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ANATOMICAL FINDINGS IN SENILE DEMENTIA: A
DIAGNOSTIC STUDY BEARING ESPECIALLY ON
THE GROUP OF CEREBRAL ATROPHIES.*

BY E. E. SOUTHARD, M. D.

(From the Laboratory of the Danvers State Hospital, Hathorne, Massa-
chusetts; and the Department of Neuropathology, Harvard

Medical School.)

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* Read in part at the Annual Session of the American Medico-Psycho-

logical Association, Atlantic City, N. J., June, 1909.

Appeldorn's data

Ratios of actual to calculated weights of brain and of heart,

liver, kidneys (combined)....

Comments of Alzheimer....

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Other chronic conditions.

The cause of death..................

Discussion and microscopic analysis.....

"Neuronophagia " and Metchnikoff's hypothesis..

Positions assumed by satellite cells.......
Relation of vascular to atrophic changes.

Conclusions
References

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I have lately possessed the unusual advantage of reviewing a considerable collection of autopsies (247) upon cases of mental disease introduced at various times in the years 1904-1908 at the daily clinics of the Danvers State Hospital, Massachusetts. The cases introduced in these clinics are of particular value, because the often divergent opinions of several diagnosticians, from three to eight or more, are recorded in each instance. The staff has varied from time to time, but has at all times contained members familiar in our recent American psychiatric literature, such as Prof. A. M. Barrett (now of Ann Arbor), Dr. H. A. Cotton (now of Trenton, New Jersey), Dr. H. W. Mitchell (now of the Eastern Maine Hospital for the Insane), Dr. H. M. Swift, and Dr. Charles Ricksher, as well as the moderator, Superintendent Charles W. Page. The clinical diagnoses which I have considered have not been those chosen for the statistical records required for the Board of Insanity, but all the diagnoses rendered for each case.

For more minute examination I have naturally resorted to those cases in which all the staff agreed, holding the opinion that uniformity in diagnosis by several men is of more value than that induced by a single chief of clinic.

To establish the degree of accuracy in diagnosis at these clinics, I may mention (what I have dealt with more specifically before the American Neurological Association) the 85 per cent accurate diagnoses where all agreed to general paresis. Only 6 out of 41 cases unanimously diagnosed general paresis turned out to be cases of

something else. The reasons for these 6 incorrect diagnoses I shall present in extenso elsewhere,' but they do not militate against the general accuracy of diagnosis in the Danvers daily clinics.

I was the more astonished to find that, on accepted anatomical criteria, our success in the diagnosis of senile dementia at these clinics was not at all comparable with our surprisingly good results in general paresis. On the hypothesis that cerebral atrophy is a necessary feature in senile dementia, our diagnoses turned out to be only 38 per cent correct. On the hypothesis that cortical arteriosclerosis is a necessary feature in senile dementia, our diagnoses were but 48 per cent correct. And, in fact, 14 of the 42 cases in which the diagnosis of uncomplicated senile dementia was rendered, viz., 33 per cent, proved to show neither sclerosis of terminal arteries nor cerebral atrophy, so that our general percentage of accuracy, as established by the finding of either cerebral atrophy or cortical arteriosclerosis (or both), was 66 per cent for senile dementia.

The general analysis of this material may be presented in the following table, which deals with the data of 42 uncomplicated cases in a total of 71 cases of probable senile dementia in a grand total of 247 cases of various types of mental disease subject to anatomical review:

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These 42 cases have been subjected to closer analysis with the object of determining the necessary features in a case of senile dementia.

It does not appear that the anatomical and histological characters of senile dementia are as clear-cut and ready of diagnosis

as the post-mortem characters of general paresis. But there is a widely current opinion that the brains of senile dements show | well-marked cerebral atrophy. Other descriptions give equal prominence to arteriosclerotic lesions. Frequently the literary student gains the impression that both kinds of disease characterize the brains of senile dements, or even obtains a thinly-veiled conception that the brain atrophy is somehow due to arteriosclerosis.

CEREBRAL ATROPHY.

With respect to cerebral atrophy, it appears that there is actually no standard by which to determine the amount of loss in weight which shall signify atrophy. Thirteen of the brains in the 42 uncomplicated cases of senile dementia, remarkably enough, yielded weights above the averages ordinarily assigned for male (1358 grams) and female (1235) grams. Thus, unless some of these 13 cases possessed unusually large brains at the outset (of which there is no evidence otherwise), we need consider only 29 cases as belonging possibly in the cerebral atrophy group.

There is, however, no warrant for the diagnosis of cerebral atrophy in every case which is somewhat underweight with respect to the assigned averages of the books, since we must take into account initial differences in brain weight (variations according to race, body weight, stature, age). Thus brain weights ranging from 1461 to 1265 have been assigned to average normal males, and weights from 1341 to 1112 to average normal females.*

It is obvious, therefore, that the degree of loss which is to warrant the diagnosis "atrophy" is hard to determine. Perhaps, in the last resort, we should be dissatisfied with any result which did not depend on an obviously impossible calculation-namely, the degree of loss from the original weight in the given case.

If in this series we adopt the arbitrary standard sometimes advocated—namely, a conceived loss of one-sixth the original weight' -and take the ordinarily assigned averages as original weights, we at once reduce the cases showing brain atrophy to II. Thus only 26 per cent of 42 cases diagnosed as senile dementia would show atrophic brains.

Perhaps it is better to trust the qualitative data with respect to the diagnosis, cerebral atrophy. Upon collation of the qualitative findings, paying attention to the occurrence of both diffuse and

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focal atrophies of convolutions, the same result as before recorded (on the criterion of weights) was registered for the incidence of brain atrophy. There were 13 cases which could not be regarded as atrophic and 29 which showed either diffuse or focal convolutional atrophy. The distribution of these classes was almost the same as the distribution of the weight classes. Two cases were carried over from the larger class (29) to the smaller (13). (The first on the score of focal atrophy of one frontal region, the second on the score of a focal lesion (possibly aplasia) of the frontal lobes). And two cases were carried in the reverse direction from the smaller class (13) to the larger (29) on the basis of exact gross descriptions, suggesting approximate normality of convolutions.

But the atrophies which were employed to separate these two classes were not all diffuse atrophies such as we have in mind in the current definitions of senile dementia. Only 20 of these cases showed an obvious diffuse cerebral atrophy, and of these four showed a slight or a questionable atrophy. Thus, if the gross qualitative differentiæ are adopted, 16 out of 42 cases of senile dementia (or 38 per cent) showed cerebral atrophy of a convincing character.

CORTICAL ARTERIOSCLEROSIS.

A review of the gross and microscopic findings indicates that we cannot safely exclude cerebral arteriosclerosis of greater or less degree in any single case of this series of 42 cases. (Four cases in which no specific note was made of cerebral arteriosclerosis yield other data, gross or microscopic, from which some degree of such change can be assumed.) Similar statements probably hold good of many brains in the non-insane in advanced age.

But it is evident that there are important theoretical differences between cases which show sclerosis of the larger anastomosing arteries and those which show sclerosis of terminal arteries. Sclerosis of the terminal arteries of the brain, whether leading to infarctions or not, obviously means much more from the standpoint of the integrity of the cerebral functions. In fact it would seem difficult to exclude with certainty cases of extensive small-branch arteriosclerosis from the group of organic dementia.

Twenty out of 42 cases diagnosed senile dementia proved to

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