Excitability of human motor and visual cortex before, during, and after hyperventilation

Abstract

Sparing R, Dafotakis M, Buelte D, Meister IG, Noth J. Excitability of human motor and visual cortex before, during, and after hyperventilation. J Appl Physiol 102: 406 -411, 2007. First published September 21, 2006; doi:10.1152/japplphysiol.00770.2006.-In humans, hyperventilation (HV) has various effects on systemic physiology and, in particular, on neuronal excitability and synaptic transmission. However, it is far from clear how the effects of HV are mediated at the cortical level. In this study we investigated the effects of HV-induced hypocapnia on primary motor (M1) and visual cortex (V1) excitability. We used 1) motor threshold (MT) and phosphene threshold (PT) and 2) stimulus-response (S-R) curves (i.e., recruitment curves) as measures of excitability. In the motor cortex, we additionally investigated 3) the intrinsic inhibitory and facilitatory neuronal circuits using a short-interval paired-pulse paradigm. Measurements were performed before, during, and after 10 min of HV (resulting in a minimum end-tidal PCO2 of 15 Torr). HV significantly increased motor-evoked potential (MEP) amplitudes, particularly at lower transcranial magnetic stimulation (TMS) intensities. Pairedpulse stimulation indicated that HV decreases intracortical inhibition (ICI) without changing intracortical facilitation. The results suggest that low PCO 2 levels modulate, in particular, the intrinsic neuronal circuits of ICI, which are largely mediated by neurons containing ␥-aminobutyric acid. Modulation of MT probably resulted from alterations of Na ϩ channel conductances. A significant decrease of PT, together with higher intensity of phosphenes at low stimulus intensities, furthermore suggested that HV acts on the excitability of M1 and V1 in a comparable fashion. This finding implies that HV also affects other brain structures besides the corticospinal motor system. The further exploration of these physiological mechanisms may contribute to the understanding of the various HV-related clinical phenomenona. partial pressure of carbon dioxide; phosphenes; threshold; pairedpulse transcranial magnetic stimulation; intracortical facilitation; intracortical inhibition HYPERVENTILATION (HV) (or hyperpnea) is the state of breathing faster or deeper than necessary, thereby reducing the CO 2 concentration of the blood below normal. What is usually referred to as HV is, in fact, hypocapnia. Since a reduction of arterial PCO 2 (Pa CO 2 ) below the normal level (40 Torr) is obtained by increasing the alveolar ventilation, HV became synonymous with hypocapnia (32). HV is known to have various effects on human physiology (for a review, see Ref. 6).For instance, a reduction in Pa CO 2 increases the excitability of sensory and motor axons in the peripheral nervous system (21,23,28).The aim of the present study was to investigate further the neural mechanisms of the HV-induced changes in cortical excitability. As measures of primary motor cortex (M1) excitability, motor threshold (MT), stimulus-response (S-R) curves (i.e., recruitment curves), intra...

Effect of graded hypoxia on supraspinal contributions to fatigue with unilateral knee-extensor contractions

“…Hypocapnia causes cerebral vasoconstriction (27) and attenuates the normal increase in cerebral blood flow in hypoxia (12). Severe hypocapnia (PET CO 2 Յ15 Torr) increases the excitability of the motor cortex (46,51). In the present study, however, cortical excitability was unaffected by the differing levels of hypocapnia; this finding is in agreement with what has been reported previously for similar levels of hypocapnia (PET CO 2 ϳ22 Torr) (32).…”

Reduced respiratory neural activity elicits phrenic motor facilitation

“…For example, brain hypocapnia/alkalosis increases neuronal excitability in the cortex (Balestrino and Somjen, 1988) and spinal cord (King and Rampil, 1994; Zhou and Turndorf, 1998). However, neuronal activity rapidly goes back to baseline levels once normal CO 2 levels are restored (Sparing et al, 2007); thus, residual CO 2 -dependent effects on motor neuron excitability likely does not account for the prolonged increase in phrenic burst amplitude observed here. Hypocapnia also results in decreased cerebral blood flow and reduced oxygen unloading at the tissues (Brian, 1998; Vogel et al, 1996), which could lead to brain hypoxia (Nwaigwe et al, 2000; Schneider et al, 1998), a stimulus known to elicit prolonged increases in respiratory motor output (Bavis and Mitchell, 2003; Blitz and Ramirez, 2002).…”

Changes in visual-evoked potential habituation induced by hyperventilation in migraine

“…But comparison between the time course of HV-induced modifications in inhibitory mechanisms as revealed by TMS studies (5–10 min after HV ends [10, 11]) and in our sensorial responses following repetitive stimulation (immediately after HV ends) renders unlikely that our HV-induced VEP amplitude changes derive from transient inhibitory cortical dysfunction.…”

“…For instance, HV slows the electroencephalogram (EEG) by increasing delta-power and decreasing alpha-power [6, 7]. It also changes somatosensory-evoked potential latency [8], reduces the long-latency somatosensory-evoked magnetic fields [9], shortens the cortical silent period [10], and reduces the phospene threshold [11] elicited by transcranial magnetic stimulation (TMS). On functional neuroimaging studies, HV decreases or even abolishes the occipital cortex response to visual stimulation [12, 13].…”