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stance, disappearance of nerve elements, gliosis and the appearance of amcboid glia cells. Alzheimer points out these findings were particularly marked in the small cell layers of the cortex. Upon these findings, Kraepelin ” explains the preservation of memory and acquired knowledge on the theory that these have their seat in the deeper layers of the cortex. To the second and third cortical layers which are affected in this disease, Kraepelin ascribes the function of the liberation or translation of perceptions into concepts, of sensations into feelings and of impulses into activity of the will. Such an interpretation, if found to be based on fact, would exactly explain the symptomatology of dementia præcox.
Southard's ” work, calling attention to the satellitosis and macroscopic areas of palpable gliosis with microgyria and visible atrophy and the microscopic evidences of sclerotic changes in nerve cells in 89 per cent of the cases examined is too well known to be more than mentioned.
Sioli " found in every one of 20 cases of undoubted dementia præcox destruction of nerve tissue and disarrangement of the normal layer formation of cortex cells, degenerative products in the perivascular and lymph spaces and amoboid cells, together with gliosis in the white matter and in the deep cortex layers.
The findings of Rosanoff," which led him to make the unequivocal statement that mental deterioration in dementia præcox goes hand in hand with brain atrophy, are also so well known that they need no more than be mentioned.
Because of the possibility that some organic basis may be found for the most striking, though usually late, symptom of dementia præcox, the work of Morse" is interesting. The dissociation between the retained intellectual functions and the emotional deterioration has a suggested explanation in her findings. Her cases died sufficiently young to make it possible to exclude the ordinary senile and arteriosclerotic changes found in brains at autopsy. The neuroglia in the optic thalami was especially investigated. Seven cases of other mental disorders were used as controls, including two cases of arteriosclerosis and senile dementia. She found increase of neuroglia, diffuse and focal, in one or more of the thalamic nuclei, cerebral cortex and in the white matter of the brain. The control cases showed none of these changes excepting the usual peripheral gliosis and perivascular increase in the
senile and arteriosclerosis cases. The writer makes the statement that "thalamic gliosis occurs more frequently in dementia præcox cases than in those with other psychoses who died at about the same age.”
What bearing this finding has on the problem of dementia præcox is suggested by analogy with numerous clinical observations made in other conditions, particularly pseudo-bulbar palsy and progressive lenticular degeneration. In these conditions, the lack of emotional control is a prominent symptom and is generally ascribed to involvement of the thalamus and other basal ganglia. This observation has been frequently confirmed by various neurologists. It is not uncommon to see cases of pseudo-bulbar palsy with completely retained mental faculties who laugh immoderately or cry uncontrollably with very little or no stimulus. The similarity between this symptom and the same condition so often met with in dementia præcox makes a striking analogy. The perusal of a review of the subject of pseudo-bulbar palsy by Tilneyis, in this connection, extremely interesting. That the analogy should not be drawn too close, however, must be mentioned, because Tilney found that the lesions in cases of pseudo-bulbar palsy were in a majority of cases multiple and occurred in the projection systems as well as in the basal ganglia or the pons or medullary nuclei. A closer analogy can be drawn in the cases of progressive lentieular degeneration described by Wilson." Concerning the matter of the mental symptoms of this disease, Wilson says, “ It is a noteworthy fact that some form of mental change or impairment is specifically referred to in at least eight of the twelve cases; its importance, therefore, must not be underestimated.” Again on page 447 he says “If the term 'dementia' is to be employed to characterize them (the mental symptoms), it must not be forgotten that this dementia is decidedly limited. . . . . It is just in
. the ordinary dementia of senility and to a less extent in dementia præcox that these symptoms are most common. .. Hence, the term 'dementia' is really not appropriate.” He refers to the absence of disorientation of time, place and person and points out that the dementia present in his cases cannot “ be likened to the steady mental involution of senile dementia or of dementia paralytica," and further says that, “it can be readily distinguished from dementia præcox. The mental symptoms are a lowered
capacity for retaining impressions with a constriction of the mental horizon. The powers of perception and recognition are good. There are no delusions or hallucinations." He refers to these patients as being “ easily tickled, pleased and amused without insight into their condition, for their cheerfulness is incompatible with knowledge of the seriousness of their illness.
The patient seems to be unable to deliberate or pass judgment on what is presented to him." Regarding the involuntary laughter or crying, Wilson says (page 472) that the association of these emotional states with the basal ganglia has long been recognized and he refers to their incidence in double hemiplegia and pseudo-bulbar palsy and even in simple hemiplegia. He further says, “On some occasions at least the patients did not appear to express the emotion which their musculature seemed to express.” Despite the fact that Wilson says that these symptoms can readily be distinguished from dementia præcox, their striking similarity to the late symptoms of this disease can readily be appreciated. Reference to this subject may be concluded by drawing attention to the pathology of this condition which seems to be limited to a symmetrically bilateral lenticular degeneration, particularly of the putamen. The globus pallidus, caudate and some of the fibers of the thalamus which come from the corpora striata are often involved. The extent of the involvement of the thalamus appears to be more marked in some cases than in others but these striothalamic fibers regularly show a secondary degeneration.
No attempt is made here to draw an analogy between dementia præcox and affections of the basal ganglia. I simply desire to point out that the anatomical changes which seem to have been found in dementia præcox by Kleist, Nissl, Alzheimer, Southard and Morse are capable of explaining at least some of the characteristic symptoms of dementia præcox. In the presence of such evidence as these investigators present, it would be extremely unwise to take a decided stand for or against the organicity of this disease. Of late years some teachers of psychiatry and many writers on this subject have been too prone to overlook the possibility that psychobiological interpretations and purely psychological explanations of the pathogenesis of this condition may not be the only considerations possible. It seems to me that the writings of Freud, Jung, Adler and others who are responsible for this state of affairs have retarded investigation of other phases of this important problem. What can be done to bring our attitude of this matter to a state where anatomopathological and physiological investigations will replace dogmatic, empirical, psychological explanations? It seems that the first desideratum is to demonstrate the falsity or the correctness of the stand that the psychoanalytic viewpoint has solved the problem. The best method to determine whether this disease is primarily a functional one and dependent on improper mental habits or perversions of the sex instinct with conflicts arising therefrom is to apply the therapeutic test. If this is true then the principles of psychoanalysis as laid down by the Teutonic writers, if applied to early cases of dementia præcox, should result in cures, or at least prolonged remissions, with more or less perfect adjustment of the individual affected. Just as unhelpful as is the attitude of those who refuse to concede the possibility of a causative influence of the organic findings in the development of this disease is the attitude of those who refuse to give any part in the production of the disease picture to psychobiological influences. Occupational, educational and custodial care have resulted in a discouragingly poor percentage of recovery in dementia præcox. Let us consider giving a free hand to competent persons so that they may practice the principles of psychoanalysis and apply them to sufferers from dementia præcox under supervision in our state hospitals and sanitariums. Before doing this, however, the psychoanalysts should be prepared to investigate these cases in the broadest way, taking into consideration all the available data. They should be prepared to give us information on the part that all the instincts play in the synthesis of dementia præcox, because the true psychoanalyst does not limit himself to a consideration of the sex instinct alone. The matters diseussed by Trotter concerning the Herd Instinct and principles of masculinity-femininity and the masculine protest of Adler. together with the broader aspects of the libido and life interest of Jung, and finally the investigations of the sex instinct according to Freud should all play a part in these investigations. If early cases of dementia præcox are referred to psychoanalysts and they are given unlimited opportunity for investigation and attempts at bringing about adjustment, we must then be willing to abide by the results. No one has yet given statistical data of a large number of cases treated by such psychoanalytic methods. It is high time
that this should be done. The suggestion is made that psychoanalysts be given in various parts of the country a number of cases sufficiently large to permit of fruitful observations and that in three, four or five years they be required to publish their data in statistical form for consideration. The cases should be undoubted examples of dementia præcox, presented at staff meetings or after consultation, and standardized for diagnosis according to the conceptions of Meyer, Kraepelin and Tanzi. They should be, as Tanzi " says, “patients who present the fundamental symptom of dementia præcox; namely, stolidity of conduct.” Concerning the diagnosis, Tanzi further says, “that whatever may be the clinical variety to which his malady belongs, the patient suffering from dementia præcox displays the disorder of his intelligence not so much by what he says and thinks as by what he does; even when he expresses and seemingly thinks something contradictory, absurd or foolish, as often occurs, the unprejudiced observer easily perceives that the patient is not faithfully conveying his own thoughts, but is to all appearances falsifying them purposely, either from ostentation, as a joke, or owing to an involuntary treachery on the part of the volitional function.” These disorders of the will and the emotions are the sine qua non of dementia præcox.
The views of Kraepelin“ on this point may be worthy of attention because psychoanalysts have been too prone to a loose interpretation of what we mean by dementia præcox. Despite the fact that we must admit that dementia præcox has no absolute clinical, pathological or anatomical signs, it is just these mental characteristics which are definite. Kraepelin states that “this peculiar and fundamental want of any strong feeling of the impressions of life, with unimpaired ability to understand and to remember, is really the diagnostic symptom of the disease we have before us." Again on page 26 he says, “We have a state of dementia before us in which the faculty of comprehension and the recollection of knowledge previously acquired are much less affected than the judgment and especially than the emotional impulses and the acts of volition which stand in close relation to those impulses.. They are invariable and permanent fundamental features of dementia præcox, accompanying the whole evolution of the disease.” These matters, which are clear to every one of us, seem to have es