Chronic pain, chronic stress and substance use: overlapping mechanisms and implications PMC

• Nov 02, 2021
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One additional concern is that if a person is acutely intoxicated and receives opioid medication, the combination can lead to problems in monitoring therapeutic or toxic effects of the opioids, as well as effects of the traumatic injury. Our next recommendation is to adequately medicate patients for their pain, regardless of their history of addictive behaviors. We have evidence that patients will seek other means, often illicit, of managing their own pain when pain is not adequately controlled. We can expect that patients with current addictions may have lower pain thresholds and may develop a tolerance to opioids more quickly. Rather than offering them less medication, they may need higher doses than expected to adequately control pain. This may be particularly important for patients with addictions who are not used to experiencing the full range of emotions when sober.

Consideration of conjoint treatment of AUD and pain is essential, especially given the bidirectional relationship between the two, including the dampening effect of alcohol on pain perception, which may lead to drinking as a coping mechanism, and thus, poor AUD treatment outcomes. This point may be particularly relevant for individuals exhibiting pain within the context of a more severe na vs aa health problem, such as HIV or sickle cell disease (Levenson et al., 2007; Merlin et al., 2015; Merlin et al., 2014). Impaired cognition can modulate the cognitive-evaluative dimension of pain experiences, both as a reinforcing factor for alcohol-seeking behavior (as alcohol is known to alleviate pain) and also in how pain is perceived. Additionally, physiological cues accompanying alcohol consumption can influence drinkers through modulating their expectancy. It should be noted that this model does not rule out or ignore the role of biological factors in the development of chronic pain, but instead emphasizes the significance of reinforcement and learning in the development and maintenance of chronic pain (Gatzounis, Schrooten, Crombez, & Vlaeyen, 2012). For instance, it is likely that dopamine release in the mesocorticolimbic dopamine system (precipitated by consuming alcohol) is responsible for relief from acute pain.

He also noted that it has been very difficult to know how adequate analgesia might affect addiction patterns, because most of these patients simply do not receive sufficient doses of narcotics. Unfortunately, very few studies have investigated crosstolerance between alcohol and opioids at a practical level or in humans. The only class of drugs known to have a direct crosstolerance with alcohol are the benzodiazepines.

Both conditions involve dysfunction of extended reward and oversight circuitry, and do alcoholics have big noses particularly prefrontal cortex. Wesson et al. state that patients who have a previous history of alcohol or drug abuse, but are not currently using, can also be effectively managed with opioids [37]. In reviewing this literature, one study found that patients who had a history of alcohol abuse alone and were active members of Alcoholics Anonymous showed no evidence of opioid prescription abuse [30]. The risk of returning to a previous addiction after using opioids to treat acute pain seems to be relatively low.

The latter highlights the need to consider domains of coping and self-regulation in exploring the neural mechanisms of chronic pain and to develop not only a greater understanding of chronic pain, but also to identify specific components that must be addressed in its treatment. 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. Opioids in particular may not be appropriate for managing pain in individuals with AUD, as they probably engage the same brain reward pathways as in AUD. Indeed, there is evidence for the involvement of the endogenous cannabinoid system in the pharmacological and behavioral effects of alcohol (Perra et al., 2005). However, gabapentin, a GABA analogue anticonvulsant medication that also is used to treat pain, has been shown to have the benefit of reducing cravings and to significantly delay relapse in individuals with AUD (Brower et al., 2008).

Alcohol Fuels Pain: Study Reveals Link Between Drinking and Chronic Pain

1. In the alcohol-dependent mice, allodynia (in which a harmless stimulus is perceived as painful) developed during alcohol withdrawal, and subsequent alcohol intake significantly decreased pain sensitivity.
2. The patients’ low expectations directly impact the issue of inadequate pain management because they may not be asking for pain medications when they need them.
3. Separately, about half of the mice that were not dependent on alcohol also showed signs of increased pain sensitivity during alcohol withdrawal but, unlike the dependent mice, this neuropathy was not reversed by re-exposure to alcohol.
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5. Similar studies should examine the potential influence of chronic alcohol problems on pain management prescriptions and doses delivered.
6. In dependent mice, allodynia developed during alcohol withdrawal, and subsequent alcohol access significantly decreased pain sensitivity.

The first recommendation is to obtain routine blood alcohol level and toxicology screening on trauma patients in the emergency department. Staff may also want to consider collecting other biochemical markers of chronic use, including a γ-glutamyl transferase. Dosing of opioids will probably need to be altered if a person is either acutely intoxicated or has impaired liver function due to chronic use. This information can also be useful in conducting brief interventions geared toward changing alcohol use. A major trauma is a life-changing event that may be used as an impetus to change addictive behaviors.

3. Chronic stress and pain co-occurrence in a large community sample

The chronic intermittent ethanol vapor-two bottle choice (CIE-2BC) mouse model used in this study paves the way for more research in this area. When Roberto’s group then measured levels of inflammatory proteins in the animals, they discovered that while inflammation pathways were elevated in both dependent and non-dependent animals, specific molecules were only increased in dependent mice. It also suggests which inflammatory proteins may be useful as drug targets to combat alcohol-related pain. Cornell Medical Index is a questionnaire that poses “yes” or “no” questions about individuals’ current occurrence of physical and emotional health symptoms, including specific types of pain symptoms. In addition to current symptoms, it also asks subjects to indicate whether they have been diagnosed with specific illnesses, and about health habits, like smoking (45).

Effect of acute and chronic alcohol abuse on pain management in a trauma center

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. The analgesic effects of alcohol on pain perception have been measured in a variety of ways, including examining pain threshold, tolerance, and pain ratings (e.g., intensity). Regarding ratings of discomfort versus intensity of pain, alcohol alleviates discomfort at lower doses and to a greater extent than intensity, suggesting the effect of alcohol may vary across components of pain. In addition, pain is influenced by alcohol dose and blood alcohol concentration (BAC), with the magnitude of the analgesic effects increasing at higher BACs (Cutter et al., 1976; Gustafson & Kallmen, 1988; Horn-Hofmann et al., 2015; Stewart, Finn, & Pihl, 1995; Thompson, Oram, Correll, Tsermentseli, & Stubbs, 2017).

This sex difference in opioid analgesic tolerance in preclinical studies is consistent with findings in clinical studies of women and men (21). Not only does early what are whippets and protracted abstinence induce a type of pain characteristic of early recovery, but it also has the tendency to exacerbate dysregulated nociception (Egli et al., 2012). In cases where pain among AUD individuals results from a comorbid condition (e.g., cancer, neuralgia, fibromyalgia), abstinence of any duration can reveal the presence and intensity of pain that was previously being masked by the analgesic effects of alcohol. This dynamic can present unique challenges for recovering individuals suffering from acute and/or chronic pain, as well as for the physicians responsible for treating both conditions.

We also consider recent evidence that will shape future investigations into novel treatment mechanisms for pain in individuals suffering from AUD. When levels of inflammatory proteins were measured, the researchers discovered that while inflammation pathways were elevated in both dependent and non-dependent mice, specific molecules were only increased in dependent mice. It also indicates which inflammatory proteins may be useful as potential targets for intervention to combat alcohol-related pain.

How does alcohol cause pain?

AUD may share common neural pathways with chronic pain, which may facilitate pain affecting alcohol use patterns, or facilitate modulatory effects of alcohol on pain processing, thereby precipitating the risk of chronic pain development. It is influenced by a host of familial, biological, environmental, and socioeconomic mediators that affect drinking behavior and susceptibility to pain disorders. These findings support the hypothesis that cummulative and chronic stress may negatively impact the VmPFC, compromising self-regulatory control over the stress-pain circuit, leading to risk of greater physical pain symptoms. Together, these findings also support the hypothesis that VmPFC may serve as a a common overlapping neural region that may underlie the high association between chronic stress and increased vulnerability to chronic pain. On the basis of this neurobiological overlap, a heuristic feed-forward model on the overlap of chronic pain, chronic stress and substance misuse risk is proposed in Figure 4, wherein chronic stress states alter VmPFC related circuits that regulate stress, reward and pain.

Family history of AUD also could be a mediating risk factor for comorbid affective disorders in pain patients. In a study on the relationship between fibromyalgia and familial history of depression and AUD in first-degree relatives (Katz & Kravitz, 1996), patients who had both fibromyalgia and depression also had higher odds of AUD in their first-degree relatives. Another family history study on prepubertal children suggested that the risk of prepubertal onset of major depressive disorder in families with a high aggregation of affective disorders is higher when there also is a high prevalence of AUD in the families (Puig-Antich et al., 1989). The interrelationship between chronic pain and AUD resides in the intersection of etiological influences, mental experiences, and neurobiological processes.

Separately, about half of the mice that were not dependent on alcohol also showed signs of increased pain sensitivity during alcohol withdrawal but, unlike the dependent mice, this neuropathy was not reversed by re-exposure to alcohol. The investigators found that, of the problem drinkers, approximately 43% of men and 44% of women reported experiencing moderate to severe pain, but in nonproblem drinkers, only 28% of men and 33% of women reported that level of pain. Likewise, pain interfered with daily activities ‘moderately’ to ‘extremely’ among 34% of men and 29% of women with drinking problems, compared to 16% and 19% of the men and women without drinking problems. Importantly, almost 38% of current problem drinkers reported using alcohol to manage pain, whereas in contrast, only 15% of nonproblem-drinking men and 13% of nonproblem-drinking women did so. Among the problem drinkers who experienced moderate to severe pain, almost 57% of men and 59% of women reported using alcohol for pain management, compared to 21% of nonproblem-drinking men and women with the same level of pain. Dysfunction in descending pain modulatory circuits is thought to play an important role in the chronification of pain (Ossipov et al., 2014).