Olga N Kokiko1, Robert J Hamm. 1. Department of Psychology, Virginia Commonwealth University, Richmond, Virginia, USA.
Abstract
PRIMARY OBJECTIVE: We provide a review of recent chronic and delayed rehabilitative pharmacological treatments examined in experimental models of traumatic brain injury. There is a specific emphasis on studies aiming to enhance cognitive recovery. MAIN OUTCOMES AND RESULTS: Decreased neuronal activity is believed to contribute to persistent cognitive disabilities. Neurotransmitter based rehabilitative treatments that increase neuronal activity may assist in the recovery of cognitive function. However, timing and dosage of drug treatment are influential in cognitive enhancement. Drug treatments that affect single and multiple neurotransmitter systems have the ability to significantly influence recovery of function following brain injury. CONCLUSIONS: Understanding the relationship between neural disturbances and functional deficits following brain injury is challenging. Cognitive impairment may be the result of a single event or multiple events that occur after the initial insult. Increasing neuronal activity during the chronic phase of injury seems to be an effective treatment strategy for facilitating cognitive recovery. Pharmacological agents do not necessarily display the same effects in an injured brain as in a non-injured brain. Thus, further research is needed to establish the effectiveness of rehabilitative drug treatments.
PRIMARY OBJECTIVE: We provide a review of recent chronic and delayed rehabilitative pharmacological treatments examined in experimental models of traumatic brain injury. There is a specific emphasis on studies aiming to enhance cognitive recovery. MAIN OUTCOMES AND RESULTS: Decreased neuronal activity is believed to contribute to persistent cognitive disabilities. Neurotransmitter based rehabilitative treatments that increase neuronal activity may assist in the recovery of cognitive function. However, timing and dosage of drug treatment are influential in cognitive enhancement. Drug treatments that affect single and multiple neurotransmitter systems have the ability to significantly influence recovery of function following brain injury. CONCLUSIONS: Understanding the relationship between neural disturbances and functional deficits following brain injury is challenging. Cognitive impairment may be the result of a single event or multiple events that occur after the initial insult. Increasing neuronal activity during the chronic phase of injury seems to be an effective treatment strategy for facilitating cognitive recovery. Pharmacological agents do not necessarily display the same effects in an injured brain as in a non-injured brain. Thus, further research is needed to establish the effectiveness of rehabilitative drug treatments.
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