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Vol. 299, Issue 3, 811-817, December 2001
Departments of Physiology and Pharmacology, and
Anesthesiology, Wake Forest University School of Medicine,
Winston-Salem, North Carolina
Chronic pain represents a mixture of pathophysiologic mechanisms,
a complex assortment of spontaneous and elicited pain states, and a
somewhat unpredictable response to analgesics. Opioids remain the
mainstay of treatment of moderate to severe chronic pain, although
there is little systematic examination to guide drug selection.
Cyclooxygenase inhibitors play primarily an adjunctive role in chronic
pain treatment. Agents with little activity in the treatment of acute
pain, such as antidepressants, antiepileptics, and i.v. administered
local anesthetics, are initiated in many patients and have significant
long-term efficacy in some patients with chronic pain. The
N-methyl-D-aspartate antagonist ketamine and
the
2-adrenergic agonist clonidine exhibit activity in
patients with acute or chronic pain and reduce opioid consumption, but are often poorly tolerated due to side effects. Topical treatment with
capsaicin or lidocaine exhibits efficacy in a subset of patients, and
invasive intrathecal treatment with opioids as well as clonidine, neostigmine, and adenosine may have advantages in some patients. Several laboratory models have been developed to mimic chronic pain
states found in humans. Nerve injury has been induced in rats by a
variety of means, resulting in mechanical allodynia and thermal
hyperalgesia. A number of arthritic states have also been produced by
means of chronic joint inflammation in rats. The pharmacology of these
neuropathic and arthritic pain models generally resembles that found in
the respective human conditions. Additional models of chronic pain,
particularly visceral pain, have been developed; however, the
pharmacology of these models is not well established at this time.
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