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Dorsal Frontal, Orbital and Mesial Frontal Cortical Lesion and Amygdaloid Kindling in Cats

Published online by Cambridge University Press:  15 November 2018

J. A. Wada  and
Akira Wake
J. A. Wada*
Affiliation:
University of British Columbia, Health Sciences Center Hospital, Vancouver, British Columbia, Canada
Akira Wake
Affiliation:
University of British Columbia, Health Sciences Center Hospital, Vancouver, British Columbia, Canada
*
2075 Wes-brook Place, U.B.C. Campus, Vancouver, B.C. Canada V6T 1W5
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Summary

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Bilateral anteromesial or orbital cortical lesions do not affect sequential pattern of amygdaloid seizure development. However, orbital cortex lesions appear to significantly participate in the elaboration of a Stage 6 seizure pattern.

Amygdaloid kindling ipsilateral to the side of anterodorsal cortical lesion or in animals with the same bilateral lesion appears to predispose them for the development of spontaneous, non-convulsive (partial complex) seizures. It also significantly modifies clinical ictal patterns with practical omission of Stages 2, 3 and 5, and largely lateralizes AD propagation to the stimulated hemisphere.

The latter two features are strikingly reminiscent of the electroclinical manifestations of secondary site AM kindling in intact animals or AM kindling in animals with forebrain commissure bisection.

Nonconvulsive (partial complex) status epilepticus was readily arrested by placement of electrolytic lesions ipsilateral to the AM stimulation, suggesting that MRF is essential for the perpetuation of the recurrent spontaneous seizure.

Finally, the presence and absence of positive and negative aftereffects respectively, in animals with anterodorsal cortical lesion is consistent with the view that transfer and interference effects are mediated through the brain stem and forebrain commissures respectively.

Résumé

Résumé

Des lésions anteromédianes bilatérales ou du cortex orbital n’affectent pas le réroulement séquentiel du développement des crises de l’amygdale. Cependant, les lésions du cortex orbital semblent participer significativement dans l’élaboration de la Phase 6 des convulsions.

Le “kindling” amygdalien ipsilatéral au côté de la lésion corticale anterodorsale ou chez les animaux avec la même lésion bilatérale

Semble les prédisposer au développement d’attaques spontanées, non convulsives (complexes partiels) Modifie signifieativement le mode ictal clinique avec en fait omission des Phases 2, 3 et 5 Latéralisé largement la propagation de AD à l’hémisphère stimulé.

Les deux dernières caractéristiques rappellent remarquablement les manifestations électro-cliniques de kindling du site AM secondaire chez les animaux intacts ou de kindling AM chez les animaux avec une bisection de la commissure antérieure.

L’état de mal épileptique non-convulsif (complexe partiel) est facilement contrôlé en plaçant des lésions électrolytiques ipsilatérales à la stimulation AM, suggérant que le MRF est essentiel à la persévérance des attaques spontanées périodiques.

Finalement, aucune des lésions corticales créée ne produisait d’effet sur le transfert. Les résultats sont compatibles avec l’hypothèse voulant que le transfert et les effets d’interférence sont transmis à travers les commissures du tronc cérébral et du télencéphale respectivement.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 4 , Issue 2 , May 1977 , pp. 107 - 115
Copyright
Copyright © Canadian Neurological Sciences Federation 1977

References

Brazier, M. A. B., Crandall, P. H. and Walsh, G. O. (1976). Enhancement of EEG lateralizing signs in temporal lobe epilepsy Exp. Neurol. 51: 241–258.Google Scholar
Corcoran, M. E., Urstad, H. McCaughran, J. A. and Wada, J. A. (1975). Frontal lobe and kindling in the rat. Can. J Neurol. Sci. 2: 501–508.Google ScholarPubMed
Goodfellow, E. F. and Niemer, W. T. (1961). The spread of afterdischarge from stimulation of the rhinencephalon in the cat. EEG J. 13: 710–721.Google Scholar
Jacobson, S. and Trojanowski, J. Q. (1975). Amygdaloid projections to prefrontal granular cortex in rhesus monkey demonstrated with horseradish peroxidase. Brain Research 100: 132–139.Google Scholar
Krettek, J. E. and Price, J. L. (1974). A direct input from the amygdala to the thalamus and the cerebral cortex. Brain Research 67: 169–174.Google Scholar
McCaughran, J. A. (1976). Role of the forebrain commissures in amygdaloid kindling. Unpublished M.Sc. thesis, University of British Columbia.Google Scholar
McIntyre, D. C. (1975). Split Brain Rat: Transfer and interference of kindled amygdala convulsions. Can. J. Neurol. Sci. 2: 429–438.Google Scholar
Wada, J. A. and Osawa, T (1976). Spontaneous recurrent seizure state induced by daily electric amygdaloid stimulation in Senegalese baboons (Papio papio). Neurology 26/3: 273–286.Google ScholarPubMed
Wada, J. A., Osawa, T. and Mizoguchi, T (1975). Recurrent spontaneour seizure state induced by prefrontal kindling in Senegalese baboons, Papio papio. Can. J. Neurol. Sci. 2: 477–492.Google Scholar
Wada, J. A. and Sato, M. (1974). Generalized convulsive seizures induced by daily electrical stimulation of the amygdala in cats. Neurology 24/6: 565–574.Google Scholar
Wada, J. A. and Sato, M. (1975). Generalized convulsive seizure state induced by daily electrical stimulation of the amygdala in split brain cats. Epilepsia 16: 417–430.Google Scholar
Wake, A. and Wada, J. A. (1975). Frontal cortical kindling in cats. Can. J. Neurol. Sci. 2: 493–499.Google Scholar
Wake, A. and Wada, J. A. (1977). Transfer & interference in amygdaloid kindling in cats. Can. J. Neurol. Sci. 4: 5–11 CrossRefGoogle ScholarPubMed
Wada, J. A., Sato, M. and McCaughran, J. A. (1975). Cortical electrographic correlates of convulsive seizure development induced by daily electrical stimulation of the amygdala in rats and cats. Folia Psychiatrica et Neurologica Japonica 29/4: 329–339.Google Scholar
Wada, J. A. and Sato, M. (1975). Effects of unilateral lesion in the midbrain reticular formation on kindled amygdaloid convulsion in cats. Epilepsia 16: 693–697 Google Scholar