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
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
.