Recent Advances in Pathophysiology of Traumatic Brain Injury

被引:326
作者
Kaur, Parmeet [1 ]
Sharma, Saurabh [1 ]
机构
[1] ISF Coll Pharm, Dept Pharmacol, Moga 142001, Punjab, India
关键词
Traumatic brain injury; secondary injury; primary brain injury; oxidative stress; excitotoxicity; inflammation; SEVERE HEAD-INJURY; CEREBRAL-BLOOD-FLOW; OXIDATIVE STRESS; CEREBROSPINAL-FLUID; MITOCHONDRIAL DYSFUNCTION; CNS INJURY; POSTTRAUMATIC HYDROCEPHALUS; INTRACRANIAL HYPERTENSION; GLUTAMATE EXCITOTOXICITY; PERMEABILITY TRANSITION;
D O I
10.2174/1570159X15666170613083606
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background: Traumatic brain injury (TBI) constitutes the primary reason for mortality and morbidity in persons worldwide below 45 years of age. 1.7 million Traumatic events occur yearly in the United States alone, considering for 50,000 deaths. In severe traumatic brain injury sufferers, a considerable achievement attained in treating short-term consequences; but till date, huge failures are occurring in researcher's capability to render severe traumatic brain injury sufferers to an elevated degree of performing. Methods: Initial damage force results in Primary brain injury, causing tissue destruction and distortion in the early post-injury period. These secondary injuries from TBI cause changes in cell performance and dissemination of trauma via activities like free-radical generation, depolarization, and formation of edema, excitotoxicity, and disruption of blood brain barrier, calcium homeostasis, and intracranial hematoma. The expectation for developing effect in TBI sufferers is the best knowledge of these activities and enhancement of remedies that restrict secondary brain damage. Results: The focal point of this study is on knowing the complex outburst of secondary impairments and studying the pathophysiology of TBI which provides alternative treatment benefits. Conclusion: While injured persons demonstrate dissimilar levels of harm and every case is novel with specific recovery profiles, this article strengthens the recent pathophysiological sight of TBI mainly attention on oxidative stress, excitotoxicity, cerebral oxygenation and cerebral blood flow (CBF), development of edema, and inflammatory activities. For initial research acknowledgment of these recurring factors could permit clarification of possible beneficial targets.
引用
收藏
页码:1224 / 1238
页数:15
相关论文
共 146 条
[1]   Traumatic Brain Injury Pathophysiology and Treatments: Early, Intermediate, and Late Phases Post-Injury [J].
Algattas, Hanna ;
Huang, Jason H. .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2014, 15 (01) :309-341
[2]   GLUTAMATE-INDUCED NEURONAL DEATH - A SUCCESSION OF NECROSIS OR APOPTOSIS DEPENDING ON MITOCHONDRIAL-FUNCTION [J].
ANKARCRONA, M ;
DYPBUKT, JM ;
BONFOCO, E ;
ZHIVOTOVSKY, B ;
ORRENIUS, S ;
LIPTON, SA ;
NICOTERA, P .
NEURON, 1995, 15 (04) :961-973
[3]  
[Anonymous], 1990, CAN DIS WKLY REP
[4]   Differential activation of ERK, p38, and JNK MAPK by nociceptin/orphanin FQ in the potentiation of prostaglandin cerebrovasoconstriction after brain injury [J].
Armstead, WA .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2006, 529 (1-3) :129-135
[5]  
Baethmann A, 1998, Curr Opin Anaesthesiol, V11, P193, DOI 10.1097/00001503-199804000-00013
[6]   Enhanced oxidative stress in iNOS-deficient mice after traumatic brain injury: support for a neuroprotective role of iNOS [J].
Bayir, H ;
Kagan, VE ;
Borisenko, GG ;
Tyurina, YY ;
Janesko, KL ;
Vagni, VA ;
Billar, TR ;
Williams, DL ;
Kochanek, PM .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2005, 25 (06) :673-684
[7]   Cerebral hyperglycolysis following severe traumatic brain injury in humans: A positron emission tomography study [J].
Bergsneider, M ;
Hovda, DA ;
Shalmon, E ;
Kelly, DF ;
Vespa, PM ;
Martin, NA ;
Phelps, ME ;
McArthur, DL ;
Caron, MJ ;
Kraus, JF ;
Becker, DP .
JOURNAL OF NEUROSURGERY, 1997, 86 (02) :241-251
[8]   Dissociation of cerebral glucose metabolism and level of consciousness during the period of metabolic depression following human traumatic brain injury [J].
Bergsneider, M ;
Hovda, DA ;
Lee, SM ;
Kelly, DF ;
McArthur, DL ;
Vespa, PM ;
Lee, JH ;
Huang, SC ;
Martin, NA ;
Phelps, ME ;
Becker, DP .
JOURNAL OF NEUROTRAUMA, 2000, 17 (05) :389-401
[9]  
Betz A., 1992, BRAIN EDEMA BLOOD BR
[10]   BRAIN LACTATE DURING PARTIAL GLOBAL-ISCHEMIA AND REPERFUSION - EFFECT OF PRETREATMENT WITH DICHLOROACETATE IN A RAT MODEL [J].
BIROS, MH ;
DIMLICH, RVW .
AMERICAN JOURNAL OF EMERGENCY MEDICINE, 1987, 5 (04) :271-277