Article

Longitudinal diffusion tensor imaging and neuropsychological correlates in traumatic brain injury patients

Geriatric Research and Education Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison WI, USA.
Frontiers in Human Neuroscience (Impact Factor: 2.9). 06/2012; 6:160. DOI: 10.3389/fnhum.2012.00160
Source: PubMed

ABSTRACT Traumatic brain injury (TBI) often involves focal cortical injury and white matter (WM) damage that can be measured shortly after injury. Additionally, slowly evolving WM change can be observed but there is a paucity of research on the duration and spatial pattern of long-term changes several years post-injury. The current study utilized diffusion tensor imaging to identify regional WM changes in 12 TBI patients and nine healthy controls at three time points over a four year period. Neuropsychological testing was also administered to each participant at each time point. Results indicate that TBI patients exhibit longitudinal changes to WM indexed by reductions in fractional anisotropy (FA) in the corpus callosum, as well as FA increases in bilateral regions of the superior longitudinal fasciculus (SLF) and portions of the optic radiation (OR). FA changes appear to be driven by changes in radial (not axial) diffusivity, suggesting that observed longitudinal FA changes may be related to changes in myelin rather than to axons. Neuropsychological correlations indicate that regional FA values in the corpus callosum and sagittal stratum (SS) correlate with performance on finger tapping and visuomotor speed tasks (respectively) in TBI patients, and that longitudinal increases in FA in the SS, SLF, and OR correlate with improved performance on the visuomotor speed (SS) task as well as a derived measure of cognitive control (SLF, OR). The results of this study showing progressive WM deterioration for several years post-injury contribute to a growing literature supporting the hypothesis that TBI should be viewed not as an isolated incident but as a prolonged disease state. The observations of long-term neurological and functional improvement provide evidence that some ameliorative change may be occurring concurrently with progressive degeneration.

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    • "The authors not only demonstrated increased atrophy during this time period, but also negatively correlated outcomes on the Glasgow Outcome Scale (Sidaros et al., 2009). In other studies, Hudak et al. (2011) found that decreases in brain volume correlated with depressive symptoms in the post-acute phase, and Farbota et al. (2012) demonstrated that diffusion tensor imaging findings (fractional anisotropy values) and neuropsychological task performance were positively correlated. Given mounting evidence revealing post-acute decline, we suggest that it is important at this stage of research to begin to consider what factors may hold the potential to influence, and in particular, offset this decline. "
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    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.
    Neuropsychology Review 12/2014; 24(4):409–427. DOI:10.1007/s11065-014-9273-6 · 5.40 Impact Factor
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    • "CTE shows some similarity to the chronic effects of moderate and severe traumatic brain injury (TBI). There is demonstrated evidence for neurodegeneration in the chronic phase of moderate to severe TBI, ensuing months to years after brain injury with sub-acute atrophy within the limbic system hippocampi (Ng et al., 2008) and elsewhere (Greenberg et al., 2008; Farbota et al., 2012; Green et al., 2014). The corpus callosum (unmyelinated axons in particular) is vulnerable to the deposition of protein post-TBI, suggesting "
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    ABSTRACT: While generalized cerebral atrophy and neurodegenerative change following traumatic brain injury (TBI) is well recognized in adults, it remains comparatively understudied in the pediatric population, suggesting that research should address the potential for neurodegenerative change in children and youth following TBI. This focused review examines original research findings documenting evidence for neurodegenerative change following TBI of all severities in children and youth. Our relevant inclusion and exclusion criteria identified a total of 16 articles for review. Taken together, the studies reviewed suggest there is evidence for long-term neurodegenerative change following TBI in children and youth. In particular both cross-sectional and longitudinal studies revealed volume loss in selected brain regions including the hippocampus, amygdala, globus pallidus, thalamus, periventricular white matter, cerebellum, and brain stem as well as overall decreased whole brain volume and increased CSF and ventricular space. Diffusion Tensor Imaging (DTI) studies also report evidence for decreased cellular integrity, particularly in the corpus callosum. Sensitivity of the hippocampus and deep limbic structures in pediatric populations are similar to findings in the adult literature and we consider the data supporting these changes as well as the need to investigate the possibility of neurodegenerative onset in childhood associated with mild traumatic brain injury (mTBI).
    Frontiers in Human Neuroscience 03/2014; 8:139. DOI:10.3389/fnhum.2014.00139 · 2.90 Impact Factor
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    • "The authors not only demonstrated increased atrophy during this time period, but also negatively correlated outcomes on the Glasgow Outcome Scale (Sidaros et al., 2009). In other studies, Hudak et al. (2011) found that decreases in brain volume correlated with depressive symptoms in the post-acute phase, and Farbota et al. (2012) demonstrated that diffusion tensor imaging findings (fractional anisotropy values) and neuropsychological task performance were positively correlated. Given mounting evidence revealing post-acute decline, we suggest that it is important at this stage of research to begin to consider what factors may hold the potential to influence, and in particular, offset this decline. "
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    ABSTRACT: Objectives: While a growing number of studies provide evidence of neural and cognitive decline in traumatic brain injury (TBI) survivors during the post-acute stages of injury, there is limited research as of yet on environmental factors that may influence this decline. The purposes of this paper, therefore, are to (1) examine evidence that environmental enrichment (EE) can influence long-term outcome following TBI, and (2) examine the nature of post-acute environments, whether they vary in degree of EE, and what impact these variations have on outcomes. Methods: We conducted a scoping review to identify studies on EE in animals and humans, and post-discharge experiences that relate to barriers to recovery. Results: One hundred and twenty-three articles that met inclusion criteria demonstrated the benefits of EE on brain and behavior in healthy and brain-injured animals and humans. Nineteen papers on post-discharge experiences revealed that variables such as insurance coverage, financial, and social support, home therapy, and transition from hospital to home, can have an impact on clinical outcomes. Conclusion: There is evidence to suggest that lack of EE, whether from lack of resources or limited ability to engage in such environments, may play a role in post-acute cognitive and neural decline. Maximizing EE in the post-acute stages of TBI may improve long-term outcomes for the individual, their family and society.
    Frontiers in Human Neuroscience 04/2013; 7:31. DOI:10.3389/fnhum.2013.00031 · 2.90 Impact Factor
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