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Bursts of 15-30 Hz oscillations following noxious laser stimulus originate in posterior cingulate cortex
A. Stančák, H. Poláček, S. Bukovský
Jazyk angličtina Země Nizozemsko
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- bolest patofyziologie MeSH
- časové faktory MeSH
- cingulární gyrus patofyziologie MeSH
- dospělí MeSH
- elektroencefalografie MeSH
- evokované potenciály MeSH
- funkční lateralita MeSH
- korová synchronizace MeSH
- lasery škodlivé účinky MeSH
- lidé MeSH
- mapování mozku MeSH
- mozek patofyziologie MeSH
- noha (od hlezna dolů) patofyziologie MeSH
- obličej patofyziologie MeSH
- periodicita MeSH
- počítačové zpracování signálu MeSH
- ruka patofyziologie MeSH
- třísla patofyziologie MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mužské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Previous EEG studies reported the presence of synchronised 15-30 Hz oscillations in vertex electrodes following innocuous somatosensory stimulation and noxious laser stimulation. The purpose of the present study was to analyse the sources of poststimulus increases of 15-30 Hz oscillations during noxious laser stimulation of four different body regions and to compare the sources of the poststimulus synchronisation with the sources of the N2 component of laser-evoked potential (LEP). In 10 healthy subjects, moderately painful laser stimuli were applied to the dorsum of the right hand, dorsum of the right foot, right groin, and right side of the face. EEG data, recorded from 111 scalp sites, were analysed using event-related desynchronisation method and source dipole analysis. A profound amplitude increase of 15-30 Hz oscillations peaking 1-2 s after noxious laser stimulation was found during stimulation of each body part. The sources of these oscillations were located in the dorsal posterior cingulate cortex and showed no somatotopic arrangement. The sources of the N2-LEP component were located in the anterior mid-cingulate cortex 25-30 mm rostral to the sources of 15-30 Hz oscillations. The amplitude of the poststimulus synchronisation of 15-30 Hz oscillations correlated (P<0.05) with the amplitude of N2-LEP component. Results show that noxious laser stimuli induce bursts of 15-30 Hz oscillations in the posterior cingulate cortex. The poststimulus increases of 15-30 Hz oscillations may stand for transient cortical inhibition possibly aiding temporary suppression of motor programs that have been primed by noxious stimulation.
Citace poskytuje Crossref.org
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- $a Previous EEG studies reported the presence of synchronised 15-30 Hz oscillations in vertex electrodes following innocuous somatosensory stimulation and noxious laser stimulation. The purpose of the present study was to analyse the sources of poststimulus increases of 15-30 Hz oscillations during noxious laser stimulation of four different body regions and to compare the sources of the poststimulus synchronisation with the sources of the N2 component of laser-evoked potential (LEP). In 10 healthy subjects, moderately painful laser stimuli were applied to the dorsum of the right hand, dorsum of the right foot, right groin, and right side of the face. EEG data, recorded from 111 scalp sites, were analysed using event-related desynchronisation method and source dipole analysis. A profound amplitude increase of 15-30 Hz oscillations peaking 1-2 s after noxious laser stimulation was found during stimulation of each body part. The sources of these oscillations were located in the dorsal posterior cingulate cortex and showed no somatotopic arrangement. The sources of the N2-LEP component were located in the anterior mid-cingulate cortex 25-30 mm rostral to the sources of 15-30 Hz oscillations. The amplitude of the poststimulus synchronisation of 15-30 Hz oscillations correlated (P<0.05) with the amplitude of N2-LEP component. Results show that noxious laser stimuli induce bursts of 15-30 Hz oscillations in the posterior cingulate cortex. The poststimulus increases of 15-30 Hz oscillations may stand for transient cortical inhibition possibly aiding temporary suppression of motor programs that have been primed by noxious stimulation.
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