The most common form of neck pain is caused by cervical paraspinal muscle spasm, usually secondary to minor strain or prolonged, unconscious muscle contraction associated with emotional stress. The problem is usually self-limited. Neck pain caused by minor muscle ligament strain is usually self-limited if aggravating activities are avoided. A relapsing clinical course is not uncommon. Muscle spasm also occurs with cervical degenerative disease (see later discussion).

Severe neck strain is seen in cervical hyperextension (whiplash) injury, which is typically sustained in an automobile accident. Sudden hyperextension of the neck followed by hyperflexion can result in significant musculoligamentous strain. The cervical segments are forced beyond their physiologic limits, resulting in tissue failure. Shearing and compressive forces tear muscle fibers and ligaments and exert excessive pressure on the disks and zygapophyseal joints. Soft tissue bleeding, swelling, severe muscle spasm, and joint and disk injury ensue, triggering pain. Symptoms typically increase over several hours, often becoming most severe the day after the acute event. The anterior or posterior ligaments of the cervical spine may be disrupted, but neurologic deficits are rare unless a cervical spine fracture is present that leads to root or cord compression. Refractory pain lasting more than 6 months may represent injury to a zygapophyseal joint, although other causes include the psychological stress of ongoing litigation and pending legal proceedings. The use of conventional seat belts does not prevent whiplash; force is still translated to the neck. Head restraints, if set too low, may exacerbate the hyperextension.

The clinical course is a function of the severity of injury and any preexisting mechanical or psychosocial pathology. Persons with a history of chronic pain complaints are likely to experience a prolonged course even after relatively minor injury. The same is true for those with concurrent psychosocial stress. Most other individuals experience relief within 6 months of the accident.

Degenerative disease is a key factor, accounting for nearly 75% of cervical radiculopathy cases. Age-related reduction in disk height and degenerative changes in adjacent facet joints lead to subluxation (cervical spondylosis), narrowing of the neuroforamina, and encroachment on the cervical nerve roots and dorsal root ganglia. Immobility and consolidation of the joint may ensue. Usually, the process is localized to the lower cervical levels, such as C-4 to C-5, C-5 to C-6, or C-6 to C-7. Degenerative changes and spurring at the cervical disk spaces are prominent. The condition presents as recurring neck stiffness and mild aching discomfort, with progressive limitation of neck motion over months to years. Lateral rotation and lateral flexion of the neck toward the painful side are limited; pain is precipitated or increased by such motions.

Cervical disk herniation can also lead to a narrowing of the neural foramina and the impingement of nerve roots. Herniation of the nucleus pulposus accounts for less than a one fourth of cervical radiculopathy cases. When there is concurrent compression of the dorsal root ganglia, radicular pain invariably ensues; compression of the root alone may not always trigger pain; inflammatory mediators appear to play a role in the generation of pain. Pain radiates in the distribution of the affected nerve root, and paresthesias, numbness, and weakness may be associated. The C-5, C-6, and C-7 nerve roots are most often affected. C-5 root compression results in the development of pain, paresthesias, and numbness in the anterosuperior shoulder and anterolateral aspect of the upper arm and forearm; a decreased biceps jerk and weakness of elbow flexion are found on examination. Compression of the C-6 nerve root produces symptoms in the dorsoradial aspect of the forearm and thumb, whereas C-7 impingement is indicated by altered sensation in the middle of the hand. The brachioradialis tendon reflex is affected by conditions altering C-5 and C-6, and the triceps jerk by injury to the C-7 and C-8 roots. The sensory symptoms and pain may follow different distributions, with the former being dermatomal and the latter being myotomal (see Chapter 167).

Rheumatoid disease can produce neck pain; it is typically worse in the morning. Concurrent symmetric polyarthropathy and subluxation at C-1 to C-2 (identifiable on plain films of the neck in flexion and extension) are characteristic. In the spondyloarthropathies, neck pain occurs in the context of diffuse back and sacroiliac discomfort. The earliest radiologic signs are those of sacroiliitis visible on sacroiliac joint films; advanced disease produces syndesmophytes. In polymyalgia rheumatica, neck pain may accompany the aching discomfort and stiffness of the shoulders and hip girdle that predominate in this condition. Polymyalgia complicated by giant-cell arteritis with carotid artery involvement can produce focal neck tenderness along one or both carotid arteries, sometimes referred to as carotodynia.

Tumor may infiltrate the spinal cord or the vertebral bodies and produce pain that is worse at night or while lying down. Cord involvement may be heralded by neurologic deficits in addition to the nocturnal pain.

Neck pain radiating to the jaw is characteristic of coronary ischemia, which is usually precipitated or worsened by physical activity. Concurrent arm pain may simulate a cervical radiculopathy. Esophageal disease may produce pain referable to the neck; if a cancer of the esophagus extends into the prevertebral space, posterior pain may develop.

Inquiry should focus on elucidating precipitating events, aggravating and alleviating factors (particularly specific neck movements), area of maximal tenderness, radiation of pain, presence of numbness or weakness in the extremities, course, past history of similar problems, history of prior or current malignancy, and previous therapeutic efforts. Warning symptoms of serious underlying pathology include concurrent fever and chills, unexplained weight loss, persistent nocturnal pain, and nuchal rigidity. Also of importance is screening for the development of myelopathy, which might be suggested by bilateral hand weakness or clumsiness, difficulty with balance, and new onset of urinary difficulties. Checking for symptoms and risk factors for myocardial ischemia rounds out the initial inquiry.

Blood tests add little to workup, except in the setting of suspected infection. Similarly, plain films of the neck are of limited value, except to detect fracture in persons with serious trauma or to confirm the presence of suspected degenerative disease and spondylosis, but findings may bear little relation to symptoms. In cases of nontraumatic neck strain, no imaging studies are necessary (the only finding would be loss of the normal lordotic curve).

Magnetic resonance imaging (MRI) is the test of choice when persistent neurologic compromise accompanies radicular neck pain, especially if symptoms are persistent for more than 6 to 12 weeks or steadily worsening and interventional or surgical therapy is being contemplated. Prompt MRI is indicated if there is concern about myelopathy from cervical cord compression. The test should not be ordered routinely for neck pain because test specificity is poor (up to half of asymptomatic persons have disk herniations on MRI) and cost is high. MRI has largely replaced bone scan for detection of spinal cord tumor. Computed tomographic (CT) scan is reserved for instances in which details of bony change (spurs, foraminal narrowing) or ligamentous calcification are desired.