TY - JOUR
T1 - Cortical excitability in drug-naive patients with partial epilepsy
T2 - A cross-sectional study
AU - Varrasi, C.
AU - Civardi, C.
AU - Boccagni, C.
AU - Cecchin, M.
AU - Vicentini, R.
AU - Monaco, F.
AU - Cantello, R.
PY - 2004/12/14
Y1 - 2004/12/14
N2 - Objective: To use paired-pulse transcranial magnetic stimulation (TMS) to investigate cortical excitability in drug-naive patients with partial epilepsy. Methods: 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 χ2 or Fisher exact tests. Results: 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). Conclusions: Intracortical inhibition, which was impaired in one-third of the patients, reflects γ-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.
AB - Objective: To use paired-pulse transcranial magnetic stimulation (TMS) to investigate cortical excitability in drug-naive patients with partial epilepsy. Methods: 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 χ2 or Fisher exact tests. Results: 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). Conclusions: Intracortical inhibition, which was impaired in one-third of the patients, reflects γ-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.
UR - http://www.scopus.com/inward/record.url?scp=10444290767&partnerID=8YFLogxK
U2 - 10.1212/01.WNL.0000145770.95990.82
DO - 10.1212/01.WNL.0000145770.95990.82
M3 - Article
SN - 0028-3878
VL - 63
SP - 2051
EP - 2055
JO - Neurology
JF - Neurology
IS - 11
ER -