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Differential Opioid Action on Sensory and Affective Cerebral Pain Processing
Author(s) -
Oertel BG,
Preibisch C,
Wallenhorst T,
Hummel T,
Geisslinger G,
Lanfermann H,
Lötsch J
Publication year - 2008
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/sj.clpt.6100441
Subject(s) - insular cortex , amygdala , sensory system , somatosensory system , opioid , parahippocampal gyrus , functional magnetic resonance imaging , anesthesia , psychology , alfentanil , secondary somatosensory cortex , medicine , neuroscience , temporal lobe , receptor , epilepsy , propofol
Low doses of morphine, the most commonly used opioid analgesic, have been shown to significantly reduce the affective but not the sensory intensive dimension of pain. This suggests differential dose–response relationships of opioid analgesia on the sensory and affective components of pain. We investigated the effects of different alfentanil plasma concentration levels (0, 19.6±2.7, 47.2±7.6, and 76.6±11.3 ng/ml) on pain‐related brain activation achieved by short pulses of gaseous CO 2 delivered to the nasal mucosa, using functional magnetic resonance imaging (fMRI) on a 3.0 T MRI scanner in 16 non‐carriers and 9 homozygous carriers of the μ‐opioid receptor gene variant OPRM1 118A>G. Increasing opioid concentrations had differential effects in brain regions processing the sensory and affective dimensions of pain. In brain regions associated with the processing of the sensory intensity of pain (primary and secondary somatosensory cortices, posterior insular cortex), activation decreased linearly in relation to alfentanil concentrations, which was significantly less pronounced in OPRM1 118G carriers. In contrast, in brain regions known to process the affective dimension of pain (parahippocampal gyrus, amygdala, anterior insula), pain‐related activation disappeared at the lowest alfentanil dose, without genotype differences. Clinical Pharmacology & Therapeutics (2008); 83 , 4, 577–588.doi: 10.1038/sj.clpt.6100441