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November 1992

Alcohol Exacerbates Behavioral and Neurochemical Effects of Rat Spinal Cord Trauma

Author Affiliations

From the Departments of Neurology (Mr Halt and Dr Faden) and Pharmacology, Georgetown University School of Medicine, Washington, DC (Dr Faden); and Veteran's Administration Medical Center, San Francisco, Calif (Dr Swanson).

Arch Neurol. 1992;49(11):1178-1184. doi:10.1001/archneur.1992.00530350096025

• Acute alcohol intoxication may exacerbate the consequences of central nervous system trauma, although the mechanism is uncertain. Effects of acute ethanol administration on behavioral and neurochemical changes were examined in rats after traumatic spinal cord injury. Survival rates were reduced and posttraumatic neurologic function worsened in ethanol-treated as compared with salinetreated controls. Ethanol-treated rats had significantly lower tissue levels of excitatory amino acids and higher levels of free fatty acids, thromboxane, and lactic acid than did controls. Tissue magnesium concentration was significantly reduced by trauma and recovered more slowly in ethanoltreated rats. Enhanced phospholipid hydrolysis with free fatty acid and thromboxane accumulation, increased release of excitatory amino acids, and decreased tissue magnesium levels may each serve to worsen secondary tissue damage and diminish neurologic recovery after spinal cord injury associated with acute alcohol intoxication.

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