PERIODIC EEG COMPLEXES IN SUBACUTE PANENCEPHALITIS: REACTIVITY, RESPONSE TO DRUGS AND RESPIRATORY RELATIONSHIPS.
1964
Abstract 1. 1. Stimuli, as applied in the present study, failed to change either the pattern or the periodicity of panencephalitic EEG complexes. It seems that the periodic EEG manifestations of panencephalitis cannot be elicited by means of extraneous stimuli once their periodicity has become stable. 2. 2. Intravenous injection of Evipan was not followed by the fast waves which characterize the incipient phase of barbiturate anaesthesia, a phenomenon attributed to a panencephalitic lesion of the cortex. 3. 3. Convulsive potentials following injections of Megimide appeared at first only with the periodic complexes, a phenomenon justifying the conclusion that these complexes indicate a state of increased excitability which facilitates the appearance of convulsive potentials. 4. 4. There is a statistically significant difference between the large number of EEG complexes during inspiration and expiration and their small number between two respirations. If we suppose that a discharge of inspiratory and expiratory bulbo-pontine neurons facilitates the appearance of panencephalitic complexes, it is logical to infer that the primary lesion responsible for them must be situated in the bulbo-pontine portion of the reticular formation or, at least, in a system closely connected therewith. 5. 5. Intravenous administration of Relaxil-G caused the characteristic periodicity of the complexes to disappear in some cases: it was replaced by the diffuse polymorphous delta activity which is usual in the final stage of panencephalitis. This effect of Relaxil permits the conclusion that the rhythmicity of the periodic complexes is regulated by the diffuse thalamic system, so that the appearance of periodic complexes depends on the relatively unimpaired condition of this system. 6. 6. Differences existing between the periodic complex on the one side, and the K complex and the secondary response of Forbes on the other, justify the statement that these electroencephalographic manifestations cannot be regarded as identical phenomena.
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