variations in amount within a given brain are more striking than the variations shown by the neuroglia cell pigments.

17. That these three loci for the deposition of pigment tend at last to a species of saturation is indicated by the fact that the even degrees of moderate or of marked pigment deposit in all loci begin to appear in the later years of life (one case at 49 years, one at 56, and the rest from 59 to 75 years).

18. The fresh point of view thus obtained for the problem of involution-melancholia by our study of fifth-decade insanities may be stated as follows:

Involution-melancholia has been regarded as possibly akin to manic-depressive insanity or even identical therewith or as possibly something quite different. Perhaps the majority of psychiatrists would regard it as a disease akin to manic-depressive insanity but modified by climacteric or presenile changes and distinguished from manic-depressive insanity by the peculiar tendency to depression which has given it its name. The novel feature of our investigation has been to study the age-factor. We have studied unselected cases arising in the fifth decade of life, excluding all coarse organic cases of brain lesion. Our resultant group is, we believe, although small, otherwise ideally representative of the conditions underlying mental disease at this age-level. Our group includes a sufficient number of the familiar cases of involution-melancholia as well as cases of delusional insanity without melancholia. The striking fact is that the melancholia cases prove also delusional. In so far as our group is representative of the fifth decade, we believe that the essential psychopathia involutionis is characterized by delusions, that in the large majority of cases melancholia is a feature superadded to the delusions, and that in a smaller majority of cases hallucinosis also occurs. The fact that melancholia may assert itself as the most prominent symptom in the clinical foreground fails to controvert the possible genetic importance of the delusions. As to the cause of psychopathia involutionis, it is easy to invoke the glands of internal secretion; and of their disorder there is actually some sign in a number of cases. Whether such disorder or some unknown factor determines the over-pigmentation (lipoid accumulations) in the cortex above noted, and whether these deposits have a direct relation to the symptoms must rest with the future.

REFERENCES.

1. Southard and Mitchell: Melancholia with Delusions of Negation: Three Cases with Autopsy. Journ. Nervous and Mental Diseases, May, 1908, Vol. XXXV, No. 5, p. 300.

2. Southard and Mitchell: Clinical and Anatomical Analysis of 23 Cases of Insanity Arising in the Sixth and Seventh Decades, with especial Relation to the Incidence of Arteriosclerosis and Brain Atrophy and to the Distribution of Cortical Pigments. Am. Journ. Insanity, Vol. LXV, No. 2, Oct., 1908.

3. Bevan Lewis: A Text-Book of Mental Diseases with Special Reference to the Pathological Aspects of Insanity: Part III, Pathological Section, General Pathology and Morbid Anatomy. Two editions, 1890, 1899.

4. Alois Alzheimer: Beitrag zur Kenntnis der pathologischen Neuroglia und ihrer Beziehungen zu den Abbauvorgängen in Nervengewebe. Histologische und Histopathologische Arbeiten über die Grosshirnrinde. Vol. III, 1910, p. 412.

5. Alford: Ten Obscure Cases of Mental Diseases: A Clinical and Anatomical Study, Boston Med. Surg. Jour., 163, 1910 (being contribution No. 4, Charles Whitney Page Series, Danvers State Hospital Papers).

THE DISTRIBUTION OF THE LESIONS OF GENERAL

PARALYSIS.

By SAMUEL T. ORTON, M. D.,

Pathologist, Worcester State Hospital, Worcester, Mass.

This analysis of the distribution of the lesions in general paralysis was taken up with the hope of adding to the data of the anatomical distribution of the lesions and possibly of throwing some light on the mechanism of infection. The gross appearance of the brain gives by means of the pial thickening and atrophy some indication of the relative severity of the process, but microscopic examination will in many instances show that the meningeal involvement is not a safe guide to the amount of cortical damage, and atrophy is at best a coarse index which reveals only the more advanced changes.

Tuczek on the basis of work done by the Weigert myelin sheath method arrived at the conclusion that the anterior part of the brain was most severely attacked, that the vertex was prone to suffer early and that the occipital region was less involved though not always free. Shaffer using the same methods suggested that the brunt of the lesions was borne by the association centers leaving the sensory cortices relatively free thus grouping the attack as a sort of system disease. Kaes held that the process was an outspoken diffuse one spread over the whole cortex, but variable in its intensity. Alzheimer on the data obtained from his classical study, and based on a wide variety of methods including cell and glia preparations, concludes that in the rapidly progressive cases the lesions are widespread and of approximately equal intensity. In the majority of the cases, however, the orbital gyri suffer the most and next in order the frontal pole and frontal half of the convexity. The occipital pole is commonly though not always the region showing the least severe involvement. In long standing cases with advanced dementia, marked paresis, etc., the distribution is again widespread. Mott has made the suggestion that the distribution is due to the relation of the venous return from

the cortex into the superior longitudinal sinus and that those areas in which the return system favors congestion are the earliest and most severely attacked.

For the present study the index used was a combined one based on the amount of perivascular infiltration and the degree of stratigraphic disturbance. This method is open to the objection that it does not take into account the glial changes nor the less prominent cell losses which, when diffuse, may be of considerable amount and yet not readily recognized except by accurate cell counts which would prove too laborious for such a large series of cases as the present.

The routine adopted in the laboratory of the Worcester State Hospital includes sections fixed and stained by three standard methods for the display respectively of the cell, fiber and glia content from six areas of each hemicerebrum in all cases except those reserved for more intensive or special study. These areas are precentral, postcentral, frontal, temporal, occipital and the hippocampus and cornu ammonis.'

The material used was for the most part from material fixed in alcohol and stained by Nissl's method. The remainder was formalin material and was stained in thionin. All sections were cut in paraffin at 10μ and should be fairly comparable.

In order to reach some comparison of the severity of the involvement in various areas some empiric standard was necessary, and the following scheme was adopted. A zero indicates those areas where the lesions were of such minor grade that one would hesitate to accept them without further data as diagnostic of paresis. In this group the meningeal lesions were purposely omitted from consideration. A single plus sign designates areas with lesions of sufficient severity for ready diagnosis, but without noticeable cell disturbances. A double plus sign refers to sections showing advanced perivascular infiltration with or without slight disturbances of lamination. A triple plus sign indicates advanced vascular lesions with distinct stratigraphic disturbance.

Fifty cases were reviewed in this way and the results may be recorded in tabular form.

'The exact location of these sections is diagrammatically indicated and the technical methods are described in an article by the writer in the Am. Jour. of Insan., Vol. LXIX, No. 2, Oct., 1912.