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Effects of 1, 1-Dimethylhydrazine (UDMH) on Evoked Cerebral Neuroelectric Responses

Report Number: AMRL TR 67-67
Author(s): W. R. Goff; T. Allison, Y. Matsumiya
Corporate Author: Yale University School of Medicine
Laboratory: Aerospace Medical Research Laboratories
Date of Publication: 1967-09
Pages: 16
Contract: AF 33(615)-2822
Project: 6302
Task: 630202
AD Number: AD0663764

The neural mechanisms of UDMH intoxication were studied by analyzing changes in cortical, subcortical, and cerebellar neuroelectric potentials evoked by peripheral nerve stimulation. Results showed that the negative component of the primary somatosensory cortical evoked potential was markedly potentiated by UDMH intoxication while the positive component of this response together with the response from the specific somatic sensory thalamic relay and from the cerebellum were unaffected. The potentiation almost always occurred in the absence of other evoked or spontaneous neuroelectric changes and preceded epileptiform seizure by several minutes. Thus it was usually the sole predictor of seizure. Motor paralysis markedly prolonged seizure onset. These results indicate the UDMH intoxication increases intracortical excitability acting primarily at axo-dendritic synapses to block inhibitory post-synaptic potentials. The resulting positive sensory-motor feedback is an important element in the production of seizures.

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