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Ever since Claude Bernard implicated the sympathetic nervous
system in sensation, its role in nociception has been the subject
of debate.1 No one would argue with the fact that
the sympathetic nervous system is intimately involved with the preservation
of homeostasis and noxious challenges in humans, although the manner
in which it influences the sensation of pain has, until recently,
escaped explanation.2 Anatomically, the sympathetic
nervous system constitutes a highly complex arrangement of preganglionic
and postganglionic neurons that subserve specific and diverse functions
of target organs, including enteric neurons, smooth muscle, syncytial
muscle, and striated muscle.3 Physiologically,
the sympathetic nervous system is associated in some way with both
systemic and specific local reactions, which are expressed by supratentorial
and confrontational aspects that are represented in the periaquaductal
gray matter of the midbrain (e.g., non-opioid analgesia).4,5 In
contrast, rest and quiescence are represented in the ventrolateral
periaquaductal gray matter, being associated with endogenous opioid
analgesia.
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The stress response described by Selye,6 “fight
or flight,” involves both spinal levels of integration,
with hypothalamo-mesencephalic centers, but is associated with adrenocortical
and hypothalamo-hypophyseal responses designed to protect the organism
under normal biologic conditions. A secondary set of responses to
sympathetic activity that can be considered pathophysiologic and
occur with or without obvious nerve injury are those changes in
blood flow, sudomotor and muscle activity, with subsequent trophic changes
and abnormal sensation long after the noxious event.7,8 Sensory
changes include allodynia, hypoalgesia, hyperalgesia, hyperesthesia,
and hyperpathia. Why, and in what manner, the sympathetic nervous
system is involved in these changes that occur in a small but readily
identifiable group of patients is still unclear. However, recent
research has clarified some of the previous misconceptions with
regard to levels of sympathetic activity, involvement of the central
nervous system, and the possibility of preexisting immunologic factors.
Interestingly, similarities in the characteristics of complex regional
pain syndrome (CRPS) are seen in other chronic pain states, such
as irritable bowel syndrome, interstitial cystitis, nonulcer dyspepsia,
and certain cases of angina pectoris.
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During the Civil War, Weir Mitchell9 drew attention
to the exaggerated response to nerve injury that was distinct from
the neurogenic inflammation that is associated with most nerve injuries. These
patients typically suffered from a penetrating injury in the vicinity
of a major nerve, in most cases without disruption, and typically
caused by a musket shot. Mitchell called this causalgia because
of the bizarre swelling, heat (causa), and pain (algia), which were
out of all proportion to the signs and symptoms of most nerve injuries.
Leriche,10 a French surgeon, also described similar
syndromes in the lower extremities for which he developed the surgical
procedure of stripping the sympathetic nervous plexus from the large
vessels in the lower extremities. Sudeck, in a series of articles,
provided similar descriptions with detailed observations of the
bony and trophic changes following injury that came to be described ...