Abstract
Introduction: Higher brain dysfunction is the major problem of patients who recover from neurotrauma the prevents them from returning to their previous social life. Many such patients do not have focal brain damage detected with morphological imaging. We focused on studying the focal brain dysfunction that can be detected only with functional imaging with positron emission tomography (PET) in relation to the score of various cognition batteries. Methods: Patients who complain of higher brain dysfunction without apparent morphological cortical damage were recruited for this study. Thirteen patients with diffuse axonal injury (DAI) or cerebral concussion was included. They underwent a PET study to image: 1) glucose metabolism by ^<18>F-FDG, and 2) central benodiazepine receptor (cBZD-R) (marker of neuronal body) by ^<11>C-flumazenil, together with cognition measurement by WAIS-R, WMS-R, and WCST etc. PET data were compared with age matched normal controls using SPM2. Results: 1) DAI patients had a significant decrease in glucose matabolism and cBZD-R distribution in the cingulated cortex than normal controls. 2) Patients diagnosed with concussion because of shorter consciousness disturbance also had abnormal FDG uptake and cBZD-R distribution. 3) Cognition test scores were variable among patients. Degree of decreased glucose metabolism and cBZD-R distribution in the dominant hemishphere corresponded well to the severity of cognitive disturbance. Conclusions: PET molecular imaging was useful to depict focal cortical dysfunction of neurotrauma patients even when morphological change was not apparent. This method may be promising to clarify the pathophysiology of higher brain dysfunction of patients with diffuse axonal injury or chronic traumatic encephalopathy.
