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MRS Detects Metabolic Dysfunction after Brain Injury

MRS 检测脑损伤后代谢功能障碍

基本信息

批准号：
7555356
负责人：
Paul M Vespa
金额：
$ 32.67万
依托单位：
UNIVERSITY OF CALIFORNIA LOS ANGELES
依托单位国家：
美国
项目类别：
财政年份：
2006
资助国家：
美国
起止时间：
2006-01-10 至 2010-12-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7555356
关键词：
Acute Anatomy Area Atrophic Benign Brain Brain Injuries Brain Part Brain region Cell Death Cell Respiration Cells Cerebrum Clinical Cognitive Coma Contusions Critical Care Decision Making Diagnostic Due Process Energy Supply Ethics Functional disorder Future Human Image Impairment Individual Injury Knowledge Lead Magnetic Resonance Imaging Magnetic Resonance Spectroscopy Measurement Measures Metabolic Metabolism Methods Microdialysis Mitochondria Monitor N-acetylaspartate Neurologic Outcome Outcome Measure Oxygen Patients Positron-Emission Tomography Production Pyruvate Pyruvates Research Personnel Risk Site Spatial Distribution Surrogate Markers Synaptic Transmission Technology Therapeutic Intervention Tissues Trauma Traumatic Brain Injury base brain metabolism brain tissue brain volume cerebral atrophy clinical care cognitive function design follow-up frontal lobe meetings metabolic abnormality assessment neurochemistry predictive modeling programs standard of care

项目摘要

The main aim of this proposal is to determine if mitochondria! dysfunction as reflected by low rates of oxidative metabolism is predictive of eventual brain volume loss after traumatic brain injury (TBI). TBI is a condition of widespread brain dysfunction in which secondary cell death and brain atrophy occur in normal appearing tissue despite a relatively confined area of primary anatomical damage. The mechanism of delayed brain atrophy is not clear but may be related to early and persistent impaired oxidative metabolism that is endemic after TBI. Reduced oxidative metabolism (CMRO2) is a result of impaired mitochondrial function and has been measured in TBI by positron emission tomography (PET). Our preliminary studies indicate that 1) CMRO2 is reduced in normal appearing brain regions as well as adjacent to contusions, 2) reduction in CMRO2 in normal regions can be monitored by cerebral microdialysis lactate/pyruvate values, 3) delayed atrophy is related to the duration of abnormal lactate/pyruvate values, and 4) delayed atrophy is related to neurologic/cognitive outcome. Hence, a persistent deficit in energy supply may be related to eventual cell loss and poor outcome. TBI provides a unique opportunity to study human brain tissue with invasive cerebral microdialysis monitoring and PET imaging, thus enabling independent measurements of mitochondrial function in space (PET) and acrosstime (microdialysis). The proposed studies will 1) Determine the magnitude and spatial distribution of impaired oxidative metabolism after TBI using PET and microdialysis, 2) Determine if brain regions of reduced oxidative metabolism are destined for brain atrophy on follow-up MR),3) Determine if acute impaired oxidative metabolism corresponds to poor clinical outcome, 4) Evaluate the validity of magnetic resonance spectroscopy N-Acetyl-Aspartate as a non-invasive surrogate marker of oxidative metabolism. The fourth aim is intended to be exploratory but could lead to widespread application of MRS in clinical care for TBI patients in centers lacking oxygen PET technology. This study can only be done within the context of traumatic brain injury, in which invasive monitoring methods are standard of care. The knowledge from the proposed studies will have widespread application to critical care of neurotrauma patients.

这项提议的主要目的是确定线粒体！功能障碍反映在低比率的