Metabolic Response of Pediatric Traumatic Brain Injury

被引:15
作者
Prins, Mayumi L. [1 ,2 ]
Matsumoto, Joyce [3 ]
机构
[1] Univ Calif Los Angeles, Dept Neurosurg, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Brain Injury Res Ctr, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, Dept Pediat, Div Pediat Neurol, Los Angeles, CA 90095 USA
关键词
traumatic brain injury; pathophysiology; child; ISCHEMIA-REPERFUSION INJURY; CEREBRAL GLUCOSE-METABOLISM; KETONE-BODY UTILIZATION; CORTICAL IMPACT INJURY; CLOSED-HEAD INJURY; KETOGENIC DIET; RAT-BRAIN; DOCOSAHEXAENOIC ACID; COGNITIVE DEFICITS; TEMPORAL WINDOW;
D O I
10.1177/0883073814549244
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Traumatic brain injury (TBI) in the pediatric brain presents unique challenges as the complex cascades of metabolic and biochemical responses to TBI are further complicated ongoing maturational changes of the developing brain. TBIs of all severities have been shown to significantly alter metabolism and hormones which impair the ability of the brain to process glucose for cellular energy. Under these conditions, the brain's primary fuel (glucose) becomes a less favorable fuel and the ability of the younger brain to revert to ketone metabolism can an advantage. This review addresses the potential of alternative substrate metabolic intervention as a logical pediatric TBI neuroprotective strategy.
引用
收藏
页码:28 / 34
页数:7
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