2017
DOI: 10.1016/j.pmr.2016.12.001
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Pathophysiology of Traumatic Brain Injury

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Cited by 187 publications
(126 citation statements)
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References 79 publications
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“…For iNOS, which is an inflammatory product similar to eNOS, significant differences were observed between trauma group (131 ± 18) and the OC-treated groups (p<0.001) and also between the trauma group and the group treated with 30 mg continued apoptosis (6). To date, many agents have been used to prevent secondary injury after TBI.…”
Section: Histopathological Findingsmentioning
confidence: 99%
“…For iNOS, which is an inflammatory product similar to eNOS, significant differences were observed between trauma group (131 ± 18) and the OC-treated groups (p<0.001) and also between the trauma group and the group treated with 30 mg continued apoptosis (6). To date, many agents have been used to prevent secondary injury after TBI.…”
Section: Histopathological Findingsmentioning
confidence: 99%
“…More than half of the severe TBI survivors are severely disabled within one year after injury, and some patients have devastating neurological disorders, including cognitive or memory impairment, and motor, sensory or emotional function obstacles [2]. In addition, for some patients with mild repetitive TBI, such as athletes in contact sports may develop chronic traumatic encephalopathy in later life [3]. The pathophysiological mechanism of TBI has two aspects, the primary injury caused by direct mechanical force and the secondary injury of neurons.…”
Section: Introductionmentioning
confidence: 99%
“…The mechanical force of the impact directly impairs the axon and a part of a neuron. The mechanism involved in secondary injury is more complicated [3][4][5]. It includes delayed cell death (such as the newly discovered ferroptosis [6]), brain edema, metabolic defects [7], and blood-brain barrier damage caused by biochemical and physiological changes after trauma [8].…”
Section: Introductionmentioning
confidence: 99%
“…Penetration to the brain can tear axons and damage neuron conduction, and vascular damage could lead to blood and leukocyte migration into the normally immune-privileged brain [11]. Primary brain injuries include contusions, intracranial hematomas, diffuse axonal injuries, direct cellular damage, loss of electrochemical function, and blood-brain-barrier (BBB) dysfunction.…”
Section: Primary Brain Injuriesmentioning
confidence: 99%