Abstracts

Rationale: Focal cortical dysplasia type II (FCD) is a malformation of cortical development which is often associated with medically refractory epilepsy. Three specific electrographic patterns have been identified: spikes and polyspikes sometimes followed by a wave / slow wave with a rhythmic and subcontinuous modality (Pattern 1), short bursts of high voltage spikes followed or not by high amplitude slow waves interrupted by relative flat periods (Pattern 2), and discharges of high frequency, low-voltage rhythmic activity with regular morphology (Pattern 3). Although some studies mention descriptively the different patterns during slow wave and REM sleep, studies which characterize systematically these changes over the different sleep stages are lacking. This study aims to describe how the typical intracerebral patterns of FCD change across the different sleep stages. Methods: The charts and recordings of all patients who underwent presurgical evaluation with combined scalp-intracranial electroencephalography (EEG) at the Montreal Neurological Institute and Hospital between January 2010 and June 2014 were reviewed. For this analysis, patients with unequivocal imaging or a histological diagnosis of FCD type II as well as the typical intracerebral EEG pattern were selected. The first sleep cycle was manually scored in the scalp EEG according to AASM 2.0. The intracranial EEG was semiquantitatively analyzed according to the frequency of patterns 1 - 3 across the different sleep stages (wake, N1, N2, N3, REM) ranging from pattern absent or rare, occasional (not present on every 30 sec. page), frequent (present on every 30 sec. page) to semicontinuous or continuous. Results: We identified 5 patients (3 women; mean age: 27 years; 4 frontal lobe epilepsies, 1 parietal lobe epilepsy) with a histologically confirmed diagnosis of FCD type II (4 type IIb and 1 type IIa). The mean epilepsy duration was 11 years. Pattern 1 was the clearly predominant pattern during wakefulness, but also during N1 and REM sleep. Of note, the EEG amplitude of this pattern was markedly reduced during REM sleep. In contrast, pattern 2 increased with sleep depth and was most prominent during N3 sleep. Pattern 3 was comparatively rare and present during N2 and N3 sleep. The semiquantitative distribution of the 3 EEG patterns across the different sleep stages is given in Figure 1. Conclusions: The previously described 3 specific EEG patterns of FCD type II were present in all patients. The 3 patterns followed a typical distribution over the different sleep stages with pattern 1 being most prominent during wake, N1 and REM sleep, and pattern 2 the hallmark of deep sleep suggesting that sleep is an important modulator of the manifestation of quasi continuous pathological EEG patterns such as present in FCD type II. Furthermore, despite the presence of an almost continuous epileptic discharge, regions of FCD are influenced by the thalamo-cortical mechanisms involved in generating sleep patterns.