Alcohol and Pain: A Translational Review of Preclinical and Clinical Findings to Inform Future Treatment Strategies
Neural substrates involved in initiating and maintaining chronic pain include dysfunction in descending pain pathways and reward network circuitry. Neural substrates of AUD involve widespread mesocorticolimbic and cerebro-cerebellar networks. Both conditions involve dysfunction of extended reward and oversight circuitry, and particularly prefrontal cortex. The acute effects of alcohol consumption on injury risk are mediated by how regularly the individual drinks. People who drink less frequently are more likely to be injured or to injure others at a given BAC compared with regular drinkers, presumably because of less tolerance (Gmel et al. 2010). This correlation was demonstrated with respect to traffic injuries in a reanalysis (Hurst et al. 1994) of a classic study conducted in Grand Rapids, Michigan (Borkenstein et al. 1974).
Dysregulation of the Mesocorticolimbic Reward Network.
Listen to relatives, friends or co-workers when they ask you to examine your drinking habits or to seek help. Ultimately, the best way to prevent alcohol-related neurologic disease is to not drink alcohol. Your chances for DMT Dimethyltryptamine Abuse Signs & Symptoms of DMT Abuse recovery depend on how early the disease is diagnosed and how much damage has already occurred.
Impact on your health
In the case of an ischemic stroke, this is caused by blockage of a blood vessel that prevents the blood from reaching neighboring brain areas. In the case of a hemorrhagic stroke, rupture of a blood vessel and bleeding into the brain occurs, which prevents normal blood supply to other brain regions. Zero (0) indicates that fewer than 500 alcohol-attributable DALYs in the disease category. PsychiatryOnline subscription options offer access to the DSM-5-TR® library, books, journals, CME, and patient resources.
More than 30 conditions listed in the WHO’s International Classification of Diseases, 10th Edition (ICD–10) (WHO 2007) include the term “alcohol” in their name or definition, indicating that alcohol consumption is a necessary cause underlying these conditions (see table 1). The most important disease conditions in this group are alcohol use disorders (AUDs), which include alcohol dependence and harmful use or alcohol abuse.3 AUDs are less fatal than other chronic disease conditions but are linked to considerable disability (Samokhvalov et al. 2010d). Overall, even though AUDs in themselves do not rank high as a cause of death globally, they are the fourth-most disabling disease category in low- to middle-income countries and the third-most disabling disease category in high-income countries (WHO 2008). Thus, AUDs account for 18.4 million years of life lost to disability (YLDs), or 3.5 percent of all YLDs, in low- and middle-income countries and for 3.9 million YLDs, or 5.7 percent of all YLDs, in high-income countries. However, AUDs do not affect all population subgroups equally; for example, they mainly affect men, globally representing the second-most disabling disease and injury condition for men.
Additionally, people with alcohol use disorder experience allodynia during alcohol withdrawal. Many people with alcohol use disorder hesitate to get treatment because they don’t recognize that they have a problem. An intervention from loved ones can help some people recognize and accept that they need professional help.
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If your pattern of drinking results in repeated significant distress and problems functioning in your daily life, you likely have alcohol use disorder. However, even a mild disorder can escalate and lead to serious problems, so early treatment is important. In the U.S., moderate alcohol consumption is defined as one drink per day for women and two drinks per day for men.
- Bi-directional arrows are used to acknowledge that reciprocal influences may occur across associations between pain and alcohol use, and dashed lines are used to illustrate the modest causal evidence derived from the current literature.
- Chronic alcohol intoxication and withdrawal, intense and/or untreated injury, or intense and/or unresolved trauma are each capable of increasing allostatic load (indicated by the dashed arrow) to the extent that a dysfunctional state emerges (symbolized by the lower inner oval) characterized by persistent hyperkatifeia and hyperalgesia.
- Finally, management of chronic pain in AUD patients cannot be optimized without considering the reciprocal risks and benefits of the treatment choices on exacerbating drinking patterns or increasing the risk of relapse.
- Thus, for example, a glass of wine often contains more than 5 fluid ounces and therefore may correspond to one and a half or even two standard drinks.
Follow-up studies are focused on how these molecules might be used to diagnose and more effectively treat alcohol-related chronic pain conditions. Conceptualization of bi-directional relations between pain and alcohol use that integrates two lines of empirical inquiry (i.e., effects of alcohol on pain and effects of pain on alcohol use), accounts for varying levels of alcohol consumption, and summarizes potential mechanistic factors identified in the current review. A recent review on the topic of alcohol withdrawal and hyperalgesia in animal models identified down-regulation of adenosine receptors, and up-regulation of L-type calcium channels, as likely mediators of alcohol withdrawal-induced hyperalgesia (Gatch, 2009). For example, co-administration of alcohol and theophylline (i.e., an adenosine receptor antagonist) has been shown to attenuate development of hyperalgesia during withdrawal, presumably because theophylline promotes up-regulation of adenosine A1 receptors (Gatch & Selvig, 2002). Co-administration of L-type calcium channel blockers and alcohol has also been shown to reduce hyperalgesia during alcohol abstinence, possibly because L-type calcium channel blockers prevent up-regulation of L-type calcium channels that would otherwise occur in the context of chronic alcohol administration (Gatch, 2009). Despite consistent evidence from the animal literature, and well-documented historical use of alcohol as an anesthetic (e.g., Shealy & Cady, 2002), only a few experimental studies have been conducted among humans to test the causal effects of acute alcohol administration on laboratory pain reactivity.
Analgesic effects have also been observed for electric shock pain (Stewart, Finn, & Pihl, 1995) and mechanical pressure pain (Woodrow & Eltherington, 1988) in the context of orally-administered alcohol. Although we identified two additional studies that demonstrated acute analgesic effects of alcohol (James, Duthie, Duffy, McKeag, & Rice, 1978; Wolff, Hardy, & Goodell, 1941), neither utilized an experimentally-rigorous design, and one study (Wolff et al., 1941) was conducted using only the three authors as subjects. Excessive alcohol consumption is also a known causal agent in the development of alcohol-related neuropathy, which can be characterized by damage to sensory, motor, and autonomic nerves, potentially due to direct neurotoxic effects of alcohol on the central and peripheral nervous systems (e.g., Chopra & Tiwari, 2012). Pain is a predominant and early feature of alcohol-related neuropathy, and treatment typically requires both acute and long-term pain management (Chopra & Tiwari, 2012; Njamnshi & Wisysonge, 2010). The estimated prevalence of alcohol-related neuropathy is 25%–66% among persons who meet criteria for AUD (Chopra & Tiwari, 2012).
Nevertheless, via the prevalence of alcohol exposure the prevalence of alcohol-attributable and relative risk for the wider, unspecific liver cirrhosis and alcohol-induced disease categories (Rehm et al. 2010a). Acceptance and Commitment Therapy (ACT) and Dialectical Behavior Therapy (DBT) are evidence-based approaches that incorporate mindfulness practices. ACT emphasizes building psychological flexibility and emphasizes values-congruent practices, while DBT emphasizes the development of emotional regulation and distress tolerance skills. These approaches transform our relationship with our thoughts, emotions, and physical sensations, including pain.
