with the patients than we doourselves.

" Low " intelligence we haveallotted to unemployable mentaldefects. " High " intelligence weregard as university standard.The other grades are self-explan-atory. The distribution of theoatients was:

and, as one might expect, thelower end of the scale is weighted.Car DrivingNone of our patients drove

either with or without a licence,and none had been involved in aroad accident as the result of afit.

Discussion

In Tempest’s series (1956)epileptics formed 7% of thetotal admissions to a burnsunit and 7 % of the domesticcases. In the present seriesno fewer than 10% of thetotal cases admitted were theresult of an epileptic fit, while

Fig. I-Total admissions to the burns unit, show-ing age and sex of patients, and distinguishingthe industrial from the domestic cases.

Fig. 3-A comparison of burns and scalds amongthe total admissions.

--- ’ !1111

Fig. 2-Age and sex distribution of domestic cases,comparing epileptics with total admissions.

Fig. 4-A comparison of burns and scalds amongthe epileptic admissions.

1300

the figure for the domestic cases was as high as 14%.Since the incidence of epilepsy in the general populationis only 0-4%, an epileptic is clearly in considerably greaterdanger of being burned than are other members of thepopulation.

There is no significant difference in the sex ratio ofepileptics in general (Gowers 1901, Lennox and Lennox1960, Lancet 1961, Walshe 1963), but we have seen inthis series that the females outnumbered the males byapproximately 3/2. None of our epileptics was burned atwork, and the greater number of burned females is pos-sibly a reflection of the greater risks they run in the courseof their housework.

It is commonly believed that after a burn, an epilepticmay have a long period of freedom from fits. This wasnot the experience of any of the 1.6 patients in our serieswho had been burnt previously, and furthermore manyof the whole group of patients included in this study hadfits in hospital, though less often. We have attributed thisimprovement to regular anticonvulsive therapy.Of 130 epileptic outpatients questioned by Phemister

(1961), about two-thirds of the men who were not inade-quate or unemployable admitted to driving. They claimedthat they would not have a fit while driving or would haveadequate warning. If they are to be believed, none hadhad a serious accident, which, as Phemister comments," is a remarkable enough finding in any comparable groupof ’ normal’ drivers ". Not all epileptic drivers are sofortunate, as borne out by Elliott (1963), who reportedfive accidents caused by epileptic drivers having fits whilein charge of a motor vehicle, in a period of 31/2 years inKent alone.

In view of Phemister’s remarks, we became interestedin auras for their value as a protective mechanism againstburning. Obviously prodromata cannot be expected tobe of much help. Some interesting facts emerge fromcloser consideration of the 6 patients who experiencedauras which should have protected them. In 2 of these

patients, the aura was only an occasional feature and didnot precede the fits in which they were burned. Theyhad both been burned previously in a fit, 1 of them once,and the other on two occasions. A 3rd patient who is inthe habit of lying down when the aura comes on admittedthat sometimes " she thinks she’ll chance it ", and in factdid so once too often, sustaining very severe burns. The4th patient was a man who always sits or lies down whenhe experiences the aura. When he was burned he hadonly just got out of bed and he was still half asleep, andhe said that this was the first fit he had ever had without

any warning. The other 2 patients who claim to haveauras are both of extremely low intelligence and mightnot be expected to take suitable action.Gowers (1901) found that 57% of a series of 2013

epileptics experienced auras-a figure which agrees veryclosely with Lennox and Cobb’s 56% of 1359 cases (1933).In the present series only 17% of the patients had auras,and, as explained above, the effective figure is probablyeven lower. This seems to substantiate the view that ina reasonably intelligent patient, an aura is in fact a veryvaluable protective mechanism.

Because the patient who is burned in an epileptic fit isunable to remove himself from the source of heat while heis unconscious, it follows that the burns he sustains are

commonly very deep indeed. The epileptic who falls withhis head in the fire sustains a burn so characteristicallydeep and horrible as to make him immediately recognisableas an epileptic from the nature of his burns alone (fig. 5).

Fig. 5-Typical epileptic burns of face and scalp soon after

adnzission.

Fig. 6-The type of burn sustained by an epileptic which will resultin at least permanent loss of function.

Similarly, a hand or foot may be completely charred by thetime the unfortunate patient recovers sufficiently to removeit from the fire, or is discovered by a relative (fig. 6).Furthermore, the clothing may be ignited and the patientunable to beat out the flames.

For all these reasons it is absolutely imperative that allopen fires, and this includes electric radiators, should beadequately guarded. It is desirable from all points of viewfor the epileptic to lead as normal a life as possible, and itis unreasonable and impracticable to expect an epilepticwoman to give up all housework. Nevertheless, we feelthat the dangers are so great, that no epileptic should tendan open fire, this particular chore being delegated to someother member of the family.Tempest (1956) pointed out that many epileptics suffer

mental deterioration, and for this and other reasons theyneglect to take their drugs. Our findings accord withthis view.

Conclusions

We have been surprised ourselves at the magnitude ofthe problem which the burned epileptic presents in thecommunity. Quite apart from humanitarian considera-tions, this 10% of admissions places a heavy load on aburns service, not only because of the numbers involvedbut also because of the severity of many of these burns,which may entail years of reconstructive surgery after skincover is obtained. ,

The problem is largely one of preventive medicine whichfalls within the sphere of family doctors and public-healthauthorities. We make a plea to all who come in contactwith epileptics and their families to warn them of thedangers, and to instruct them in preventive measures. Itseems that the epileptic who never or only occasionally haswarning of an impending fit is especially at risk, and thismight profitably be pointed out. All patients should be

1301

encouraged to install adequate guards on all open fires, andto avoid tending the fires themselves.Because of the important preventive implications of the

findings, we have enlisted the assistance of Prof. Andrew B.Semple, medical officer of health for the city of Liverpool.He has very kindly agreed to undertake a full study of homeconditions and other relative features of burned epilepticsin Liverpool, and we hope that the findings of this studywill contribute to the prevention of these cases.

SummaryOf 351 patients admitted to a regional burns unit in a

period of twenty-one months, 34 or nearly 10% were thereas the direct result of an epileptic fit.The sex ratio, incidence of auras, previous burns, use of

adequate fire guards, and other features in the epilepticsare described.These patients were admitted under the care of Mr. A. H. M.

Littlewood and Mr. L. B. Scott, to whom we are grateful for per-mission to publish. The photographs were taken by Mr. R. R. Greenand our thanks are also due to Mrs. G. Hayes for secretarial assistance.

REFERENCES

Central Health Services Council (1956) Report of the Sub-committee on theMedical Care of Epileptics. H.M. Stationery Office.

Elliott, A. (1963) Brit. med. J. i, 1334.Gowers, W. R. (1901) Epilepsy and Other Chronic Convulsive Diseases:

Their Causes, Symptoms and Treatment. London.Lancet (1961) i, 438.Lennox, W. G., Cobb, S. (1933) Arch. Neurol. Psychiat. 30, 374.

— Lennox, M. A. (1960) Epilepsy and Related Disorders. London.Phemister, J. C. (1961) Lancet, i, 1276.Tempest, M. N. (1956) Brit. med. J. i, 1387.Walshe, F. M. R. (1963) Diseases of the Nervous System. Edinburgh and

London.

SEROLOGICAL FINDINGS IN

CARCINOMATOUS NEUROMYOPATHY

P. C. WILKINSONM.B. Lond.

LECTURER IN BACTERIOLOGY,DEPARTMENT OF BACTERIOLOGY, THE LONDON HOSPITAL, E.1*

"Present address: Department of Bacteriology, Western Infirmary, Glasgow.

ALTHOUGH the non-metastatic neurological syndromesassociated with carcinoma in man have become increasinglywell recognised (Denny Brown 1948, Brain et al. 1951,Henson et al. 1954, Brain 1963), very little work suggestinga possible mechanism for their setiology has been pub-lished. In recent years, increasing attention has been paidto the role of immune mechanisms in diseases of thenervous system, stimulated particularly by work on

experimental allergic encephalomyelitis (Kies and Alford1959) and neuritis (Waxman and Adams 1955) in animals.Recently Melnick (1963) has reported circulating anti-bodies to neuronal tissue in man in the Guillain-Barre

syndrome and has suggested that they may occur in otherneuropathies. The present paper describes the serologicalfindings in a group of patients with malignant diseasewho presented with neuromyopathy. It forms part of aclinical, histological, and experimental survey of thesesyndromes, some clinical findings from which have alreadybeen published (Croft and Wilkinson 1963). All patientswere screened and classified clinically by a neurologicalteam before they were included in the series, and

necropsies were performed on the majority of patientswho died.

Materials and Methods

34 cases of carcinomatous neuromyopathy were studied.Complement-fixation Test (C.F.T.).-A complement-fixation

technique identical to that described by White et al. (1961) wasemployed. Two minimal hasmolytic doses of complement wereincubated overnight at 4°C with appropriate dilutions of testserum and antigen. 2% of sheep cells were added next day, and

the test was read after incubation at 37°C for 30 minutes. All

positive sera were titrated to the end-point, and only thoseshowing complete fixation at a dilution of 1/16 or higher wereincluded in the series as positive.

Sera were taken from 10-15 ml. of blood and stored at-20°C.Tissue antigens were made up from normal human brain,

sciatic nerve, thyroid, liver, skeletal muscle, placenta, lung, andlung carcinoma, and from guineapig brain. 25% (weight/volume) saline extracts were made up by homogenisation in0-15M buffered sodium chloride at pH 7-0. These extractswere spun at 3000 r.p.m. in an angle centrifuge, and after over-night storage at -20°C the supernates were spun again at

10,000 r.p.m. The resultant clear solutions were stored in smallaliquots at either -20°C or +4°C with 0-03% sodium azide aspreservative. Fresh brain extracts were made up at frequentintervals because they were found to lose their activity rapidlywhether stored at +4°C, -20°C, or -70°C.

In a number of tests the preparation of antigens wasmodified to test the effect of simple physicochemicalprecedures on their ability to give complement-fixationreactions with positive sera.

Heat.-Saline brain extracts were either heated to 56°C for60 minutes or autoclaved at 10 lb. per sq. in. for 20 minutes.

Alcohol and acetone.-One aliquot of fresh brain was homo-genised in 10 volumes of absolute alcohol, and another in 10volumes of acetone. The homogenates were incubated at 37°Cfor 2 hours and then spun. The precipitates were washed threetimes in saline, and saline extracts were made up from them.

Formalin was added to saline extracts of human brain tofinal concentration of 0-1%. The anti-complementary effect ofthese extracts was slightly increased by this manoeuvre.

Clostridium welchii filtrate.-A saline brain extract was in-cubated at 37°C for 24 hours with an equal volume of a Seitzfiltrate of an overnight iron-strip-broth culture of Cl. welchii.This extract was used at double strength in complement-fixation tests, which included a control tube with Cl. welchii-filtrate-treated brain but without complement to test for directhasmolytic activity by the filtrate.

Brain Results

The results of complement-fixation tests against wholehuman brain in carcinomatous neuromyopathy and invarious other conditions are shown in table i. Organ-specific antibodies were those reacting with brain aloneand not with the other tissues tested (thyroid, muscle,liver, placenta, gastric mucosa, and lung). Non-organ-specific antibodies were those reacting with many or allof these other tissues as well as with brain. Only thosepatients in whom the diagnosis was confirmed by a clinicalneurological team or at necropsy were included in the

carcinomatous-neuromyopathy group. These patientswere examined by Dr. Marcia Wilkinson, or by Dr. P. B.Croft, who previously reported the clinical findings in thisgroup of cases (Croft and Wilkinson 1963). All other caseswere classified as doubtful. The " other neurologicalTABLE I-COMPLEMENT-FIXATION TESTS AGAINST BRAIN IN CARCINO-

MATOUS NEUROPATHY AND OTHER GROUPS (SERUM TITRE 1/16OR HIGHER)

*Case of systemic lupus erythematosus.