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 alpha(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.