Human Spinal Cord Retains Substantial Structural Mass in Chronic Stages After Injury
- 1 June 1999
- journal article
- research article
- Published by Mary Ann Liebert Inc in Journal of Neurotrauma
- Vol. 16 (6), 523-531
- https://doi.org/10.1089/neu.1999.16.523
Abstract
In chronic stages of human spinal cord injury, atrophy of the cord has been reported in regions both at and distant to the injury site. Local cord atrophy results from the direct effects of bony impact and ischemia, whereas distant atrophy results from anterograde (Wallerian) and retrograde axonal degeneration. However, the actual extent of degenerative changes in the chronically injured human spinal cord both at and remote from the injury site has rarely been reported, and has not been rigorously quantified to date. In the present study, we quantified the extent of spinal cord atrophy in 12 humans with chronic injury (2–34 years posttrauma) utilizing quantitative stereological assessment of spinal cord magnetic resonance images, and compared the results to uninjured human spinal cords. Focal cystic atrophy of the cord, characterized by signal attenuation on T1-weighted images, was regularly present at the actual site of impact injury and replaced a mean longitudinal area equaling less than one spinal cord segment in length (2.01 ± 0.60 cm2, or a loss of 89.3 ± 17.4% of the longitudinal area of one spinal cord segment). Spinal cord segments immediately rostral to the zone of cystic degeneration showed atrophy of only 19.4 ± 7.5 % of normal cord longitudinal area, and spinal cord segments immediately caudal to the zone of cystic degeneration showed atrophy of 16.5 ± 4.1% of normal cord longitudinal area. Extensive spinal cord atrophy extending beyond the region of injury occurred in two of twelve cases (16.7%), and both were caused by late syrinx formation. Thus, spinal cord atrophy after trauma remains primarily restricted to the original site of injury. Experimental neural repair strategies should take into account the importance of "bridging" relatively short zones of cystic atrophy, then promoting axonal regeneration through potentially long segments of remaining cord parenchyma.Keywords
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