J. Neurol. Neurosurg. Psychiat., 1965, 28, 344

A peculiar type of post-concussive 'blackout'LEONARD D. OSLER AND MICHAEL G. FUSILLO'

From the Department of Neurology, Boston University School of Medicine,Boston, Mass., U.S.A.

The purpose of this paper is to call attention to anunusual form of post-concussive 'blackout' and topresent two case reports which illustrate the syn-drome. One report includes a description of awitnessed attack and this encourages us to publishthese case reports. One of the reasons why so little iswritten and known about post-concussive 'black-outs' is that they are seldom seen by a doctor whocan examine the patient at the time of the attack.Although blackouts of one sort or another are

common after head injury, the type we describe israre. We have not found any previous description ofsuch cases, though little attempt is made to differen-tiate types of attack in the descriptions of post-concussive blackouts in the literature.The attacks we describe occur in people of good

previous personality of any age and either sex. Theyare characterized by severe headache preceding theblackout, complete and sudden loss of consciousnesswith falling and injury to the patient, absence ofphysical signs and E.E.G. changes, and the persist-ence of attacks for years without response to anyform of treatment.

CASE REPORTS

CASE 1 A 51-year-old, married, white housewife wasfirst seen on 13 October 1959 complaining of recurrentblackouts with headache, following a head injury on2 June 1959.While working as a sales clerk in a grocery store, she

slipped on a patch of jam from a broken jar and struckher head, and remembers falling to the floor striking herhead. She was unconscious after the accident until sheawoke in a community hospital 30 minutes later and re-covered normal consciousness at once without confusion(post-traumatic amnesia 30 minutes). There was noretrograde amnesia. Physical examination at that timewas normal except for bruising of the face. She wasdescribed as worried and anxious. Skull and chest radio-graphs, E.E.G., and lumbar puncture showed no abnor-mality. She remained in hospital three weeks and duringthe first week 'blacked out' twice in bed without warning.The attacks were not described in detail.1 Supported in part by a grant from the National Institutes of Health(TlNB-5126-07-897).

There was no previous history of serious illness oraccidents, and she had not visited a doctor for nine years.She was a happily married woman with 10 children, andthere was no family history of migraine, seizures, orfainting attacks.She was first examined by one of us (L.D.O.) on 10

October complaining of recurrent 'blackouts' and head-aches since the accident. The headache was temporal andoccipital in distribution, of dull aching character, oftenpresent on waking in the morning and unaccompanied bynausea or visual symptoms. Although she was seldom freeof headache, it became much worse for several hoursbefore each blackout.

Blackouts occurred suddenly two or three times a weekand she was forewarned by exacerbation of the headache.She would suddenly fall unconscious and on variousoccasions had cut her scalp, scraped her knees, broken herdentures, and acquired a black eye. In one attack, whilesitting at supper with the family, she fell forward with herhead on the table. The family stated that she was limpand unconscious for three minutes without frothing,tongue biting, enuresis, or convulsion. She was tired andcold after the attack, but not confused. The family hadnoted tension and irritability, poor concentration andsleep disorder since the accident, in this previouslyplacid person.

Physical examination showed a pleasant, well-nourishedwhite woman with a scar on the left forehead from arecent fall. The temperature and pulse rate were normal.The blood pressure was 140/80 mm. Hg. No abnormalitywas found on general or neurological examination andthe mental state was normal. There were no intracranialbruits. An E.E.G. was normal.The diagnosis of post-concussive syndrome with an

unusual seizure disorder was made and she was treatedwith dilantin and phenobarbitol.Over the next eight months she was seen at monthly

intervals and the blackouts gradually decreased innumber to four or five per month, without other changesin her condition. The following drugs in full dosagewere tried without effect: Dilantin, phenobarbitol,Equanil, Ergomar, ephedrine sulphate, Mysoline, Darvon,and Mesantoin. A high-calorie diet for six weeks, with50 g. of glucose at times of exacerbation of headache hadno effect.On 4 July 1960 the patient was admitted to the

Massachusetts Memorial Hospitals for full investigation.Physical examination showed no abnormality on admis-sion.

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A peculiar type ofpost-concussive 'blackout'

Routine blood examination, urine analysis, and stoolexamination were normal. The blood Hinton test wasnegative. Fasting blood sugar and two-hour post-prandialblood sugar levels were 81 mg.% and 117 mg.% re-spectively. The blood urea nitrogen was 8 mg. %. Lumbarpuncture gave clear fluid under normal pressure contain-ing 0 cells, protein 17 mg. %, and sugar 54 mg. %. The E.E.G., skull, and chest radiographs were normal. A cardiolo-gist found no abnormality of the cardiovascular systemand normal E.C.G. A pneumoencephalogram was normal.The patient was discharged unchanged.

Follow-up examinations at monthly intervals revealeda decrease in the number of blackouts to two or three amonth over the next year. They remained unchanged incharacter and unaffected by treatment.

In September 1961, for the first time a blackout wasfollowed by a complete right-sided hemisensory losswhich persisted for 48 hours. Her local doctor found noother physical signs. This right-sided sensory- loss alsofollowed two or three subsequent blackouts, clearingwithin 24 hours each time.On 14 January 1963, during a blackout, she fell and

stru&k her head on a concrete step with severe bruising,and was re-admitted to the Massachusetts MemorialHospitals.

Physical examination on admission was negative exceptfor severe bruising of the forehead. On the secondhospital day a blackout was witnessed by one of us (M.F.)during a physical examination.

The attack The patient had left her bed 15 secondspreviously and was standing at the time. Without warningshe became limp and unresponsive and would have fallenwithout support. She was returned to bed. The bloodpressure was 200/70 mm.Hg. The pulse rate was regularat 110 per minute. Respiratory rate was 16 per minute,regular and deep. There was no response to deep pain orpinprick stimulus. The pupils were equal and reacted tolight: there was no resistance to eye opening. Bothplantar reflexes were down-going. The trunk and extremi-ties showed no temperature change, and there was nopallor or sweating. After two minutes of unconsciousnessthe patient said, 'Oh, my God', opened her eyes, heldher forehead in both hands, and complained of severeheadache. After four to five minutes she regained fullconsciousness and complained of extreme tiredness.On questioning she was unaware of the attack except byinference from the severity of her headache. She was con-

fused at first and thought she had left her bed to go to thebathroom, but rapidly remembered that a physical exam-ination was in progress, and she soon recognized theexaminer. Throughout the attack the pulse and respiratoryrates did not change and the blood pressure remainedconstant. Unfortunately an E.E.G. could not be obtainedat the time but early the next day it was normal.

Routine investigations, including serum phosphorusand calcium estimations, were all normal, except for amild iron-deficiency anaemia. An electroencephalogramtaken on the tilt table with carotid artery compressionresulted in no change of pulse rate or blood pressure.However, the patient became unresponsive for a fewseconds and on awakening showed a transient weaknessof the right arm and leg. No definite change in the electro-

encephalogram accompanied this episode, but the recordwas marred by artefact and difficult to interpret.-For this reason a left carotid arteriogram was made on

11 March 1963 by Dr. Edward Spatz and proved normal.From the date of discharge onwards blackouts oc-

curred at the rate of one per month through the firstfour months of 1964. There have been none since April1964 to the present date. The legal case was concluded,and a cash settlement made in March 1964.

CASE 2 A 55-year-old, married, white, male, realestate brokerwas admitted to the Massachusetts MemorialHospitals on 3 December 1962 under the care of Dr.Charles Kane, complaining of blackouts preceded bysevere headache for the previous two years.

His illness began at midnight one day in November1960 when he was assaulted on the street, stabbed in thechest wall, and knocked unconscious for several minutes.There was no retrograde amnesia. He was confused onrecovering consciousness and drove home at night with-out headlights. The following day he noticed pain andswelling over the left parietal area of the skull, and he wasconfused until 1.30 p.m. Thus, the period of post-trau-matic amnesia lasted 13j hours. Three days later he beganto have blackouts, all similar in character, occurringonce or twice a week. His attacks began with a sensationof warmth in the epigastrium and excessive sweatingfollowed by a sharp pain over the left side of the headlasting for one minute. In some attacks, he was confusedduring the minute preceding the blackout. He then fellunconscious for several minutes, without convulsion,tongue biting or enuresis, but often bruising himself inthe attack. He was confused and drowsy after the attack.

In the two years before admission, the patient had beenadmitted to other Boston hospitals on three occasionsfor diagnostic study. Physical examination, skull radio-graphs, lumbar punctures, and electroencephalogramswith sleep study and carotid compression on a tilt tablehad all been normal. Bilateral carotid arteriograms andtwo pneumoencephalograms had been normal.He had been treated with Dilantin, Mysoline, Mesan-

toin, Librium, Dexamyl, Ritalin, Tofranil, and Bellergalin full dosage without effect.

His previous medical history included concussiveinjuries 26 years and seven years before admission,each without sequelae. There was a history of excessivedrinking many years previously, with one withdrawalseizure 22 years before. For 17 years he had been practic-ally a total abstainer, except for a short period followingthe death of a daughter 12 years ago. He had sufferedfrom jaundice, pneumonia with empyema, and influenzain childhood. There was an old history of duodenal ulcer.The family history was negative for epilepsy, migraine,

fainting attacks, and psychiatric illness.Physical examination revealed a well-developed, well-

nourished, alert, right-handed white man in no distress.The pulse rate, temperature, and respiratory rate were allnormal. The blood pressure was 130/70 mm. Hg. Apartfrom an amblyopic left eye present since childhood andinability to elicit the abdominal reflexes, the physical andneurological examination was normal. The mental statewas normal.

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Routine blood investigation, urine analysis, fastingblood sugar, blood urea nitrogen, blood Hinton test,total serum protein, and albumin-globulin ratio, skulland chest radiographs, electrocardiogram, and sleepelectroencephalogram were all normal. A radiograph ofthe cervical spine showed minimal hypertrophic osteo-arthritic change. Upper gastro-intestinal radiographsshowed a small hiatus hernia and scarring of the duodenalbulb. Bilateral brachial arteriograms showednormalfillingof subclavian, vertebral, and right internal and commoncarotid arteries. The left carotid arteries had beennormally filled on previous carotid arteriography.The patient had no blackouts during his six days in

hospital and was discharged unchanged.Follow-up examinations to the present date show that

the blackouts persist twice weekly, and that no medica-tion has influenced them.

REVIEW OF THE LITERATURE

In the best known series (Russell, 1932; Ascroft,1941; Denny-Brown, 1944; Penfield and Shaver,1945; Quadfasel and Walker, 1947; Rowbotham,1949; Walker, Caveness, Barrow and Allen, 1954;Wertheimer, 1956; Dereux and Dereux, 1958;Gurdjian andWebster, 1958 ;JennettandLewin, 1960;Lennox and Lennox, 1960; Paillas, Courson, Naquet,and Paillas, 1962) of open and closed head injuries inthe literature we have been unable to find anyreference to the type of blackout we describe, and webelieve this is the first detailed report of such cases.

Gastaut and Gastaut (1957) are two of the fewphysicians who have discussed the more unusualtypes of post-concussive blackout following closedhead injury. However, they confine themselves toattacks of syncope occurring within hours or days ofa head injury and ceasing within a year. Such attacksdo not resemble those in the two previous casereports.Walker and Jablon (1959), in a follow-up study of

932 cases of head injury in World War II, described12 cases with what they called 'borderline' attacks.The attacks were characterized by dizziness, light-headedness, and a faint or vague feeling without lossof consciousness, and the electroencephalogram wasnormal. They considered that the attacks fell intothe group described by Gowers as vaso-vagal attacks.In a second group of the 12 cases there were thosewhose dizzy spell led to a short period of un-consciousness called a 'blackout' but without fallingor injury. We do not feel that these cases are com-parable with our own.Hagenmuller (1960), in a statistical study of

2,941 cases of head injury, found 470 cases of post-traumatic epilepsy. Amongst these, 65 patientssuffered from 'falling attacks' without other stigmataof grand mal. He comments that in this group of 65cases there are many with the symptoms of a post-

concussive syndrome and unexplained blackouts.He feels that in some of these cases symptoms whichappear psychiatric may be masking true post-traumatic epilepsy. In the absence of detailed de-scription of these cases it is hard to assess theirstanding, but the group may well include cases suchas ours.

Jennett (1962) discussed 282 cases of closed headinjury, including 13 cases with so-called 'akinetic'general attacks. These patients suffered attacks ofunconsciousness lasting five to 30 minutes in whichthere was no convulsion and the patient was inertand limp. Although no further details of the attackare given and there is no mention of headache inrelation to the 'blackouts', it seems possible that thisgroup may include cases like those we describe. Thereare insufficient data to confirm this idea.Walker and Jablon (1961), in another follow-up

study of 739 cases with head wounds from WorldWar II, found 20 cases which showed '. . . epigastricfeelings, staring or blank spells, associated withdefinite loss of consciousness for as long as a minuteso that 10 of them fell down but did not convulse'.They consider that these 20 cases properly belong tothe convulsive group, although the type of epilepsyis not clear either from the case histories or theelectroencephalograms, which were abnormal infour cases.Symonds (1942), discussing unusual types of

seizure following contusion, mentions varieties ofdizziness which are less easily placed: 'I would drawattention in particular to one which is often describedas a "blackout". The onset is sudden, there is dim-ness of vision and a sense of insecurity of balancewhich may result in falling, without any descriptionof true vertigo. Consciousness is often momentarilydisturbed and may be lost. The main features ofthese attacks are syncopal rather than epileptic.Nevertheless in some cases after repetition there is atransition into epilepsy.' He then gives a case reportillustrating this type of blackout. The main featuresof our own cases suggest epilepsy rather than syn-cope.Matthews (1963), in a chapter discussing black-

outs under the subheading, 'The undiagnosableblackout', describes a case which closely resemblesour case 1, though without preceding concussion.'A woman of46 has suffered for 10 years from attacksof unconsciousness in which she falls, having fromone to six attacks a month. There is no warning, noconvulsion or incontinence, and she is unconsciousfor about five minutes. There do not appear to beany precipitating causes. Investigation has virtuallyruled out any of the causes described in this chapter,and anticonvulsants in great variety have neverinfluenced the frequency of the attacks.' This is the

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nearest description we have found in the literatureto our own case reports. Unfortunately, as in ourcases, the cause remains unexplained.The association of headache with blackout in our

cases led us to review the literature of the associationof epilepsy with migraine. Many authors (Liveing,1873; Gowers, 1907; Vining, 1922; Bramwell, 1926;Ely, 1930; Bickerstaff, 1961b; Lees and Watkins,1963) describe cases in which there is a clear anddirect transition from a migraine attack to an epilep-tic fit. However, most of these authors are agreedthat this is a rare occurrence and too much signific-ance must not be attached to the few cases in whichit occurs. The modem view is that the association ofmigraine with epilepsy may well be coincidental.Nevertheless, it certainly occurs, and this is ofimportance in considering later the possible causesof the attacks we are describing.

In brief then, a study of the literature revealsgroups of cases in many of the large series of headinjuries, which are hard to classify in the absence ofdetailed descriptions. Most authors regard theseblackouts as atypical convulsive disorders, but nomention is made of associated headache or theresponse of such cases to treatment.

DISCUSSION

In this paper we have attempted to isolate oneparticular form of post-concussive blackout andconsider its peculiar features in detail. These are:severe headache or head pain before an attack,unconsciousness without convulsion, persistence ofattacks for many years, lack of response to anti-convulsants or other drugs, and absence of E.E.G.abnormality. We must emphasize that there is noreport of an E.E.G. taken during an attack.The whole subject of these odd forms of post-

concussive blackout is a neglected one and meritsfurther study. Although we cannot be sure of thecause of the type we describe, certain possibilitiesdeserve discussion. These are syncope or faintingattacks, vasovagal attacks (Gowers), cerebrovascularinsufficiency attacks, hypoglycaemic attacks, cardiacattacks, functional or hysterical attacks, post-trau-matic epileptic attacks, and epileptic attacks pre-ceded by vascular change.We feel certain that the attacks are not simple

faints. Headache is unusual before fainting attacks,and the more common symptoms of dry mouth,blurred vision, sweating, and lightheadedness whichprecede a faint are not seen in these attacks. Theattacks are too sudden for faints and they result infalling with injury. Some of them occurred in bed orwhen the patient was sitting and they were associatedwith confusion. Finally the attack we witnessed had

none of the features of a faint, the patient's colourand blood pressure remaining normal.

Vasovagal attacks as described by Gowers (1907)were prolonged attacks attributed to disorder of themedullary centres. 'The attacks are never really brief.They seldom last less than ten minutes, and moreoften continue for half an hour or more.' 'Thesymptoms comprehend subjective gastric, respira-tory, and cardiac discomfort, sometimes cardiacpain and even a sense of impending death.' Suchattacks are quite unlike those we describe.The whole subject of cerebrovascular insufficiency

is poorly understood. Basically it implies disease ofcerebral or extra-cerebral arteries with periods whenthe blood pressure is inadequate to maintain cere-bral blood flow. During the attack witnessed by us,our patient, while still unconscious, showed no fallof blood pressure, no localizing signs, and the pulserate was rapid and the skin colour normal. Arterio-graphy was normal in both patients and the restingblood pressure was also normal. There would seemto be no serious basis for postulating that cerebro-vascular insufficiency caused the attacks.

Hypoglycaemia, as a cause, can be dismissed.Neither patient ever showed an abnormally lowblood sugar level, nor were the attacks related in anyway to meals. Case 1 was given a high calorie dietfor six weeks and advised to take sugar at the onsetof headache without any effect whatsoever on theattacks.

It is well known that various types of cardiacdisease may cause sudden blackouts. This cause wascarefully eliminated in our patients. Cardiologistsfound no evidence of heart disease in either patientand both showed normal electrocardiograms.Of major appeal to insurance company lawyers is

the explanation of such attacks on a functional orhysterical basis. Certainly many of the symptoms ofthe 'post-concussive syndrome' closely resemblethose found in patients of hysterical personality.

'Pressure type' headaches, dizziness, insomnia,faints, poor concentration, irritability, and alteredpersonality recur again and again in the post-con-cussive syndrome in persons whose personalitiesbefore the accident, though differing widely in type,show no evidence of hysterical illness. Indeed it isthis very repetition of the same group of symptoms incase after case of concussion regardless of age, sex,and previous personality, which convinces us that thepost-concussive syndrome has an organic basisrather than a psychological one. This is not todeny that secondary neurotic symptoms maybecomesuperimposed later. However, it is known that braininjury or disease in a person of normal personalitymay manifest itself by the appearance of floridhysterical symptoms long before any organic signs

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of the underlying brain change have becomeapparent. Knowing that brain tumour, multiplesclerosis, or the onset of arteriosclerosis may causea reversion from a normal to a more immature orhysterical personality, it is not unreasonable tosuppose that concussion can do the same. What wedo not believe is that patients in middle age andpreviously normal will show hysterical symptomsfor the first time, unless some organic change hasoccurred in the brain. Sargant and Slater (1963)have summed the matter up very clearly: '. . . inter-ference with bodily well being makes a man more,not less, liable to be disturbed by psychogenicstimuli. In the war neuroses, the psychological causesofanxiety and hysteria, till then relatively inoperative,began to have a greater effect when the man had lostseverely in weight. The change in physique had al-tered his disposition and his ability to adapt. Headinjuries illustrate the same phenomenon. Psychia-trists and neurologists are very apt to discover in theheadaches of the post-concussive the operation ofpsychological factors, and to conclude, therefore,that the proper treatment is psychotherapeutic.The change that has escaped notice is that the psy-chogenic stimuli which now produce symptomswould not have been effective before the injury. Thereal disability is not a hysterical headache, but anincreased susceptibility to hysteria: not the faints,attacks of giddiness, or ill temper which are soclearly due to the circumstances of the moment, butthe raised autonomic lability.'While we would accept this hypothesis as a reason-

able explanation of many of. the symptoms, in-cluding some faints and blackouts, which occur aspart of the post-concussive syndrome, we cannotaccept it for the type of blackout we are discussing.The sudden onset of these blackouts, the lack of aprecipitating cause, the injuries and severe bruisingwhich accompany the falls, and the severely painfulheadache which precedes the attack, make themunlike the type of blackout which represents aretrogression to a more infantile or hysterical per-sonality after head injury. In our experience suchblackouts seldom result in true unconsciousness orinjury, have a precipitating psychogenic stimulusand respond eventually to psychiatric help of onesort or another. Moreover in the attack witnessedby us there were no features of any typeof hystericalattack with which we are familiar. There was noprecipitating cause, the patient was unconscious,the eyes could be opened without resistance, and theattack was followed by confusion. Certainly neitherpatient showed a hysterical personality before theinjury. But it must be admitted that case 1 after theinjury did develop a hemisensory loss following someof her blackouts which would certainly be called

functional or hysterical. And though the attacksdiminished in frequency steadily over the years incase 1, it is a remarkable fact that they ceased en-tirely one month after the legal settlement. However,for the reasons given, we cannot easily accept theidea that these blackouts are functional, though wecertainly cannot unequivocally disprove it.

This brings us to the last two possibilities. Arethese attacks an unusual form of post-traumaticepilepsy, or some form of vascular headachewhich leads on to an epileptic seizure? In favour ofepilepsy is the suddenness of the attacks with falling,the injuries sustained by the patient, and the tran-sient confusion which follows them. It is well knownthat certain types of epileptic attack are not convul-sive, and the association of headache with epilepticseizure is also well known. The objections to a diag-nosis of post-traumatic epilepsy are first that theE.E.G. remains normal (though unfortunatelythere are no reports of any taken during a seizure),and secondly that the attacks are stubbornly re-sistant to all forms of anticonvulsant therapy. Ifthese are post-traumatic epileptic attacks then theyrepresent a form of short, non-convulsive, 'akinetic'attack unresponsive to the usual forms oftreatment.The remaining possibility is that concussion in

some way alters the autonomic control of bloodvessels leading to vascular headache and subsequentblackout. Certainly head injury may lead to morefrequent vascular headaches or 'migraine' in sus-ceptible people, i.e., those of migrainous personality.The difficulty comes in relating the preceding head-ache to the blackout. The modern view of the rela-tion of epilepsy to migraine is that it is coincidentaland that there is no evidence that the vascularchanges of migraine result in epileptic seizureexcept in predisposed persons. Bickerstaff (1961a)has described basilar artery migraine in which un-consciousness may result from the attack, but thereare well-marked preceding symptoms of basilarartery insufficiency in those cases, and nothing ofthis kind occurs in the type of blackouts we aredescribing. Finally no form of migraine therapy hasbeen of value in our cases.To sum up, we feel that the probable cause of the

attacks is one of the last two possibilities we havediscussed. Either the attacks arise from post-traumatic autonomic change of some sort, or theyare an unusual form of post-traumatic epilepsy.

Finally we wish to stress the need for furtherinvestigation of the post-concussive blackout. Werequire more information about the electroence-phalogram during or immediately following attacks.The medico-legal aspects of these cases demandgreater attention than they have received in the past.

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A peculiar type ofpost-concussive 'blackout'

SUMMARY

Two cases with an unusual type of post-concussiveblackout are described, with a report of a witnessedattack in one case. This type of blackout is precededby severe headache, refractory to all forms of treat-ment, persistent for many years, and seen in patientswithout physical signs or E.E.G. changes.The literature of the post-concussive blackout is

reviewed and its possible causes discussed. The con-clusion is reached that the attacks are probablyepileptic and may possibly be precipitated by achange in the autonomic control of cerebral bloodvessels.The need for further investigation and the medico-

legal importance of the subject is stressed.

We wish to thank Dr. Charles Kane for permission toreport case 2.

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Bickerstaff, E. R. (1961a). Basilar artery migraine. Lancet, 1, 15-17.(1961b). Impairment of consciousness in migraine. Ibid., 2,1057-1059.

Bramwell, E. (1926). Discussion on migraine. Brit. med. J., 2, 765-769.Denny-Brown, D. (1944). The clinical aspects of traumatic epilepsy.

Amer. J. Psychiat., 100, 585-592.Dereux, J., and Dereux, J. F. (1958). Les sequelles centrales des

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Ely, F. A. (1930). The migraine-epilepsy syndrome. A statisticalstudy of heredity. Arch. Neurol. Psychiat (Chic.), 24, 943-949.

Gastaut, H., and Gastaut, Y. (1957). Etude electroclinique des syn-copes post-traumatiques. Rev. Neurol., 96, 423-425.

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Lees, F., and Watkins, S. M. (1963). Loss ofconsciousness in migraine.Lancet, 2, 647-650.

Lennox, W. G., and Lennox, M. A. (1960). Epilepsy and RelatedDisorders. Little, Brown, Boston.

Liveing, E. (1873). On Megrim, Sick-Headache, and Some AlliedDisorders. Churchill, London.

Matthews, W. B. (1963). Practical Neurology. Blackwell, Oxford.Paillas, J. E., Courson, B., Naquet, R., and Paillas, N. (1962).

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Penfield, W., and Shaver, M. (1945). The incidence of traumaticepilepsy and headache after head injury in civil practice.Res. Publ. Ass. nerv. ment. Dis., 24, 620-634.

Quadfasel, F. A., and Walker, A. E. (1947). Problems of post-traumatic epilepsy in an army general hospital. Ibid., 26, 461-475.

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Wertheimer, P. (1956). tpilepsie traumatique. Reflexions a proposde 158 observations. Lyon chir., 52, 130-140.

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