Tomaszczyk Jennifer C, Green Nathaniel L, Frasca Diana, Colella Brenda, Turner Gary R, Christensen Bruce K, Green Robin E A
Research Department, Toronto Rehabilitation Institute - University Health Network, Toronto, ON, Canada.
Neuropsychol Rev. 2014 Dec;24(4):409-27. doi: 10.1007/s11065-014-9273-6. Epub 2014 Nov 25.
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.
基于在损伤慢性阶段脑容量损失和有害白质改变的越来越多的研究发现,研究人员认为中重度创伤性脑损伤(TBI)可能通过降低储备能力和诱导神经退行性变来使大脑“老化”。这些变化与较差的认知和功能结果相关的证据证实了慢性TBI的这种渐进性特征。借鉴为解释认知老化而开发的一个框架(Mahncke等人,《脑研究进展》,157,81 - 109,2006a;Mahncke等人,《美国国家科学院院刊》,103(33),12523 - 12528,2006b),我们在此提出环境因素(特别是环境匮乏和认知不用)促成了负面神经可塑性变化的恶性循环,这可能调节上述大脑变化。在此背景下,我们回顾支持原始老化框架及其外推至慢性TBI的新文献。我们得出结论,负面神经可塑性可能是慢性TBI中认知和神经衰退的潜在机制之一,但存在一些干预点,可减轻这种衰退并改善长期临床结果。