Klinische Neurophysiologie 2004; 35 - 152
DOI: 10.1055/s-2004-832064

Clinical and EEG Findings in Eleven Patients with Insular Epilepsies

B Kruse 1, I Tuxhorn 2, J Schmitt 3, R Schulz 4, F Wörmann 5, A Ebner 6
  • 1Bielefeld
  • 2Bielefeld
  • 3Bielefeld
  • 4Bielefeld
  • 5Bielefeld
  • 6Bielefeld

Purpose: We have attempted to study auras, seizure semiology, and EEG findings in insular epilepsies. Methods: We reviewed the clinical and EEG data of eleven patients with epileptogenic lesions in the insular region. Ten patients underwent EEG-video intensive monitoring with surface electrodes and three patients subsequently underwent invasive EEG recording with subdural grid electrodes. One outpatient had only a routine EEG taken. Clinical data of two patients were excluded: One patient was too handicapped to report auras reliably. The other patient had an additional large extrainsular lesion making it unclear if seizures arose from the insular or extrainsular cortex. Results: All patients experienced auras: they were epigastric in nature in five, „tingling“ in the whole body in four, psychic (fear, mood disturbances) in three, somatosensible (tingling in the contralateral arm) in two, and complex visual in one patient. Two had additional autonomic signs (flush, tachycardia). Seizures were characterized by oral and manual automatisms in seven, hypermotor symptoms in five, and focal tonic seizures of the contralateral arm in two patients. The interictal and ictal epileptiform activity occurred ipsilateral over temporal lateral (three patients), temporal mesial (two patients), frontal, centrotemporal, centroparietal, parietolateral and median regions. Seizure patterns were found over the temporal region in four patients (one with a fast propagation to the frontal region); they were frontal, parietolateral, frontotemporal, or diffuse. One patient had no seizure pattern. Conclusions: Patients with insular epilepsies show a great variety of auras and other seizure symptoms and EEG findings. Seizure semiology and EEG findings can mimic other epilepsies, e.g., temporal or frontal lobe epilepsy.