Cervical Myelopathy

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Search Strategy

Databases Searched: Pubmed, Web of Knowledge, PEDro
Keywords: Cervical myelopathy, Physical Therapy, Treatment, Management, Cervical Stenosis, CSM, Differential diagnosis

Definition/Description

Cervical myelopathy is the result of spinal cord compression in the cervical spine. Any space occupying lesion within the cervical spine with the potential to compress the spinal cord can result in this degenerative disease of the spinal cord. [3,11] Cervical compression in myelopathy is predominantly due to pressure on the anterior spinal cord with ischaemia and to deformation of the cord by anterior herniated discs, spondylitic spurs or an ossified posterior longitudinal ligament. [20] Human histological studies revealed degeneration of the anterior horns, cavity formation, and demyelination in the severely compressed spinal cord. The spontaneous course of myelopathy is characterized either by long periods of stable disability followed by episodes of deterioration or a linear progressive course. The presentation of a cervical myelopathy varies in accordance to the severity of the spinal cord compression, and it's location. [1]

Clinically Relevant Anatomy

There are seven cervical vertebrae and eight cervical nerve roots. [5,11] The spinal cord is the extension of the central nervous system outside the cranium. It is encased by the vertebral column and begins at the foramen magnum. [2] The spinal cord is an extremely vital part of the central nervous system, and even a small injury to it can lead to severe disability. [4]
A complex system of ligaments serves to stabilize and protect the cervical spine. For example, the ligamentum flavum that extends from the anterior surface of the cephalic vertebra to the posterior surface of the caudal vertebra and connects to the ventral aspect of the facet joint capsules. A ligament that is also often involved in this condition is the posterior longitudinal ligament. It is situated within the vertebral canal, and extends along the posterior surfaces of the bodies of the vertebræ, from the body of the axis, where it is continuous with the membrana tectoria, to the sacrum. [4]

Epidemiology /Etiology

Cervical spondylotic myelopathy is the most common disorder of the spinal cord in persons older than 55 years of age. [5,7,9] Radiologic spondylotic changes increase with patient age; 90% of asymptomatic persons older than 70 years have some form of degenerative change in the cervical spine. Both sexes are affected equally. Cervical spondylosis usually starts earlier in men (50 years) than in women (60 years). It causes hospitalization at a rate of 4.04 per 100,000 person-years. [5,10]

Zhang et al. divided the cause of cervical myelopathy into different categories [12]:
• Static factors: A narrowing of the spinal canal size can result from disc degeneration, spondylosis, stenosis, osteophyte formation at the level of facet joints, segmental ossification of the posterior longitudinal ligament and yellow ligament hypertrophy, calcification or ossification. Patients with a congenitally narrow spinal canal (<13mm) have a higher risk for the development of symptomatic cervical myelopathy. [1,10,15]
• Dynamic factors: due to mechanical abnormalities of the cervical spine or instability.[1]
• Vascular and cellular factors: Spinal cord ischemia affects oligodendrocytes, which results in demyelination exhibiting features of chronic degenerative disorders. Also glutamatergic toxicity, cell injury and apoptosis may occur.[1]

Characteristics/Clinical Presentation

Cervical myelopathy can cause a variety of signs and symptoms. Spinal cord symptoms caused by cervical spondylosis are divided into two groups: long-tract and segmental symptoms. Early symptoms of this condition are ‘numb, clumsy, painful hands’ and disturbance of fine motor skills [1]. As spinal cord degeneration progresses, lower motor neuron findings in the upper extremities, such as loss of strength, atrophy of the interosseous muscles and difficulty in fine finger movements, may present. Additional clinical findings may include: neck stiffness (decreased ROM, especially extension), shoulder pain, paresthesia in one or both arms or hands, signs of radiculopathy, Babinski and Hoffman's sign, ataxia and dexterity loss. [5,6,21] Typical neurological signs of long-tract involvement are exaggerated tendon reflexes (knee and ankle), presence of pathological reflexes, spastic quadriplegia, sensory loss and bladder-bowel disturbance. [15]
Once the disorder is diagnosed, complete remission to normality never occurs, and spontaneous remission to normal normality is uncommon. In 75% of the patients, episodic worsening with neurological deterioration occured, 20% had slow steady progression, whereas 5% had rapid onset progression. [1]

Differential Diagnosis

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Examination

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