期刊
PAIN
卷 150, 期 1, 页码 93-102出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1016/j.pain.2010.04.001
关键词
Temporal summation; Human; Functional imaging; Thalamus; Cortex; Psychophysics; Heat pain
资金
- Dept. of Veteran's Affairs, the Veteran's Educational and Research Association of Michigan, NIH [AR46045]
- Bonica Fellowship
- IBRO Fellowship
- WHO/NINDS Fellowship
- University of Michigan Medical School SBRP
Noxious cutaneous contact heat stimuli (48 degrees C) are perceived as increasingly painful when the stimulus duration is extended from 5 to 10 s, reflecting the temporal summation of central neuronal activity mediating heat pain. However, the sensation of increasing heat pain disappears, reaching a plateau as stimulus duration increases from 10 to 20 s. We used functional magnetic resonance imaging (fMRI) in 10 healthy subjects to determine if active central mechanisms could contribute to this psychophysical plateau. During heat pain durations ranging from 5 to 20 s, activation intensities in the bilateral orbitofrontal cortices and the activation volume in the left primary (S1) somatosensory cortex correlated only with perceived stimulus intensity and not with stimulus duration. Activation volumes increased with both stimulus duration and perceived intensity in the left lateral thalamus, posterior insula, inferior parietal cortex, and hippocampus. In contrast, during the psychophysical plateau, both the intensity and volume of thalamic and cortical activations in the right medial thalamus, right posterior insula, and left secondary (S2) somatosensory cortex continued to increase with stimulus duration but not with perceived stimulus intensity. Activation volumes in the left medial and right lateral thalamus, and the bilateral mid-anterior cingulate, left orbitofrontal, and right S2 cortices also increased only with stimulus duration. The increased activity of specific thalamic and cortical structures as stimulus duration, but not perceived intensity, increases is consistent with the recruitment of a thalamocortical mechanism that participates in the modulation of pain-related cortical responses and the temporal summation of heat pain. Published by Elsevier B. V. on behalf of International Association for the Study of Pain.
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