Hypocapnia related changes in pain-induced brain activation as measured by functional MRI.

Full Abstract

Stress, acute pain and chronic pain may often result in hyperventilation (HV) which produces hypocapnia. The aim of this fMRI-study was to investigate the influence of hypocapnia on cortical activation during noxious stimulation in 14 healthy volunteers. The intensity of voluntary HV was controlled by capnometry Three tasks were performed in the fMRI sessions: (I) three 3-min HV periods with 7-min periods of recovery in between; (II) mechanically induced phasic pain stimulation--pain task (PT); (III) tapping--motor task (MT). The last two of these protocols were performed under normocapnic and hypocapnic conditions. HV decreased the fMRI signal by 3-7% in all regions of the cortex and subcortical nuclei. This decrease was most prominent in the opercular, frontal and temporal areas. When the PT was performed during hypocapnia a strong reduction in cluster sizes and lower t-values in S1 and insular cortex were found. In contrast MT was accompanied by an increase in cluster sizes and higher t-values. From this we conclude that hypocapnia significantly influences the BOLD signal in nociceptive and motor systems, indicating that either the coupling between the BOLD effect and neuronal processing changed or that the activity in the cortical network which represents the pain processing is decreased. These effects should be considered for functional brain imaging studies on the nociceptive system.

Author information

Author/s: Terekhin, Pavel (P); Forster, Clemens (C);

Affiliation: Department of Physiology & Pathophysiology, University of Erlangen/Nuernberg, Universitaetsstr. 17, D-91054 Erlangen, Germany.

Journal and publication information

Publication Type: Comparative Study; Journal Article

Journal: Neuroscience letters (Neurosci Lett), published in Ireland. (Language: eng)

Reference: 2006-May; vol 400 (issue 1-2) : pp 110-4

Dates: Created 2006/05/08; Completed 2006/08/04; Revised 2006/11/15;

PMID: 16517071, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

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