BRITISH MEDICAL JOURNALLONDON SATURDAY JULY 2 1960

DISEASE OF MIND AND DISORDER OF BRAIN*BY

Sir CHARLES SYMONDS, K.B.E., C.B., D.M., F.R.C.P.Honorary Consultant Physician, National Hospital, Queen Square; Consulting Physician Emeritus for Nervous Diseases,

Guy's Hospital, London

The centenary of the foundation of the NationalHospital, Queen Square, is a fitting occasion for thepraise of famous men, and it is opportune that the SirWilliam Gowers Memorial Lecture falls due to bedelivered at this time. My predecessor in this task drewfor us, in his brilliant and inimitable style, a picture ofGowers better than any I could present to you, andpointed the contrast between Gowers and HughlingsJackson, the naturalist and the philosopher (Walshe,1956). It is to the fortunate association in the earlydays of the Hospital of two men of genius so differentin their outlook, yet alike in their aims, that we owe inlarge measure the tradition which has inspired theirsuccessors to this day. It is difficult to know which hashad the greater influence, for their interests werecomplementary and combined to form a discipline ofclinical neurology at a scientific level far higher thanthat generally obtaining in medicine at that time.Jackson's has been the greater fame. We have, perhaps,taken too much for granted what we owe to Gowers,both for his own minute and accurate descriptions ofdisease and the methods of observation he developedand enjoined upon others. If in this lecture I refer toJackson as often as to Gowers it is because theircontributions to my subject were of equal importanceand closely linked.

The Biochemical LesionGowers's greatest interest was in the patterns of

nervous disorder and their classification. He soughtespecially for symptoms and signs that could be relatedto structural lesions and was convinced that in diseasessuch as paralysis agitans more refined methods ofobservation would show structural damage at the timeunseen. He did not, however, believe that themicroscope would necessarily reveal such lesions evenin the most severe interruption of neural function ifthis were reversible. Thus he was impressed by thefailure to discover any histological abnormality in fatalcases of acute ascending paralysis of the Landry type,and by his observation of occasional rapid recoveryfrom the illness. The interpretation he put forward wasthat the paralysis was due to some toxic influence actingupon "the ramification . . . in which the pyramidalfibres must end in the grey matter and by which theyare connected with the lower segment" (Gowers, 1886).He adduced, as an example of the kind of effect he hadin mind, the abolition of the function of nerve-endingsin muscle by curare. This is an instance of his ability,from his wide knowledge of medicine and its*Gowers Memorial Lecture given at B.M.A. House, London,

on June 23, 1960.

physiological background, to give whatever speculationin which he might indulge a foundation in fact. Heenvisaged what we should to-day call a biochemicallesion.Many other examples might be quoted of his power

of deducing a principle from clinical observation andfollowing it through to its logical conclusion. Indiscussing the selective, symmetrical incidence of leadpalsy, after rejecting other hypotheses he says:

"It can alone be due to some slight inherentdifference in the minute constitution of the nerveswhich enables the atoms of lead to join with theatoms and molecules of these nerves and derange theprocess of their nutrition, acting on these nerve fibresand not on others. . . When we think of the fact howgreat is its significance. Those nerve fibres, for somereason, have not the power of resistance to a morbidchemical agent as other nerves have. They differin their behaviour when a molecule of a metallicpoison is presented to them, although they are thesame in the minutest scrutiny we can give them, thesame to every other test we can apply. . . The variouseffects of different poisons bring before us in almoststartling clearness how profound is the influence ofdifferences far beyond our powers of scrutiny."

(Gowers, 1895.)

Evidence for a Physical BasisGowers was also an ardent collector of cases in which

the phenomena of nervous disorder were mainly orwholly subjective but presented features sufficientlydistinct to be clearly recognizable in a group of suchcases. This for him was convincing evidence of aphysical, as opposed to a psychogenic, basis. Nowhereis this conviction more clearly expressed than in hiscomment on the subjective phenomena of what hecalled the vaso-vagal attack. "To dismiss it," he says," as a hysterical fancy is simply to push it out of sightwith the foot. So definite a feeling must have adefinite origin" (Gowers, 1907).

His insistence on the rule that symptoms should notbe regarded as hysterical because they are strange ledhim to many valuable conclusions, some of which arestill neglected. His description of what he calledencephalic vertigo as an occasional occurrence inlabyrinthine disease could not be clearer. " It differsfrom the ordinary sensation of subjective vertigo inseeming to be within the skull, not to involve the headas a whole. The brain seems to the sufferer to beturning over and over or round and round. . . . It isnot only strange in character but peculiarly distressing."

5191B

2 JULY 2, 1960 DISEASE OF MIND AND DISORDER OF BRAIN

(Gowers, 1907.) He presents illustrative cases. Yethalf a century later patients with this symptom are oftendiagnosed as hysterical simply because it is so strange.

In common with other writers of his time, Gowersobserved a distinction between organic and functionalnervous diseases. He was careful, however, to definewhat he meant by these terms. "The term organicdisease," he writes in the introduction to his textbook," as commonly used means visible disease. Butvisibility is partly relative: it depends upon the meansof vision." He goes on to remark upon the use of themicroscope and the development of staining methodswhich have rendered visible changes that could notbefore be seen, but adds: "Molecular changes innutrition, considered as such, must be colossal to bedetected. Such alterations not sufficient to be seen

probably constitute the morbid process in many diseasesthat are commonly regarded as functional. Hence we

may distinguish a class of 'nutritional disease ' fromthose that consist in a mere derangement of function.While distinguishing these two classes we cannotentirely separate them, because nutrition and functionare mutually dependent, and prolonged functionaldisturbances may determine nutritional change."Gowers wrote little about mental disorder. It almost

seems as if he found the subject distasteful. Indiscussing the mental symptoms of organic disease ofthe brain he writes : "With the much disputed relationof mind to brain the physician has nothing to do"(Gowers, 1886). Nevertheless, some of his observationsand conclusions-the validity of subjective symptomsas evidence of a physical cause, the selective action ofpoisons upon a group of apparently identical neurones,

and the concept of the invisible lesion-have an

important bearing upon the psychological symptoms offunctional nervous disorder.

Examples of Psychical DisorderJackson wrote much about psychological disorder and

repeatedly insisted upon the distinction betweenpsychical and physical phenomena, but applied to bothhis concept of dissolution as a process which as theresult of a loss of function permitted the appearance

of positive symptoms representing the action of thehealthy parts remaining. The simplest example of thiskind illustrating psychical disorder is agnosia, and it isin the most restricted forms of agnosia that there isgreatest opportunity for observation. Such cases are

rare, and this must be my justification for recallingone that I have previously recorded. The patient was

a soldier aged 21, intelligent, quiet, and reserved. Asthe result of a very small penetrating gunshot woundin the occipital region he lost the perception of distancewithout any other disability. The evidence for this isto be found in the report to which I have alluded(Symonds, 1945).

This young man, who came under our observation a

fortnight after his injury, was then ambulant and active.He made no complaint of anything wrong, but peculiar-ities in his behaviour attracted attention. He was

disinclined to move about, and, when he did so,

progressed in a slow, hesitant manner. When he walked

along a corridor in which there was a corner he

approached the wall facing him with his arms out-

stretched, turning only when he felt it. He was examined

his behaviour was hysterical. It is to the credit of Dr.Charles Phillips that he first suggested the true explana-tion, but this at first was doubted because of curiousdiscrepancies. When the patient was asked to estimatethe distance of a wall opposite to him in the emptyroom in which he was examined he could not do so.

But when he stood at one end of his ward and was

asked to judge the length of it he did so, after an oddpause, with fair accuracy. The explanation, whenprovided by himself, was simple. He knew roughly whatwas the usual width of a bed and the distance betweenbeds, and by multiplying this by the number of bedshad arrived at his estimate. There were many otherinstances of this kind of behaviour.

I have related this case as an example of psychologicaldisorder which at first, because it was so peculiar, was

thought to be hysterical, but in fact represented theattempt of the mind to work when deprived of one ofits tools. I submit that psychological disorder of muchgreater complexity deserves examination from this pointof view.

In the case mentioned there was a demonstrablerelation between local brain damage and psychicalsymptoms. The next group of cases to be consideredis that in which there are psychical symptoms of aparticular kind associated with evidence of organicdisease of the brain, but with no demonstrable localiza-tion. Of the many possible examples I shall take two.The first is that of encephalitis, leaving in its wake avery distinct pattern of intellectual impairment com-prising a persistent retrograde amnesia covering severalyears, and gross defect of recent memory with littleinterference with other intellectual functions. Immediateretention is unimpaired, and skills and knowledgeacquired before the illness are preserved. The patientis therefore able to achieve a good score on intelligencetests, failing only on those requiring recent memory.He is able, for example, to retain eight digits, do serialsubtractions and similar tasks quite well, and yet failsto remember any item of a name, address, and flowergiven to him five minutes previously. Recognition isaffected as well as recall, and learning of new materialis impossible. Comparable symptoms have beenobserved after bilateral temporal lobe resection.Of equal interest is the defect of moral sense resulting

in children from encephalitis lethargica. Manyexamples were recorded at the time of the epidemicwithout recognizable impairment of intellectual function,and sometimes without any of the physical sequelaecommonly observed after the illness. There can be no

doubt of the organic basis of the defect, which is usuallyirreversible, though we have no clues in this instance forlocalization. What is most remarkable is that thissequel did not occur in adults, suggesting that whateverstructures are involved are essential for learning todistinguish between right and wrong but not necessary

for the preservation of such distinction, or, to put it inanother way, if learning has continued long enough theprocess involved has produced physical changes in sucha widespread net of neurones that local damage has notthe same effect as it would have at an earlier stage ofthe process. Whatever the interpretation may be, we

seem to be dealing with a kind of moral agnosia, andobserve the mind deprived of this sense proceeding to themost ruthless extremes of antisocial conduct. In thisthere is reasoned direction, and often great skill inescaping detection and puniishment. Granted the defect,

by several experienced observers, who concluded that

BIuTISHMEDICAL JOURNAL

thought, feeling, and behaviour are rational.

DISEASE OF MIND AND DISORDER OF BRAIN BRrrIH 3MEDICAL JOURNAL

Functional PsychosesWe now come to the much larger category of

psychical disorders in which there is no direct evidenceof cerebral disease, of which the most important are

the functional psychoses. Before embarking on thissubject I shall refer to what Jackson had to say uponit in his essay on " The Factors of Insanities " (Jackson,1894).

"In every insanity more or less of the highestcerebral centres is out of function, temporarily or

permanently, from some pathological process; for mypresent limited purpose it m-atters little what thatprocess may be. It only matters as the pathologicalprocesses produce loss of function, that is dissolution,of more or less of the highest centres. I do not usethe term function in the sense often given to it inclinical accounts of nervous maladies, as, for example,when it is said of a patient that ' his case is entirelyfunctional.' I do not believe that there is such a

thing as loss or defect of function of any nervouselements without a proportionate material alterationof their structure and nutrition. Of course the separa-tion into structure, nutrition and function of thenervous system is artificial; it is merely a convenientdevice, just as the separation into the surface, weightand mass of a body is."He then goes on to enumerate what he calls the four

factors of insanities as they may be applied to the con-

fusion and allied conditions in terms of his theory ofdissolution, and continues thus:

" Although I speak of dissolution of the highestcerebral centres as if it were uniform-as if all thedivisions of these centres were ' evenly ' affected-itis clear enough that there are local dissolutions ofthose centres. That there are different kinds as wellas different degrees of insanity is evident-melancholiaand general paralysis for two examples. Differentregions of the highest cerebral centres undergo disso-lution in different kinds of insanity."He ends his essay with the surmise that the causes

of certain of the insanities may be found to lie notwithin the brain itself, but in the organs which supplyits nourishment.Although their approach is different we find little

divergence between the conclusions arrived at byGowers and by Jackson about what is meant byfunctional nervous disorder. Jackson, however, wentmuch farther along the road that leads from neurologytowards psychiatry. It is, I think, natural that he shouldhave taken melancholia as one of his examples of localdissolution, for the clinical pattern of this illness in itssevere forms is remarkably constant and distinct. " Sodefinite a feeling must have a definite origin." Gowers'sdictum is all the more applicable if the psychosis isregarded not only as a disorder of mood but a disorderof feeling which will account for the great variety ofdysaesthesiae that may be observed in the illness-headdiscomforts, general malaise, bodily aching, and disturb-ance of visceral feeling, for example. In the milderdegrees of the illness it is of symptoms of this kindthat the patient may chiefly complain. The increasingrecognition of these milder degrees and of their greatfrequency has led to difficulties in terminology, whichhave not yet been solved. Those patients who are mildlyaffected are obviously not insane, yet the illness is oftencalled psychotic so that the affective disorder may bedistinguished from that which is termed neurotic.

Affective and Schizophrenic IllnessConcerning the distinction between endogenous and

reactive forms of depressive illness I will say nothingexcept that I am doubtful of its validity. It will sufficefor my present argument if it is admitted that there aremany cases both of the severe and of the mild degreein which the onset is without discoverable cause,physical or psychogenic. They are endogenous so faras we can see. I would like to add, however, that thisis equally true of some cases in which the disorder ofaffect is not depression but fear; for these patients,because they are anxious instead of depressed andbecause anxiety is a pure form is not generally acceptedas a characteristic of endogenous affective disorder, areoften regarded as suffering from a neurosis.The arguments for supporting Jackson's assumption

that this disease of mind represents a regional disorderof function in the brain are many. We may first con-sider the evidence in favour of believing that the illnesshas a physical basis irrespective of localization. Someof the arguments are equally applicable to the otherfunctional psychosis-schizophrenia, and I will take firstthose observations which are relevant to both diseases.The absence of psychogenic cause is notable, though itmust be regarded critically owing to the possibility ofemotional stress which the subject is concealing or ofwhich he is unaware. Much has been made ofunconscious emotional disorder in the aetiology of thepsychoses, especially by the psychoanalytic school.Demonstrable proof of this is lacking, and it is, I think,fair to assume that the patient who complains that hefeels sad although he has a satisfactory job, a goodwife, and a comfortable home, and believes that he hasno reason whatever for unhappiness, is usually speakingthe truth. The illness is as much a foreign body as hethinks. In the schizophrenic it is harder to estimatepsychogenic factors in the aetiology owing to his thoughtdisorder; but again, when all the facts are considered,psychogenesis is conspicuously absent in most cases.The distinct clinical pattern of the illness has alreadybeen mentioned. It is again more readily observed inthe affective disorder than in schizophrenia, but of eitherillness it may be said that the symptoms have as muchvalidity for the experienced clinician as those of a

duodenal ulcer or angina.The strongest evidence, however, for a physical basis

is the genetic factor as demonstrated especially by thestudy of uniovular twins. In Kallmann's (1953) seriesthe percentage of twin partners similarly affected bymanic-depressive psychosis was for uniovular twins96% and for binovular twins 25% ; in the case of schizo-phrenia the concordance for uniovular twins was 86%and for binovular twins 15%. Slater's figures for con-

cordance in a similar investigation of the affectivedisorder, analysed by Fonseca (1959), were in uniovulartwins 75%, in binovular twins 38%. These figures com-pare with an expected incidence for the generalpopulation of 0.4% for manic-depressive psychosis and0.8% for schizophrenia.

Spontaneous recovery from an episode of manic-depressive illness-as much endogenous as the onset-is further evidence for a reversible physical disorder.Moreover, the response of depressive illness to electricconvulsion therapy, mysterious though it be, is clearlya physical effect. On the other side, it must be observedthat in neither the affective disorder nor in schizophreniahas there been any histological proof of cerebral disease,

JULY 2, 1960

4 JULY 2, 1960 DISEASE OF MIND AND DISORDER OF BRAIN

with the possible exception in schizophrenia of the dwarfcells in the thalamus found by the Vogts. In the affectivedisorder one might accept without difficulty the absenceof histological change; for the illness, however severe

and of whatever duration, may be reversible. I havemyself observed recovery from a certifiable depressiveillness of ten years' duration in a woman at that timeaged 60. Once improvement began recovery was com-

plete in a few weeks. This was before the advent ofE.C.T. In schizophrenia histological lesions are more

to be expected. Perhaps they may yet be seen. It isnot yet certain that the lesions responsible for paralysishave been identified. On the other hand, the lesion,though irreversible, may be biochemical, without visiblechange, as Gowers surmised might be true of many

functional disorders.We have to conclude that in neither of the functional

psychoses is there proof of organic cerebral disease or

even of selective biochemical disorder. The evidencefor their physical basis is strong but circumstantial. Itis nevertheless worth pursuing the inquiry further andasking what evidence may be found for supposing thatif a physical basis does exist it is of a focal or regionalkind. I use these terms not in a morphological sense,

but to indicate the possibility that particular systems ofneurones may be involved. Here again the distinctnessof the clinical pattern may be put forward as a reason

for supposing that in each of the diseases under consider-ation particular, and different, neurophysiologicaldispositions are involved. Further evidence has becomeavailable in recent years from the use of drugs.

Specific Patterns Produced by DrugsOne of the most interesting experiences for

neurologists of my own generation was the appearanceof Parkinsonism and other stereotyped motorphenomena after encephalitis lethargica. Here was an

example, comparable with that of a lead palsy, of a

remarkable selective action upon particular units of thecentral nervous system by a new neurotropic virus.Equally remarkable has been the experience in recentyears of witnessing identical symptoms, including theoculogyric crisis, after the administration of new drugs(Heaton-Ward, Carpenter, and Jancac, 1959). We may

conclude that the disease and the drug have each affectedthe same region, and this observation is likewise relevantto the effect of drugs in causing specific patterns ofpsychical disorder.For some years it had been noted that mescaline would

produce in normal subjects psychological disorder insome respects resembling that of schizophrenia. It wasby chance, however, that Hofman, in 1943, in the pursuitof chemical experiments with L.S.D.25, discovered inhimself remarkable effects, which he subsequentlyproved to be reproducible by the ingestion of minutequantities of this drug. Out of this work has evolveda considerable literature dealing with the resemblanceof the psychological disorder thus produced to that ofschizophrenia. The hallucinations, thought disorder,and disturbance of affect and behaviour have beenregarded by many as representing a model of schizo-phrenic psychosis, but critical consideration of thepublished data makes this doubtful. The fact remains,however, that L.S.D.25 can cause psychological disorderof a very complex and fairly constant pattern. Whetherthe experimental psychosis exactly resembles schizo-phrenia or not, the experiment has shown that a

psychosis of this type can be produced by the action

of a particular chemical substance, which may bepresumed to act upon a particular region of the brain.

It is also worthy of remark that certain drugs, ofwhich imipramine is the current example, can have a

specific action in relieving depressive illness. On theother side, it has been learned by chance that Rauwolfiaserpentina prescribed for arterial hypertension may

sometimes cause an illness hardly distinguishable froma depressive psychosis.

Manifestations of EpilepsyEpilepsy, as Jackson was the first to observe, provides

an opportunity of studying psychological symptoms ofvaried and distinct patterns, and establishing some

degree of correspondence of the pattern with the regionof the brain involved in the epileptic discharge. Owinglargely to the work of Penfield and his collaborators,a considerable body of data has been accumulated on

this subject. I shall first consider those observationsthat are relevant to endogenous effective disorder. Theyhave been studied in detail by Denis Williams (1956).That a paroxysmal disorder of mood may occur as a

manifestation of epilepsy was recognized by Jacksonand has repeatedly been observed since, and it isgenerally agreed that fear is the most frequent experi-ence. This is commonly described by the sufferer as

irrational and without relation to any relevant thoughtor memory. The patient tells us simply that he isintensely frightened of he knows not what. He recog-nizes the emotion as unnatural. He may even say thatit seems to be coming from inside him. The subjectiveexperience, except for its brevity, seems identical withthat of the patient with an endogenous fear state, whocomplains of a state of fear and foreboding for whichthere is no cause.

Ictal depression is less often met with, but again, apartfrom its duration, is indistinguishable from the descrip-tions given by patients with affective disorder. Theexperience described may be simply a feeling of intensesadness or may have some reference as in the case of a

boy aged 13 whose minor attacks were preceded by a

feeling which he described as " like a guilty conscienceas if you'd murdered someone or stolen something,"At the same time he had an epigastric aura. His headthen turned to the left and he lost his senses for a fewseconds. As he came to himself he would sometimeswonder what he had stolen or whom he had killed.The resemblance between forced thinking and

hallucinatory experience occurring as ictal phenomena,and similar subjective symptoms in schizophrenia, hasbeen the subject of an important paper by Karagullaand Robertson (1955), who record the various gradua-tions from amorphous thoughts to auditory or visualhallucinations observed in temporal-lobe seizures. Theyhave stressed the difficulty patients have in describingsuch experiences. My own observations include severalof a schizophrenic character. Of particular interest are

ideas of reference and passivity. One of my patients,if at the onset of a minor seizure she was in conversa-

tion, felt that the other person was repeating what was

in her own mind. Another described " somethingdirecting me to do something I don't want to do. It

may be something about the house I'm going to do. Mymind somehow tells me not to do it." In another case

the warning of a major seizure was of voices rapidlyrepeating, "Yes, you did, No, you didn't," etc., for a

second or two. As Kinnier-Wilson (1927-8) observed,I epilepsy cannot call into being physiological processes

BRxITiMEDICAL JOURNAL

JULY 2, 1960 DISEASE OF MIND AND DISORDER OF BRAIN BRMDC OMEDICJKL IOURUL

that do not exist. It may be argued, therefore, that thepsychical symptoms which have been described aredependent upon the isolated and therefore distortedevocation of functions regionally represented.Of further interest in relation to schizophrenia is the

occurrence of chronic mental disorder in epilepticsresembling very closely the ordinary schizophrenicpsychosis. Mayer-Gross, Slater, and Roth (1960) haveobserved feelings of passivity with ideas of reference,paranoid moods, hallucinations, and catatonicphenomena. They conclude that the close clinicalsimilarity to schizophrenic symptomatology must besignificant and is more likely to be accounted for by alike regional site than by any common factor in thepathology.Association of Schizophrenia with Cerebral TumourIf the symptoms of schizophrenia are the result of

disordered function in a particular region of the brainit might be expected that they would occasionally resultfrom coarse disease-for example, a tumour. Such anoccurrence might be exceedingly rare, for it would beessential for the appearance of such symptoms not onlythat certain functions should be put out of action, butthat other functions should remain in action, and in thehypothetical case it is probable that the anatomicalsubstrata of these functions are closely related. Thecoarse lesion is not selective enough; it destroys toomuch. For the same reasons one would expect, in thecase of a growth, that if such symptoms occurred theymight be of transient duration, disappearing as thedestruction increased. This sequence I have observedin a few cases of cerebral tumour. The occurrence isso rare that it has been dismissed as coincidence. Yetthe sudden appearance at the same time of the symptomsof tumour and schizophrenia is sometimes impressive.

In one of my cases there was further evidence of avery suggestive nature. This patient was a man aged 35,a scientific worker of high intelligence, with no previousevidence of mental abnormality, who in the fortnightbefore his admission to hospital had had several attacksof an epileptic character. During this period he hadalso developed symptoms which, on admission, wereindistinguishable from those of a schizophrenicpsychosis. He showed the incongruity of thought andaffect, thought disorder, and bizarre delusional ideascharacteristic of the condition without, so far as couldbe judged, any clouding of consciousness. Subsequentlyhe became drowsy, with signs suggesting a left frontaltumour, and died a fortnight after his admission tohospital after ventriculography and biopsy. At thenecropsy a tumour was found involving the corpuscallosum and extending forward into the left frontallobe. Histologically this was a glioblastoma.Two years previously this patient's sister, then aged

34, had come under the care of Dr. Hugh Garland onaccount of occasional epileptic seizures. She was aschool-teacher with no mental abnormality. In thecourse of time physical signs developed, leading to thediagnosis of a left posterior frontal tumour, and fiveyears after the first symptom an exploratory craniotomyby Mr. W. R. Henderson revealed an infiltrating gliomain this situation. Histologically this was an oligodendro-glioma. After the operation she rapidly developedsymptoms of mental disorder and was transferred to amental hospital, from which, through the courtesy ofDr. R. W. Bryson, I have been able to obtain particulars.These I need not describe in detail. They were typicalof a schizophrenic psychosis.

It is a remarkable coincidence that brother and sistershould both have had a cerebral tumour and that ineach case the same area should have been involved.The tumours were of different histological types, and,in any case, evidence of a familial incidence of cerebralgliomas, apart from those that may occur in neuro-fibromatosis, is, so far as I am aware, lacking. Probably,therefore, we must accept coincidence thus far. But itis difficult to accept further coincidence as the explana-tion of the schizophrenic psychosis in both cases. Inthis direction it is natural to look for a genetic factor,having regard to the observation that if one sibling hasschizophrenia the chance of another being similarly.affected is 14% as compared with the incidence of 0.8%for the whole population. We may then argue that thegenetic factor somehow operated in determining thepattern of mental activity in what Jackson called thehealthy parts remaining after the destructive lesion. Itso, was the site of the destructive process, similar inthe two cases, significant ? We cannot be sure that itwas, for account must be taken of epileptic activity inthe brains of both patients, and of the possibility ofdiffuse interference with cerebral function by increasedintracranial pressure. The question of regional signifi-cance should, however, be pursued further. A study ofthe incidence of schizophrenic symptoms in patientswho have had gunshot wounds of the brain mightpossibly yield information.

ConclusionsExamples have been given of specific patterns of

psychological disturbance caused by organic cerebraldamage. Evidence has been presented which suggeststhat the two diseases of mind which we call affectiveand schizophrenic are the effects of functional disorderin the brain, and that each represents what Jacksoncalled a local dissolution, the region being different inthe two cases. Neurologists hitherto have not takenmuch part in the investigation of these conditions,partly because they have been busy with other problems.partly for lack of opportunity. The opportunity hasfortunately been provided at the National Hospital bythe establishment of a psychiatric unit, which, it is to behoped, will in due course expand. Jackson saw no moreincongruity in classing together progressive muscularatrophy and insanity, upon the basis for advancingscientific knowledge, than in the botanist's classificationof the bamboo with common grass. If he was right,neurology has a duty to contribute its share towards theunderstanding of these diseases of mind which fill morehospital beds than all other nervous disorders combined.

REFERENCESFonseca, A. F. da (1959). Analise Heredo-Clinica das Pertubaceos

Afectivas. Imprensa Portuguesa, Porto.Gowers, W. R. (1886). A Manual of Diseases of the Nervous

System. Churchill, London.(1895). Clinical Lectures on Diseases of the Nervous System.

Churchill, London.(1907). The Border-Land of Epilepsy. Churchill, London.

Heaton-Ward W. A. Carpenter, W. H. K., and Jancac, J. (1959).Brit. med. J., 2,'407.

Jackson, J. Hughlings (1894). Reprinted in Selected Writings ofJohn Hughlings Jackson, edited by James Taylor, 1932.Hodder and Stoughton, London.

Kallmann, F. J. (1953). Heredity in Health and Mental Disorder.Norton, New York.

Karagulla, S., and Robertson, E. E. (1955). Brit. med. J., 1, 748.Mayer-Gross, W., Slater, E., and Roth, M. (1960). Clinical

Psychiatry, 2nd ed. Cassell, London.Symonds, C. P. (1945). Trans. Ophthalmol. Soc. U.K., 65, 3.Walshe, Sir F. (1956). Lancet, 2, 1059.Williams, D. (1956). Brain, 79, 29.Wilson, S. A, K. (1927-8). J. Neurol. Psychopath., 8, 332.