Power spectral analysis of EEG characteristics during sleep in epileptics.
Power spectral analysis of spontaneous EEG activity recorded during non-rapid eye movement (REM) sleep was employed in an effort to identify characteristic EEG substrate abnormalities in epileptics. All-night polygraphic recordings were obtained from 10 poorly controlled subjects with mixed and generalized seizures. Similar data were obtained from 10 matched nonepileptic subjects. Continuous 10 min samples of non-REM sleep were identified at the beginning and end of these all-night recordings. EEG activity recorded during these periods from left sensorimotor and parieto-occipital bipolar leads was digitized, subjected to the fast Fourier transform, and then sorted into successive 4 Hz frequency bands between 0 and 23 Hz. Mean spectral density was determined for each frequency band from both samples in both groups. Comparison of these values disclosed both similarities and differences between the two groups. All subjects showed a significant "time-of-night effect," with power at 0-3, 4-7, and 8-11 Hz greater at the beginning of the night. This finding was related to a similar observation in developing infants and attributed to a circadian influence on neuronal generators. In group comparisons, epileptics showed selective differences in common when compared with nonepileptics. These differences were reduced when data from a small group of unmedicated epileptic subjects were partialled out. Medicated epileptics showed differences restricted to the early morning non-REM sleep sample, which included significantly greater power at 4-7 Hz and significantly lower power at 12-15 Hz. Unmedicated subjects showed these differences in both samples and also showed significantly greater power in the 0-3 Hz band. It was suggested that anticonvulsant medications may exert a general normalizing influence on EEG characteristics during sleep, particularly at the beginning of the night in proximity to their administration. The documentation of significant EEG deviations restricted to two basic rhythmic patterns during sleep suggests a disturbance of underlying thalamocortical mechanisms.
D000293:Adolescent; D000328:Adult; D002220:Carbamazepine / Q000627:therapeutic use; D002940:Circadian Rhythm; D004569:Electroencephalography; D004827:Epilepsy / Q000188:drug therapy / Q000503:physiopathology*; D005013:Ethosuximide / Q000627:therapeutic use; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D008991:Monitoring, Physiologic; D010634:Phenobarbital / Q000627:therapeutic use; D010672:Phenytoin / Q000627:therapeutic use; D011324:Primidone / Q000627:therapeutic use; D012895:Sleep, REM / Q000502:physiology*
D011324:Primidone; D002220:Carbamazepine; D005013:Ethosuximide; D010672:Phenytoin; D010634:Phenobarbital