Journal article
Dissociated changes of frontal and parietal somatosensory evoked potentials in sleep
Neurology, Vol.45(1), pp.154-160
1995
DOI: 10.1212/WNL.45.1.154
PMID: 7824107
Abstract
We studied the changes of frontal and parietal somatosensory evoked potentials (SEPs) in the awake state versus different stages of sleep in 10 normal adult subjects. Frontal and parietal SEP components were affected differentially as sleep stages progressed. In general, the amplitudes of frontal components, notably P22, were increased in sleep, whereas the amplitudes of parietal components were decreased in sleep. A sensitive waveform change from the awake state to sleep was present in the frontal response, where a subtle notched negativity, termed "N40," was present only in the awake state and quickly dissipated in all stages of sleep, including stage 1. The amplitude changes from the awake state to stage 3/4 sleep were neither linear nor parallel among SEP components. The most discordant changes occurred in stage 3/4. The amplitudes for the frontal N18-P22-N30 complex and parietal N20-P26-N32 complex increased from stage 2 to stage 3/4, while those for frontal N30-fP40 and parietal N32-pP40 decreased. In contrast to these divergent amplitude changes, the latencies of all components except P14 and frontal N18 showed progressive prolongation from the awake state to slow-wave sleep. The SEP waveforms and latencies in REM sleep approximated those in the awake state, although amplitudes for frontal peaks still remained slightly higher and amplitudes for parietal peaks slightly lower. We postulate that interactions of excitatory and inhibitory phenomena are responsible for the component-dependent and sleep-stage-dependent amplitude enhancement or depression in sleep.
Details
- Title: Subtitle
- Dissociated changes of frontal and parietal somatosensory evoked potentials in sleep
- Creators
- Y NOGUCHI - Univ. Iowa coll. medicine, dep. neurology, div. clin. electrophysiology, Iowa City IA 52242, United StatesT YAMADA - Univ. Iowa coll. medicine, dep. neurology, div. clin. electrophysiology, Iowa City IA 52242, United StatesM YEH - Univ. Iowa coll. medicine, dep. neurology, div. clin. electrophysiology, Iowa City IA 52242, United StatesM MATSUBARA - Univ. Iowa coll. medicine, dep. neurology, div. clin. electrophysiology, Iowa City IA 52242, United StatesY KOKUBUN - Univ. Iowa coll. medicine, dep. neurology, div. clin. electrophysiology, Iowa City IA 52242, United StatesJ KAWADA - Univ. Iowa coll. medicine, dep. neurology, div. clin. electrophysiology, Iowa City IA 52242, United StatesG SHIRAISHI - Univ. Iowa coll. medicine, dep. neurology, div. clin. electrophysiology, Iowa City IA 52242, United StatesS KAJIMOTO - Univ. Iowa coll. medicine, dep. neurology, div. clin. electrophysiology, Iowa City IA 52242, United States
- Resource Type
- Journal article
- Publication Details
- Neurology, Vol.45(1), pp.154-160
- Publisher
- Lippincott Williams & Wilkins; Hagerstown, MD
- DOI
- 10.1212/WNL.45.1.154
- PMID
- 7824107
- ISSN
- 0028-3878
- eISSN
- 1526-632X
- Language
- English
- Date published
- 1995
- Academic Unit
- Neurology
- Record Identifier
- 9984020888302771
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