The study of pain may be relevant to the study of chemical intolerance
(CI) in many ways. Pain is often reported as a symptom of CI
and it is defined as a subjective experience similar to many
other symptoms of CI, making its objectification difficult.
Furthermore, the CNS plastic changes that underlie the development
of persistent pain states and abnormal pain responses may share
some similarities with those involved in the sensitization to
environmental chemicals. Functional brain imaging studies in
humans demonstrate that acute pain evoked by nociceptive stimulation
is accompanied by the activation of a widely distributed network
of cerebral structures, including the thalamus and the somatosensory,
insular, and anterior cingulate cortices. Abnormal activity
within these regions has been associated with the experience
of pain following damage to the peripheral or central nervous
system (neuropathic pain) in a number of clinical populations.
In normal individuals, activity within this network is correlated
with subjective pain perception, is highly modifiable by cognitive
interventions such as hypnosis and attention, and has been associated
with emotions. Other cognitive mediators such as expectations
can also produce robust changes in pain perception (e.g., in
placebo analgesia). These effects likely depend on both higher-order
cerebral structures and descending mechanisms modulating spinal
nociceptive activity. These psychological processes can be solicited
to reduce clinical pain and we speculate that they may further
attenuate or promote central mechanisms involved in the transition
from acute to persistent pain states. The investigation of central
determinants of subjective experience is essential to assess
the possibility that higher-order brain/psychological processes
modulate and/or mediate the development of persistent pain states.
These factors may contribute to the development of symptoms
in CI.
