Abstract

Neuropathic pain is initiated or caused by a primary lesion or dysfunction in the nervous system. Neuropathic pain is composed of peripheral neuropathic pain (with a primary lesion or dysfunction in the peripheral nervous system) and central neuropathic pain (CNP; with a primary lesion or dysfunction in the central nervous system). CNP may be further subdivided into supraspinal central neuropathic pain and spinal central neuropathic pain. Opioids have a role in the pharmacologic management of neuropathic pain; however, there is a scarcity of literature on the treatment of CNP with opioids. One of the few statements in the literature regarding the analgesic efficacy of opioids for CNP suggests that despite limited data, the opioid responsiveness for neuropathic pain of central and peripheral etiologies is similar. After reviewing the extremely limited data, it is proposed that although there may be a subpopulation of patients with CNP who have a reasonable analgesic response to opioids, overall, when sensory pain rating is used as the yardstick, CNP appears to respond less well to opioids than peripheral neuropathic pain. Thus, opioids should be considered a second- or third-line agent in any algorithm of the pharmacologic treatment of CNP. Also within CAP, it appears that supraspinal central neuropathic pain may respond less well to a trial of opioids than spinal central neuropathic pain. Moreover, under close monitoring for side effects (eg, constipation), it is suggested that clinicians may want to consider titrating to higher doses of potent opioids before the trial is judged to be unsuccessful for refractory supraspinal central neuropathic pain.

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