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Interictal EEG Discoordination in a Rat Seizure Model

Neymotin, Samuel A.*; Lee, Heekyung; Fenton, André A.*†‡§; Lytton, William W.*†‡∥

Journal of Clinical Neurophysiology: December 2010 - Volume 27 - Issue 6 - p 438-444
doi: 10.1097/WNP.0b013e3181fe059e
Invited Review

Cognitive and psychiatric comorbidities are common and clinically important in medial temporal lobe epilepsy and are likely caused by ongoing abnormalities in brain activity. In addition, it is unclear how the dynamics of interictal brain activity in medial temporal lobe epilepsy contributes to the generation of seizures. To investigate these issues, the authors evaluated multisite interictal EEG from a perinatal excitotoxic, hippocampal lesion rat model of medial temporal lobe epilepsy. Sample entropy, an information theoretical measure, demonstrated decreased complexity at different time scales and across all channels in epileptic animals. However, higher-order multiarea measures showed evidence of increased variability in population correlation measures. This apparent paradox was resolved by noting that although the EEG from epileptic animals was overall more stereotyped, there were frequent periods where two or more brain areas “broke off” from ongoing brain activity in epileptic animals, producing decorrelations between areas. These decorrelations were particularly apparent across the midline, suggesting impairments of interhemispheric coordination, a form of interhemispheric diaschisis. Both the observed alterations could contribute to a reduction in brain functionality: an overall reduction in complexity and a failure of interhemispheric brain coordination, suggesting a breakdown in communication between hemispheres. The authors speculate that any tendency of areas to lose communication or break away from coordinated brain activity might predispose to seizures in these areas.

From *SUNY Downstate/Poly-NYU Joint Biomedical Engineering Program; †Neural and Behavioral Science Program; Departments of ‡Physiology & Pharmacology and §Neurology, SUNY Downstate, Brooklyn; and ∥Center for Neural Science, New York University, New York, New York, and the Department of Neurology, Kings County Hospital Center, Brooklyn, New York.

Supported by National Institute of Mental Health (R01MH084038) and National Institute of Neurologic Disorders and Stroke (R42NS064474).

Address correspondence and reprint requests to William W. Lytton, 450 Clarkson Ave., Box 31, Brooklyn, NY 11203-2098; e-mail:

Copyright © 2010 American Clinical Neurophysiology Society