Changes in cerebral glucose metabolism in patients with posttraumatic cognitive impairment after memantine therapy: a preliminary study

Objective To investigate the changes in cerebral glucose metabolism in patients with posttraumatic cognitive impairment after memantine therapy. Methods We performed serial F-18 fluorodeoxyglucose positron emission tomography studies before and after memantine therapy (20 mg per day) on 17 patients with posttraumatic cognitive impairment using statistical parametric mapping analysis. In addition, covariance analysis was performed to identify regions, where changes in regional cerebral glucose metabolism correlated significantly with increased Mini-Mental Status Examination scores. Results Statistical parametric mapping analysis demonstrated that, compared with baseline, significantly increased cerebral glucose metabolism occurred in both inferior, middle and superior frontal gyri, both angular gyri, both precuneus, the right middle cingulum, the left inferior parietal lobule, the left fusiform gyrus, the left precentral gyrus, the left paracentral lobule, and the left lingual gyrus after memantine therapy (P-uncorrected < 0.005). In contrast, cerebral glucose metabolism was significantly decreased in both cerebellum, the left thalamus, the left olfactory, the right middle temporal gyrus, the right amygdala, and the right insula (P-uncorrected < 0.005). In the correlation analysis, improvements in Mini-Mental Status Examination scores after memantine therapy were significantly associated with increased cerebral glucose metabolism in the inferior and middle frontal gyri and the inferior parietal lobule of the left hemisphere (P-corrected < 0.0001). Conclusions Our findings indicate that the prefrontal and the parietal association cortices may be the relevant structures for the pharmacological response to memantine therapy in patients with posttraumatic cognitive impairment.