Japanese Journal of Neurosurgery
Online ISSN : 2187-3100
Print ISSN : 0917-950X
ISSN-L : 0917-950X
Higher Brain Dysfunction due to Traumatic Brain Injury through Traffic Accident
Hideaki MASUZAWAKimiyoshi HIRAKAWAHiroki TOMITANorio NAKAMURA
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JOURNAL OPEN ACCESS

2004 Volume 13 Issue 2 Pages 104-110

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Abstract
Neuropsychological, emotional, cognitive and vocational sequelae are prominent complications after traumatic brain injury caused by traffic accident. They are comprised of cognitive impairment such as memory disturbance, impairment of multi-task execution and loss of self-awarenes, and personality changes such as easy irritability, violent behavior and childishness. These symptoms and signs have frequently been ascribed to focal brain injury, such as in the fronto-temporal lobes. However, they are probably the product of diffuse brain injury and should be attributed to diffuse loss of white matter or neural network in the brain. This dysfunction tends to be underdiagnosed or even overlooked in medical practice, because, though the cognitive part can be assessed neuropsychologically, the emotional or personality part, which has greater influence on the social outcome, often passes unnoticed by the professionals. Rather it is sensed intuitively by the family or persons who live or work close together with the victim. Close examination of the serial neuroimaging films usually disclosed either normal-appearing brain or small hemorrhage in the early days. The ventricles become dilated within a few months post-injury. This ventriculomegaly stays permanent and is highly indicative of loss of brain tissue or white matter neural network. The severity of this dysfunction is significantly correlated with the duration of initial unconsciousness and the final increase in ventricular size compared to the day-of-injury level. Varying cerebellar ataxia in gait and speech and spastic hemiplegia are frequent neurological associations. Thus, diffuse axonal injury can be regarded as the main pathology underlying the higher brain dysfunction due to traumatic brain injury. Diffuse brain injury secondary to hypoxia and secondary to mass lesion cannot be denied as another cause of this dysfunction. It is noteworthy that this dysfunction mimicks dementia pugilista and the physiologically aged brain both clinically and neuroradiologically.
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© 2004 The Japanese Congress of Neurological Surgeons

この記事はクリエイティブ・コモンズ [表示 - 非営利 - 改変禁止 4.0 国際]ライセンスの下に提供されています。
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
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