One of the most distressing symptoms of many
neuropathic pain syndromes is the enhanced
pain sensation to tactile or thermal stimulation (
hyperalgesia). In the present study we used functional magnetic resonance imaging (fMRI) and explored brain activation patterns during acute impact
pain and
mechanical hyperalgesia in the human ultraviolet (UV)-B model. To investigate pharmacological modulation, we examined potential differential fMRI correlates of
analgesic and antihyperalgesic effects of two intravenous
cyclooxygenase inhibitors, i.e.
parecoxib and
acetylsalicylic acid (ASA). Fourteen healthy volunteers participated in this double-blinded, randomized and placebo-controlled crossover study. Tactile stimuli and mechanical impact
hyperalgesia were tested at the site of a UV-B irradiation and acute mechanical
pain was tested at a site distant from the irradiated skin. These measurements were conducted before and 30 min after a 5-min
intravenous infusion of either saline (placebo),
parecoxib 40 mg or ASA 1000 mg. Acute mechanical
pain and
mechanical hyperalgesia led to widespread activations of brain areas known to comprise the human
pain matrix.
Analgesic effects were found in primary (S1) and secondary (S2) somatosensory cortices, parietal association cortex (PA), insula, anterior parts of the cingulate cortex and prefrontal cortices. These brain areas were also modulated under antihyperalgesic conditions. However, we observed a greater
drug-induced modulation of mainly PA and inferior frontal cortex during
mechanical hyperalgesia; during acute mechanical
pain there was a greater modulation of mainly bilateral S2. Therefore, the results of the present study suggest that there is a difference in the brain areas modulated by
analgesia and antihyperalgesia.