Persistent cognitive dysfunction after traumatic brain injury: A dopamine hypothesis.
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.
Bales
James W
JW
Brain Trauma Research Center, University of Pittsburgh, PA 15260, USA.
Wagner
Amy K
AK
Kline
Anthony E
AE
Dixon
C Edward
CE
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D001930:Brain Injuries / Q000188:drug therapy / Q000503:physiopathology*; D003071:Cognition / Q000502:physiology; D003072:Cognition Disorders / Q000188:drug therapy / Q000503:physiopathology*; D004298:Dopamine / Q000378:metabolism*; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000009:adverse effects / Q000494:pharmacology; D006801:Humans; D008959:Models, Neurological
D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D004298:Dopamine