Definition: Neck pain is a relatively common complaint, affecting approximately one-third of the population at some time in their lives.
Anatomic Considerations: Neck pain can derive from several structures within the neck, including cervical vertebral, zygapophyseal joints, ligaments, tendons, muscles, or spinal cord and nerve roots. Pain originating in the neck may be referred to other locations, including the suboccipital and interscapular regions or shoulder and arm. Whereas cervical rotation is primarily caused by craniocervical and C1-2 articulations, flexion and extension are largely accomplished at the C5-6 and C6-7 articulations.
Etiology: Precipitating causes for pain in these structures include degenerative arthritis, inflammatory arthritis, bony hypertrophy, trauma, muscle spasm, fibromyalgia, myelopathy, infection (e.g., osteomyelitis, septic discitis), and tumor (primary or metastatic) (Table 25). Systemic causes of neck pain are suggested by the findings of fever, chills, sweats, weight loss, and pain not relieved by rest or recumbency.
Differential Diagnosis of Neck Pain
|Soft tissue injury (sprain)Traumatic (e.g., whiplash)
Secondary to strain or overuse
Associated with other diseases (e.g., osteoarthritis)
Osteoarthritis (with or without osteophyte formation)
Ankylosing spondylitis and other spondyloarthropathies
Juvenile arthritis (juvenile rheumatoid arthritis)
Radicular (nerve root) entrapment (i.e., radiculopathy)
Diffuse idiopathic skeletal hyperostosis
Osteoporosis (with compression fracture)
Infections of bone (osteomyelitis)
Discitis Meningitis Thyroiditis
Fibromyalgia myofascial pain syndrome
Cardinal Findings: Acute onset of neck pain is often related to injury to muscle or other soft tissues. Such pain may be caused by direct trauma, indirect trauma (e.g., rapid deceleration, whiplash), or overuse. This is sometimes referred to as cervical strain. In this condition, neurologic examination should be normal. Patients often try to resist motion and will keep their head/neck in a fixed, single position. On palpation, paraspinal spasm may be evident. Acute neck pain may also result from infection, fracture, vertebral collapse, or meningitis. Chronic cervical pain (e.g., cervical OA) may also be exacerbated by any cause of soft tissue strain or spasm, thereby magnifying the patient’s overall perception of pain. Common causes of chronic neck pain also includes fibromyalgia, inflammatory arthritis (e.g., RA, AS), or bony metastases.
Patients with neck pain should be evaluated by assessing for range of motion (flexion, extension, lateral bending, lateral rotation), muscle spasm, tender trigger points (indicating myofascial pain syndrome or fibromyalgia), focal vertebral tenderness, and neurologic deficit. A detailed neurologic examination is indicated for all patients with neck pain, primarily to identify radicular causes or myelopathy. Patients with myelopathy have symptoms in all extremities, weakness, hyperreflexia, and a Babinski sign.
On examination, the anatomic source of pain should be sought. Nonradiating axial pain usually originates in facet joints or cervical disc disorders. Radicular pain denotes radiation to an extremity in a dermatomal distribution (see Dermatomal Map). Radicular pain may be inflammatory, traumatic, or degenerative in origin and manifests with weakness, loss of reflexes, and abnormal nerve conduction velocities. Focal axial pain should raise suspicion of neoplasia, mass, or infection.
Complications: Neurologic findings may result from cervical myelopathy, radiculopathy, or spinal cord trauma or transection after trauma (especially in patients with AS). Cervical myelopathy may be seen in patients with RA with C1-2 subluxation owing to destruction of the transverse ligament or erosion of the odontoid. Subaxial subluxation (usually at C4-5, C5-6) may result from apophyseal joint damage at these levels. Myelopathy should be suggested by either upper extremity weakness, paresthesias, hyperactive reflexes, or the Lhermitte sign (the induction of paresthesias or electric sensations down the thoracic spine on cervical flexion). Patients with OA of the neck may form bony spurs or ligamentous hypertrophy that may cause impingement of the spinal cord or nerve root. If such lesions are central, they may result in spinal stenosis. More commonly, bony spurs near the neural foramina impinge on the exiting nerve root, resulting in radiculopathy. Depending on the severity, there may be demonstrable impairment of neurologic function.
Diagnostic Testing: There are no specific diagnostic tests. HLA-B27 may be helpful in young adults who manifest features of spondyloarthropathy.
Imaging: Routine radiographs are not routinely recommended but may be indicated for patients with trauma, chronic complaints, suspected malignancy, or infection or if neurologic deficit is found. C1 and C2 abnormalities are common in RA and lower cervical segments (C4-7) are often involved in OA. Scintigraphy, CT and MRI may provide the extent of disease and structures involved. MRI is indicated in the evaluation if neurologic impairments are suspected (e.g., cervical spinal stenosis). Nerve conduction studies are indicated if a radiculopathy or upper extremity neuropathy is suspected.
Therapy: Several modalities may be used. Education and physical therapy are important and often overlooked. Many patients respond to NSAIDs or simple analgesics. Because muscle spasm may be an important contributor to the pain, muscle relaxants are sometimes useful adjuncts. Some patients with cervical soft tissue injury report good pain relief with short-term use of a soft cervical collar and intermittent isometric exercise. Surgical interventions are seldom indicated and usually not effective. Surgical stabilization may be indicated for patients with severe C1-2 subluxation or with marked cephalad migration of the odontoid and a neurologic deficit.
Prognosis: Most neck pain is benign. However, patients with neurologic deficits tend to have greater morbidity. Because most neck pain is mechanical in nature, at least half will improve within 4 to 6 weeks with conservative measures. More than 70% will be asymptomatic within 3 months.
Adapted from: RheumaKnowledgy