The PET (H2O)-O-15-bolus method was used to image regional brain activ
ity in normal human subjects during intense pain induced by intraderma
l injection of capsaicin and during post-capsaicin mechanical allodyni
a (the perception of pain from a normally non-painful stimulus), Image
s of regional cerebral blood flow were acquired during six conditions:
(i) rest; (ii) light brushing of the forearm; (iii) forearm intraderm
al injection of capsaicin, (iv) and (v) the waning phases of capsaicin
pain; and (vi) allodynia, Allodynia was produced by light brushing ad
jacent to the capsaicin injection site after ongoing pain from the cap
saicin injection had completely subsided. Capsaicin treatment produced
activation in many discrete brain regions which we classified as subs
erving four main functions: sensation-perception (primary somatosensor
y cortex, thalamus and insula); attention (anterior cingulate cortex);
descending pain control (periaqueductal grey); and an extensive netwo
rk related to sensory-motor integration (supplementary motor cortex, b
ilateral putamen and insula, anterior lobe and vermis of the cerebellu
m and superior colliculus), Comparison of the noxious and non-noxious
stimuli yielded several new insights into neural organization of pain
and tactile sensations. Capsaicin pain, which had no concomitant tacti
le component, produced little or no activation in secondary somatosens
ory cortex (SII), whereas light brushing produced a prominent activati
on of SII, suggesting a differential sensitivity of Sn: to tactile ver
sus painful stimuli. The cerebellar vermis was strongly activated by c
apsaicin, whereas light brush and experimental allodynia produced litt
le or no activation, suggesting a selective association with C-fibre s
timulation and nociceptive second-order spinal neurons. The experiment
al allodynia activated a network that partially overlapped those activ
ated by both pain and light brush alone. Unlike capsaicin-induced pain
, allodynia was characterized by bilateral activation of inferior pref
rontal cortex, suggesting that prefrontal responses to pain are contex
t dependent.