Reported rates of substance abuse or dependence among patients with chronic pain have been higher than those in the general population (Brown et al. 1996). For most, the substance use disorder preceded the onset of the pain disorder (Brown et al. 1996). In fact, a preexisting substance use disorder may have predisposed the individual to accidents and physical trauma, some of which may evolve into chronic pain syndromes (Polatin et al. 1993).
Of particular concern is the relationship of opioid dependence to chronic pain. It is arguable that signs of physiological dependence, i.e., demonstration of tolerance to the effects of opioids or the precipitation of withdrawal with abrupt medication cessation, would naturally result from the chronic administration of opioid analgesics and otherwise do not signal psychological dependence that accompanies dependence or addiction. Instead, psychological signs of dependence would be reflective in behaviors suggesting a loss of control over the use of opioids, e.g., using more of the opioid than intended; using the agent to acquire effects apart from analgesia, e.g., emotional effects; going to inordinate lengths to acquire, use, or recover from the opioids; and using the agent to the point of, and despite, inducing deleterious effects. Behaviors suggestive of loss of control, and therefore dependence, include lying, seeking additional prescriptions from other doctors, using street drugs, escalating doses beyond prescribed levels, seeking early refills, and manipulative behaviors displayed with the intended purpose of obtaining narcotic analgesics.
Although chronic pain patients may be vulnerable to developing new substance use disorders in the course of treatment (Dersh et al. 2002, Brown et al. 1996, Dunbar and Katz 1996), investigations assessing the presence of opioid dependence in chronic pain patients have reported contradictory conclusions. Some contend that this is an extraordinarily rare event (Zenz et al. 1992) whereas other investigators have found high rates of opioid dependence in chronic pain populations (Ives et al. 2006, Wu et al. 2006). Risk factors for opioid dependence include a prior history of substance abuse; prior physical/sexual abuse; major depression, anxiety disorders, and personality disorders (Dersh et al. 2002, Ives et al., Fishbain et al. 1998). Opioids have been a predominant focus; however, several other agents used in pain treatment are likewise prone to abuse and dependence; including the muscle relaxant carisoprodol; ketamine; ergot alkaloids and barbiturates employed in migraine treatment; and benzodiazepines.
Although challenging, effective pain management should never be withheld because of an abuse/addiction history. Effective treatment may require use of an array of pain-reducing approaches, e.g., use of adjunctive agents, or those with low abuse potential, physical, and psychological therapies, as well as participation in concurrent substance abuse treatment programs.
Treatment of pain in patients with opioid dependence can be particularly challenging, however. In fact, some evidence points to the fact that opioid dependence can enhance sensitivity to pain, i.e., opioid-induced hyperalgesia (Chang et al. 2007). Patients on long-term methadone maintenance have been shown to have less tolerance for experimentally induced pain (Doverty et al. 2001). Ongoing opioid consumption can set off a cascade of cellular responses and neurophysiology mechanisms that enhance pain sensitivity (White 2004), e.g., increasing the production and activity of neuropeptides such as dynorphin (Vanderah et al. 2001), cholecystokinin (Xie et al. 2005), and substance P (King et al. 2005). Activation of glial cells producing inflammatory cytokines also results in amplified pain (Watkins et al. 2007).
In some cases, detoxification from the substance(s) upon which one is dependent, e.g., alcohol, may be required before the initiation of treatment. The substances abused may be employed to self-medicate one's psychological distress, necessitating psychological along with prudent psychopharmacologic interventions.
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