Opportunities for neuroprotection in traumatic brain injury.
Traumatic injury of the brain in man is normally followed by little or no recovery of function by the lesioned tissue. Neuroprotective strategies employed in the acute period after traumatic CNS injury attempt to use pharmacological tools to reduce the progressive secondary injury processes that follow after the initial lesion occurs to limit overall tissue damage. Results from experimental animal studies using a variety of drugs that modulate neurotransmitter function, scavenge free radicals, or interfere with cell death cascades point toward many new opportunities for pharmacological intervention in the acute and subacute period after traumatic brain injury.
Verma
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Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA.
D000208:Acute Disease; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D001930:Brain Injuries / Q000503:physiopathology / Q000628:therapy*; D016923:Cell Death / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects; D016166:Free Radical Scavengers / Q000627:therapeutic use; D006801:Humans; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D018377:Neurotransmitter Agents / Q000037:antagonists & inhibitors / Q000502:physiology; D020127:Recovery of Function / Q000502:physiology; D013119:Spinal Cord Injuries / Q000503:physiopathology / Q000628:therapy
D016166:Free Radical Scavengers; D018696:Neuroprotective Agents; D018377:Neurotransmitter Agents