A Meta-analysis of the Cortical Silent Period in Epilepsies

•We evaluated the consistency of CSP changes in untreated patients with epilepsies.•A significant mean difference was found, with longer CSP in patients than in controls.•Meta-analysis confirms enhancement of cortical inhibitory measure in epilepsies.•CSP may reflects compensatory phenomena counteracting transition to ictal state.

ObjectiveThe cortical silent period (CSP) following transcranial magnetic stimulation reflects GABAB-mediated inhibition in the primary motor cortex (M1) and could contribute to understand the pathophysiological substrates of epileptic conditions. Increased CSP duration has been reported in idiopathic generalized epilepsy (IGE) and in partial epilepsy (PE) involving the M1, although other studies yielded discordant findings. We used meta-analysis to systematically assess the consistency of CSP changes in untreated patients with epilepsies.MethodsDatabases were searched for controlled studies evaluating the CSP in drug-naïve or drug-free patients with IGE or PE. For each study, the mean difference with 95% confidence intervals (CIs) between CSP duration obtained in patients and controls was calculated. The effect of motor threshold (MT) on the CSP duration has also been explored by meta-analysis and meta-regression.ResultsFourteen studies (267 patients and 234 controls) were included. A significant mean difference (14.16 ms, 95% CI, 1.20, 27.11 ms) was found, with longer CSP in patients than in controls. The mean difference was still greater (18.05 ms) if only the 202 IGE patients were analyzed. No MT difference emerged between patients and controls. Meta-regression showed no relationship between MT and CSP duration.ConclusionMeta-analysis confirms CSP modifications in epilepsies, with enhancement of this cortical inhibitory measure at least in most IGE patients. This provides rationale for further investigations aiming to verify the hypotheses that increased CSP reflects compensatory neural phenomena counteracting transition from the interictal to ictal state and that CSP variability reflects the pathophysiological heterogeneity of epileptic syndromes.