Premium
The Unique Histopathological Responses of the Injured Spinal Cord: Implications for Neuroprotective Therapy
Author(s) -
GUTH LLOYD,
ZHANG ZIYIN,
STEWARD OSWALD
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb08017.x
Subject(s) - wallerian degeneration , neuroprotection , spinal cord , medicine , necrosis , spinal cord injury , granulation tissue , wound healing , inflammation , lesion , degeneration (medical) , pathology , pharmacology , surgery , immunology , psychiatry
Tissue destruction at the primary site of a spinal cord injury leads to persistent necrosis that progressively enlarges the lesion. Steroids attenuate this necrotizing process and promote tissue repair even though such anti‐inflammatory drugs interfere with wound healing in non‐CNS organs. To address this paradox, the spinal cord of rats and mice was crushed extradurally and the effects of the following anti‐inflammatory agents studied by light microscopical image analysis: allopurinol, aminoguanidine, indomethacin, a bacterial lipopolysaccharide, naproxen, and pregnenolone. The contribution of Wallerian degeneration to progressive necrosis was studied in a mutant mouse strain ( Wld S ) that is characterized by delayed Wallerian degeneration. In rats, the anti‐inflammatory agents selectively attenuated progressive necrosis and encouraged wound healing. In mice, considerable tissue repair occurred without pharmacological intervention; this wound‐healing process was delayed in the mutant Wld S strain. Since spinal cord injury results in concomitant tissue necrosis and wound healing, a goal of neuroprotective therapy is to regulate the dynamic balance between these destructive and reparative processes.