Neuropathology of human spinal cord injury : the basis for new treatments

Research output: Contribution to journalArticle

Abstract

The changes which take place in the human spinal cord after injury are dynamic and continuous. At first there is oedema swelling and haemorrhage within the mechanically disrupted tissues followed by liquefaction and necrosis. Cytokines associated with the inflammatory reaction cause aggravation of the damage with spreading necrosis. Macrophages remove debris, leading in a few weeks to a glial lined cavity into which nerve root regenerations will grow after some months Wallerian degeneration with extensive loss of axons becomes visible after about a year in the descending and ascending long tracts. Treatment in the initial stages is directed to reducing oedema demyelination and secondary damage by administration of methyl prednisolone, 4-amino pyridine, and the neutralization of harmful cytokines. The lesion is different in every patient and there is a variable amount of white matter preservation across the level of the injury in most. This residual white matter is exploited by the restorative neurologist to optimize the outcome. Regeneration of long tracts is necessary to restore function in the established case. This depends upon axonal regrowth, which may be induced by trophic factors and/or inhibition of 'No-Go' using antibodies. Regenerated long axons need to reach their correct destination nuclei and function normally. This will require re-education toward which the property of CNS plasticity may be utilized to restore normal physiology. This is a mammoth undertaking and currently beyond reasonable expectations as shown by recent reports of stem cell therapy in humans. However, replacing the central grey matter and the re-establishment of a polysynaptic pathway akin to the propriospinal system by stem cells may be more likely to succeed.
Original languageEnglish
Pages (from-to)11-21
JournalAmerican journal of neuroprotection and neuroregeneration
Volume1
Issue number1
Publication statusPublished - 2009

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