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Cold‐induced limb pain decreases sensitivity to pressure‐pain sensations in the ipsilateral forehead
Author(s) -
Knudsen Lone,
Drummond Peter D.
Publication year - 2009
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1016/j.ejpain.2008.12.005
Subject(s) - forehead , cold pressor test , anesthesia , diffuse noxious inhibitory control , nociception , medicine , locus coeruleus , blood pressure , noxious stimulus , anatomy , central nervous system , heart rate , receptor
The aim of this study was to investigate the effect of unilateral limb pain on sensitivity to pain on each side of the forehead. In the first experiment, pressure‐pain thresholds and sharpness sensations were assessed on each side of the forehead in 45 healthy volunteers before and after a 10 °C cold pressor of the hand and in 18 controls who were not subjected to the cold pressor. In a second experiment, forehead sensitivity was assessed in 32 healthy volunteers before and after a 2 °C cold pressor. The assessments were repeated without the cold pressor, and before and after six successive 4 °C cold pressor tests. The 10 °C cold pressor did not influence forehead sensitivity, whereas the 2 °C cold pressor and the 4 °C cold pressor tests resulted in bilateral analgesia to sharpness and pressure. The analgesia to pressure was greater in the ipsilateral forehead. Stress‐induced analgesia and diffuse noxious inhibitory controls may have contributed to the analgesia to pressure‐pain and sharpness sensations bilaterally after the most painful cold pressor tests. The locus coeruleus inhibits ipsilateral nociceptive activity in dorsal horn neurons during limb inflammation, and thus may have mediated the ipsilateral component of analgesia. Pain‐evoked changes in forehead sensitivity differed for sharpness and pressure, possibly due to separate thalamic or cortical representations of cutaneous and deep tissue sensibility. These findings suggest that several mechanisms act concurrently to influence pain sensitivity at sites distant from a primary site of painful stimulation.