Neck Pain in Adults _________________________________________________________________________
Opioid Analgesics When severe pain requires powerful analgesic control, few options are as effective and widely available as opioids [160]. Non-opioid analgesics were examined for chronic pain efficacy in 271 randomized controlled trials. Many showed statistically significant effect sizes, but pain reduction sizes were usually not clinically relevant [161]. However, the current regulatory environment and concern regarding misuse inhibits opioid prescribing, placing clinicians with patients in severe pain in a double-bind [162]. Opioid prescribing is a complex issue that should be approached by balancing control (to prevent inappropriate use) with access (for appropriate patients). With focus on either, and neglect of the other, consequences follow. Overemphasis on access has led to increased opioid prescriptions and related addiction, diversion, and overdose deaths. Retail opioid prescriptions peaked in 2010 and by 2018 (168 million) were below population-adjusted levels for 2000 (172 million) and 1999 (161 million) [163; 164]. Prescription opioid analgesic use per capita (in MME) fell 62.3% from 2011 to 2020 [165]. Prescription opioid analgesic presence (any opioid) in drug overdose deaths was 12,940 in 2003 (4.5 per 100,000 population), 25,052 in 2013 (7.9 per 100,000 population), and 79,358 in 2023 (24.0 per 100,000 population) [166]. Until improved analgesics are developed, opioids remain the only option for severe pain in many patients [160]. Clear evidence demonstrates that screening for substance use disorder before initiating opioid therapy in patients with chronic pain minimizes its development [96; 167; 168; 169]. In addition, most fatalities involving prescription opioid analgesics occur with co-ingested benzodiazepines, alcohol, and other CNS/respiratory depressants. Prevention involves patient education and cautious or avoidance of co-prescribing CNS depressants [170; 171; 172]. In controlling severe acute neck pain, oxycodone, morphine, and hydromorphone are similarly effective. For chronic moderate-to-severe neck pain, the suggested options shift to several more recent opioid preparations with lower abuse potential, greater tolerability, and/or alternate drug delivery that increase safety in long-term use. Opioid-induced constipation is a class-wide opioid adverse effect perceived by patients as the most distressing side effect [173]. A study of chronic pain patients with opioid- induced constipation from prior opioids found patient fear of constipation led to a number taking little or no study medication and inadequate pain control, despite the study drug being designed to reduce opioid-induced constipation [174]. Unlike other opioid side effects, opioid-induced constipation does not typically resolve with continued use, becoming chronic in 40% to 45% of patients on long-term opioids and adversely affecting patient quality of life and pain control [96;
173]. Opioid-induced constipation should be anticipated and managed prophylactically. Several medications are approved by the U.S. Food and Drug Administration (FDA) for opioid- induced constipation, including naloxegol, methylnaltrexone,
lubiprostone, and naldemedine. Abuse-Deterrent Formulations
All extended-release oral opioids are available in abuse- deterrent formulations, designed to make nontherapeutic use more difficult, less attractive, or less rewarding. Abuse-deterrent formulations use physical barriers that resist crushing; chemical barriers that form into a viscous gel if mixed with liquid; and/ or opioid antagonist sequestration that product tampering activates to neutralize the agonist. Some abuse-deterrent formulations use multiple deterrence mechanisms. While abuse-deterrent formulations can deter extended-release opioid tampering to defeat the slow-release mechanism for a rapid- onset, high-dose opioid effect, they cannot prevent abuse of intact pills. Abuse-deterrent formulations are one of several approaches to minimize prescription opioid abuse ( Table 5 ), but insurance non-coverage is common, due to higher costs than standard opioid formulations [96; 175; 176]. Oxycodone/Naloxone To reduce opioid-induced constipation during long-term therapy, the opioid antagonist naloxone was combined with oxycodone extended-release in a fixed-dose 2:1 ratio. Unlike short-acting naloxone, the extended-release formulation limits systemic exposure and does not block or reverse oxycodone analgesia [183]. Combination oxycodone/naloxone (Targin) was FDA-approved in 2014 but has since been discontinued for use in the United States [173; 184; 185]. Oxycodone/ naloxone and oxycodone extended-release show similar efficacy in chronic pain. Oxycodone/naloxone reduces but does not eliminate constipation and seems more effective in new patients with opioid-induced constipation than in preventing constipation during treatment [183]. Buprenorphine Buprenorphine differs from standard opioids as a partial mu-opioid receptor agonist. This produces a respiratory depression ceiling effect, making buprenorphine safer in overdose, and a euphoria ceiling effect that lowers drug “liking.” Buprenorphine is a kappa-opioid receptor antagonist, producing an anti-hyperalgesic effect relevant to neuropathic pain that often contributes to chronic spine-related pain [186; 187; 188]. Transdermal buprenorphine is the primary form used in chronic pain treatment. The transdermal patch is effective for seven days, after which it is replaced [189]. A buccal formulation was FDA-approved in 2016 based on studies demonstrating efficacy in patients with moderate-to- severe chronic low back pain [190]. The buccal formulation is available in a wider range of doses compared with the transdermal patch and can be administered every 12 hours [191].
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