What is the pathophysiology of central cord syndrome (CCS)?

Updated: May 21, 2020
  • Author: Michelle J Alpert, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
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Answer

Central cord syndrome (CCS) most often occurs after a hyperextension injury in an individual with long-standing cervical spondylosis. (See also the Medscape Reference article Cervical Spondylosis.) Injury may result from posterior pinching of the cord by a buckled ligamentum flavum or from anterior compression of the cord by osteophytes. [14] Historically, spinal cord damage was believed to originate from concussion or contusion of the cord with stasis of axoplasmic flow, causing edematous injury rather than destructive hematomyelia. Autopsy studies subsequently demonstrated that CCS may be caused by bleeding into the central part of the cord, portending a less favorable prognosis. Studies have also shown that CCS probably is associated with axonal disruption in the lateral columns at the level of the injury to the spinal cord, with relative preservation of the grey matter.

The syndrome also may be associated with fracture dislocation and compression fracture, especially in a congenitally narrowed spinal canal. [10] These anteroposterior compressive forces also distribute the greatest damaging effect on the central mass of the cord substance.

CCS-related motor impairment results from the pattern of lamination of the corticospinal and spinothalamic tracts in the spinal cord. Sacral segments are the most lateral, with lumbar, thoracic, and cervical components arranged somatotopically, proceeding medially toward the central canal.


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