Cervical Spondylosis is often referred to as the arthritis of the neck, which includes general wear and tear that affects the cervical spine. “Cervical” refers to the seven stacked vertebral bones in the neck region. “Spondylosis” is when parts of the spine begin to wear out which is often age-related. The condition is also commonly known as “osteoarthritis” of the neck.
Cervical spondylosis (CS) is a natural consequence of aging and often appears when people are in their 30s. By 60, nine out of ten people are expected to show degenerative changes in the cervical spine. (https://my.clevelandclinic.org/health/diseases/17685-cervical-spondylosis)
What is the etiology of CS?
The primary risk factor and contributor to the incidence of CS is age-related degeneration of the intervertebral disc and cervical spine elements. Degenerative changes in surrounding structures including the uncovertebral joints, facet joints, posterior longitudinal ligaments (PLL) and ligamentum flavum all combine towards narrowing of the spinal canal and intervertebral foramina. Consequently, the spinal cord, spinal vasculature and nerve roots can be compressed resulting in the 3 clinical syndromes of cervical spondylosis: axial neck pain, cervical myelopathy and cervical radiculopathy.
Factors that can contribute to an accelerated disease process and early-onset cervical spondylosis include exposure to significant spinal trauma, a congenitally narrow vertebral canal, dystonic cerebral palsy affecting cervical spine musculature manual labor and specific high impact athletic activities like rugby or horse-back riding. (https://www.ncbi.nlm.nih.gov/books/NBK551557/)
What is the pathophysiology of CS?
The pathogenesis of cervical spondylosis involves a degenerative cascade that produces biomechanical changes in the cervical spine, manifesting as secondary compression of neural and vascular structures. An increase in the keratin-chondroitin ratio prompts changes to the proteoglycan matrix resulting in loss of water, protein, and mucopolysaccharides within the intervertebral disc. Desiccation of the disc causes the nucleus pulposus to lose its elasticity as it shrinks and becomes more fibrous. As the nucleus pulposus loses its ability to maintain weight-bearing loads effectively, it begins to herniate through the fibres of the annulus fibrosus and contributes to the loss of disc height, ligamentous laxity, and buckling, and compression of the cervical spine. With further disc desiccation, the annular fibres become more mechanically compromised under compressive loads, producing significant alterations in the load distribution along the cervical spine. The result is a reversal of the normal cervical lordosis. Progression of the kyphosis causes the annular and Sharpey’s fibres to peel off from the vertebral body edges, resulting in reactive bone formation. These bone spurs or osteophytes can form along the ventral or dorsal margins of the cervical spine, which can then project into the spinal canal and intervertebral foramina. Furthermore, disruption in the load balance along the spinal column generates greater axial loads onto the uncovertebral and facet joints which triggers hypertrophy or enlargement of the joints and accelerates bony spur formation into the surrounding neural foramen. These degenerative changes lead to loss of cervical lordosis and movement, as well as a reduction in the spinal canal diameter. (https://www.ncbi.nlm.nih.gov/books/NBK551557/)
What are the symptoms of CS?
How is CS diagnosed?
If there is radiating pain down the upper limb with head extension and ipsilateral head rotation to the affected side, then it’s considered a positive Spurling`s test for cervical radiculopathy. In some cases, manual neck distraction might alleviate radicular pain.
The key parameters are osteophyte formation, intervertebral disc height narrowing and vertebral end-plate sclerosis.
How will imaging help?
How is CS treated?
Choice of treatment depends on severity of patient`s symptoms. In the absence of red flags and significant myelopathy, the goals of treatment are to relieve pain, improve functional mobility and participation id daily activities. Non-operative management includes:
Few studies have shown symptom reduction with use of trigger point injection over myofascial trigger points. A systematic review done in 2019 show patient having significant pain relief following epidural steroid injection. Long-term pain relief was also seen in a systematic review done in 2015 to study effects of radiofrequency lesioning, medial branch block and facet joint injection in CS cases.