_________________________________________________________________________ Neck Pain in Adults
Muscle Relaxants Appropriate for muscle spasm with pain, there is strong evidence that muscle relaxants can provide short-term pain relief in acute low back pain (and by extension, neck pain due to spasm). Clinicians should consider the side effects of drowsiness or dizziness. Carisoprodol is not recommended because its active metabolite, meprobamate, is a drug with abuse potential [103]. NSAIDs NSAIDs are endorsed universally as first-line therapy for acute mild-to-moderate pain of any origin and broadly as first-line therapy for diverse chronic pain conditions, including neck pain. NSAIDs have similar pharmacology but diverse molecular structure. Patient response to specific NSAIDs varies, and several trials of different NSAIDs may be needed to identify an effective agent [103]. A meta-analysis evaluated 35 randomized controlled trials for NSAID efficacy in low back, neck, and sciatica pain. Pain and disability outcomes of NSAIDs or placebo were pooled and averaged, and differences were compared using a 0–10 scale. No study reported outcomes beyond 12 weeks. Only two neck pain studies were found, and the outcomes of these studies were for less than four weeks [130]. NSAIDs surpassed placebo in neck pain reduction by 1.6, a minimally important difference to patients in pain. NSAIDs surpassed placebo by 1.2 in disability reduction. Average differences between NSAIDs and placebo in low back pain/ sciatica were lower than neck pain. In aggregate, six participants required treatment with NSAIDs, instead of placebo, for one additional participant to achieve clinically important pain reduction [130]. Another review of NSAIDs in spine pain found two neck pain studies. One involved intravenous NSAIDs, but the other study found greater pain reduction with indomethacin and piroxicam over placebo, and no difference between NSAIDs [47]. NSAIDs inhibit cyclooxygenase-1 and -2 (COX-1 and COX-2), enzymes that convert arachidonic acid to pro-inflammatory prostanoids. COX-2 inhibition reduces inflammation and pain. Prostanoids also play key roles in maintaining normal physiologic processes; their inhibition accounts for the adverse effects of NSAIDs [131; 132]. COX-1 inhibition suppresses prostaglandins that protect the gastric mucosa and thromboxanes that promote platelet aggregation. COX-2 inhibition suppresses prostacyclins in vascular endothelium that inhibit platelet aggregation [133]. Thus, serious or fatal GI, cardiovascular, or renal adverse effects can result from NSAIDs use [132]. In 1997, 16,500 deaths from upper GI bleeding/perforation were linked to NSAIDs [134; 135]. This prompted introduction of COX-2-selective NSAIDs to reduce GI risks, which became
linked to cardiovascular adverse effects. The view emerged that COX-2 selective NSAIDs had greater risk of cardiovascular toxicity and lower risk of GI toxicity than traditional NSAIDs. Greater accrual of patient outcomes demonstrated all NSAIDs carry GI and cardiovascular risks [131; 136; 137; 138]. Celecoxib has the least GI toxicity but high, dose-related cardiovascular risk. Naproxen has the best cardiovascular safety, but greatest GI toxicity [138]. Concurrent NSAID and selective serotonin reuptake inhibitor (SSRI) use increases upper GI bleeding risks [139; 140]. Adding a proton pump inhibitor or switching NSAIDs to celecoxib is recommended to mitigate upper GI risks [141]. Despite greater awareness, NSAIDs cause 7,000 to 10,000 GI hemorrhage fatalities annually [142]. All NSAIDs increase risks of fatal and non-fatal cardiovascular and cerebrovascular events and renal failure, especially in elderly patients. Serious adverse effects can occur within one month of regular therapy. Long-term NSAID use is not recommended, and NSAIDs should be used at the lowest effective dose for the shortest duration possible [103; 133; 143]. Given the risk profile, clinicians should reconsider using NSAIDs for pain and limit their use to pain with inflammation [144]. Antidepressants Noradrenergic projections form a key component of descending pain inhibition pathways. Impaired descending pain inhibition can facilitate and maintain chronic pain. Drugs that inhibit norepinephrine reuptake can enhance spinal noradrenergic efficiency to reduce chronic pain, including some antidepressants and the opioids tramadol and tapentadol [69; 122]. Tricyclic antidepressants (TCAs) and selective serotonin/ norepinephrine reuptake inhibitors (SNRIs) are recommended first-line options in chronic neuropathic pain disorders and in chronic pain with a neuropathic component [67; 69; 71]. Tricyclic Antidepressants The first antidepressants used in pain treatment, TCAs may also produce analgesia by blocking NMDA-induced hyperalgesia, voltage-gated sodium channels, and delta-opioid receptor interaction [145; 146; 147]. Amitriptyline is the most studied, endorsed, and prescribed TCA in chronic pain, and some evidence suggests it may be the most effective analgesic antidepressant [68; 70; 71; 79]. Other TCAs (e.g., nortriptyline, desipramine) are better tolerated but lack the evidence base of amitriptyline. Analgesic effects are independent of antidepressant effect, and analgesic dosing is 20% to 33% of antidepressant doses [147]. SNRIs Duloxetine and venlafaxine are the most-studied SNRIs in chronic pain, with duloxetine the most widely endorsed agent [79]. SNRIs inhibit reuptake of serotonin and norepinephrine,
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