Departments of Psychology (Drs Belchev and Gilboa), Public Health Sciences (Dr Binns), Medical Imaging (Dr Mikulis), and Psychiatry (Dr Green), University of Toronto, Toronto, Ontario, Canada; Rotman Research Institute at Baycrest, Toronto, Ontario, Canada (Drs Belchev, Gilboa, and Binns); Toronto Rehabilitation Institute, Toronto, Ontario, Canada (Drs Belchev, Gilboa, and Green and Mss Colella and Glazer); and Krembil Research Institute, Toronto, Ontario, Canada (Dr Mikulis).
J Head Trauma Rehabil. 2022;37(3):E144-E156. doi: 10.1097/HTR.0000000000000696. Epub 2021 Jun 15.
To examine the trajectory of structural gray matter changes across 2 chronic periods of recovery in individuals who have sustained severe traumatic brain injury (TBI), adding to the growing literature indicating that neurodegenerative processes occur in the months to years postinjury.
Patients who experienced posttraumatic amnesia of 1 hour or more, and/or scored 12 or less on the Glasgow Coma Scale at the emergency department or the scene of the accident, and/or had positive brain imaging findings were recruited while receiving inpatient care, resulting in 51 patients with severe TBI.
Secondary analyses of gray matter changes across approximately 5 months, 1 year, and 2.5 years postinjury were undertaken, using an automated segmentation protocol with improved accuracy in populations with morphological anomalies. We compared patients and matched controls on regions implicated in poorer long-term clinical outcome (accumbens, amygdala, brainstem, hippocampus, thalamus). To model brain-wide patterns of change, we then conducted an exploratory principal component analysis (PCA) on the linear slopes of all regional volumes across the 3 time points. Finally, we assessed nonlinear trends across earlier (5 months-1 year) versus later (1-2.5 years) time-windows with PCA to compare degeneration rates across time. Chronic degeneration was predicted cortically and subcortically brain-wide, and within specific regions of interest.
(1) From 5 months to 1 year, patients showed significant degeneration in the accumbens, and marginal degeneration in the amygdala, brainstem, thalamus, and the left hippocampus when examined unilaterally, compared with controls. (2) PCA components representing subcortical and temporal regions, and regions from the basal ganglia, significantly differed from controls in the first time-window. (3) Progression occurred at the same rate across both time-windows, suggesting neither escalation nor attenuation of degeneration across time.
Localized yet progressive decline emphasizes the necessity of developing interventions to offset degeneration and improve long-term functioning.
研究经历严重创伤性脑损伤（TBI）后两个慢性恢复期的个体结构灰质变化轨迹，这增加了表明神经退行性过程发生在受伤后数月至数年的不断增长的文献。
招募了在住院治疗期间经历了 1 小时或更长时间的创伤后遗忘、或在急诊室或事故现场格拉斯哥昏迷量表评分 12 或更低、或有阳性脑成像发现的患者，共 51 名严重 TBI 患者。
使用具有改进的形态异常人群准确性的自动分割协议，对损伤后约 5 个月、1 年和 2.5 年的灰质变化进行二次分析。我们比较了患者和匹配对照组在与较差的长期临床结局相关的区域（伏隔核、杏仁核、脑干、海马体、丘脑）。为了模拟大脑整体变化模式，我们随后对所有区域体积的线性斜率进行了探索性主成分分析（PCA）。最后，我们通过 PCA 评估了早期（5 个月-1 年）和晚期（1-2.5 年）时间窗之间的非线性趋势，以比较随时间的退化率。慢性退化在皮质和皮质下脑内广泛预测，并在特定感兴趣区域内预测。
（1）从 5 个月到 1 年，与对照组相比，患者在伏隔核中显示出明显的退化，在杏仁核、脑干、丘脑和左侧海马体中则表现出边缘退化，当单侧检查时。（2）代表皮质下和颞叶区域以及基底节区域的 PCA 成分在第一个时间窗中与对照组明显不同。（3）两个时间窗之间的进展速度相同，表明随时间没有退化的加剧或衰减。
局部但进行性的下降强调了开发干预措施以抵消退化和改善长期功能的必要性。
