• Yong Wook Kim, Ji-Cheol Shin, and Young-sil An.
• Department and Research Institute of Rehabilitation Medicine, Yonsei University College of Medicine, 250 Seongsanno, Seoul, Korea. ywkim1@yuhs.ac
• Clin Neuropharmacol. 2009 Nov 1;32(6):335-9.

ObjectivesTo evaluate the effects of methylphenidate on cerebral glucose metabolism in patients with impaired consciousness after acquired brain injury.MethodsFourteen patients with impaired consciousness after acquired brain injury were enrolled in our study. We evaluated the level of consciousness with the Glasgow Coma Scale upon initial evaluation and at the 6-week follow-up after methylphenidate medication (0.3 mg/kg per day, which was administered twice daily). Positron emission tomography was performed before and after 6 weeks of medication, and the effects of methylphenidate on cerebral glucose metabolism were analyzed using statistical parametric mapping.ResultsThe statistical parametric mapping analysis indicated that significant increases of the cerebral glucose metabolism after methylphenidate therapy, compared with the initial positron emission tomographic image, were most evident in the left precuneus, the right posterior cingulated and the right retrosplenial cortices, and the right inferior parietal cortex (P < 0.001). In addition, cerebral glucose metabolism was significantly increased in the right precuneus, the right superior and middle temporal gyri, and bilateral middle occipital gyri (P < 0.005). In the correlation analysis, improvement of the Glasgow Coma Scale scores after methylphenidate medication was significantly associated with increased cerebral glucose metabolism in the bilateral precuneus, the bilateral middle occipital gyri, and right middle frontal gyrus.ConclusionsOur findings suggest that the posteromedial parietal cortex, which is part of the neural network for consciousness, may be the relevant structure for the pharmacological response to methylphenidate treatment in patients with impaired consciousness after acquired brain injury.

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