Experimental brush-evoked allodynia activates posterior parietal cortex

To study the brain activation pattern of coexisting experimental ongoing pain and brush-evoked allodynia (pain evoked by innocuous brush) with the use of PET.

Neuropathic pain usually has two essential phenomena: ongoing pain and brush-evoked allodynia, which coexist and may influence each other. Capsaicin induces both ongoing pain and brush-evoked allodynia.

Eight healthy right-handed volunteers participated in eight H2(15)O PET scans with two blocks of four randomized conditions: 1) rest, 2) brush, 3) capsaicin pain, and 4) capsaicin pain + brush (brush-evoked allodynia). Capsaicin was injected intradermally on the nondominant forearm and the subjects rated pain intensity and unpleasantness on 100-mm visual analogue scales.

Pain intensity and unpleasantness were significantly higher during brush-evoked allodynia (74 +/- 4 and 67 +/- 4 mm) compared with capsaicin pain alone (60 +/- 4 and 51 +/- 5 mm). Brush-evoked allodynia, but not capsaicin pain alone, increased blood flow significantly in the contralateral right sensory association cortex Brodmann area (BA) 5/7, and in bilateral prefrontal cortex BA 9/10/47 and insula. No significant activity was seen in thalamus or primary somatosensory cortex (SI). Direct comparison between capsaicin pain and brush-evoked allodynia revealed significant increase in contralateral BA 5/7 only.

The specific activation of contralateral BA 5/7 indicates that this brain region is important to the processing of brush-evoked allodynia. The involvement of BA 5/7 in brush-evoked allodynia is claimed to reflect multisensory input to this region, its role in conscious pain perception, and its neuroplastic properties.