TY - JOUR
T1 - Global hippocampal and selective thalamic nuclei atrophy differentiate chronic TBI from Non-TBI
AU - Sandry, Joshua
AU - Dobryakova, Ekaterina
N1 - Publisher Copyright:
© 2021 Elsevier Ltd
PY - 2021/12
Y1 - 2021/12
N2 - 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 R2 = .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 non-uniform, 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 (r2 = .23, p = .038), thalamus (r2 = .36, p = .007) and ventral diencephalon (r2 = .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.
AB - 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 R2 = .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 non-uniform, 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 (r2 = .23, p = .038), thalamus (r2 = .36, p = .007) and ventral diencephalon (r2 = .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.
KW - Atrophy
KW - Chronic brain injury
KW - Head injury
KW - Hippocampus
KW - Neurodegeneration
KW - Nuclei
KW - Subcortical gray matter
KW - Subfields
KW - Thalamus
KW - Trauma
UR - http://www.scopus.com/inward/record.url?scp=85117399706&partnerID=8YFLogxK
U2 - 10.1016/j.cortex.2021.08.011
DO - 10.1016/j.cortex.2021.08.011
M3 - Article
C2 - 34689031
AN - SCOPUS:85117399706
SN - 0010-9452
VL - 145
SP - 37
EP - 56
JO - Cortex
JF - Cortex
ER -