ABSTRACT
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.
