====== Cervical Degenerative Disc Disease Pathophysiology ====== [[Pathogenesis]] of [[Cervical Degenerative Disc Disease]] is controversial. Theories include the following alone or in combination: 1. Direct cord compression between osteophitic bars and hypertrophy or infolding of the ligamentum flavum, especially if superimposed on congenital narrowing of cervical subluxations 2. Ischemia due to compression of vascular structures ((TAYLOR AR. VASCULAR FACTORS IN THE MYELOPATHY ASSOCIATED WITH CERVICAL SPONDYLOSIS. Neurology. 1964 Jan;14:62-8. PubMed PMID: 14112448. )) arterial deprivation ((Bohlman HH, Emery SE. The pathophysiology of cervical spondylosis and myelopathy. Spine (Phila Pa 1976). 1988 Jul;13(7):843-6. Review. PubMed PMID: 3057649.)) and/or venous stasis ((Kim RC, Nelson JS, Parisi JE, Schochet SSJ, In : Spinal cord pathology. Principles and Practice of Neuropathology. St. Louis: Mosby, 1993:398-435.)). 3. Repeated local cord trauma by normal movements in the presence of disc protusion and/or osteophytic bars (cord and root injuries ((Jeffreys RV. The surgical treatment of cervical myelopathy due to spondylosis and disc degeneration. J Neurol Neurosurg Psychiatry. 1986 Apr;49(4):353-61. PubMed PMID: 3701345; PubMed Central PMCID: PMC1028758. )) ). a. cephalad/caudal movement with flexion extension ((Adams CB, Logue V. Studies in cervical spondylotic myelopathy. I. Movement of the cervical roots, dura and cord, and their relation to the course of the extrathecal roots. Brain. 1971;94(3):557-68. PubMed PMID: 5111717. )). b. anterior/posterior traction on the cord by dentate ligaments ((Levine DN. Pathogenesis of cervical spondylotic myelopathy. J Neurol Neurosurg Psychiatry. 1997 Apr;62(4):334-40. PubMed PMID: 9120444; PubMed Central PMCID: PMC1074087. )) and nerve roots c. diameter of spinal canal varies during flexion and extension Increased stenosis is more common in extension. Unstable segments may sublux (so-called pincer mechanism) ((Benzel EC. Biomechanics of Spine Stabilization. Rolling Meadows, IL: American Association of Neurological Surgeons Publications; 2001.)). Histologicallly ((Ogino H, Tada K, Okada K, Yonenobu K, Yamamoto T, Ono K, Namiki H. Canal diameter, anteroposterior compression ratio, and spondylotic myelopathy of the cervical spine. Spine (Phila Pa 1976). 1983 Jan-Feb;8(1):1-15. PubMed PMID: 6867846. )) there is a degeneration of the central gray matter at the level of compression, degeneration of the posterior columns above the lesion (particularly in the anteromedial portion), and demyelination in the lateral columns (especially the corticospinal tracts) below the lesion. Anterior spinal tracts are relatively spared. There may be atrophic changes in the ventral and dorsal roots and neurophagia of anterior horn cells.