Pathophysiology of Cervical Spondylosis, Radiculopathy, and Myelopathy

Cervical Spondylosis

Cervical spondylosis encompasses a spectrum of degenerative conditions affecting the cervical spine and is a characteristic process of aging. Radiographically, it is observed in approximately 10% of people by age 25 years, increasing to nearly 95% of people by age 65 years. ^, Multiple authors near the end of the 19th century initially described it as an inflammatory process and potentially infectious in origin, and therefore referred to it as cervical spondylitis. It was not until 1952 that Brain identified this condition as a degenerative process of aging and coined the now commonly used term cervical spondylosis. Cervical spondylosis can result in axial neck pain caused by degenerative disc disease, as well as facet arthrosis. Additionally, cervical spondylosis can result in neural symptoms of cervical radiculopathy or cervical myelopathy. The pathophysiology of spondylosis, radiculopathy, and myelopathy is critical for clinical practitioners to appreciate, and aids in the understanding of clinical manifestations, as well as treatment options for these conditions.

Pathology

Degeneration associated with spondylosis begins at the intervertebral disc, unlike degenerative arthritis, which is associated with inflammation of the synovial lining of joints. The nucleus pulposus consists of proteoglycan aggregates composed of hydrophilic hyaluronic chains with side chains containing chondroitin sulfate and keratin sulfate. Repeated mechanical stresses and aging of the nucleus pulposus lead to multiple pathological changes. ^, Histologically, there is loss of hydrophilic mucopolysaccharides, resulting in desiccation along with an increase in keratin sulfate, leading to disc shrinkage, loss of elasticity, kyphotic alignment, and transfer of compressive loading forces peripherally onto the annulus and posteriorly onto the facet joints. As surrounding structures undergo increasing mechanical stresses, they develop reactive changes, such as uncovertebral bone spurs, posterior annulus disc–osteophyte complexes, and facet hypertrophy, which can additionally lead to spinal cord and/or nerve root compression. End plates, uncovertebral joints, and facet joints form osteophytes as a biomechanical mechanism to increase the weightbearing surface area in an attempt to increase stability. The ligamentum flavum and posterior longitudinal ligament (PLL) can additionally undergo hypertrophy; however, the compressive aspects of the ligamentum flavum and annulus may be primarily caused by buckling secondary to disc height loss.

Cervical Spondylosis and Axial Neck Pain

Axial neck pain is a common presenting chief complaint seen by the general practitioner. Contributing anatomic sources of neck pain are multiple and include neck musculature, tendons, ligaments, facet joints, intervertebral discs, and cervical vasculature. The most common cause of nondegenerative isolated neck pain is cervical strain—as frequently seen with whiplash injury—resulting from injury to neck muscles, tendons, and ligaments. Referred pain, or sclerotomal pain, from the cervical spine often presents with shoulder and temporomandibular joint pathology. The anatomic source of isolated neck pain in patients with cervical spondylosis vary. The intervertebral disc is an important and common source of axial pain. ^, The intervertebral disc is innervated ventrally by branches from the sympathetic plexus and dorsally by the sinuvertebral nerve, which arises from the ventral nerve root. ^{, ,} The sinuvertebral nerve also innervates the PLL, dura, and a substantial portion of the vertebral body periosteum. ^, Tears in the annulus may stimulate the sinuvertebral nerve, and injection of local anesthetic in the disc space can temporarily relieve pain in some patients. ^, The facet joints are another potential source of axial pain. ^, Cervical facet joints are innervated by branches arising from the dorsal ramus. Stimulation of subaxial facet joints generates reproducible neck pain patterns in normal volunteers. However, facet steroid injections and percutaneous radiofrequency neurotomy have demonstrated variable results. ^,

Acute neck pain may be related to inflammation or muscle injury, and warrant a trial of nonsteroidal antiinflammatory drugs (NSAIDs) and short-term muscle relaxants if needed. A temporary soft neck collar can provide comfort as well. Isolated axial pain that fails to respond to initial conservative therapy can be further evaluated with cervical radiographs. Cervical spondylotic changes on radiograph are ubiquitous in the aging population and include loss of disc height, osteophyte formation, kyphosis, and subluxation. ^, However, although multiple studies have demonstrated good results in operative management of axial pain, surgical management for axial neck pain is controversial. ^, Radiculopathy can have a significant component of scapular and trapezial pain, but is commonly associated with upper extremity radicular pain and/or neurological symptoms. However, C3‒C4 radiculopathy is a source of unilateral axial pain without upper extremity pain or neurological findings that may be associated with a positive Spurling sign. C3‒C4 radiculopathy that causes axial pain may respond well to nerve root injections or surgical decompression. Additionally, pseudarthrosis from previously attempted fusion can also lead to significant axial pain with or without recurrent radiculopathy and may benefit from revision stabilization and fusion procedures. Chronic neck pain, however, can be managed with NSAIDs and physical therapy exercises to strengthen the cervical musculature, and opioid therapy should be avoided. Surgery for chronic neck pain without commonly accepted indications, such as radiculopathy, myelopathy, pseudarthrosis, and unstable traumatic injuries, should be avoided. Additionally, patients undergoing surgery with chronic neck pain should be counseled of the likely possibility of continued neck pain postoperatively and that the relief of chronic neck pain with fusion is unreliable.