机构：[1]Department of Neurosurgery, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, USA[2]Department of Neurology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, USA[3]Department of Molecular and Medical Pharmacology, and UCLA-DOE Center for Molecular Medicine, David Geffen School of Medicine, University of California at Los Angeles,Los Angeles, California, USA[4]Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China神经外科首都医科大学宣武医院
Chronic brain atrophy after traumatic brain injury (TBI) is a well-known phenomenon, the causes of which are unknown. Early nonischemic reduction in oxidative metabolism is regionally associated with chronic brain atrophy after TBI. A total of 32 patients with moderate-to-severe TBI prospectively underwent positron emission tomography (PET) and volumetric magnetic resonance imaging (MRI) within the first week and at 6 months after injury. Regional lobar assessments comprised oxidative metabolism and glucose metabolism. Acute MRI showed a preponderance of hemorrhagic lesions with few irreversible ischemic lesions. Global and regional chronic brain atrophy occurred in all patients by 6 months, with the temporal and frontal lobes exhibiting the most atrophy compared with the occipital lobe. Global and regional reduction in cerebral metabolic rate of oxygen (CMRO2), cerebral blood flow (CBF), oxygen extraction fraction (OEF), and cerebral metabolic rate of glucose were observed. The extent of metabolic dysfunction was correlated with the total hemorrhage burden on initial MRI (r = 0.62, P = 0.01). The extent of regional brain atrophy correlated best with CMRO2 and CBF. Lobar values of OEF were not in the ischemic range and did not correlate with chronic brain atrophy. Chronic brain atrophy is regionally specific and associated with regional reductions in oxidative brain metabolism in the absence of irreversible ischemia. Journal of Cerebral Blood Flow & Metabolism (2010) 30, 883-894; doi:10.1038/jcbfm.2009.263; published online 23 December 2009
基金：
Grant nos NS049471, NS02089, and the California State Neurotrauma Initiative.
第一作者机构：[4]Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China
通讯作者：
通讯机构：[*]Departments of Neurosurgery and Neurology, David Geffen School of Medicine at UCLA, Ronald Reagan UCLA Medical Center, 757 Westwood Blvd, Room RR 6236A, Los Angeles, CA 90095, USA.
推荐引用方式(GB/T 7714)：
Yueqiao Xu,David L McArthur,Jeffry R Alger,et al.Early nonischemic oxidative metabolic dysfunction leads to chronic brain atrophy in traumatic brain injury[J].JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM.2010,30(4):883-894.doi:10.1038/jcbfm.2009.263.
APA：
Yueqiao Xu,David L McArthur,Jeffry R Alger,Maria Etchepare,David A Hovda...&Paul M Vespa.(2010).Early nonischemic oxidative metabolic dysfunction leads to chronic brain atrophy in traumatic brain injury.JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM,30,(4)
MLA：
Yueqiao Xu,et al."Early nonischemic oxidative metabolic dysfunction leads to chronic brain atrophy in traumatic brain injury".JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM 30..4(2010):883-894
医学