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Repeated noxious
balloon distensions of the colorectal region in humans evoke painful
responses that increase pain sensitivity and expand the area of
pain referral to the overlying somatic areas of the body (Ness
et al., 1990). Animal studies support the findings observed
in human studies.
Activity recorded
from neurons in the lower thoracic gray matter during distension
of the gall bladder show that some neurons respond only to somatic
input and not to the visceral stimulus while another population
responds to both somatic input and distension (Cervero
et al., 1992). In the latter group of neurons, but not the
former, the region of skin that could be stimulated to excite
the neurons was greater in the presence of the visceral stimulus
than it was when the visceral stimulus was not present. That is,
the spinal neurons became sensitized to a larger region of skin
if there was enhanced activity in visceral afferents. The visceral
stimulus is selective, because only those neurons responsive to
visceral stimulation change their sensitization to the somatic
input.
An additional
important characteristic of these responsive neurons is that the
somatic referral of visceral pain that produced the changes tended
to outlast the duration of the noxious visceral stimulus. This
observation correlates well with the clinical experience that
hyperalgesia is felt after the painful episode has passed. These
results raise the possibility that central sensitization of spinothalamic
tract cells, and perhaps other ascending pathways, could intensify
the pain experience resulting from angina pectoris.
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