Traumatic brain injury: Mechanisms, manifestations, and visual sequelae

被引:20
|
作者
Rauchman, Steve H. [1 ]
Zubair, Aarij [2 ]
Jacob, Benna [2 ]
Rauchman, Danielle [3 ]
Pinkhasov, Aaron [2 ]
Placantonakis, Dimitris G. [4 ]
Reiss, Allison B. [2 ]
机构
[1] Fresno Inst Neurosci, Fresno, CA USA
[2] NYU, Long Island Sch Med, Mineola, NY 11501 USA
[3] Univ Calif Santa Barbara, Dept Neurosci, Santa Barbara, CA USA
[4] NYU, Grossman Sch Med, New York, NY USA
关键词
traumatic brain injury; light sensitivity; contrast sensitivity; neuroinflammation; visual acuity; headache; oxidative stress; CELL-DEATH MECHANISMS; PSYCHOGENIC NONEPILEPTIC SEIZURES; FIELD LOSS INCREASES; OXIDATIVE STRESS; OLDER-ADULTS; MENTAL FATIGUE; RISK-FACTORS; HEAD TRAUMA; HIPPOCAMPAL NEUROGENESIS; POSTTRAUMATIC EPILEPSY;
D O I
10.3389/fnins.2023.1090672
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Traumatic brain injury (TBI) results when external physical forces impact the head with sufficient intensity to cause damage to the brain. TBI can be mild, moderate, or severe and may have long-term consequences including visual difficulties, cognitive deficits, headache, pain, sleep disturbances, and post-traumatic epilepsy. Disruption of the normal functioning of the brain leads to a cascade of effects with molecular and anatomical changes, persistent neuronal hyperexcitation, neuroinflammation, and neuronal loss. Destructive processes that occur at the cellular and molecular level lead to inflammation, oxidative stress, calcium dysregulation, and apoptosis. Vascular damage, ischemia and loss of blood brain barrier integrity contribute to destruction of brain tissue. This review focuses on the cellular damage incited during TBI and the frequently life-altering lasting effects of this destruction on vision, cognition, balance, and sleep. The wide range of visual complaints associated with TBI are addressed and repair processes where there is potential for intervention and neuronal preservation are highlighted.
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页数:18
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