1993 - bumke - la disolucion de la demencia precox

8/19/2019 1993 - Bumke - La Disolucion de La Demencia Precox

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History of Psychiatry

DOI: 10.1177/0957154X93004013081993; 4; 133History of Psychiatry

Oswald BumkeDie Auflösung der Dementia Praecox: (The dissolution of dementia praecox

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OSWALD BUMKE

(Director of the Department of Psychiatry and Neurology in Leipzig)

Die Auflösung der Dementia Praecox

(The dissolution of dementia praecox)

The older among you will still remember the apparently triumphal progressmade by the dementia praecox concept some twenty years ago. The ground hadbeen prepared by Kahlbaum and Hecker, and Kraepelin gave this concept itsoriginal shape. This was the time when Moebius said, in a review of Kraepelin’stextbook: ’The dementia praecox has grown rather fat.’ As a matter of fact, thisnew illness had swallowed up a number of old ones. We might still consider thisa good thing. The bringing together of various ’juvenile dementing disorders’meant that several rather superficial and casual similarities (mood, delusions,hallucinations, etc.), which had once been tentatively used in classification, were

replaced by better criteria. This development, however, has finally and more orless automatically destroyed the boundaries that were supposed to enclose thisnew clinical creation. What is left, instead of ’dementia praecox’, is theschizothymic constitution according to a common view; I prefer the idea of

schizophrenic reactions.Bleuler’s excellent monograph on schizophrenia (1911) is a milestone in this

development. At that time we already knew that the diagnostic importance ofcatatonic symptoms had been overrated in an unacceptable way, but we stilllacked the new integrated point of view under which all the different clinicalvarieties of ’dementia praecox’ allowed themselves to be ranged. It was thereforean important advance that the emphasis had now been shifted towards theschizophrenic personality, and towards the analysis of schizophrenic thinking.

This was followed by a shift of scientific interest away from the grossanomalies of thinking and the more conspicuous emotional disturbances indementia praecox, towards the finer shades of the schizophrenic self. During

t Published in Klinische Wochenschrift, iii (1924), 437-40. The following footnote is translated fromthe original:

Paperread at the

meetingof ’Central German

psychiatristsand

neurologists’, Leipzig,28 October

1923.


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this development, however, the disease concept of dementia praecox tended tomelt away in our hands. Even before this, Bleuler had let his schizophreniashade off into normality, by way of certain forms of psychopathy as well asseveral unusual varieties of personality; today he will, however, in completeagreement with Kretschmer, perceive nothing in dementia praecox but themorbid condensation of normal mental reactions.

This view of the matter is closely akin to the one long maintained by myselfwith regard to the hysterical, the nervous, the manic-depressive, and theparanoid constitutions. These dispositions are in fact connected with normalityby way of indefinite transitional stages: we are apparently dealing with trulyquantitative deviations from normal mental processes, such as are continuallybeing produced anew by the mechanisms of heredity, and which always bear thestamp of this

originfrom the earth and soil of the normal

psyche.But their origin, as well as their transitions into normality, imply that theprocesses leading to these abnormal constitutions cannot be organic braindisorders. We should certainly assume that there are deviations in the function ofthe brain tissue, but these deviations will arise from the normal somaticdisposition in just the same way as their mental counterparts are related tonormal behaviour. Mental disorders which are ’functional’ in this sense can andmust shade off into normal human psychology. It is, on the other hand, hardlylikely that the gradual dilution of an organic disease would end up in a normaltemperament.

It is a fact, however, ’that anatomicalchanges

can

alwaysbe demonstrated in

the brains of patients with dementia praecox’, and also that every one of thesepsychoses represents a process ’taking place in a brain which was originally, asfar as we can know, anatomically healthy’ (H. Josephy). We might as wellmention here that this anatomical process does not seem to be the same in allcases. The anatomy, then, shows the organic nature of the schizophrenicpsychoses, but it does not demonstrate that they constitute a ’disease entity’.

I shall return to this theme later on. At this moment my task is to indicate that

there are grave objections to the now prevalent, purely psychological view ofschizophrenia, and that this view is probably mistaken when referrering to therelations between this disorder and the normal

psyche.I would not

denythat we

can find suggestions of schizophrenic symptoms in many persons; but it seems tome that Bleuler’s original conception, that schizophrenia may appear in disguise,just as there are cases of latent pulmonary tuberculosis, is still a betterrepresentation of the facts than is the notion of a schizoid temperament. Ifdementia praecox is an organic process, then schizoid psychopaths evidentlyhave partly recovered from - or are the victims of an abortive form of - thisdisease. They may therefore be compared to incipient cases of general paresis,or to people approaching senility, but not to those hysterical characters who mayarbitrarily be regarded as either ill or not ill. Among the relatives of

schizophrenics, moreover,we find not

onlycases of mental

disorders,but

sometimes also intellectual defects. As I see it, this is further evidence that we




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are dealing with organic and exogenous disturbances, and not with endogenousand functional ones.

I should add that I remain thoroughly sceptical about the concept of a normalinitial stage of dementia praecox, as put forward by Kretschmer, Hoffmann andBleuler. My reasons for this are also founded on clinical and psychologicalexperience. So far I have not been able to convince myself that the traits ofcharacter requisitioned by these authors for their concepts of schizoidia andschizothymia are anything else than normal peculiarities of the human mind,such as can be found wherever we look for them, albeit more or less pronounced.Kretschmer himself made a concession which I feel is important in thisconnection: ’We cannot separate the pre-psychotic, the psychotic and the non-psychotic (namely in the schizoids).’ Certainly not, for the non-psychotic do notshow schizoid traits, and such traits are incorrectly attributed to the normalhistorical personages whom Kretschmer uses as examples.There certainly remains a lot of work to be done in this field. As I said before,

we should try to exclude from the domain of psychopathy those cases who are inactual fact schizophrenics in disguise. In this way it is possible that cranks, forinstance, and some eccentric fanatics, dominated by an idea, totally lacking in

flexibility, tolerance, empathy, and without any sense of humour, that suchcases will some day be finally excluded from the category of psychopaths. Manyasocial cases, found among tramps and the work-shy, have even now beenreclassified as cases of dementia praecox thanks to the studies by Wilmanns. YetI don’t believe that this development could ever go so far as envisaged byKretschmer, who thinks that everything he has described as schizoid characterwill somehow turn out to be connected with dementia praecox. And when

Bleuler even promises to find schizoid traits in every human being, he is justcalling everybody a schizoid without proving anything apart from the fact thatsome universal human traits are preserved also in confirmed cases of

schizophrenia.I am convinced that those cool, unimpassioned people, who soberly calculate

everything, whose emotions never run high, and who may be - according totheir other temperamental qualities - either cold egoists or socially very valuablehard workers, that they are no more ’schizoid’ or ’schizothymic’ than those

gloomy, reserved characters who are inwardly misanthropic. The ’coldaristocrats’, however, ’the passionate idealists’, and the ’cold despots’, in whomKretschmer perceives variants of the schizoid temperament, are from my pointof view simply mentally healthy, and I don’t believe that their temperament, ortheir social attitude (which is a different thing), should be thought to have

anything to do with dementia praecox. If someone is oversensitive and cold atthe same time, however, and does not merely keep a straight face to hide his

sensitivity, or if he is stubborn and fitful, hot and sluggish - in other words: ifhe shows this psychologically incomprehensible unpredictability which ischaracteric of schizophrenics, I would not regard this as a (normal) temperament,but only as illness. And if this illness cannot be diagnosed in this man, but only




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in his brother, I would assume that his condition is due to an unrecognized phaseof illness, or to an abortive form.

It appears to me that Kretschmer’s schizoid is an artificial construct which

arbitrarily and inorganically fits some schizophrenic symptoms into the normalhuman mind. I certainly know that many colleagues do not agree with this viewof the matter. But these scientists will have to resolve the contradiction betweenthe acceptance of the idea of a schizoid temperament on the one hand, and thefacts of anatomical lesions in dementia praecox on the other. As far as I know,there is not a single example of such an attempt. According to Kahn, theschizoid temperament and the schizophrenic process psychosis should be not

only quantitatively, but also qualitatively different. He, too, regards the schizoidas a particular form of psychopathy, connected with normality via indefiniteintermediate stages, and

probablyinherited as a dominant trait. Dementia

praecox itself, according to this author, is a true disease process (as also assumed

by Josephy, for anatomical reasons); and this process requires not only theschizoid disposition, but also another (recessive) hereditary factor.

It is also evident that the ’schizoid’ of Kahn cannot be identical with that of

Kretschmer, Hoffmann and Bleuler, even though there is considerable

psychological agreement between these concepts. Kretschmer regardsschizothymia as a normal kind of temperament which is found in every human

being, excepting only the cycloids. Bleuler, however, finds at least a suggestionof schizoidia in everybody, without exception. It would be rather senseless to

inquireinto the mode of inheritance of such a

trait;the ’schizoid’

genotypewould simply be identical with that which gives rise to a human being.Kahn could not very well have wished to demonstrate a dominant inheritance

of this kind of schizoidia. His conclusions are evidently based on the assumptionthat his schizoidia is not present in every human being and that it is not the sameas the notion of Kretschmer, Hoffmann and Bleuler: ’a kind of mental being andmental reactions, present in everybody to some extent, which appears as

schizophrenia in cases of a morbid intensification, but is usually regarded asschizoid psychopathy in intermediary cases’ (Bleuler). As I see it, Kahn hasnot so far been able to delimit an alternative schizoidia which might offer a

solid basis for genetic studies. We shall therefore have to await the results offuture studies, which should first and foremost start from clearly defined

concepts.It seems to me doubtful whether the time for such investigations has yet come,

because those genetic studies of dementia praecox published so far have in

general to be interpreted with the greatest caution. I would not deny that thecareful and thorough work done in this area has sometimes reminded me ofVirchow’s remark that even scabies was regarded as a hereditary disease until itscause had been discovered. To be sure, we would all agree that there is at least a

subgroup of dementia praecox cases in which the disease is hereditary, as

demonstrated particularly by Rudin’s cautious and reliable observations. Butthis is valid for a small group of clinically homogeneous cases, like Rudin’s




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probands, and it certainly does not have to apply to all the schizophrenias, aproportion of which might have been acquired after conception.

If the facts accumulated so far are reconsidered from this point of view, it is

noteworthy that dementia praecox is never inherited through several generationsin a dominant fashion. Transmission from parents to children is rare, and even in

the case of two schizophrenic parents the children do not invariably becomeschizophrenic (Kahn). Finally, sibs of probands do not fall ill quite as often asshould be expected according to those rules of inheritance that seem to be validin other situations.

All these facts, to which might be added others which are no less conflicting,have already given rise to several rather complex hypotheses; there is just onething that has only rarely been considered. What if dementia praecox simply doesnot exist? ’What would we say’, asked P. Schroeder, ’if someone when studyingthe causes, the initial stages, the Abderhalden reaction, the course, and theheredity, were to deal with the whole of the organic disorders - general paresis,senile dementia, etc. - all together as one disease?’ Well,this design whichSchroeder rightly describes as foolish has been used often enough in the olderstatistical studies of heredity, and their results have been neither less, nor more

contradictory than those of recent contributions to the question of theinheritance of schizophrenic disorders. All these contradictions, however, would

instantly vanish if the nature of heredity were considered, namely that thismechanism can only transmit specific characteristics. A similar course of events

might be expected in the present case: if we let go of the idea that dementia

praecox is a disease entity, and speak instead of schizophrenic reactions whichmight be elicited in different ways, the whole picture will immediately becomeclearer. A group of cases with a recessive mode of inheritance might then

conceivably exist, who are clinically similar to other, non-genetic cases simplybecause the brains of all, or at least many human beings are predisposed to thiskind of reaction to various harmful influences. It is also possible that in each caseof dementia praecox not two genes, but inherited as well as acquired factors- constitution and an exogenous influence - are both necessary. I might perhapsremind you of pulmonary tuberculosis, in the severe forms of which a hereditaryfactor is important, in addition to exogenous factors. If we take a similar view ofcertain schizophrenic reactions, there is actually no need for the second

recessively inherited factor assumed by Rfdin.There is today little reason to doubt that dementia praecox will meet the fate

predicted for so many mental disorders by Hoche in his theory ofsyndromes. Buteven this is no longer simple and straightforward. Neither the functional

syndromes of psychopathy, nor the exogenous reactions described by Bonhoefferhave remained ’diseases’ in the sense of the clinical school. Where does dementia

praecox belong? Will it, like neurasthenia and hypochondria, neuropathy,mania, melancholia, hysteria and paranoia, join the large group of abnormalreactions and constitutions in which we

may occasionallyobserve the

developmentof psychoses through a morbid intensification of mental dispositions that are in




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themselves normal? This view is refuted, as I see it, not only by the findings ofacquired anatomical lesions, but also by the fact that all of the various

schizophrenic conditions are closely related to other disorders of an organicorigin. But it is hardly disputed that every case of dementia praecox, whether thecauses be endocrine or not, still has an organic basis. The question is whetherschizophrenia should be regarded as a ’disease entity’ among the organicdisorders, and whether all schizophrenic psychoses have the same causes and thesame biological basis. We have already heard that so far histopathology has atleast not shown that there is such a uniformity of pathogenesis - and we addedthat no support for an assumption of homogeneity can be found in genetics.There are quite a few clinical observations which point in the opposite direction.Several schizophrenic syndromes are known to occur not only in dementia

praecox, but also in intoxications and infections, in various somatic disordersand after serious brain injury; they are thus found in the ’symptomatic’ psychoseswhich have all along been regarded as prototypes of Bonhoeffer’s exogenousreactions.

I readily admit that the schizophrenic conditions hold a special position amongthese exogenous reactions. But it seems to me that we would tackle various

clinical problems much more realistically if we would first of all regard thesesyndromes as reactions which are latent in the brain - or at least in many brains -and with which human beings may respond to several different noxiousinfluences. Our ability to perceive certain connections which are possibleaccording to clinical experience has been blocked for years by the dogma thatthere are only disease entities in psychiatry, and that the ’unity’ of these diseasesalways has to do with course and outcome. From this latter point of view, it wouldseem unthinkable that the same damage to the brain might in one case lead to a

transitory ’symptomatic’ psychosis, while in another case the result might be anincurable defect.

We have, however, got used to the fact that a primary tuberculosis of the lungwill heal completely in one patient, while in another it leads to phthisis anddeath. Similarly, we cannot distinguish among cases of delirium tremens theminority of patients who will end up with a defect of the Korsakov type. Whyshould schizophrenic

syndromesbe exempt from this kind of

variability?There

is no longer any doubt that the majority of cases formerly diagnosed as acutehallucinosis or amentia, respectively, will reach an end state of schizophrenicdementia. Nobody has yet proved that these ’cases of dementia praecox’ havenothing in common with, for instance, those ’symptomatic psychoses’ of the

puerperium which initially show the same symptoms but eventually lead to

recovery. We may thus confidently reconsider the possibility that, even in this

field, course and outcome of illnesses are determined by the strength of theircauses relative to the resistance of the organism. This means that manyschizophrenic disease processes might well be the more malignant or evenincurable

analogiesof the same events which

giverise to

symptomatic psychosesif the brain is more resistant, or the injury not so serious.




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Support for this assumption can also be found in symptomatology. Incoherence,for example, which is an important symptom in psychosis with acute infectious

disease, differs from the fragmentation seen in schizophrenia in only a singlerespect, namely that the former invariably occurs in a setting of cloudedconsciousness, while the latter is not connected with other obvious signs of sucha disturbance of consciousness. Is it really the case that these two symptoms have

nothing to do with each other? Would it not be possible to regard schizophrenicfragmentation as the residue of a syndrome which in the acute phase alsoincludes deficiencies of perception and attention, a tendency to concrete

thinking etc., simply all the other signs of a clouded consciousness? The two

symptoms might in this respect be connected in the same way as the one pointedout by Bonhoeffer and Schroeder for the delirious and the amnestic syndromes.The amnestic syndrome is always included in the delirious syndrome: when the

clouding subsides, it sometimes appears for a while as the only residue.It is time for me to finish. It is possible to develop quite similar ideas in several

areas where the problem is to draw a line between ’dementia praecox’ and other

exogenous disorders, e.g., some involutional paranoid psychoses, alcoholic

hallucinosis, and alcoholic dementia. The similarities between some epilepticpsychoses and schizophrenia would also be relevant here. But I don’t have thetime to explore all this. The task I had set myselffor today was to indicate that it

might be a good thing to reconsider the relations between the schizophrenicprocesses and the organic disorders. I am also convinced that ’dementia praecox’

will,in the event, lose more than hitherto of its

solidityand

unity.I expect it to

join the exogenous reactions, and not the psychopathic constitutions.There is, to be sure, a bridge between these two points of view which

otherwise seem irreconcilable. We know according to Kleist, for example, that

many people have a particular bent for symptomatic psychoses and maytherefore fall ill several times in response to different infections. In such cases

constitution thus has an important role, in the organic area. As the particularcharacteristics, furthermore, of a psychosis which has been provoked by an

exogenous factor, are in many cases partly determined by individual dispositions, itis after all conceivable that constitution is partly responsible also in the

schizophrenicreactions. I have

alreadyindicated this

possibilityin the

discussion of hereditary factors. If this is the truth of the matter, it would beeasier than it seems at first to reconcile Kahn’s notion of schizoidia as well as

Kretschmer’s theory of bodily constitution with my idea of the exogenouscharacter of schizophrenic syndromes. I should like to remind you once more of

pulmonary tuberculosis, and of the relations between this exogenous process andcertain somatic predispositions.


1993 - bumke - la disolucion de la demencia precox

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