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Review
. 2016 Jan 18;7(1):20-9.
doi: 10.5312/wjo.v7.i1.20.

Mechanical and cellular processes driving cervical myelopathy

Roisin T Dolan  1 , Joseph S Butler  1 , John M O'Byrne  1 , Ashley R Poynton  1
Affiliations
Review

Mechanical and cellular processes driving cervical myelopathy

Roisin T Dolan et al. World J Orthop. .

Abstract

Cervical myelopathy is a well-described clinical syndrome that may evolve from a combination of etiological mechanisms. It is traditionally classified by cervical spinal cord and/or nerve root compression which varies in severity and number of levels involved. The vast array of clinical manifestations of cervical myelopathy cannot fully be explained by the simple concept that a narrowed spinal canal causes compression of the cord, local tissue ischemia, injury and neurological impairment. Despite advances in surgical technology and treatment innovations, there are limited neuro-protective treatments for cervical myelopathy, which reflects an incomplete understanding of the pathophysiological processes involved in this disease. The aim of this review is to provide a comprehensive overview of the key pathophysiological processes at play in the development of cervical myelopathy.

Keywords: Cervical myelopathy; Cervical spine; Neck pain.

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Figures

Figure 1
Figure 1
Degenerative changes that contribute to extrinsic compression of the spinal cord in cervical myelopathy. OPLL: Ossification of the posterior longitudinal ligament.
Figure 2
Figure 2
Determination of the anteroposterior compression ratio in patients with cervical myelopathy. AP = b/a × 100. Reprinted with permission. AP: Anteroposterior compression ratio.
Figure 3
Figure 3
Cellular mechanisms involved in cervical myelopathy. The hypoxia/ischemia cascade results from chronic progressive compression of the cervical spinal cord. This induces extracellular (TNF-α) and intracellular pro-apoptotic pathways (p-53, JNK), induces neuroinflammation and ultimately, neuronal and oligodendrocyte destruction. Additionally, compromise of the BSCB results from ischemia-induced endothelial cell loss. Increased BSCB permeability alters the cellularity of the spinal cord microenvironment and is thought to further potentiate neuroinflammation. These mechanisms contribute to the upper limb dysfunction, spasticity, and gait disturbances observed in human cervical spondylotic myelopathy. BSCB: Blood-spinal cord barrier; TNF-α: Tumor necrosis factor-α.
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