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Negative Neuroplasticity in Chronic Traumatic Brain Injury and Implications for Neurorehabilitation

机译:慢性创伤性脑损伤中的负性神经可塑性及其对神经康复的影响

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摘要

Based on growing findings of brain volume loss and deleterious white matter alterations during the chronic stages of injury, researchers posit that moderate-severe traumatic brain injury (TBI) may act to "age" the brain by reducing reserve capacity and inducing neurodegeneration. Evidence that these changes correlate with poorer cognitive and functional outcomes corroborates this progressive characterization of chronic TBI. Borrowing from a framework developed to explain cognitive aging (Mahncke et al., Progress in Brain Research, 157, 81-109, 2006a; Mahncke et al., Proceedings of the National Academy of Sciences of the United States of America, 103(33), 12523-12528, 2006b), we suggest here that environmental factors (specifically environmental impoverishment and cognitive disuse) contribute to a downward spiral of negative neuroplastic change that may modulate the brain changes described above. In this context, we review new literature supporting the original aging framework, and its extrapolation to chronic TBI. We conclude that negative neuroplasticity may be one of the mechanisms underlying cognitive and neural decline in chronic TBI, but that there are a number of points of intervention that would permit mitigation of this decline and better long-term clinical outcomes.
机译:基于在受伤的慢性阶段大脑体积减少和有害的白质变化的不断增长的发现,研究人员认为中度至重度创伤性脑损伤(TBI)可能通过降低储备能力和诱导神经变性而“使大脑老化”。这些变化与较差的认知和功能结局相关的证据证实了慢性TBI的这种进行性特征。借用开发用于解释认知衰老的框架(Mahncke等人,Progress in Brain Research,157,81-109,2006a; Mahncke等人,美国国家科学院院刊,103(33) ),12523-12528,2006b),我们在此建议环境因素(尤其是环境贫困和认知障碍)导致负性神经增生性变化的下行螺旋形,可能会调节上述脑部变化。在这种情况下,我们回顾了支持原始衰老框架的新文献及其对慢性TBI的推断。我们得出结论,负性神经可塑性可能是慢性TBI认知和神经衰弱的潜在机制之一,但是有很多干预措施可以减轻这种下降并改善长期临床疗效。

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