Published online Jan 18, 2016. doi: 10.5312/wjo.v7.i1.20
Peer-review started: December 29, 2014
First decision: February 10, 2015
Revised: October 12, 2015
Accepted: November 3, 2015
Article in press: November 4, 2015
Published online: January 18, 2016
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.
Core tip: The pathophysiology of cervical myelopathy involves a combination of mechanical static and dynamic factors, triggering a cascade of biomolecular changes to include ischemia, excitotoxicity, neuroinflammation and apoptosis. Development of targeted neuro-protective treatment strategies, specifically modulating these molecular pathways, may optimize neurological recovery following surgical decompression. The aim of this review is to provide an overview of the pathophysiological processes at play in the development of cervical myelopathy.