Dolan RT, Butler JS, O’Byrne JM, Poynton AR. Mechanical and cellular processes driving cervical myelopathy. World J Orthop 2016; 7(1): 20-29 [PMID: 26807352 DOI: 10.5312/wjo.v7.i1.20]
Corresponding Author of This Article
Dr. Roisin T Dolan, MA, MD, MRCSI, Department of Trauma and Orthopaedic Surgery, Waterford Regional Hospital, Dunmore Rd., X91 ER8E Waterford, Ireland. roshdolan@hotmail.com
Research Domain of This Article
Orthopedics
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Orthop. Jan 18, 2016; 7(1): 20-29 Published online Jan 18, 2016. doi: 10.5312/wjo.v7.i1.20
Mechanical and cellular processes driving cervical myelopathy
Roisin T Dolan, Joseph S Butler, John M O’Byrne, Ashley R Poynton
Roisin T Dolan, Department of Trauma and Orthopaedic Surgery, Waterford Regional Hospital, X91 ER8E Waterford, Ireland
Joseph S Butler, National Spinal Injuries Unit, Department of Trauma and Orthopaedic Surgery, Mater Misericordiae University Hospital, D07 AX57 Dublin, Ireland
John M O’Byrne, Department of Trauma and Orthopaedic Surgery, Royal College of Surgeons in Ireland, Cappagh National Orthopaedic Hospital, D11 K316 Dublin, Ireland
Ashley R Poynton, Department of Trauma and Orthopaedic Surgery, Mater Private Hospital, D07 WKW8 Dublin, Ireland
Author contributions: All authors had significant contributions to the conception and design of the review article; Dolan RT and Butler JS contributed to drafting the article; O’Byrne JM and Poynton AR were responsible for revising it critically for important intellectual content.
Conflict-of-interest statement: The authors declare no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Roisin T Dolan, MA, MD, MRCSI, Department of Trauma and Orthopaedic Surgery, Waterford Regional Hospital, Dunmore Rd., X91 ER8E Waterford, Ireland. roshdolan@hotmail.com
Telephone: +353-51-858000 Fax: +353-51-858001
Received: December 26, 2014 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
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.
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.
