Cortical excitability in drug-naive patients with partial epilepsy: a cross-sectional study

To use paired-pulse transcranial magnetic stimulation (TMS) to investigate cortical excitability in drug-naive patients with partial epilepsy. Twenty-one drug-naive patients with partial epilepsy and 15 control subjects were studied. The relaxed threshold to TMS, the central silent period, and the i...

Full description

Saved in:
Bibliographic Details
Published inNeurology Vol. 63; no. 11; p. 2051
Main Authors Varrasi, C, Civardi, C, Boccagni, C, Cecchin, M, Vicentini, R, Monaco, F, Cantello, R
Format Journal Article
LanguageEnglish
Published United States 14.12.2004
Subjects
Online AccessGet more information

Cover

Loading…
More Information
Summary:To use paired-pulse transcranial magnetic stimulation (TMS) to investigate cortical excitability in drug-naive patients with partial epilepsy. Twenty-one drug-naive patients with partial epilepsy and 15 control subjects were studied. The relaxed threshold to TMS, the central silent period, and the intracortical inhibition/facilitation were measured. Statistics implied cluster analysis methods. Also assessed were the patient interictal EEG epileptiform abnormalities (EAs) on a semiquantitative basis. Then the TMS was contrasted to the clinical and EEG findings, using chi2 or Fisher exact tests. One-third of the patients made up a "pathologic" cluster with a disrupted intracortical inhibition (p < 0.01). Two-thirds had a normal inhibition. Interictal EAs predominated in the pathologic cluster, for frequency (p < 0.04), duration (p < 0.04), and focality (p < 0.02). Intracortical inhibition, which was impaired in one-third of the patients, reflects gamma-aminobutyric acid (GABA) activity within cortical area 4. Defective GABA inhibition is a typical pathogenic factor in partial epilepsy. Transcranial magnetic stimulation proved able to detect it. The weaker cortical inhibition had a direct relation to the severity of interictal epileptiform abnormalities.
ISSN:1526-632X
DOI:10.1212/01.WNL.0000145770.95990.82