Free
This Month in Anesthesiology  |   January 2002
Pain-related Cerebral Activation Characterized by Magnetic Resonance Imaging in Healthy Volunteers.
Article Information
This Month in Anesthesiology
This Month in Anesthesiology   |   January 2002
Pain-related Cerebral Activation Characterized by Magnetic Resonance Imaging in Healthy Volunteers.
Anesthesiology 1 2002, Vol.96, 5A. doi:
Anesthesiology 1 2002, Vol.96, 5A. doi:
Pain-related Cerebral Activation Characterized by Magnetic Resonance Imaging in Healthy Volunteers. Kurata et al. (page 35)
Kurata et al.  recruited five healthy, right-handed volunteers (four men, one woman) for four sets of experiments, which included delivery of pain stimuli and cognitive tasks, while characterizing subjects’ brain activity using functional magnetic resonance imaging. The purpose of the study was not only to localize cerebral activation by various stimuli, but also to characterize the time course of signal intensity.
Study subjects took no psychoactive or analgesic medications for 24 h preceding the experiments. Each was fitted with a thermal stimulator on the right and left forearms and was trained in rating pain sensation on a scale of 0–10. After baseline pain thresholds were established, each subject was examined with four cycles of 15-s hot (47.2–49.0°C) pain stimulus (alternated with a 30-s control stimulus), first on one forearm and then on the other. The hot pain stimulus (“on phase”) was limited to 15 s to reduce head motion–related artifacts on magnetic resonance imaging. Images of brain activation were obtained during pain stimulus experiments and also during visual (visually guided saccade) and motor (finger tapping) tasks. Visually guided saccade and finger tapping were also conducted in cycles, i.e.  , 30 s of active task performance alternated with 30 s of rest conditions.
Voxel-wise t  statistical maps were standardized and averaged across subjects. Blood oxygenation level–dependent signal time courses were analyzed at local maxima of representative activation clusters. The researchers found that pain stimulus on the right forearm activated the brain's secondary somatosensory (S2), superior temporal, anterior cingulate, insular, prefrontal cortices, premotor, and lenticular nucleus areas. Pain stimulus on the left forearm activated similar but fewer areas at lower signal intensity. Pain-related activation was statistically weaker and showed less consistent signal time courses than visually guided saccade or finger tapping–related activation. However, the pain-related signals decayed earlier before the stimulus ended, whereas the signal plateaus induced by visually guided saccade and finger tapping were well-sustained. Although the study used a block design of repeated identical stimuli and a short-duration pain stimulus, it showed that the bilateral S2 was robustly activated by somatic thermal pain in blood oxygenation level–dependent contrast functional magnetic resonance imaging.