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Systemic Factors and Epileptic Brain Damage: Prolonged Seizures in Paralyzed, Artificially Ventilated Baboons

Brian S. Meldrum, MB, PhD; Roger A. Vigouroux, MD; James B. Brierley, MD
Arch Neurol. 1973;29(2):82-87. doi:10.1001/archneur.1973.00490260026003.
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Prolonged electroencephalographic seizures were induced by the intravenous injection of bicuculline (0.5 to 1.4 mg/kg) in adolescent Papio papio, while they were paralyzed and artificially ventilated on air or oxygen. Physiological monitoring revealed an initial increase in cerebral blood flow. Arterial oxygen tension remained steady or decreased slightly. Rectal temperature rose, but did not exceed 40.0 C.

After perfusion-fixation of the brain, light microscopy revealed neurons with ischemic cell change in seven animals who had had seizures lasting three hours 25 minutes to seven hours 30 minutes. These changes predominated in the neocortex (small pyramidal neurons), thalamus (anterior, dorsomedial, and ventral nuclei), and hippocampus (Sommer sector and endfolium).

Comparison with our previous studies in nonparalyzed baboons indicates that paralysis provides partial protection against neuronal damage in the neocortex and hippocampus. Cerebellar damage (related to hyperpyrexia and arterial hypotension) is almost totally prevented by paralysis.

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