PET Molecular Imaging to Investigate Higher Brain Dysfunction in Patients with Neurotrauma
Introduction: Many neurotrauma patients suffer from higher brain dysfunction even when focal brain damage is not detected with MRI. We performed functional imaging with positron emission tomography (PET) to clarify the relationship between the functional
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Abstract Introduction: Many neurotrauma patients suffer from higher brain dysfunction even when focal brain damage is not detected with MRI. We performed functional imaging with positron emission tomography (PET) to clarify the relationship between the functional deficit and symptoms of such patients. Methods: Patients who complain of higher brain dysfunction without apparent morphological cortical damage were recruited. Thirteen patients underwent PET study to image glucose metabolism by 18F-FDG, and central benzodiazepine receptor (cBZD-R) by 11C-flumazenil, together with measurement of cognition. Results: Diffuse axonal injury (DAI) patients have a significant decrease in glucose metabolism and cBZD-R distribution in the cingulated cortex than normal controls. Score of cognition test was variable among patients. The degree of decreased glucose metabolism and cBZD-R in the dominant hemisphere corresponded well to the severity of cognitive disturbance. Patients with a milder type of diffuse brain injury (i.e., cerebral concussion) also showed abnormal glucose metabolism and cBZD-R distribution when they suffered from cognitive deficit. Conclusion: PET molecular imaging was useful for depicting the cortical dysfunction of neurotrauma patients T. Nariai (*), M. Inaji, Y. Tanaka, and K. Ohno Department of Neurosurgery, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan e-mail: [email protected] M. Hiura Faculty of Sports and Health Science, Hosei University, Tokyo, Japan C. Hosoda Department of Cortical Function Disorders, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan K. Ishii Positron Medical Center, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo, Japan
even when morphological change was not apparent. This method may be promising in clarifying the pathophysiology of higher brain dysfunction of patients with neurotrauma, but without morphological abnormality. Keywords Diffuse brain injury • Cerebral concussion • PET • FDG • Flumazenil • Brain cognition
Introduction Higher brain dysfunction is a major problem for patients who have recovered from neurotrauma as it prevents them from returning to their previous social life. Many patients with diffuse brain injury such as diffuse axonal injury, cerebral concussion, and chronic traumatic encephalopathy (CTE) [1, 2] do not have their focal brain damage detected with morphological imaging. In such cases, the lack of concrete evidence to connect symptoms and focal brain lesions often causes medical and social problems. Positron emission tomography (PET) is a powerful tool for depicting the abnormal pathology of the brain using various molecular probes. In the clinical study of cognitive disorders such as Alzheimer’s disease, functional or pathological changes are known to be detected in the early stages when there is no brain atrophy and the cognitive deficit is only mild [3, 4]. We considered that the use of PET molecular imaging is also useful in depicting the cognitive deficit of patients with diffuse brain injury, eve
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