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The Journal of Neuroscience, February 18, 2009, 29(7):2103-2112; doi:10.1523/JNEUROSCI.0980-08.2009

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Neurobiology of Disease
Development of Spontaneous Recurrent Seizures after Kainate-Induced Status Epilepticus

Philip A. Williams,¹ Andrew M. White,^2,3 Suzanne Clark,¹ Damien J. Ferraro,¹ Waldemar Swiercz,^2,3 Kevin J. Staley,^2,3 and F. Edward Dudek¹

¹Department of Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523, and Departments of ²Pediatrics and ³Neurology, University of Colorado Health Sciences Center, Denver, Colorado 80262

Correspondence should be addressed to Dr. F. Edward Dudek, Department of Physiology, University of Utah School of Medicine, 420 Chipeta Way, Suite 1700, Salt Lake City, UT 84108-1297. Email: ed.dudek{at}hsc.utah.edu

Acquired epilepsy (i.e., after an insult to the brain) is often considered to be a progressive disorder, and the nature of this hypothetical progression remains controversial. Antiepileptic drug treatment necessarily confounds analyses of progressive changes in human patients with acquired epilepsy. Here, we describe experiments testing the hypothesis that development of acquired epilepsy begins as a continuous process of increased seizure frequency (i.e., proportional to probability of a spontaneous seizure) that ultimately plateaus. Using nearly continuous surface cortical and bilateral hippocampal recordings with radiotelemetry and semiautomated seizure detection, the frequency of electrographically recorded seizures (both convulsive and nonconvulsive) was analyzed quantitatively for 100 d after kainate-induced status epilepticus in adult rats. The frequency of spontaneous recurrent seizures was not a step function of time (as implied by the "latent period"); rather, seizure frequency increased as a sigmoid function of time. The distribution of interseizure intervals was nonrandom, suggesting that seizure clusters (i.e., short interseizure intervals) obscured the early stages of progression, and may have contributed to the increase in seizure frequency. These data suggest that (1) the latent period is the first of many long interseizure intervals and a poor measure of the time frame of epileptogenesis, (2) epileptogenesis is a continuous process that extends much beyond the first spontaneous recurrent seizure, (3) uneven seizure clustering contributes to the variability in occurrence of epileptic seizures, and (4) the window for antiepileptogenic therapies aimed at suppressing acquired epilepsy probably extends well past the first clinical seizure.

Key words: convulsion; EEG; epilepsy; latent period; radiotelemetry; seizure clusters

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Received Oct. 2, 2008; revised Dec. 29, 2008; accepted Jan. 5, 2009.

Correspondence should be addressed to Dr. F. Edward Dudek, Department of Physiology, University of Utah School of Medicine, 420 Chipeta Way, Suite 1700, Salt Lake City, UT 84108-1297. Email: ed.dudek{at}hsc.utah.edu

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