Alcohol dependence as a chronic pain disorder

Abstract

Dysregulation of pain neurocircuitry and neurochemistry has been increasingly recognized as playing a critical role in a diverse spectrum of diseases including migraine, fibromyalgia, depression, and PTSD. Evidence presented here supports the hypothesis that alcohol dependence is among the pathologies arising from aberrant neurobiological substrates of pain. In this review, we explore the possible influence of alcohol analgesia and hyperalgesia in promoting alcohol misuse and dependence. We examine evidence that neuroanatomical sites involved in the negative emotional states of alcohol dependence also play an important role in pain transmission and may be functionally altered under chronic pain conditions. We also consider possible genetic links between pain transmission and alcohol dependence. We propose an allostatic load model in which episodes of alcohol intoxication and withdrawal, traumatic stressors, and injury are each capable of dysregulating an overlapping set of neural substrates to engender sensory and affective pain states that are integral to alcohol dependence and comorbid conditions such as anxiety, depression, and chronic pain.

Glucocorticoid receptor antagonism decreases alcohol seeking in alcohol-dependent individuals

“…Alcoholism, or alcohol use disorder, is a complex psychiatric condition characterized by craving, compulsive seeking, and excessive drinking of alcohol, as well as the emergence of negative emotional states during withdrawal (2)(3)(4). Allostatic changes in brain reward and stress systems are thought to mediate many of these symptoms.…”

Predator odor stress alters corticotropin-releasing factor-1 receptor (CRF1R)-dependent behaviors in rats

“…In animals, a single intense stress or chronic stress produces hyperalgesia (Boccalon et al, 2006; da Silva Torres et al, 2003; Geerse et al, 2006; Quintero et al, 2000; Zhang et al, 2012), increases anxiety-like behaviour, and produces hyperarousal in rats (Campos et al, 2013; Kinn Rød et al, 2012; Serova et al, 2013). Alcohol dependence also promotes hyperarousal and hyperalgesia (i.e., increased nociception), each of which may promote compulsive alcohol drinking (Edwards et al, 2012; Egli et al, 2012; Koob, 1999). Our lab utilizes a predator odor stress model that produces lasting increases in alcohol consumption by rats (Edwards et al, 2013), allowing for the hypothesis that hyperarousal and hyperalgesia may be important motivational factors in stress-induced escalation of alcohol drinking.…”

Correlates of prescription opioid therapy in Veterans with chronic pain and history of substance use disorder

“…It is possible that high pain ratings led clinicians to initiate opioid therapy for these participants. Indeed, previous studies demonstrated that patients with SUD are highly sensitive to pain and report greater pain severity relative to those without SUD [45][46][47]. In one scenario, elevated pain ratings in this group of participants prescribed LOT may represent reductions in pain severity from even higher pain ratings observed prior to opioid therapy initiation, albeit to levels still greater than pain ratings endorsed by those not prescribed opioids.…”