THE PRESENT STATUS OF OUR KNOWLEDGE OF THE PATHOLOGICAL HISTOLOGY OF THE CORTEX IN THE PSYCHOSES
Abstract
When we review the principal facts of the newer histological investigations of the paralysis process, we can conclude that this process is so well differentiated that it can be separated from all other diseases of the central nervous system. Our knowledge of the pathological anatomy is of extreme value for the clinical symptomatology of paralysis, as it allows us to diagnose cases of an atypical and extraordinary character.
Further, the newer findings indicate that the process cannot be entirely accounted for by the inflammatory process in the blood vessels. More often independent degenerative changes are seen in the nervous tissue which go hand in hand with the inflammatory changes.
The histological investigations of the other organs of the body make it more probable that the paralytic process is not only a disease of the central nervous system, but a disease of the entire body. But more investigations are needed to prove this point.
Focal or circumscribed degeneration of the medullated sheath of the axis cylinders, particularly in the cortex, which can approach even the focal lesions of multiple sclerosis, is a frequent accompanying change in the paralytic process of the central nervous system.
It is possible to differentiate a third type of paralysis which can be added to the typical cases and atypical localized forms (Lissauer's paralysis) the stationary paralysis which is characterized by a particularly mild process in the histological and clinical picture.
The paralysis on the ground of hereditary lues is associated frequently with characteristic changes in the cerebellum, particularly the abnormal form and multiple nuclei of the Purkinje cells. This characteristic finding of the Purkinje cells is so frequently found, and in so many cases, that it is impossible to class them with isolated double nucleated cells found in the cerebellum of cases of other mental diseases. It is not entirely clear from whence these cells originate. From the fact that they are occasionally found in paralysis in middle life, and after late acquired syphilis in relation to a severe cerebellar atrophy, and are similar to the cells in juvenile paralysis, at present one cannot conclude that their presence indicates paralysis hereditaria tarda. Thorough examination of particularly atrophic cerebellum in adult paralysis is necessary before we can arrive at any conclusion.
The investigations of Sibelius indicate, possibly, that in the central nervous system of paralytics, who have acquired syphilis, that frequently developmental anomalies are present. And possibly this means that there is a specific predisposition towards a later paralysis when accompanied with syphilis.
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