Neuropharmacological modulation of cognitive deficits after brain damage.
OBJECTIVE
This review discusses recent studies that have implications for potential neuropharmacological interventions which target cognitive deficits resulting from traumatic brain injury or stroke.


RESULTS
An important new study concerning the activity of N-methyl-D-aspartate (NMDA) receptors after brain injury reveals that previous influential hypotheses about an increase in glutamate triggering neuronal death may need to be revised. Furthermore, the study suggests that cognitive function may be best preserved by stimulation of NMDA receptors with agonists rather than by the use of antagonists, as previously believed. Investigations of animal models of stroke and traumatic brain injury have further demonstrated the possibility of intervening in the acute and sub-acute stages to protect specific brain systems, such as preservation of the cholinergic system (via cholinesterase inhibitors) and hippocampal neurons (via a D2 agonist). Clinical trials in humans indicate it is also possible to target these neurotransmitter systems to enhance cognitive performance in patients with chronic deficits. In particular, recent studies demonstrated that it is possible to ameliorate the effects of two common cognitive syndromes, visual neglect and aphasia.


CONCLUSIONS
Cognitive deficits are an extremely common consequence of either traumatic brain injury or stroke. Recent studies demonstrate the potential for using neuropharmacological intervention after acquired brain injury to prevent or ameliorate the effects of cognitive impairments. These treatments, however, are still in their preliminary stages and further research is required to identify the most effective compounds.
Parton
Andrew
A
Imperial College, Division of Neuroscience and Mental Health, Charing Cross Hospital, and Institute of Cognitive Neuroscience, University College London, London, UK. a.parton@imperial.ac.uk
Coulthard
Elizabeth
E
Husain
Masud
M
D000818:Animals; D001930:Brain Injuries / Q000150:complications; D003072:Cognition Disorders / Q000209:etiology / Q000517:prevention & control*; D018690:Excitatory Amino Acid Agonists / Q000627:therapeutic use*; D006801:Humans; D009480:Neuropharmacology / Q000379:methods*; D018377:Neurotransmitter Agents / Q000378:metabolism; D017448:Receptors, Dopamine D2 / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology
D018690:Excitatory Amino Acid Agonists; D018377:Neurotransmitter Agents; D017448:Receptors, Dopamine D2; D016194:Receptors, N-Methyl-D-Aspartate