Abstract
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.
Highlights
Negative Neuroplasticity in AgingCognitive and neural decline in aging have been wellestablished (Hedman et al 2012; Salthouse 2010)
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
The current paper argues that the Mahncke et al (2006a, b) framework for aging related decline can be extrapolated to TBI, with the possibility that disuse-mediated negative neuroplastic change may underlie cognitive and neural declines associated in chronic stage TBI
Summary
Cognitive and neural decline in aging have been wellestablished (Hedman et al 2012; Salthouse 2010). Increased reliance on simpler processing strengthens underlying neural pathways in a Hebbian Learning manner (i.e., “the cells that fire together wire together”; Hebb 1949) with commensurate decreases in the activity of competing, complex cognitive processes, resulting in a weakening of their underlying synaptic connectivity (Mahncke et al 2006a; Dosher and Lu 2009) They conceptualize negative plastic change as “a self-reinforcing, downward spiral of reduced interaction with challenging environments and reduced brain health” (Mahncke et al 2006a, p.86). We note that a number of other factors may possibly contribute to aging- and TBIrelated cognitive and neural decline through negative neuroplastic brain changes, Mahncke et al (2006a) focus on those factors that may be readily modifiable through behavioural interventions
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