Neck pain encompasses a variety of associated disorders, including whiplash pain and associated disorders (WAD) and other non-traumatic, traumatic, and work-related neck pain [8]. Neck pain and associated disorders account for 10.2 million physician and hospital outpatient visits in the United States each year [8].

Neck pain prevalence is slightly higher in women in their fifth decade of life, and a higher incidence is found in office/computer workers, manual laborers, and healthcare workers. Chronic neck pain is associated with psychologic factors (e.g., anxiety, poor coping skills, somatization), sleep disorders, smoking, sedentary lifestyle, and genetics [9,10,11]. Common neck pain comorbidities include headache, back pain, arthralgias, and depression [2,9].

Higher body mass index increases risk of chronic neck and shoulder pain. Obese persons may be predisposed to neck pain due to systemic inflammation, deleterious structural changes, increased mechanical stress, diminished muscle strength, greater number of psychosocial factors, and greater kinesiophobia-related disability [2,12].

As noted, neck pain is the fourth leading cause of disability in the United States (behind low back pain, depression, and arthritic disorders), and in some industries, it accounts for as much time off work as low back pain [1,2,14]. In many patients, neck pain becomes chronic, with life-impairing symptoms that severely decrease quality of life and restrict work productivity and daily activities [8].

WADs result from rapid acceleration/deceleration, typically involving rear-end or side-impact motor vehicle collisions, and represent 75% of all survivable motor vehicle collision injuries [15]. WAD can also occur from falls, diving, or collisions in contact sports. The "limit of harmlessness" with rear-end collision is 5 to 10 miles per hour (MPH); many whiplash injuries involve rear-end motor vehicle collision at speeds of 14 MPH or less [16,17,18,19]. WAD is associated with significant economic costs from lost work productivity, medical care, legal services, and other disability-related expenses, mostly incurred by patients with chronic symptoms [20].

The annual rate for acute whiplash symptoms is 1 to 6 cases per 1,000 population, and an estimated 1% of adults have chronic whiplash pain. In data from nine U.S. states, 45% of patients with chronic neck pain attributed their pain to a motor vehicle collision [16,21].

Outcomes for acute idiopathic neck pain are surprisingly poor. Resolution is often incomplete, and prognosis is markedly worse than commonly believed. Statistical pooling of published outcomes showed an average pain severity score (on a 0–100 scale) of 64 at onset, decreasing to 35 at 6.5 weeks, but increasing by 12 months to 42. Disability declined from an average score (0–100) of 30 at onset to 17 by 6.5 weeks, without further improvement at 12 months [25].

After the first 6.5 weeks, no further reduction in neck pain was found. The initial decreases in pain (45%) and disability (43%) are worthwhile to some patients, but the severity of persistent pain (35–42/100 up to one year) is sufficient to interfere with functioning and quality of life. Compared with low back pain one year after onset, neck pain intensity is twice as high and disability is comparable [25,26,27].

Recovery rates from WAD have been unchanged for decades, with 50% of patients experiencing ongoing pain and disability [15]. Following acute whiplash injury, recovery is slow for pain intensity outcomes, which usually require six months or longer to decrease 20%. Recovery is no better for disability outcomes, with average scores failing to reach 20% improvement by 12 months [29]. Following acute traumatic neck pain (including WAD), patients follow one of three likely trajectories for pain and disability [29]:

During acute or subacute WAD, risk factors for persistent problems include [29]:

Many patients with cervical radiculopathy secondary to acute disk herniation have a favorable clinical course. Symptom resolution occurs over weeks to months because 40% to 76% of herniated cervical disks spontaneously resorb independent of treatment. Acute neuropathic symptoms in spinal stenosis stabilize or improve in more than 50% of patients, but anatomic derangements do not generally improve without treatment [29,35,36].

In cervical whiplash, diverse symptoms develop following a rapid sequence of injuries [16,19,62]. The first is cervical hyperextension injury. A driver/passenger is struck from behind, which throws the body forward, but the head lags to hyperextend the neck. When the head and neck reach maximum extension, the neck snaps into flexion. The head is then thrown forward, flexing the cervical spine and resulting in rapid deceleration injury. The chin truncates forward flexion, but it can remain sufficient to cause longitudinal distraction and neurologic damage. Hyperextension may occur in the subsequent recoil. Within 100 ms, the cervical spine is compressed from below; as lower segments extend with upper segments flexed, the cervical spine assumes an S-shaped curve. In a split-second, all cervical segments are forced backward into extension. Whiplash-like loads of combined shear, bending, and compression forces can injure facet joints/capsules, and facet injury is the most common source of chronic post-whiplash pain. Spinal bones, ligaments, muscles, tendons, and disks may also become injured [41,63,64].

Neuropathic pain can develop when nerve fibers in any segment of the somatosensory system become dysfunctional or transmit signals inappropriately—without lesion or disease [95,96]. The painDETECT questionnaire (PDQ) was developed to identify neuropathic components in patients with chronic low back pain considered nociceptive [67,87,97]. This tool characterizes "altered nociception" as a distinct pain phenotype in chronic low back pain. In these patients, neuropathic-like signs and symptoms reflect maladaptive nervous system functioning and central rather than peripheral pain mechanisms [94,98].

Neuropathic pain can develop when nerve fibers in any segment of the somatosensory system become dysfunctional or transmit signals inappropriately—without lesion or disease [95,96]. The painDETECT questionnaire (PDQ) was developed to identify neuropathic components in patients with chronic low back pain considered nociceptive [67,87,97]. This tool characterizes "altered nociception" as a distinct pain phenotype in chronic low back pain. In these patients, neuropathic-like signs and symptoms reflect maladaptive nervous system functioning and central rather than peripheral pain mechanisms [94,98].

The Tampa Scale of Kinesiophobia (TSK), the Fear Avoidance of Pain Scale (FAPS), the Patient Health Questionnaire-9 (PHQ-9), and the Hospital Anxiety and Depression Scale (HADS) measure "yellow flags," psychosocial conditions that may predispose the patient to a more complex clinical course, chronicity, or disability [8,19,103]. The following psychologic factors should be identified and measured using the associated tools:

Diagnostic imaging has an essential role in some neck pain presentations. However, imaging findings of bulging disks or degenerative changes are common in asymptomatic persons and increase with age [14,103]. In some patients, the imaged abnormality is causing their neck pain. In most patients with acute neck pain, imaging fails to identify a pathologic cause or pathologic findings have uncertain relevance or do not change the course of treatment [29].

Magnetic resonance imaging (MRI) is the imaging study of choice for most cervical spinal abnormalities. MRI can add important information about soft tissue injuries related to bony injuries seen on x-ray or computed tomography (CT) or disk or ligamentous injuries suggested by x-ray, CT, or clinical findings [109]. It can also distinguish hematoma from edema. MRI is highly accurate in identifying disk injury and ligament injuries [19,110]. It is able to detect ligament disruption and subtle vertebral fracture, but is unreliable in depicting sources of cervical diskogenic pain because significant annular tears can escape MRI detection [16,41].

Systematic reviews of guideline-recommended analgesics for neck pain have found acetaminophen ineffective and NSAIDs minimally effective, compared with placebo. Systematic reviews have also found minimal benefit in other analgesics considered effective. These results may reflect true ineffectiveness or possible limitations with randomized controlled trial evaluation of analgesics, including [120,121]:

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 [103,134,144]. Given the risk profile, clinicians should reconsider using NSAIDs for pain and limit their use to pain with inflammation [145].

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 [146,147,148]. 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 [148].

Antiepileptic drugs are diverse, but pregabalin and gabapentin are the only widely studied agents in chronic low back pain. As with antidepressants, few neck pain studies are available and chronic low back pain outcomes are used to inform decisions.

Pregabalin and gabapentin are widely recommended first-line agents in neuropathic pain disorders, such as painful diabetic neuropathies and postherpetic neuralgia [70]. Analgesic, anxiolytic, and anticonvulsant effects arise from binding to alpha-2/delta-1 subunits of calcium channels, highly expressed in brainstem structures where descending pain modulatory pathways originate and a likely key analgesic target of pregabalin/gabapentin [68].

Until improved analgesics are developed, opioids remain the only option for severe pain in many patients [161]. Clear evidence demonstrates that screening for substance use disorder before initiating opioid therapy in patients with chronic pain minimizes its development [96,166,167,168]. 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 [169,170,171].

Tapentadol is a mu-opioid receptor agonist and norepinephrine reuptake inhibitor combined in a single molecule. Tapentadol extended-release was extensively investigated in Europe, with the finding that the formulation is effective in diverse chronic pain, with or without neuropathic pain component, in evaluations up to two years [190,191]. Researchers found function, health status, and quality of life improved during long-term treatment. The drug has a good safety profile, with GI tolerability more favorable than other opioids and a low risk of withdrawal after cessation. To date, analgesic tolerance has not been found in long-term data.

In studies, tapentadol was as effective as oxycodone in nociceptive and neuropathic chronic low back pain, with better GI tolerability and treatment adherence [71,192,193,194]. Earlier gains in function, health status, and quality of life maintained over one year in 1,154 patients receiving open-label tapentadol extended-release after completing randomized controlled trials, including average pain scores (3.9 start, 3.7 end) [195].

Vertebral artery dissection caused by high-velocity, low-amplitude thrusting is a rare but recognized outcome. Vascular accidents following extension and rotation of the neck beyond the physiologic range lead to a cascade of events including thrombosis, stroke, and death [221]. More than 400 cases following cervical manipulation have described arterial dissection, brain stem injury, cerebellar injury, spinal cord injury, thrombosis, locked-in syndrome, joint dislocation, and death. Risk of these rare but catastrophic events can be minimized by avoiding extension-based high-velocity, low-amplitude thrust [16].

Joint mobilization techniques incorporate a low-velocity and small- or large-amplitude oscillatory movement, within a joint's passive range of motion [8]. A mobilization treatment consists of passive movement involving oscillatory motions to the vertebral segment(s). The passive mobility is performed in a graded manner (I, II, III, IV, or V), which depicts the speed and depth of joint motion during the maneuver. Mobilization may include skilled manual joint tissue stretching [103]. Other modalities include myofascial releases, counterstrain, and indirect or direct muscle energy techniques [16]. Indications include the need to improve joint play, segmental alignment, or intracapsular arthrokinematics or to reduce pain associated with tissue impingement. Mobilization should be accompanied by active therapy [103].

A 2015 Cochrane review of mobilization therapy in neck pain noted anterior-posterior mobilization may favor pain reduction over rotatory or transverse mobilizations at immediate follow-up in patients with acute and subacute neck pain [220]. For those with subacute and chronic neck pain, cervical mobilization alone may not be different from ultrasound, TENS, acupuncture, and massage in improving pain, function, quality of life, and participant satisfaction at immediate and intermediate follow-up. Multiple sessions of TMD manual therapy may be more effective than cervical mobilization in improving pain/function at immediate and intermediate follow-up for patients with chronic cervical headache and TMD.

Traction is popular among patients with cervical radiculopathy, but it is contraindicated with tumor, infection, fracture, or dislocation [103]. Mechanical traction is widely used to promote cervical immobilization and widen the foraminal openings. Cervical traction may relieve radicular pain from nerve root compression, but it does not improve pain from soft-tissue injury. Hot packs, massage, or electrical stimulation should be applied before traction to relieve pain and relax muscles [65].

Exercise combined with any blend of manipulation, mobilization, muscle energy, and stretching is more effective in reducing neck pain and disability than any single approach used alone [103]. A systematic review of exercise efficacy in neck pain disorders concluded that use of strengthening and endurance exercises for the cervico-scapulothoracic region and shoulder may be beneficial in reducing pain and improving function; and that stretching exercises alone are not beneficial [225]. In acute radiculopathy, cervical stretch, strengthening, and stabilization exercises show a small benefit in pain reduction. For chronic neck pain, the authors identified five modalities with some evidence of efficacy for neck pain [225]:

The second trial compared cervical and scapulothoracic stabilization exercises alone or plus connective tissue massage. Both decreased pain intensity and anxiety levels, but combination therapy led to significantly greater improvements in pain intensity at night, pressure pain threshold, state anxiety, and mental health than exercises alone [227]. At six-month follow-up, patients with chronic nonspecific neck pain showed significantly greater reductions in pain and disability from global postural re-education than manual therapy (nine 1-hour sessions for both) [228].

Consensus indicates that exercise therapy is beneficial for chronic pain, but the lack of endogenous analgesia in some chronic pain disorders should not be ignored and clinicians should account for this when treating patients with chronic pain [230]. General exercise is frequently recommended for WADs. In contrast to other musculoskeletal pain conditions, a review of high-quality studies concluded general exercise does not reduce pain or disability in patients with WAD [223].

Exercise-induced hypoalgesia describes the desired effect of reduced pain sensitivity following exercise. The effect of acute exercise on pain sensitivity in chronic pain conditions is controversial, because hypoalgesia, unchanged pain sensitivity, and hyperalgesia (impaired exercise-induced hypoalgesia) have all been reported. Evidence suggests impaired exercise-induced hypoalgesia is evident in WAD following aerobic exercise [231].

In patients with chronic WAD, exercise-induced hypoalgesia responses to isometric (3-minute wall squat) or aerobic (30 minute bicycling) exercise were compared by recording neck and leg pressure pain thresholds before and after exercises. Pressure pain threshold increases were found at both areas after isometric, but not aerobic, exercise. Isometric exercises directed at non-painful muscles may reduce local and remote pain sensitivity in patients with chronic WAD and mild-to-moderate neck pain and disability [232].

The persistence of therapeutic effects following a course of acupuncture was evaluated in a meta-analysis of 29 randomized controlled trials of diverse chronic pain. Depending on the control group (no-acupuncture versus sham acupuncture), 50% to 90% of acupuncture benefit was sustained 12 months after treatment and did not seem to decrease importantly in chronic pain [241]. Patients can generally be reassured that treatment effects persist. Questions of acupuncture cost-effectiveness can take these findings into account.

Facet joint interventions identify and treat facet-mediated pain. To identify facet joints as the pain source, inter-articular injections of local anesthetic are placed into facet joints or along their innervating nerve fibers (sensory medial branch). A separate comparative block is performed on a different date to confirm the level of involvement and reduce placebo response. Pain relief from both medial branch nerve blocks confirms facet origin, and radiofrequency ablation is indicated for extended pain control [50,250].

Trigger point injection with a local anesthetic (with or without corticosteroid) is widely used in treating myofascial pain. With trigger point injection, the trigger point in the taut muscle band is palpated, slightly stretched to prevent it from moving, and injected. The needle is redirected in the area to ensure injectate distribution. The fast-in/fast-out method is the most successful in eliciting a local twitch response (which helps confirm diagnosis) and reducing myofascial pain [57]. Sedation is not needed for trigger point injection [103]. The efficacy of this approach is enhanced when immediately followed by a myofascial intervention [57,103].