Abstracts

Rationale: EPC is caused by a limited etiologic repertoire of rolandic lesions. Prominent among these is FCD. Despite anticipated severe motor deficits, surgical resection of highly epileptogenic rolandic cortex is usually needed to control the continuous seizures. Unexpectedly, some patients may then present with EPC in the other hemibody, strongly suggesting unsuspected bilateral symmetrical dysplastic lesions.Objective: To report three patients with well documented FCD-related EPC involving one hemibody which shifted to the other hemibody following resection of the original rolandic lesion. Methods: Three female patients, aged between 6 and 26 years of age when evaluated, presented with medically refractory unilateral EPC. All underwent comprehensive neurophysiological and neuroimaging presurgical evaluation. One had ictal SPECT before and after the initial resection. Resection of motor cortex of the contralateral hemisphere was then performed, under acute ECoG monitoring. Histological analysis of the resected tissue was available in all. Results: One patient had an increased signal in a portion of the rolandic cortex, and MRI of the other two were normal. Ictal SPECT in one patient showed hyperperfusion of the motor cortex contralateral to the initial EPC. Between one day and one year following complete resection of one motor cortex, EPC started in the contralateral hemibody. One patient died of infectious complications after reappearance of EPC in the other hemibody and the other two continue with contralateral EPC. Post-resection ictal SPECT in one patient showed hyperperfusion in the contralateral motor cortex. Histopathology showed Taylor-type FCD in the resected tissue of all patients. Conclusions: Caution must be exercised when surgically treating EPC due to rolandic FCD. EPC may start ‘de novo’ in the contralateral hemibody, strongly suggesting disinhibition of the epileptogenic potential of unsuspected contralateral, roughly symmetrical, rolandic EPC.