This review focuses on white matter (WM) changes in mild traumatic brain injury (mTBI) as assessed by multimodal MRI. All the peer reviewed publications on WM changes in mTBI from January 2011 through September 2016 are included in this review. This review is organized as follows: introduction to mTBI, the basics of multimodal MRI techniques that are potentially useful for probing the WM integrity, summary and critical evaluation of the published literature on the application of multimodal MRI techniques to assess the changes of WM in mTBI, and correlation of MRI measures with behavioral deficits. The MRI–pathology correlation studies based on preclinical models of mTBI are also reviewed. Finally, the author’s perspective of future research directions is described.
About 2% of the US population is affected by traumatic brain injury (TBI) which results in an annual healthcare cost of $76.5 billion . Based on clinical symptoms, TBI can be categorized as either mild or moderate or severe . Focal TBI generally results in contusion or laceration to cortical and subcortical structures and intracranial bleeding and results in severe TBI. In contrast, diffuse injury is the result of stretching and tearing of axons due to linear and angular acceleration/deceleration. Linear acceleration causes less severe axonal shearing than angular acceleration/deceleration . Traumatic axonal injury (TAI) is thought to be a major pathologic event in TBI and may be responsible for much of the observed cognitive deficits [4–12]. Diffuse axonal injury (DAI) may be considered as a subset of TAI. Diffuse axonal injury has some histopathological characteristics that occur immediately and within hours and days of injury. Axons in white matter (WM) are vulnerable to diffuse injury because of their small diameter (∼3 μ) and long projections. DAI could result in mechanical breaking of the axonal cytoskeleton that could affect axonal transportation which in turn affects communication between different brain structures. WM pathology, and especially that detected with neuroimaging, is also influenced by other factors such as blood flow/edema, metabolic aberrations, excitotoxicity and secondary degeneration, Wallerian degeneration, and other factors, which occur under the umbrella of TAI and coalesce over time, not just what occurs within the acute time frame. Depending on the severity of DAI, TBI victims could experience cognitive and behavioral deficits. Advances in biomechanical modeling identified WM pathways that are most vulnerable to stretch and shear injury. These pathways include corona radiata (CR), internal capsule (IC), cerebral peduncle (CP) and corpus callosum (CC) [13–15].
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