Effects of voluntary hyperventilation on cortical sensory responses - Electroencephalographic and magnetoencephalographic studies

Citation
J. Huttunen et al., Effects of voluntary hyperventilation on cortical sensory responses - Electroencephalographic and magnetoencephalographic studies, EXP BRAIN R, 125(3), 1999, pp. 248-254
Citations number
30
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EXPERIMENTAL BRAIN RESEARCH
ISSN journal
00144819 → ACNP
Volume
125
Issue
3
Year of publication
1999
Pages
248 - 254
Database
ISI
SICI code
0014-4819(199904)125:3<248:EOVHOC>2.0.ZU;2-K
Abstract
It is well established that voluntary hyperventilation (HV) slows down elec troencephalographic (EEG) rhythms. Little information is available, however , on the effects of HV on cortical responses elicited by sensory stimulatio n. In the present study, we recorded auditory evoked potentials (AEPs) and magnetic fields (AEFs), and somatosensory evoked magnetic fields (SEFs) fro m healthy subjects before, during, and after a 3- to 5-min period of volunt ary HV. The effectiveness of HV was verified by measuring the end-tidal CO2 levels. Long-latency (100-200 ms) AEPs and long-latency AEFs originating a t the supratemporal auditory cortex, as well as long-latency SEFs from the primary somatosensory cortex (SI) and from the opercular somatosensory cort ex (OC), were all reduced during HV. The short-latency SEFs from SI were cl early less modified, there being, however, a slight reduction of the earlie st cortical excitatory response, the N20m deflection. A middle-latency SEF deflection from SI at about 60 ms (P60 m) was slightly increased. For AEFs and SEFs, the center-of-gravity locations of the activated neuronal populat ions were not changed during HV. All amplitude changes returned to baseline levels within 10 min after the end of HV. The AEPs were not altered when t he subjects breathed 5% CO2 in air in a hyperventilation-like manner, which prevented the development of hypocapnia. We conclude that moderate HV supp resses long-latency evoked responses from the primary projection cortices, while the early responses are less reduced. The reduction of long-latency r esponses is probably mediated by hypocapnia rather than by other nonspecifi c effects of HV. It is suggested that increased neuronal excitability cause d by HV-induced hypocapnia leads to spontaneous and/or asynchronous firing of cortical neurones, which in turn reduces stimulus-locked synaptic events .