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A PATHOLOGIC CONTRIBUTION TO THE CONCEPT OF NEUROSOMATIC DETERIORATION IN EPILEPSY, WITH RECORD OF TWO CASES
Morgan B. Hodskins; Paul I. Yakovlev
Am J Psychiatry 1931;87:663-666.
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Monson State Hospital, Palmer, Mass.

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Abstract

These cases, clinically, seem quite different; however, both show the same essential features: epilepsy and the symptomatologic pattern of neurosomatic deterioration. In the first case—a child— deterioration developed more rapidly and was more destructive, in nine years leading to the ultimate stage of neurosomatic deterioration; namely, profound dementia and cerebral flexion paraplegia. In the second case—a man 66 years of age, with late epilepsy—the neurologic picture characteristic of neurosomatic deterioration developed more slowly, was not so dramatic, and the symptomatologic pattern was one that could be identified with the arteriosclerotic Parkinsonism.Pathologically, in both cases was found evidence of a primary vascular cerebral lesion which was, in the first case, an acute lesion—meningo-encephalitis; in the second case, a chronic lesion— cerebral-arteriosclerosis. In both cases the primary pathologic lesion was the starting point of the same chronic degenerative process affecting principally the frontal cortex (third layer) and basal ganglia (pallidum and peduncular-hypothalamic formation). This last chronic degenerative and atrophic secondary process appears to be the most plausible cause of the clinical symptoms of neurosomatic deterioration. The predominant localization of this process in the third layer of the cortex and in the pallidum appear to agree with the fundamental features of the clinical syndrome which was manifested by disturbances in the psychomotor sphere; namely, dementia and progressive rigidity.

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