Document Detail


Development of spontaneous recurrent seizures after kainate-induced status epilepticus.
MedLine Citation:
PMID:  19228963     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 approximately 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.
Authors:
Philip A Williams; Andrew M White; Suzanne Clark; Damien J Ferraro; Waldemar Swiercz; Kevin J Staley; F Edward Dudek
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  29     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-02-20     Completed Date:  2009-04-16     Revised Date:  2014-09-20    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2103-12     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Action Potentials / physiology
Animals
Brain / physiopathology*
Chronic Disease
Convulsants / pharmacology
Disease Models, Animal
Electric Stimulation
Epilepsy / physiopathology*
Excitatory Amino Acid Agonists / pharmacology
Hippocampus / physiopathology
Kainic Acid / pharmacology
Male
Neurons / physiology
Rats
Rats, Sprague-Dawley
Recurrence
Seizures / etiology*,  physiopathology*
Signal Processing, Computer-Assisted
Status Epilepticus / chemically induced,  complications*,  physiopathology*
Telemetry
Time Factors
Grant Support
ID/Acronym/Agency:
NS045144/NS/NINDS NIH HHS; R01 NS045144/NS/NINDS NIH HHS; R01 NS045144-06/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Convulsants; 0/Excitatory Amino Acid Agonists; SIV03811UC/Kainic Acid
Comments/Corrections
Comment In:
Epilepsy Curr. 2009 Sep-Oct;9(5):144-5   [PMID:  19826508 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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