Journal
CORTEX
Volume 145, Issue -, Pages 37-56Publisher
ELSEVIER MASSON, CORP OFF
DOI: 10.1016/j.cortex.2021.08.011
Keywords
Chronic brain injury; Trauma; Head injury; Subcortical gray matter; Hippocampus; Thalamus; Subfields; Nuclei; Neurodegeneration; Atrophy
Funding
- New Jersey Commission on Brain Injury Research [CBIR201RG027, CBIR17PIL022]
- New Jersey Health Foundation [PC103-17]
- Consortium of Multiple Sclerosis Centers
- Kessler Foundation
Ask authors/readers for more resources
This study evaluated the importance of subcortical gray matter atrophy in differentiating chronic moderate-severe TBI from non-TBI participants, finding extensive atrophy across nearly all brain regions for chronic TBI individuals. The data supported an accelerated aging hypothesis in chronic moderate-severe TBI coinciding with a similar neuropathological profile found in neurodegenerative diseases that was observed in the study.
Traumatic brain injury (TBI) may increase susceptibility to neurodegenerative diseases later in life. One neurobiological parallel between chronic TBI and neurodegeneration may be accelerated aging and the nature of atrophy across subcortical gray matter structures. The main aim of the present investigation is to evaluate and rank the degree that subcortical gray matter atrophy differentiates chronic moderate-severe TBI from non-TBI participants by evaluating morphometric differences between groups. Forty individuals with moderate-severe chronic TBI (9.23 yrs from injury) and 33 healthy controls (HC) underwent high resolution 3D T1-weighted structural magnetic resonance imaging. Whole brain volume was classified into white matter, cortical and subcortical gray matter structures with hippocampi and thalami further segmented into subfields and nuclei, respectively. Extensive atrophy was observed across nearly all brain regions for chronic TBI participants. A series of multivariate logistic regression models identified subcortical gray matter structures of the hippocampus and thalamus as the most sensitive to differentiating chronic TBI from non-TBI participants (McFadden R-2 = .36, p < .001). Further analyses revealed the pattern of hippocampal atrophy to be global, occurring across nearly all subfields. The pattern of thalamic atrophy appeared to be much more selective and nonuniform, with largest between-group differences evident for nuclei bordering the ventricles. Subcortical gray matter was negatively correlated with time since injury (r = -.31, p = .054), while white matter and cortical gray matter were not. Cognitive ability was lower in the chronic TBI group (Cohen's d = .97, p = .003) and correlated with subcortical structures including the pallidum (r(2) = .23, p = .038), thalamus (r(2) = .36, p = .007) and ventral diencephalon (r(2) = .23, p = .036). These data may support an accelerated aging hypothesis in chronic moderate-severe TBI that coincides with a similar neuropathological profile found in neurodegenerative diseases. (C) 2021 Elsevier Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available