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  • Updated 10.16.2023
  • Released 09.21.1998
  • Expires For CME 10.16.2026

Cervical spondylotic myelopathy

Introduction

Overview

Cervical spondylotic myelopathy is a progressive noninflammatory disease process occurring in middle-aged and elderly patients, predominantly affecting the intervertebral discs and facets joints. Narrowing of the spinal canal by osteophytic spurring produces myelopathy by compression of the spinal cord and radiculopathy by compression of the nerve roots. In this updated article, the author presents proper diagnostic criteria, presentation, differential diagnoses, pathophysiology, and treatment options, including the latest imaging criteria and a review of anterior and posterior surgical approaches.

Key points

• Cervical spondylotic myelopathy is an arthritic condition affecting the cervical facet joints and discs producing bony ridging in the central canal and neural foramina, resulting in compressive signs and symptoms of spinal cord and nerve root compression.

• Presenting features may involve a mix of upper and lower motor neuron dysfunction in the arms and hands, and upper motor neuron dysfunction in the legs.

• The diagnosis is established by combining clinical findings with the imaging characteristics of bony narrowing of the central and lateral aspects of the cervical spinal canal, as seen on MRI and CT.

• Treatment is directed at controlling arthritic axial neck pain, and surgical decompression with or without fusion is considered if signs and symptoms of myelopathy are present.

Historical note and terminology

Cervical spondylosis, often referred to as “hard cervical disc disease,” is a process involving a combination of degenerative changes in the intervertebral disc, the facet joints, and the ligamentum flavum. Cervical spondylotic myelopathy is the most serious consequence of this degenerative process, especially when associated with a congenitally narrow cervical vertebral canal (57). As Benzel has shown, spondylosis is a natural process of aging, is seen in 10% of individuals by the age of 25 years and in 95% by the age of 65 years, and is often preceded by mild segmental instability (16; 98). Dehydration of the disc leads to hardening and calcification with loss of disc resilience; ligamentous laxity provides a compensatory range of motion to the spine; the facet joints tend to enlarge to better share the stress loads, as the ligamentum flavum thickens in an attempt to stabilize the spine (34). The combination of these degenerative changes causing narrowing of the cervical spinal canal (spondylosis) and spinal cord injury (myelopathy) gives rise to the term “cervical spondylotic myelopathy.” It is technically not an arthritis, as degeneration of the intervertebral disc does not primarily involve the synovial membrane. Although the pathological existence of intervertebral disc herniation was realized as early as 1929 by Schmorl and Andrae (26), its clinical correlation with well-described syndromes of compressive myelopathy was not thoroughly reviewed until 1956, when only posterior decompressive surgeries were employed (26). Direct surgical attack on the anterior compressive disc-spur complex was not developed until the late 1950s with the work of Smith and Robinson (99) and Cloward (27). Cervical disc disease with progression to bony ridging and calcification of the posterior longitudinal ligament may occur anywhere in the cervical spine and over several levels, but most commonly is seen at C4-5, C5-6, and C6-7. Because it is a disease process, there is often a combination of stages of degeneration in the individual patient, such that one level may be predominantly a “soft disc” rupture and compression, whereas a more chronically degenerative level may exhibit “hard disc” compression. Either may be centrally located, causing spinal cord compression (myelopathy), laterally protruding into a narrowed foramen causing root compression (radiculopathy), or anterolateral with a mixed clinical picture of myeloradiculopathy.

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