Date Published: December 22, 2012
Publisher: Hindawi Publishing Corporation
Author(s): Chester K. Yarbrough, Rory K. J. Murphy, Wilson Z. Ray, Todd J. Stewart.
Cervical spondylotic myelopathy (CSM) refers to impaired function of the spinal cord caused by degenerative changes of the cervical spine resulting in spinal cord compression. It is the most common disorder in the United States causing dysfunction of the spinal cord. A literature review of the natural history of mild cervical myelopathy is undertaken. Clinical presentation and current concepts of pathophysiology are also discussed. While many patients with mild signs of CSM will stabilize or improve over time with conservative treatment, the clinical course of a specific individual patient cannot be predicted. Asymptomatic patients with cervical stenosis and abnormalities on electrophysiologic studies may be at higher risk for developing myelopathy.
Cervical spondylosis refers to osteoarthritic degeneration of the cervical spine. Brain et al. suggested symptomatology, whether radiculopathy or myelopathy, resulted from disc protrusion and associated soft tissue abnormalities [1, 2]. Although degeneration can occur secondary to various causes, years of motion and activity, commonly referred to as “wear and tear,” is the most common etiology. Several studies have shown in animal models and in humans that excessive motion and repetitive micro-trauma accelerates degenerative changes [3–9]. The accumulation of degenerative changes affects both canal diameter and sagittal mobility of the cervical spine . Additionally, a congenitally narrow spinal canal may predispose one to formation of CSM [11–14]. In current understanding, cervical spondylosis encompasses degenerative changes affecting the uncovertebral joints, facet joints, intervertebral discs, and the other soft tissue and bony components of the cervical spine. While it may affect only a single level, spondylosis has been shown to commonly begin at lower levels with subsequent progressive involvement of multiple spinal levels .
Several authors have described pathologic findings associated with CSM in cadaveric studies of patients with CSM [36–38]. Pathologic findings include atrophy, neuronal loss in gray matter, and demyelination in the surrounding white matter. Interestingly, these findings are similar to those found in patients with transient hypoperfusion. The magnitude of pathologic findings correlates with the length of myelopathy and directly relates to the degree of canal stenosis [36–38]. Several authors have found that imaging findings including diffusion tensor imaging and apparent diffusion coefficient maps also show white-matter tract changes at the corresponding levels of compression [39–41].
CSM may present with divergent clinical findings depending on the levels affected, involvement of the neural foramina, and long tract involvement. A variety of neurological signs and symptoms may be present, including sensory changes, reflex abnormalities, decreased dexterity, weakness, gait instability, bowel and bladder dysfunction, spasticity, presence of Hoffman’s and/or Babinski’s sign, axial neck pain, radiculopathy, and even acute spinal cord injury [42–44]. The variation in symptoms caused by involvement of the various cervical levels results in a large possibility of clinical presentations affecting almost any muscle of the body.
Cervical spondylotic myelopathy occurs in age-dependent fashion as degenerative changes occur in the cervical spinal cord. Presenting signs and symptoms are highly variable and may stabilize or improve over time with conservative management. Abnormal electrophysiology and presence of radiculopathy may portend an increased chance of progression from asymptomatic cervical spondylosis to myelopathy.