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Bilateral Pathological Damage in Temporal Lobe Epilepsy

Published online by Cambridge University Press:  18 September 2015

Thomas L. Babb
Thomas L. Babb*
Affiliation:
Department of Neurology and the Brain Research Institute, UCLA School of Medicine, University of California, Los Angeles
*
Department of Neurology, University of California, Los Angeles, California, U.S.A. 90024
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Abstract:

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Patients with drug-refractory temporal lobe epilepsy can be treated successfully with surgical resection of one temporal lobe, especially when the resection includes the hippocampus. Although intrahippocampal recordings usually localize seizure onsets to one hippocampus, there are bilaterally-independent interictal spikes, occasional contralateral seizure onsets and post-resection seizures that implicate contralateral damage and epileptogenicity. Post-mortem onquantified studies of both hippocampi in epileptics have revealed incidences of bilateral hippocampal sclerosis, mostly being asymmetric. The present paper reports on two post-mortem cases of bilateral, asymmetric cell loss in patients with physiologically-verified hippocampal epilepsy. In one patient the damage was severe bilaterally, but only slightly greater damage in one hippocampus. In the second patient, damage in one hippocampus was as severe as in the first patient; however the contralateral hippocampus appeared undamaged. However, cell counts revealed losses of over 30% in three different hippocampal subregions, indicating a mild form of asymmetric bilateral damage in patient two.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 18 , Issue S4 , November 1991 , pp. 645 - 648
Copyright
Copyright © Canadian Neurological Sciences Federation 1991

References

REFERENCES

1.Babb, TL, Brown, WJ. Pathological findings in epilepsy. In: Engel, J Jr, ed. Surgical Treatment of the Epilepsies. New York: Raven Press 1987; 511–540.Google Scholar
2.Engel, J Jr, Crandall, PH, Rausch, R. The partial epilepsies. In: Rosenberg, RN, Grossman, RG, Schochet, S. et al., eds. The Clinical Neurosciences. New York: Churchill-Livingstone, 1983; 1349–1380.Google Scholar
3.Wilson, CL, Isokwa-Akesson, M, Babb, TL, et al. A comparative view of local and interhemispheric limbic pathways in humans: an evoked potential analysis. In: Engel, J Jr, ed. Fundamental Mechanisms of Human Brain Function. New York: Raven Press 1987; 27–38.Google Scholar
4.Demeter, S, Rosene, DL, Van Hoesen, GW. Interhemispheric pathways of the hippocampal formation, presubiculum, and entorhinal and posterior parahippocampal cortices in the rhesus monkey: the structure and organization of the hippocampal commissures. J Comp Neurol 1985; 233: 30–47.CrossRefGoogle ScholarPubMed
5.Amarai, DG, Insausti, R, Cowan, WM. The commissural connections of the monkey hippocampal formation. J Comp Neurol 1984; 224: 307–336.CrossRefGoogle Scholar
6.Engel, J Jr, Crandall, PH. Falsely localizing ictal onsets with depth EEG telemetry during anticonvulsant withdrawal. Epilepsia 1983; 24: 344–355.CrossRefGoogle ScholarPubMed
7.Brazier, MAB, Crandall, PH. Tests of the predictive value of EEG recording from within the brain in the partial epilepsies. In: Cobb, WA, Van Duijn, H, eds. Contemporary Clinical Neurophysiology. Amsterdam: Elsevier Scientific Publishing Co. 1978; 83–103.Google Scholar
8.Babb, TL, Lieb, JP, Brown, WJ, et al. Distribution of pyramidal cell density and hyperexcitability in the epileptic human hippocampal formation. Epilepsia 1984b; 25: 721–728.CrossRefGoogle ScholarPubMed
9.Mouritzen-Dam, A. Epilepsy and neuron loss in the hippocampus. Epilepsia 1980; 21: 617–629.Google Scholar
10.Margerison, JH, Corsellis, JAN. Epilepsy and the temporal lobes. Brain 1966; 89: 499–530.CrossRefGoogle ScholarPubMed
11.Sano, K, Malamud, N. Clinical significance of sclerosis of the cornu ammonis. Arch Neurol Psychiatry 1953; 70: 40–53.CrossRefGoogle ScholarPubMed
12.Babb, TL, Brown, WJ, Pretorius, J, et al. Temporal lobe volumetric cell densities in temporal lobe epilepsy. Epilepsia 1984a; 25: 729–740.CrossRefGoogle ScholarPubMed
13.Bouchet, and Cazauvieilh, . De l’épilepsie considérée dans ses rapports avec l’aliénation mentale. Recherche sur la nature et le siège de ces deux maladies; mémoire qui a remporté le prix au concours établi par M. Esquirol. Arch Gen Med 1825; 9: 510–542.Google Scholar
14.Bratz, EAmmonshornbefunde der epileptischen. Arch Psychiatr Nervenkr 1899; 31: 820–836.CrossRefGoogle Scholar