Neck pain affects approximately 10% of the American population. It is one of the most common neuromusculoskeletal conditions seen by health care practitioners. Sources of neck pain include conditions that compress, destroy, or irritate pain-sensitive tissues such as the annulus fibrosis, posterior longitudinal ligament, and the zygapophyseal joint capsule. Cervical nerve root involvement usually results in pain and neurological findings along the distribution of the nerve. Referred pain can occur from visceral involvement and may also be confused with primary shoulder conditions and peripheral nerve entrapment.1
Common conditions associated with neck pain are degenerative disc disease, disc herniations, and degenerative joint disease of the zygapophyseal joints. The exact cause of neck pain in an individual can be unclear. This is due to the fact that approximately 50% of the population has degenerative joint disease. These are often incidental findings that are observed in patients following whiplash injuries and in repetitive occupational injuries.2 A history of whiplash injury is a significant contributor in the development of chronic neck pain.3 The chronic pain associated with cervical sprain/strain are most likely to effect the facet joints, the intervertebral disc, and the upper cervical ligaments. C2-3 is most commonly associated with occipital headaches and C5-6 is most often associated with cervical, axial, and referred arm pain.
Cervical facet joint involvement can be responsible for a significant portion of chronic neck pain. The pain associated with facets overlap both myofascial and discogenic patterns.4 Neuro-anatomic studies reveal that the facet joint is richly innervated and contains both free and encapsulated nerve endings. The facet capsule is richly innervated with C-fiber and A-delta fibers. Many of these nerves are at a high threshold and likely to generate pain. Local pressure and capsular stretch can mechanically activate these nerves.
These neurons can also be sensitized or excited by naturally occurring inflammatory agents, including substance P and phospholipase A. Physiological changes in the spinal cord, particularly the complexes of the dorsal horn, implicate excitatory amino acids such as substance P, glutamate, gamma-aminobutyric acid (GABA), and N-methyl-D-aspartate (NMDA).5
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