Introduction

Chronic spinal cord injury (SCI) can lead to an insidious clinical decline in individuals even years after the initial injury and is accompanied by a slow and progressive cytoarchitectural destruction known as post-traumatic syringomyelia. At present, no pathological mechanisms satisfactorily explain the ongoing degeneration.

Results

Here, I document the first report of a progressive dilation of the central canal lumen cranial to the epicenter of injury in a rodent contusion model of chronic SCI, presumably due to distensile forces within the canal. This ascending pathology may represent a tertiary form of injury arising from disturbances in CSF flow near the epicenter of injury due to dural scarring. This slow and progressive pathology may be the histologic correlate of the ascending clinical decline seen in patients.

Progressive central canal dilation was also accompanied by an empirically predictable disruption in the surrounding ependymal region, a known stem cell niche capable of gliogenesis. Ependymal region cells play an important role in CSF homeostasis, cellular signaling and wound repair in the spinal cord. Therefore, the progressive disruption of the ependymal region by mechanical and cytotoxic means is presented a novel pathogenic step in spinal cord injury.

The clinical significance of these findings and some possible therapeutic interventions will be discussed.

Methods

Adult female Sprague-Dawley rats were anesthetized, laminectomized at T10 and received spinal cord contusion injuries with a force of 250 kilodynes using an Infinite Horizon Impactor. Animals were randomly distributed into 5 groups and killed 1 (n=4), 28 (n=4), 120 (n=4), 450 (n=5), or 540 (n=5) days after injury.  Morphometric and immunohistochemical studies were then performed.  

Conclusions

This study documents progressive ependymal region destruction as a novel step in the pathogenesis of chronic spinal cord injury and identifies the ependymal region as a novel therapeutic target, through cellular rescue or replacement. Moreover, these histologic findings share many features of chronic hydrocephalus suggesting that early monitoring and restoration of favorable CSF hydrodynamics in spinal cord injury may be necessary to prevent this ongoing destruction and provide an environment more hospitable for repair.

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Copyright 2004 Milan Radojicic MD.  All rights reserved.