Neck Pain in Adults _________________________________________________________________________
Cervical Strain/Sprain Cervical strain is injury to the muscle-tendon unit, while cervical sprain is injury to ligamentous structures. Cervical strain/sprain injuries involve flexion, extension, or rotation, with or without axial loading. Acute neck pain frequently involves injury to cervical muscle-tendon or ligamentous structures, which can expand into a range of secondary effects [47]. For instance, edema, hemorrhage, and inflammation can follow elongation and tearing of muscles or ligaments in cervical strain/sprain. Many cervical muscles do not terminate in tendons, but attach to the periosteum (membrane covering a bone surface). Muscles respond to injury by contracting, and recruit surrounding muscles to “splint” the injured muscle. This reflexive tightening (spasm) of paraspinal muscles can cause excruciating pain [56]. Chronic pain following cervical strains usually originates from facet joints, disks, or ligaments [41]. Cervical Myofascial Pain Cervical myofascial pain also relates to overuse, injury, or trauma and originates from cervical muscles and their surrounding fascia that support the shoulders and neck [57]. Cervical myofascial pain may result as a secondary muscle tissue response to disk or facet-joint injury [41]. Myofascial pain is common in the general population, with 21% of patients in general orthopedic clinics and 85% to 93% of patients in specialty pain management centers having a myofascial pain component. Cervical myofascial pain incidence is disproportionately high in women and peaks in midlife and declines after middle age [57]. Trigger points—the hallmark feature of myofascial pain—are hyperirritable areas in palpable, taut bands of skeletal muscle fiber that elicit local or referred pain. Rapid palpation may elicit a local twitch response, a brisk contraction of muscle fibers around the taut band. Active trigger points generate spontaneous or movement-provoked pain; latent trigger points produce pain when compressed [57]. In cervical myofascial pain, other muscles in the functional unit compensate, promoting a more widespread, chronic problem. Chronicity and disability are strongly linked to pain duration. Recurrence decreases with early treatment initiation to prevent muscle compensation patterns. Migraine and muscle contraction headache frequently co-occur, and TMD can be myofascial in origin [57]. Cervical Disk Disorders Disk disorders can develop acutely from neck injury or trauma, or through chronic degenerative processes. The C6–C7 disk is the most frequent herniation site [51]. More common cervical disk disorders include herniated nucleus pulposus, degenerative disk disease, and internal disk disruption.
Cervical spine nerve roots exit through small vertebral ports called the foraminal space, above their same-numbered vertebral body; the first cervical spine nerve exits above C1, and the eighth between C7 and T1 [46; 48]. The longitudinal ligaments keep the seven vertebrae and atlanto-occipital joint behaving as a single unit. The ligamentum flavum connects annular fibers (laminae) of adjacent vertebrae and helps the vertebral column resume upright posture after flexion [46]. Nociceptors are sensory receptors of primary neurons in cervical spinal tissue. Nociceptors respond to harmful pressure, temperature, or biomechanical stress (noxious stimuli) by transmitting signals (nociception) to the spinal cord and brain. CERVICAL SPINE PATHOPHYSIOLOGY Neck pain can develop from chronic overuse or strain, injury, trauma, or degenerative processes involving bony, articular (disks, facets), nerve (root, spinal cord), or soft (ligament, tendon, muscle) tissues of the cervical spine. In this section, pathologic processes are described that can result in neck pain, starting with acute-onset conditions followed by chronic, degenerative conditions. Facet-Mediated Pain Facet joints and capsules are richly innervated by nociceptors sensitive to local stretch or compression. These neurons are activated by abnormal loading or excessive biomechanical stress from whiplash injury or fracture, and sensitized by inflammation and locally released inflammatory promoters (e.g., substance P, phospholipase A). Facet joint pain can develop from degenerative disk or facet joint changes; inflammatory cytokines are found at high levels in facet joint tissue when a degenerative disorder is present. Facet joints are covered by hyaline cartilage and enclosed by synovial capsules, features of other joints that make facet joints vulnerable to osteoarthritis (facet joint arthropathy) [50; 52]. Facet joint pain accounts for 36% to 55% of neck pain and 60% of whiplash pain [50]. The C5–C6 facet joint is the most common origin of cervical, axial, and referred arm pain. Facet joints/capsules largely underlie chronic neck pain, and referred facet pain overlaps with myofascial and diskogenic pain patterns [41]. Cervicogenic Headache Cervicogenic headache is defined as a unilateral, non- throbbing, non-lancinating head pain caused by referred cervical spine pain. Approximately 70% of cervicogenic headaches originate from the C2–C3 facet joint [53; 54; 55]. The lifetime prevalence of cervicogenic headache is as high as 4.1% in the general population, 17.5% in patients with severe headaches, and 53% in patients with post-whiplash headache [53]. Cervicogenic headache occurs at rates four times higher in women, and the average patient age is 43 years. Migraines often have a cervical pain component and can co-occur with cervicogenic headache [53].
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