Neurobiological aspects of pain in the context of alcohol use disorder.

Abstract

Alcohol is an effective and widely utilized analgesic. However, the chronic use of alcohol can actually facilitate nociceptive sensitivity over time, a condition known as hyperalgesia. Excessive and uncontrollable alcohol drinking is also a hallmark feature of alcohol use disorder (AUD). Both AUD and chronic pain are typically accompanied by negative affective states that may underlie reinforcement mechanisms contributing to AUD maintenance or progression. Frequent utilization of alcohol to relieve pain in individuals suffering from AUD or other chronic pain conditions may thus represent a powerful negative reinforcement construct. This chapter will describe ties between alcohol-mediated pain relief and potential exacerbation of AUD. We describe neurobiological systems engaged in alcohol analgesia as well as systems recruited in the development and maintenance of AUD and hyperalgesia. Although few effective therapies exist for either chronic pain or AUD, the common interaction of these conditions will likely lead the way for promising new discoveries of more effective and even simultaneous treatment of AUD and co-morbid hyperalgesia. An abundance of neurobiological findings from multiple laboratories has implicated a potentiation of central amygdala (CeA) signaling in both pain and AUD, and these data also suggest that attenuation of stress-related systems (including corticotropin-releasing factor, vasopressin, and glucocorticoid receptor activity) would be particularly effective and comprehensive therapeutic strategies targeting the critical intersection of somatic and motivational mechanisms driving AUD, including alcohol-induced hyperalgesia.