Sustained limbic seizures induced by intraamygdaloid kainic acid in the baboon: Symptomatology and neuropathological consequences

Sustained limbic seizures induced by intraamygdaloid kainic acid in the baboon: Symptomatology... In Papio papio baboons chronically prepared for cortical and deep electroencephalographic recording, injection of kainic acid into the amygdala (7 animals) or temporal pole (2 animals) gave rise to focal epileptic discharges lasting 15 to 150 hours. Electrographically, the seizure activity spread ipsilaterally and contralaterally within the limbic system but did not become generalized. The principal associated motor signs were arrest of movement and oral automatisms. Histological examination after two to ten days demonstrated lesions (neuron loss and gliosis) at the injection site that varied according to the amount of kainic acid injected (2 to 68 μg). “Remote” lesions occurred in the ipsilateral hippocampus (end‐folium and Sommer sector) and neocortex (occipital and frontal regions). The hippocampal lesions were comparable to those previously described as consequent to status epilepticus. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Neurology Wiley

Sustained limbic seizures induced by intraamygdaloid kainic acid in the baboon: Symptomatology and neuropathological consequences

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Publisher
Wiley
Copyright
Copyright © 1980 American Neurological Association
ISSN
0364-5134
eISSN
1531-8249
DOI
10.1002/ana.410080507
Publisher site
See Article on Publisher Site

Abstract

In Papio papio baboons chronically prepared for cortical and deep electroencephalographic recording, injection of kainic acid into the amygdala (7 animals) or temporal pole (2 animals) gave rise to focal epileptic discharges lasting 15 to 150 hours. Electrographically, the seizure activity spread ipsilaterally and contralaterally within the limbic system but did not become generalized. The principal associated motor signs were arrest of movement and oral automatisms. Histological examination after two to ten days demonstrated lesions (neuron loss and gliosis) at the injection site that varied according to the amount of kainic acid injected (2 to 68 μg). “Remote” lesions occurred in the ipsilateral hippocampus (end‐folium and Sommer sector) and neocortex (occipital and frontal regions). The hippocampal lesions were comparable to those previously described as consequent to status epilepticus.

Journal

Annals of NeurologyWiley

Published: Nov 1, 1980

References

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