• Takayuki Kato, Noriyuki Nakayama, Yuto Yasokawa, Ayumi Okumura, Jun Shinoda, and Toru Iwama.
• Chubu Medical Center for Prolonged Traumatic Brain Dysfunction, Kizawa Memorial Hospital, Minokamo City, Gifu, Japan. nou-taka@a.email.ne.jp
• J. Neurotrauma. 2007 Jun 1;24(6):919-26.

AbstractThe aim of this study was to explore the regional cerebral glucose metabolism (rCM) in patients with chronic stage traumatic brain injury (TBI) compared with normal controls. We also investigated the relationship between regional cerebral glucose metabolism and cognitive function. We performed 2-[(18)F]fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) study using statistical parametric mapping (SPM) analysis in 36 diffuse axonal injury (DAI) patients (mean age +/- SD, 36.3 +/- 9.8 years). At 6 months or more after head injury, all patients underwent FDG-PET study and neuropsychological batteries to assess cognitive function. Thirty healthy, gender-matched control subjects who were comparable in age were also studied. Between the TBI patients and normal controls, group comparisons showed regional metabolic decreases in the bilateral frontal lobes, temporal lobes, thalamus, as well as the right cerebellum in the TBI group. Only full-scale Intelligence Quotient (IQ) (mean +/- SD, 78.5 +/- 11.9) correlated positively with rCM in the right cingulate gyrus and the bilateral medial frontal gyrus. In other examinations, the correlation was not provided. DAI may induce functional disconnection and decreased neuronal activity, and finally lead to diffuse glucose hypometabolism. Low full-scale IQ scores may be related to significantly different underlying cognitive impairment. In supporting cognitive function following TBI, which showed diffuse cerebral metabolic reduction compared with normal controls, medial prefrontal cortex and anterior cingulate cortex may be an important component.

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