Persistent cognitive dysfunction after traumatic brain injury: A dopamine hypothesis

Neurosci Biobehav Rev. 2009 Jul;33(7):981-1003. doi: 10.1016/j.neubiorev.2009.03.011. Epub 2009 Apr 1.

Abstract

Traumatic brain injury (TBI) represents a significant cause of death and disability in industrialized countries. Of particular importance to patients the chronic effect that TBI has on cognitive function. Therapeutic strategies have been difficult to evaluate because of the complexity of injuries and variety of patient presentations within a TBI population. However, pharmacotherapies targeting dopamine (DA) have consistently shown benefits in attention, behavioral outcome, executive function, and memory. Still it remains unclear what aspect of TBI pathology is targeted by DA therapies and what time-course of treatment is most beneficial for patient outcomes. Fortunately, ongoing research in animal models has begun to elucidate the pathophysiology of DA alterations after TBI. The purpose of this review is to discuss clinical and experimental research examining DAergic therapies after TBI, which will in turn elucidate the importance of DA for cognitive function/dysfunction after TBI as well as highlight the areas that require further study.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain / drug effects
  • Brain / physiopathology
  • Brain Injuries / drug therapy
  • Brain Injuries / physiopathology*
  • Cognition / physiology
  • Cognition Disorders / drug therapy
  • Cognition Disorders / physiopathology*
  • Dopamine / metabolism*
  • Dopamine Agonists / pharmacology
  • Dopamine Antagonists / adverse effects
  • Dopamine Antagonists / pharmacology
  • Humans
  • Models, Neurological*

Substances

  • Dopamine Agonists
  • Dopamine Antagonists
  • Dopamine