
PsychiatryOnline subscription options offer access to the DSM-5-TR® library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. The researchers found that there was a significant increase in drinking behavior in the group of mice that were dependent on alcohol compared to the non-dependent group. Pain perception is a subjective, complex, and distributed process that involves multiple structures involved in sensory, emotional, and cognitive processing that interact together concurrently to form the perceived pain experience (Chapman, 2005).
Nociplastic Pain and Pain-Motivated Drinking in Alcohol Use Disorder
This function of pain contrasts with the stress-induced analgesia that is typically produced by acute stressors (Butler and Finn, 2009; also see Knoll and Carlezon, 2010). Relevant to the interface with alcoholism, chronic pain-induced activation of the amygdala is accompanied by alterations in mPFC function and production of cognitive deficits (Ji et al., 2010; Ji and Neugebauer, 2011; Sun and Neugebauer, 2011). Such executive system deficits are hypothesized to play a critical role in the aberrant decision-making that accompanies the transition from drug use to dependence (George and Koob, 2010), and by this mechanism individuals suffering from chronic pain may be more susceptible to alcohol misuse and poor pain management. Despite numerous reports on multi-directional associations between chronic pain disorders and depression or alcohol abuse [1,2,6,7,9,15,16,17], it is not clear if depressive disorders carry a different burden for those with and without a history of alcohol abuse in the presence of chronic pain. Consideration of the brain reward system may help to clarify the links among chronic pain, depression, and alcohol abuse by showing their overlapping neuroanatomy. For example, the dysregulation of brain reward circuitry may play a role in the interrelatedness of depression, chronic pain, and alcohol abuse [6].
Approach to the pharmacological management of chronic pain in patients with an alcohol use disorder
Another facet of this relationship is revealed in studies showing that people experiencing chronic pain turn to alcohol presumably for relief (e.g., Brennan et al., 2005; Riley and King, 2009). Dysfunction in the brain reward system seems to be considered as the prominent shared pathological link among these conditions [38]. However, it is not clear why despite the overlap between neural pathways underlying chronic pain and alcohol abuse, as well as the high comorbidity of both of those conditions with depression, the burden of depressive disorders is greater in people with ALC.
Other Factors Associated with Pain and Alcohol Use
Evidence derived from both animal and human studies indicates that acute alcohol administration may confer short-term pain-inhibitory effects. For example, animal models have consistently demonstrated increased pain threshold following acute ethanol administration, with some data suggesting a dose-response effect (e.g., Ibironke & Oyekunle, 2012). These animal models further demonstrated that acute pain-inhibitory effects of alcohol tended to diminish following 10–12 days of ethanol administration, which suggests that short-term analgesic effects may be reduced in the context of chronic alcohol exposure (Gatch & Lal, 1999).

Future research may also examine other relevant third variables (e.g., comorbid medical conditions, emotional distress) that could further inform our evolving conceptualization of reciprocal relations between pain and alcohol use. The goal of the current review was to integrate evidence derived from relevant psychological, social, and biological empirical literatures to generate testable hypotheses that may inform future research and the development of novel interventions. The current review extends previous work by examining associations between pain and various levels of alcohol consumption (including low-to-moderate levels of drinking), and by identifying psychosocial mechanisms that may underlie these relations. We begin by providing an overview of the background and terminology relevant to the study of both pain and alcohol, reviewing data regarding the co-occurrence of pain and alcohol use disorder, and discussing potential confounds and relevant third variables. We then review studies examining both the effects of alcohol on pain and the effects of pain on alcohol use, and integrate these findings to conceptualize a series of reciprocal interrelations between pain and alcohol. Chronic pain affects an estimated 116 million American adults and costs the nation up to $635 billion each year (Committee on Advancing Pain Research, Care, and Education; Institute of Medicine, 2011).
Alcohol’s Effects on the Body
Biomarkers of alcohol abuse include carbohydrate-deficient transferrin (CDT) and phosphatidylethanol (PEth). CDT is an indirect metabolite of ethanol and constitutes either a marker of prolonged, heavy alcohol consumption or a marker of relapse. Peth on the other hand is a direct alcohol metabolite that can be measured to monitor alcohol consumption as well as for the identification of early signs of alcohol-related clinical manifestations.
As such, abnormalities in those structures may provide a substrate for pain disorders, depressive disorders, and alcohol-related disorders to be manifested as comorbid conditions in vulnerable individuals. Recurrent pain is highly prevalent among treatment seeking problem drinkers (Boissoneault, Lewis, & Nixon, 2018; Sheu et al., 2008), and alcoholism is considered a risk factor, both for the development of chronic pain in patients who suffer from AUD, and for relapse in those attempting to remain abstinent. AUD patients with pain also are likely to report current opioid use (Witkiewitz & Vowles, 2018). But despite numerous reports on the associations between chronic pain and AUD, the underlying mechanisms involved in linking them remain elusive.

This will be followed by a discussion of how acute pain is typically managed in a trauma population, including a review of evidence for the undermedication of acute pain. The final section will focus on the three aforementioned groups and https://rehabliving.net/a-review-on-alcohol-from-the-central-action/ the specific challenges to managing pain in these populations. Despite these limitations, our findings may have important implications for understanding the underlying factors contributing to depressive disorders in chronic pain patients.
Indeed, a better under understanding of mechanisms by which persons in pain may be motivated to consume alcohol (e.g., expectancies for pain relief) would inform the development of tailored interventions. Third, given evidence from animal studies that acute pain-inhibitory effects may subside with chronic alcohol exposure, human trials are also warranted to determine whether tolerance to alcohol reduces acute pain-inhibitory effects. Finally, studies that have examined pain-inhibitory effects of oral alcohol administration typically utilized beverages containing sugar to conceal alcohol dosage (e.g., Brown & Cutter, 1977). Given recent evidence that sugar may reduce pain (Stevens, Yamada, Lee, & Ohlsson, 2013) and amplify the pain-inhibitory effects of other substances (Kanarek & Carrington, 2004), future research should attempt to disentangle the pain mitigating effects of alcohol relative to other constituents (e.g., sucrose). The brain and body respond to events such as alcohol intoxication, stress, and injury by activating neuronal and hormonal responses to promote physiological stability in the face of a changed set point (allostasis).
People with alcohol use disorder are unable to stop or control their alcohol consumption, even when it causes problems to their health, relationships, and work. Alcohol Use Disorder (AUD) and chronic pain are widespread conditions with extensive public health burden. This review seeks to describe neuroanatomical links and major mediating influences between AUD and chronic pain, in the service of identifying factors that predict the risk of chronic pain in precipitating or facilitating AUD. Pain management in the trauma population has been a major focus of attention for the last two decades following studies showing that patients are generally undermedicated for pain and that high rates of pain while hospitalized can lead to poorer outcomes [5,6]. The American Pain Society has developed quality assurance standards for the relief of acute pain [7]. [2] The agency’s 2016 Guideline for Prescribing Opioids for Chronic Pain, which established artificially restrictive prescribing recommendations, is a key reason why so many patients are deprived of medically necessary pain management.
Besides, the key mechanism of chronic pain includes the long-term potentiation of glutamatergic transmission. The pathophysiology of ALN involves underlying mechanisms that include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters [52,53,54]. An essential risk factor regarding the etiology of ALN is the amount of alcohol consumed throughout the years since alcohol displays direct toxicity on nerve fibers [55]. It is estimated that consumption of more than 100 ml of ethyl alcohol per day significantly increases the risk of ALN [56].
- Alcohol Use Disorder (AUD) and chronic pain are widespread conditions with extensive public health burden.
- In other words, the warning labels on prescription painkiller bottles to avoid alcohol are far more than mere suggestions; they can be life-saving.
- A classic example of neuromodulation is spinal cord stimulation, which is used to treat a variety of conditions that cause chronic pain.
- This point may be particularly relevant for individuals exhibiting pain within the context of a more severe health problem, such as HIV or sickle cell disease (Levenson et al., 2007; Merlin et al., 2015; Merlin et al., 2014).
- As illustrated in the model, intense and unresolved trauma is also predicted to contribute to allostatic load in this system to influence vulnerability to chronic pain disorders and alcohol dependence.
Dr. Roberto and her team are continuing to investigate how the inflammatory proteins identified in this study might be used to diagnose or treat alcohol-related chronic pain conditions. To date, the lack of preclinical, or animal, models of alcoholic neuropathic pain limited the investigation of pathological mechanisms underlying the onset of neuropathic pain in people with alcohol use disorder. The researchers found increased levels of IBA-1 and CSF-1 in the spinal cord tissue of mice with alcohol withdrawal-related allodynia and mice with alcohol-induced neuropathic pain. The interrelationship between chronic pain and AUD resides in the intersection of etiological influences, mental experiences, and neurobiological processes. The patient’s pain was considered to be mixed nature, primarily neuropathic, though there seemed to be some component of nociceptive and, specifically, musculoskeletal pain. Because of the patient’s reported ongoing use of alcohol, acetaminophen and NSAIDs are not considered safe alternatives.
This is a teachable moment that all trauma centers should use to the patient’s advantage, and we recommend offering these interventions through acute care. It is worth noting that peripheral neuropathy has no reliable treatment due to the poor understanding of its pathology. One reason people often self-medicate pain with alcohol, aside from the fact that it is so easy to obtain, is that they see alcohol as also a way to manage stress, and chronic pain and stress frequently go together.

Little did I know that alcohol packs a punch with seven calories per gram, almost as much as fat. This realization is just the beginning of my questioning other beliefs https://rehabliving.net/ I held about alcohol and the benefits I perceived it offers. One possible criticism here is that drug users don’t owe me or anyone else an explanation for their habits.
Additionally, acetaminophen and NSAIDs can also be used effectively to supplement opiates, thus decreasing the dose of opiates needed to manage pain. In cases of neuropathic pain, neuropathic agents, such as gabapentin, should also be considered. Finally, nonpharmacologic interventions, such as hypnosis, relaxation and distraction, should not be overlooked as adjuncts to opiates for acute pain management. Alcohol use disorder (AUD), which encompasses the conditions commonly called alcohol abuse, alcohol dependence and alcohol addiction, affects 29.5 million people in the U.S. according to the 2021 National Survey on Drug Use and Health.
The model accounts for well-documented comorbidities between alcohol and anxiety disorders (Kushner et al., 2012), anxiety, depression and chronic pain disorders (Gerrits et al., 2012; Gureje et al., 2008) as well as alcohol dependence and pain sensitivity discussed previously. It also predicts that drugs (such as CRF-1 receptor antagonists) acting upon the shared neurocircuits would likely be effective for treating alcohol dependence and pain disorders whereas other pharmacotherapies targeting disorder-specific mechanisms would be effective for one disorder, but not the others. The model also explains observed functional substitutability of acute alcohol withdrawal episodes and restraint stress in provoking social anxiety (Breese et al., 2005). A model of how alcohol intoxication and withdrawal, trauma (stress) and injury transition to the corresponding disease states of alcohol dependence, anxiety disorders/depression, and chronic pain through actions upon an overlapping set of neural circuits (symbolized by the outer oval). Under normal, homeostatic conditions (symbolized by the upper inner oval), alcohol intoxication produces emotional and sensory pain though a compensatory opponent response (i.e., withdrawal) to an initial rewarding and analgesic action. Emotional and sensory pain comprise the initial response to trauma and injury that may be followed by a compensatory analgesic/euphoric response when terminated.
For decades it has been recognized that patients are undermedicated for acute pain, particularly children, the elderly and substance abusers. When a patient has a substance abuse problem, either current or past, these factors become even more complicated and the optimal management of acute pain becomes an even bigger challenge. 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).
In the meantime, while chronic pain should always be evaluated by a medical professional, there are many options for medication/opioid-based treatment, drawing on complementary and alternative approaches. It’s not unusual for people with chronic pain to consume alcohol to self-medicate—to drink to help sand down the sharp edges of their pain and turn down the volume of their discomfort. However, what starts out as something that seems like a solution often becomes part of the problem and can even make chronic pain worse. A Scripps Research team showed how both alcohol intake and alcohol withdrawal can lead to increased pain and hypersensitivity. Additionally, the study sheds light on the pathways involved in alcohol withdrawal-related allodynia and alcohol-induced neuropathic pain. Since previous research has shown that the immune system is activated in response to peripheral alcohol neuropathy, the researchers also examined the activation of the immune response in non-dependent mice with neuropathic pain.
Psychotherapy be extremely beneficial in dealing with chronic pain’s mental and emotional aspects. Because physical and emotional pain are related and activate one another, addressing depression, sadness, frustration, irritability, anger, anxiety, and fear has multi-level benefits. By shifting perspective and adjusting one’s thinking, it’s possible to change emotional responses and, in turn, dramatically decrease the level of suffering. This can significantly reduce the stress and suffering connected to chronic pain, which helps calm the sympathetic division of the autonomic nervous system and decrease pain perceptions. Research has shown that chronic alcohol use can cause long-term, painful nerve damage, known as alcoholic neuropathy. It is estimated that 50% to 60% of the total variance in risk for AUD is accounted for by variation in genetic factors (Rietschel & Treutlein, 2013).