Department of Neurophysiology and Clinical Neurology, Grenoble University Hospital Inserm U398, Faculty of Medecine, Strasbourg, France
Recent clinical and experimental studies have suggested that the basal ganglia are involved in epileptic seizures as a propagation pathway or as a remote inhibitory control circuit. The present case report may provide additional evidence from post‐ictal magnetic resonance imaging (MRI) supporting this hypothesis. A healthy 13 year‐old boy was admitted for a complex partial status epilepticus. MRI, performed one week later, revealed bilateral T2 hyperintense signals in the striata and a left temporal arachnoid cyst. Left temporal slow waves were noted on EEG recording. No obvious metabolic alterations were identified. During the next six years of follow‐up, no seizure occurred and striatal alterations progressively disappeared. The clinical characteristics of the seizures, EEG slow waves, and probably the presence of an arachnoid cyst suggest that seizures originated from the left temporal lobe. The long‐lasting MRI changes suggest that bilateral striatal alterations may have been secondary to an inflammatory process, which in turn could have disrupted a striatal inhibitory control over seizures. On the basis of these arguments, we speculate involvement of basal ganglia in epileptic seizures, as a part of a modulatory control system over seizures rather than a propagation pathway. Future reports will support or invalidate our hypothesis.