Effects of voluntary hyperventilation on cortical sensory responses
Electroencephalographic and magnetoencephalographic studies |
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Authors: | J Huttunen H Tolvanen E Heinonen J Voipio H Wikström R J Ilmoniemi R Hari K Kaila |
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Institution: | (1) BioMag Laboratory, Medical Engineering Centre, P.O. Box 508, Helsinki University Central Hospital, FIN-00029 HYKS, Finland e-mail: huttunen@biomag.helsinki.fi, Tel.: +358-9-471-5542, Fax: +358-9-471-5781, FI;(2) Department of Biosciences, Division of Animal Physiology, University of Helsinki, Finland, FI;(3) Brain Research Unit, Low Temperature Laboratory, Helsinki University of Technology, Espoo, Finland, FI |
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Abstract: | It is well established that voluntary hyperventilation (HV) slows down electroencephalographic (EEG) rhythms. Little information
is available, however, on the effects of HV on cortical responses elicited by sensory stimulation. In the present study, we
recorded auditory evoked potentials (AEPs) and magnetic fields (AEFs), and somatosensory evoked magnetic fields (SEFs) from
healthy subjects before, during, and after a 3- to 5-min period of voluntary 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 at the supratemporal auditory cortex, as well as
long-latency SEFs from the primary somatosensory cortex (SI) and from the opercular somatosensory cortex (OC), were all reduced
during HV. The short-latency SEFs from SI were clearly less modified, there being, however, a slight reduction of the earliest
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 populations 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 the
subjects breathed 5% CO2 in air in a hyperventilation-like manner, which prevented the development of hypocapnia. We conclude that moderate HV suppresses
long-latency evoked responses from the primary projection cortices, while the early responses are less reduced. The reduction
of long-latency responses is probably mediated by hypocapnia rather than by other nonspecific effects of HV. It is suggested
that increased neuronal excitability caused by HV-induced hypocapnia leads to spontaneous and/or asynchronous firing of cortical
neurones, which in turn reduces stimulus-locked synaptic events.
Received: 14 October 1997 / Accepted: 28 October 1998 |
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Keywords: | Hyperventilation Magnetoencephalography Somatosensory cortex Auditory cortex Somatosensory evoked response Auditory evoked response Human |
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