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: 3.63). 06/2012; 6:160. DOI: 10.3389/fnhum.2012.00160
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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- " between the acute and 6 - month follow - up scan , but there was no evidence for continued improvement at 2 - year follow - up . To date , there is insufficient data to draw conclusions about the temporal window of recovery , but two group studies have indicated continued recovery up to a year ( Sidaros et al . , 2008 ) and 4 years after injury ( Farbota et al . , 2012 ) . Perhaps most striking in this regard is a case study of a patient with severe TBI who emerged from a minimally conscious state 19 years post - injury and was subsequently scanned on two occasions 18 months apart ( Voss et al . , 2006 ) . During that time , normalization of FA was seen in several regions , which was thought to repres"
ABSTRACT: Recent advances in neuroimaging methodologies sensitive to axonal injury have made it possible to assess in vivo the extent of traumatic brain injury (TBI) -related disruption in neural structures and their connections. The objective of this paper is to review studies examining connectivity in TBI with an emphasis on structural and functional MRI methods that have proven to be valuable in uncovering neural abnormalities associated with this condition. We review studies that have examined white matter integrity in TBI of varying etiology and levels of severity, and consider how findings at different times post-injury may inform underlying mechanisms of post-injury progression and recovery. Moreover, in light of recent advances in neuroimaging methods to study the functional connectivity among brain regions that form integrated networks, we review TBI studies that use resting-state functional connectivity MRI methodology to examine neural networks disrupted by putative axonal injury. The findings suggest that TBI is associated with altered structural and functional connectivity, characterized by decreased integrity of white matter pathways and imbalance and inefficiency of functional networks. These structural and functional alterations are often associated with neurocognitive dysfunction and poor functional outcomes. TBI has a negative impact on distributed brain networks that lead to behavioral disturbance.
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- "Two commonly used diffusion metrics, fractional anisotropy (FA) and mean diffusivity (MD), are obtained by fitting the diffusion tensor model to diffusion data (Basser et al., 1994; Mori and Zhang, 2006). DTI is widely used in neuroimaging studies (Le Bihan et al., 2001) and has been applied in studies of brain development (Cascio et al., 2007), aging (Charlton et al., 2010), Alzheimer's disease (Sexton et al., 2011), multiple sclerosis (Harrison et al., 2011), and traumatic brain injury (Farbota et al., 2012). "
ABSTRACT: Diffusion tensor imaging (DTI) measures are commonly used as imaging markers to investigate individual differences in relation to behavioral and health-related characteristics. However, the ability to detect reliable associations in cross-sectional or longitudinal studies is limited by the reliability of the diffusion measures. Several studies have examined reliability of diffusion measures within (i.e. intra-site) and across (i.e. inter-site) scanners with mixed results. Our study compares the test-retest reliability of diffusion measures within and across scanners and field strengths in cognitively normal older adults with a follow-up interval less than 2.25 years. Intra-class correlation (ICC) and coefficient of variation (CoV) of fractional anisotropy (FA) and mean diffusivity (MD) were evaluated in sixteen white matter and twenty-six gray matter bilateral regions. The ICC for intra-site reliability (0.32 to 0.96 for FA and 0.18 to 0.95 for MD in white matter regions; 0.27 to 0.89 for MD and 0.03 to 0.79 for FA in gray matter regions) and inter-site reliability (0.28 to 0.95 for FA in white matter regions, 0.02 to 0.86 for MD in gray matter regions) with longer follow-up intervals were similar to earlier studies using shorter follow-up intervals. The reliability of across field strengths comparisons was lower than intra- and inter-site reliability. Within and across scanner comparisons showed that diffusion measures were more stable in larger white matter regions (>1500 mm(3)). For gray matter regions, the MD measure showed stability in specific regions and was not dependent on region size. Linear correction factor estimated from cross-sectional or longitudinal data improved the reliability across field strengths. Our findings indicate that investigations relating diffusion measures to external variables must consider variable reliability across the distinct regions of interest and that correction factors can be used to improve consistency of measurement across field strengths. An important result of this work is that inter-scanner and field strength effects can be partially mitigated with linear correction factors specific to regions of interest. These data-driven linear correction techniques can be applied in cross-sectional or longitudinal studies. Copyright © 2015. Published by Elsevier Inc.
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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. "
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.