Effects of the dopaminergenic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: A study using positron emission tomography (PET)
Amantadine; Dopamine; Executive function; Frontal lobes; Positron emission tomography; Traumatic brain injury
Primary objective: This study was performed to assess effects of amantadine (AMH), a dopaminergic agent and NMDA antagonist, on chronic traumatic brain injury (TBI). The primary hypotheses were that amantadine treatment would result in executive function improvement and increased activity in pre-frontal cortex. Research design: An open-label design was used. Methods: Twenty-two subjects underwent neuropsychological testing pre- and post-12 week treatment. Six subjects also underwent PET scanning. Intervention: Amantadine 400 mg was administered per day. Results: Significant improvements on tests of executive function were observed with treatment. Analysis of PET data demonstrated a significant increase in left pre-frontal cortex glucose metabolism. There was a significant positive correlation between executive domain scores and left pre-frontal glucose metabolism. Conclusions: This is the first known study to assess amantadine in chronic TBI using PET and the data are consistent with the hypotheses. The conduction of further studies is warranted. © 2005 Taylor & Francis Group Ltd.
Kraus, M., Smith, G., Butters, M., Donnell, A., Dixon, E., Yilong, C., & Marion, D. (2005). Effects of the dopaminergenic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: A study using positron emission tomography (PET). Brain Injury, 19 (7). http://dx.doi.org/10.1080/02699050400025059