Sandry Joshua, Dobryakova Ekaterina
Psychology Department, Montclair State University, Montclair, NJ, USA.
Center for Traumatic Brain Injury Research, Kessler Foundation, East Hanover, NJ, USA; Department of Physical Medicine and Rehabilitation, Rutgers-New Jersey Medical School Newark, NJ, USA.
Cortex. 2021 Dec;145:37-56. doi: 10.1016/j.cortex.2021.08.011. Epub 2021 Sep 28.
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 = .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 (r = .23, p = .038), thalamus (r = .36, p = .007) and ventral diencephalon (r = .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.
创伤性脑损伤（TBI）可能会增加日后患神经退行性疾病的易感性。慢性TBI与神经退行性变之间的一个神经生物学相似之处可能是加速衰老以及皮质下灰质结构萎缩的性质。本研究的主要目的是通过评估两组之间的形态学差异，来评估和排序皮质下灰质萎缩将慢性中度至重度TBI与非TBI参与者区分开来的程度。40名患有中度至重度慢性TBI（受伤后9.23年）的个体和33名健康对照者（HC）接受了高分辨率3D T1加权结构磁共振成像。全脑体积被分类为白质、皮质和皮质下灰质结构，海马体和丘脑分别进一步细分为子区域和核团。在慢性TBI参与者的几乎所有脑区都观察到广泛萎缩。一系列多变量逻辑回归模型确定海马体和丘脑的皮质下灰质结构对区分慢性TBI与非TBI参与者最为敏感（麦克法登R = 0.36，p < 0.001）。进一步分析显示，海马体萎缩模式是全局性的，几乎发生在所有子区域。丘脑萎缩模式似乎更具选择性且不均匀，脑室周围核团的组间差异最为明显。皮质下灰质与受伤后的时间呈负相关（r = -0.31，p = 0.054），而白质和皮质灰质则不然。慢性TBI组的认知能力较低（科恩d = 0.97，p = 0.003），并且与包括苍白球（r = 0.23，p = 0.038）、丘脑（r = 0.36，p = 0.007）和腹侧间脑（r = 0.23，p = 0.036）在内的皮质下结构相关。这些数据可能支持慢性中度至重度TBI中的加速衰老假说，这与神经退行性疾病中发现的类似神经病理学特征相吻合。
