[Pathophysiology and treatment of spinal cord injury].

Abstract

Spinal cord injury can lead to devastating functional disability. Pathophysiological studies show that, very early after the initial trauma, secondary damage is caused by toxic phenomena involving excitatory amino acids (excitotoxicity). The use of specific antagonists can attenuate this secondary damage in murine models. However, the kinetics of this phenomenon must be precisely documented before launching clinical trials of multidrug therapy. Axonal regeneration, previously considered impossible within the mammalian central nervous system, depends on appropriate control of glial reactivity. This may be achieved through gene therapy (si RNA) targeting glial obstacles. Finally, the existence in the spinal cord of autonomous centers such as the locomotor CPG suggests that cell therapy-based approaches may also be effective.

• Authors: Alain Privat
• Journal: Bulletin de l'Academie nationale de medecine (Bull Acad Natl Med) Vol. 189 Issue 6 Pg. 1109-17; discussion 1117-8 (Jun 2005) ISSN: 0001-4079 [Print] Netherlands
• Vernacular Title: Physiopathologie du traumatisme médullaire et conséquences thérapeutiques.
• PMID: 16433437 (Publication Type: English Abstract, Journal Article, Review)

Chemical References

• Receptors, N-Methyl-D-Aspartate

Topics

• Animals
• Axons (physiology)
• Cell Death
• Humans
• Nerve Regeneration (physiology)
• Neurons (pathology)
• Receptors, N-Methyl-D-Aspartate (antagonists & inhibitors)
• Spinal Cord Injuries (physiopathology, therapy)