Abstracts

Rationale: Sleep and epilepsy are intricately linked. Sleep has profound effects on epilepsy by affecting the occurence of interictal discharges (IEDs) and seizures depending on the epilepsy syndromes. Vice versa epilepsy changes sleep by disrupting normal sleep through seizures. Sleep spindles are typically associated with an increase of IEDs. We studied the change in number and power of sleep spindles preceding nightly seizures. Methods: We retrospectively evaluated the nightly EEG recordings of presurgical epilepsy patients from our EEG-video-monitoring unit. We studied temporal lobe epilepsy (TLE) and extratemporal lobe epilepsy (XTLE) patients separately. We evaluated the 200 seconds before the EEG seizure onset for spindle density (spindles per minute) and spindle power and compared that to the interictal baseline sleep of the individual patient. Results: The spindle density and the spindle power decreased significantly in the minutes preceding the first seizure of the night. The reduction before secondarily generalized seizures (8.74±2.46; p=0.001) was more pronounced than before focal seizures (10.50±2.54; p=0.003) compared to the individual baseline (12.17±2.69) of each patient. This finding was more pronounced in XTLE than in TLE patients. The reduction of spindle power was also significant and was more pronounced in XTLE. The mean spindle density decreased significantly in all focal (10.18±1.89; p=0.001) and generalized preictal period (8.83±2.39; p=0.001) compared to the mean interictal period (12.07±2.09). The results showed a higher significance in XTLE than in TLE. Conclusions: Our data demonstrate that spindle density decreases in the minutes before the observable EEG or clinical onset of a seizure. This may be a reflection of a change in the epileptic network even before the observable onset. This finding may be helpful in understanding seizure mechanisms and in anticipating seizures. Our study supports the notion that changes in the epileptic network precede the seizure onset and have an influence on seizure generation and termination.