A CLINICAL, ELECTROENCEPHALOGRAPHIC AND ANATOMICAL STUDY OF EXPERIMENTAL JAPANESE “B” ENCEPHALITIS IN THE MONKEY

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Abstract
Seven monkeys were inoculated with the virus of Japanese "B" encephalitis intracerebrally. One or more electroencephalographic tracings were made daily. The animals were sacrificed after varying times and the nervous system examined by serial sections. The first animal, inoculated with an attenuated virus, was sacrificed 4 days later before any clinical or electrical abnormality was evident. A generalized cerebral edema was the chief anatomical lesion. Thus, a lesion of a purely exudative character, e.i., simple cerebral edema, showed no clinical nor electrical sign. The slow waves which habitually characterize cerebral edema, have a totally different significance. Paralleling the productive inflammation, these waves suggested in other circumstances a complication of intracranial hypertension (hippocampal engagement or vascular compression). Another 2 animals, inoculated with an attenuated virus, were sacrificed on the 8th day. Their eeg''s showed a bilateral delta wave dysrhythmia, continuous at first, but later tending to fragment, predominanting in the anterior and middle cortical regions, reinforced episodically by bursts of fusiform delta waves. The anatomical picture was that of a major productive reaction, with discrete signs of neuro-axonal involvement. Perivascular infiltrations and glial nodules were situated in the gray matter, though sparing, relatively, the cortex and predominating at the level of the sub-thalamus and thalamus. The transmitted character of the delta dysrhythmia points to this location as the site of the inflammatory lesions. The same electrical anomalies and the same distribution of lesions are found in human cases of Japanese "B" encephalitis. These facts have a still more general significance in that one finds in other types of encephalitis, analogous bilateral delta dysrhythmia which assumes the characteristics of a diencephalitis. Another 4 monkeys were inoculated with an extremely virulent strain. They presented a consistent clinical picture: sudden prostration of the animal, with a rapid development of coma. The anatomical lesions were characterized by a massive infiltration of the brain stem (mesencephalic tegmentum). It was from this area that the electrical and clinical anomalies arose. The sudden coma and flattening of the eeg tracing, and the electrical silence observed in one case, was thought to represent a cerebral catastrophe secondary to a massive involvement of the regulatory formations in the brain stem. In another 2 cases, the eeg showed, at once, the beginning of a typical encephalitis of gray matter since, closely correlated in time with the extension of the inflammatory process to the reticular substance of the brain stem, the electrical activity was entirely changed; being then analogous to that seen experimentally when part of the reticular system is removed.