Degenerative Cervical Myelopathy: Development and Natural History [AO Spine RECODE-DCM Research Priority Number 2]

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Authors

NOURI Aria TESSITORE Enrico MOLLIQAJ Granit MELING Torstein SCHALLER Karl NAKASHIMA Hiroaki YUKAWA Yasutsugu BEDNAŘÍK Josef MARTIN Allan R VAJKOCZY Peter CHENG Joseph S KWON Brian K KURPAD Shekar N FEHLINGS Michael G HARROP James S AARABI Bizhan RAHIMI-MOVAGHAR Vafa GUEST James D DAVIES Benjamin M KOTTER Mark R N WILSON Jefferson R

Year of publication 2022
Type Article in Periodical
Magazine / Source GLOBAL SPINE JOURNAL
MU Faculty or unit

Faculty of Medicine

Citation
Web https://journals.sagepub.com/doi/10.1177/21925682211036071
Doi http://dx.doi.org/10.1177/21925682211036071
Keywords cervical spondylotic myelopathy (CSM); cord compression; ossification of the posterior longitudinal ligament (OPLL); progression; risk factors
Description Study Design: Narrative review. Objectives: To discuss the current understanding of the natural history of degenerative cervical myelopathy (DCM). Methods: Literature review summarizing current evidence pertaining to the natural history and risk factors of DCM. Results: DCM is a common condition in which progressive arthritic disease of the cervical spine leads to spinal cord compression resulting in a constellation of neurological symptoms, in particular upper extremity dysfunction and gait impairment. Anatomical factors including cord-canal mismatch, congenitally fused vertebrae and genetic factors may increase individuals' risk for DCM development. Non-myelopathic spinal cord compression (NMSCC) is a common phenomenon with a prevalence of 24.2% in the healthy population, and 35.3% among individuals >60 years of age. Clinical radiculopathy and/or electrophysiological signs of cervical cord dysfunction appear to be risk factors for myelopathy development. Radiological progression of incidental Ossification of the Posterior Longitudinal Ligament (OPLL) is estimated at 18.3% over 81-months and development of myelopathy ranges between 0-61.5% (follow-up ranging from 40 to 124 months between studies) among studies. In patients with symptomatic DCM undergoing non-operative treatment, 20-62% will experience neurological deterioration within 3-6 years. Conclusion: Current estimates surrounding the natural history of DCM, particularly those individuals with mild or minimal impairment, lack precision. Clear predictors of clinical deterioration for those treated with non-operative care are yet to be identified. Future studies are needed on this topic to help improve treatment counseling and clinical prognostication.
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