In Vivo Characterization of Traumatic Brain Injury Neuropathology with Structural and Functional Neuroimaging

Abstract

Quantitative neuroimaging is increasingly used to study the effects of traumatic brain injury (TBI) on brain structure and function. This paper reviews quantitative structural and functional neuroimaging studies of patients with TBI, with an emphasis on the effects of diffuse axonal injury (DAI), the primary neuropathology in TBI. Quantitative structural neuroimaging has evolved from simple planometric measurements through targeted region-of-interest analyses to whole-brain analysis of quantified tissue compartments. Recent studies converge to indicate widespread volume loss of both gray and white matter in patients with moderate-to-severe TBI. These changes can be documented even when patients with focal lesions are excluded. Broadly speaking, performance on standard neuropsychological tests of speeded information processing are related to these changes, but demonstration of specific brain-behavior relationships requires more refined experimental behavioral measures. The functional consequences of these structural changes can be imaged with activation functional neuroimaging. Although this line of research is at an early stage, results indicate that TBI causes a more widely dispersed activation in frontal and posterior cortices. Further progress in analysis of the consequences of TBI on neural structure and function will require control of variability in neuropathology and behavior.

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

“…For example, a linear relationship with cerebral atrophy relates to injury severity measures such as GCS, PTA, and duration of LOC Wilde et al, 2006b). Likewise, complicated mTBI is more likely to have positive neuroimaging findings (Levine et al, 2006;McAllister et al, 2001;Vorst et al, 2007) and significant residuals (Kennedy et al, 2006). If boxing is considered a model for detecting "pre-clinical" or asymptomatic brain injury, recent diffusion tensor imaging studies have demonstrated abnormalities in boxers (Chappell et al, 2006;Zhang et al, 2006b).…”

Cognitive processing speed and the structure of white matter pathways: Convergent evidence from normal variation and lesion studies

“…Long distance transmission of signals across the cerebrum depends upon the ability of long association tracts to reduce signal degradation (Catani and ffytche, 2005). White matter diseases, such as multiple sclerosis which leads to demyelination, and wide spread damage across fiber systems, as occurs in traumatic brain injury, cause an overall slowing of cognitive processes (Levine et al, 2006;Rao, 1996).…”

Structural consequences of diffuse traumatic brain injury: A large deformation tensor-based morphometry study

“…Among the survivors, 80,000 to 90,000 individuals are left with significant long-term cognitive and motor disabilities (Jacobs, 1988;Max, Rice, & MacKenzie, 1990;McKinlay, Brooks, Bond, Martinage, & Marshall, 1981;Rutland-Brown, Langlois, Thomas, & Xi, 2006;Thomsen, 1984;Thurman, Alverson, Dunn, Guerrero, & Sniezek, 1999). However, efforts to identify the neuropathologic correlates of these deficits have gained only limited success to date (Bigler, 2001a;Levine et al, 2006). As colleagues (2002, 2006) appropriately pointed out, using more sensitive and reliable in vivo neuroimaging protocols may facilitate the identification of specific brainbehavior relationships in the TBI population.…”