Linking opioid-induced hyperalgesia and withdrawal-associated injury site pain: a case report

Abstract

Introduction and objectives:Understanding the details of one individual's experience with pain, opioid use and withdrawal may generate insights into possible relationships between opioid-induced hyperalgesia and withdrawal-associated injury site pain (WISP).Methods:This case study was extracted from a mixed methods study that characterized WISP. In 2014, the individual was recruited from a primary care clinic that prescribes opioid agonist therapy. In an interview, she completed a 35-item survey and elaborated on her own experience. Follow-up contact was made in June of 2017.Results:This 34-year-old white woman had several twisting injuries of her right knee between ages 13 and 15. The pain resolved each time in a few days, and she was pain free for 15 years. Around age 30, she initiated illicit oxycodone recreationally (not for pain) and developed an opioid use disorder. On detoxification, she experienced severe knee pain for 6 weeks that resolved postdetoxification but returned after subsequent oxycodone use and withdrawal episodes along with generalized skin sensitivity. This experience of WISP became a barrier to opioid cessation. Although nonsteroidal anti-inflammatories and gabapentin relieved WISP and methadone therapy assisted her opioid use disorder, an eventual change to sublingual buprenorphine/naloxone provided superior control of both.Conclusion:This case report illustrates that both opioid use and withdrawal can reactivate injury site pain, which can increase with dose escalation and repeated withdrawal events. The timing, trajectory, and neuropathic features of WISP reported here are consistent with those previously reported for the development of opioid-induced hyperalgesia, possibly linking these phenomena.

Knowing the Enemy Is Halfway towards Victory: A Scoping Review on Opioid-Induced Hyperalgesia

“…Whether or not OIH develops in a dose-dependent manner is not consensual [ 10 , 11 ]. The specificity of tested opioid substances, administration route and tested pain modality may also have to be considered [ 4 ] in addition to further contextual and individual variables [ 41 ].…”

Withdrawal-associated injury site pain prevalence and correlates among opioid-using people who inject drugs in Vancouver, Canada

“…Gabapentinoids and NSAIDs, among other medications, have been shown in clinical and pre-clinical trials to reduce opioid-induced hyperalgesia and withdrawal-induced hyperalgesia through a variety of mechanisms, and were named as mitigators of WISP by participants in our previous research (Arout et al, 2015;Compton et al, 2010;Dunbar et al, 2007;Kang et al, 2002;Lee et al, 2013;Ramasubbu and Gupta, 2011;Rieb et al, 2018Rieb et al, , 2016. Catecholamine release can cause neuroimmune changes leading to neuroinflammation, and has been implicated as one of the mechanisms of opioid withdrawal hyperalgesia (Arout et al, 2015;Drummond, 2001;Martelli et al, 2014;Pongratz and Straub, 2014;Raghavendra et al, 2002).…”

“…We suggested a variety of possible causal mechanisms, for example, linking WISP with central sensitization, opioid-induced hyperalgesia and withdrawal-induced hyperalgesia (Hutchinson et al, 2007;Rieb et al, 2016;Rivat and Ballantyne, 2016;Woolf, 2011). We later published a case report that described these features (Rieb et al, 2018). Non-opioid medications that have previously been identified to help relieve WISP include gabapentin and non-steroidal anti-inflammatories (NSAIDS) (Rieb et al, 2018(Rieb et al, , 2016.…”

“…We later published a case report that described these features (Rieb et al, 2018). Non-opioid medications that have previously been identified to help relieve WISP include gabapentin and non-steroidal anti-inflammatories (NSAIDS) (Rieb et al, 2018(Rieb et al, , 2016. However, the prevalence and clinical significance of WISP in various populations have yet to be reported.…”

Evolution of Analgesic Tolerance and Opioid-Induced Hyperalgesia Over 6 Months: Double-Blind Randomized Trial Incorporating Experimental Pain Models

“…15,17,45,46,56,68 Case series describe generalized hypersensitivity and even myoclonus with very high opioid doses, intrathecal administration, or concomitant phenothiazines. 13,23,24,29,36,37,43,53,60,61,64,65 Clinical diagnostic criteria for OIH have been proposed, but OIH incidence, dose threshold, and time course remain uncertain. 3,28 Does OIH produce a new pain, expand the topography of existing pain, increase pain above pretreatment levels, manifest as declining relief from each opioid dose, or some combination of the above?…”