The conundrum of opioid tapering in long-term opioid therapy for chronic pain: A commentary

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Abstract

<div class="section"> <a class="named-anchor" id="S1">  </a> <h5 class="section-title" id="d7677364e142">Background</h5> <p id="P1">In response to the opioid epidemic and new guidelines, many patients on high-dose long term opioid therapy (LTOT) for chronic pain are getting tapered off opioids. As a result, a unique clinical challenge is emerging: while many on LTOT have poor pain control, functional decline, psychiatric instability, aberrancies and misuse, these issues may often worsen with opioid tapering. Currently, a clear explanation and practical guidance on how to manage this perplexing clinical scenario is lacking. </p> </div><div class="section"> <a class="named-anchor" id="S2">  </a> <h5 class="section-title" id="d7677364e147">Methods</h5> <p id="P2">We offer a commentary with our perspective on possible mechanisms involved in this clinical phenomena and offer practical management guidance, supported by available evidence. </p> </div><div class="section"> <a class="named-anchor" id="S3">  </a> <h5 class="section-title" id="d7677364e152">Results</h5> <p id="P3">It is not well recognized that allostatic opponent process involved in development of opioid dependence can cause worsening pain, functional status, sleep and psychiatric symptoms over time, and significant fluctuation of pain and other affective symptoms due to their bidirectional dynamic interaction with opioid dependence (‘affective dynamism’). These elements of complex persistent dependence (CPD), the grey area between simple dependence and addiction, can lead to escalating and labile opioid need, often generating aberrant behaviors. Opioid tapering, a seemingly logical intervention in this situation, may lead to worsening of pain, function and psychiatric symptoms due to development of protracted abstinence syndrome. We offer practicing clinicians management principles and practical guidance focused on management of CPD in addition to chronic pain in these difficult clinical scenarios. </p> </div><div class="section"> <a class="named-anchor" id="S4">  </a> <h5 class="section-title" id="d7677364e157">Conclusion</h5> <p id="P4">Awareness of the science of the neuroplasticity effects of repeated use of opioids is necessary to better manage these patients with complex challenges. </p> </div>

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Reward and motivation in pain and pain relief.

Edita Navratilova, Frank Porreca (2014)

Pain is fundamentally unpleasant, a feature that protects the organism by promoting motivation and learning. Relief of aversive states, including pain, is rewarding. The aversiveness of pain, as well as the reward from relief of pain, is encoded by brain reward/motivational mesocorticolimbic circuitry. In this Review, we describe current knowledge of the impact of acute and chronic pain on reward/motivation circuits gained from preclinical models and from human neuroimaging. We highlight emerging clinical evidence suggesting that anatomical and functional changes in these circuits contribute to the transition from acute to chronic pain. We propose that assessing activity in these conserved circuits can offer new outcome measures for preclinical evaluation of analgesic efficacy to improve translation and speed drug discovery. We further suggest that targeting reward/motivation circuits may provide a path for normalizing the consequences of chronic pain to the brain, surpassing symptomatic management to promote recovery from chronic pain.

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Addiction and the brain: the neurobiology of compulsion and its persistence.

Garrett S Hyman, Robert Malenka (2001)

People take addictive drugs to elevate mood, but with repeated use these drugs produce serious unwanted effects, which can include tolerance to some drug effects, sensitization to others, and an adapted state - dependence - which sets the stage for withdrawal symptoms when drug use stops. The most serious consequence of repetitive drug taking, however, is addiction: a persistent state in which compulsive drug use escapes control, even when serious negative consequences ensue. Addiction is characterized by a long-lasting risk of relapse, which is often initiated by exposure to drug-related cues. Substantial progress has been made in understanding the molecular and cellular mechanisms of tolerance, dependence and withdrawal, but as yet we understand little of the neural substrates of compulsive drug use and its remarkable persistence. Here we review evidence for the possibility that compulsion and its persistence are based on a pathological usurpation of molecular mechanisms that are normally involved in memory.

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Addiction as a stress surfeit disorder.

J. Park, Ami Cohen, Cara L. Buck … (2013)

Drug addiction has been conceptualized as a chronically relapsing disorder of compulsive drug seeking and taking that progresses through three stages: binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation. Drug addiction impacts multiple motivational mechanisms and can be conceptualized as a disorder that progresses from positive reinforcement (binge/intoxication stage) to negative reinforcement (withdrawal/negative affect stage). The construct of negative reinforcement is defined as drug taking that alleviates a negative emotional state. Our hypothesis is that the negative emotional state that drives such negative reinforcement is derived from dysregulation of key neurochemical elements involved in the brain stress systems within the frontal cortex, ventral striatum, and extended amygdala. Specific neurochemical elements in these structures include not only recruitment of the classic stress axis mediated by corticotropin-releasing factor (CRF) in the extended amygdala as previously hypothesized but also recruitment of dynorphin-κ opioid aversive systems in the ventral striatum and extended amygdala. Additionally, we hypothesized that these brain stress systems may be engaged in the frontal cortex early in the addiction process. Excessive drug taking engages activation of CRF not only in the extended amygdala, accompanied by anxiety-like states, but also in the medial prefrontal cortex, accompanied by deficits in executive function that may facilitate the transition to compulsive-like responding. Excessive activation of the nucleus accumbens via the release of mesocorticolimbic dopamine or activation of opioid receptors has long been hypothesized to subsequently activate the dynorphin-κ opioid system, which in turn can decrease dopaminergic activity in the mesocorticolimbic dopamine system. Blockade of the κ opioid system can also block anxiety-like and reward deficits associated with withdrawal from drugs of abuse and block the development of compulsive-like responding during extended access to drugs of abuse, suggesting another powerful brain stress/anti-reward system that contributes to compulsive drug seeking. Thus, brain stress response systems are hypothesized to be activated by acute excessive drug intake, to be sensitized during repeated withdrawal, to persist into protracted abstinence, and to contribute to the development and persistence of addiction. The recruitment of anti-reward systems provides a powerful neurochemical basis for the negative emotional states that are responsible for the dark side of addiction. This article is part of a Special Issue entitled 'NIDA 40th Anniversary Issue'. Copyright © 2013 Elsevier Ltd. All rights reserved.

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Author and article information

Journal

Title: Substance Abuse

Abbreviated Title: Substance Abuse

Publisher: Informa UK Limited

ISSN (Print): 0889-7077

ISSN (Electronic): 1547-0164

Publication date Created: September 20 2017

Publication date (Electronic): September 20 2017

Pages: 1-10

Affiliations

[1 ] VA New England Mental Illness Research and Education Center, West Haven, Connecticut, USA

[2 ] Advanced Pact Pain Clinic, VA Hampton Medical Center, Hampton, Virginia, USA

[3 ] Department of Psychiatry, Yale School of Medicine, New Haven, Connecticut, USA

[4 ] Department of Anesthesiology and Pain Medicine, University of Washington School of Medicine, Seattle, Washington, USA

Article

DOI: 10.1080/08897077.2017.1381663

PMC ID: 6129223

PubMed ID: 28929914

SO-VID: 5e248fd2-2c46-421e-a6c6-6ff0e1fcacfd

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The conundrum of opioid tapering in long-term opioid therapy for chronic pain: A commentary

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Most cited references 44

Reward and motivation in pain and pain relief.

Addiction and the brain: the neurobiology of compulsion and its persistence.

Addiction as a stress surfeit disorder.

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