Kriukova Kseniia, Boswell Misque, Asifriyaz Tuba, Gong Joyce, Duncan Dominique, Vespa Paul
University of Southern California.
Ronald Reagan UCLA Medical Center.
Res Sq. 2024 Dec 4:rs.3.rs-5390622. doi: 10.21203/rs.3.rs-5390622/v1.
To investigate hippocampal volume changes in moderate to severe traumatic brain injury (TBI) patients compared to healthy controls and assess their association with post-traumatic epilepsy (PTE), focusing on age-related effects.
Imaging and demographic data for TBI patients were obtained from the Epilepsy Bioinformatics Study for Antiepileptogenic Therapy (EpiBioS4Rx) database; healthy controls matched by age and sex were sourced from Alzheimer's Disease Neuroimaging Initiative (ADNI), the National Institute of Mental Health (NIMH) Intramural Healthy Volunteer Dataset, the Parkinson's Progression Markers Initiative (PPMI), and the Autism Brain Imaging Data Exchange (ABIDE). MRI images for TBI subjects were obtained within 14-32 days post-injury. MRI data were preprocessed and segmented using FreeSurfer's recon-all pipeline and the hippocampal subfield segmentation module.
TBI patients showed significantly smaller average hippocampal volumes than controls (β = -191.0, p = 8.33e-04, FDR p = 1.47e-03, Cohen's d = -0.36), notably in the right and left CA1 head regions. No significant hippocampal volume differences were found between TBI+ and TBI- patients overall. In patients aged 60+, TBI+ patients had significantly larger volumes in the right CA1 head than TBI- patients (β = 57.43, p = 0.0300, FDR p = 0.040; Cohen's d = 1.06).
Hippocampal atrophy is evident in TBI patients but not directly linked to PTE development in most age groups. In patients over 60, hypertrophy in the right CA1 head may be associated with PTE, suggesting age and regional hippocampal changes influence epilepsy risk post-TBI. These findings highlight the complexity of hippocampal involvement in PTE and suggest potential shared mechanisms with neurodegenerative disorders such as Alzheimer's disease.
研究中度至重度创伤性脑损伤(TBI)患者与健康对照相比海马体积的变化,并评估其与创伤后癫痫(PTE)的关联,重点关注年龄相关影响。
TBI患者的影像学和人口统计学数据来自抗癫痫发生治疗的癫痫生物信息学研究(EpiBioS4Rx)数据库;年龄和性别匹配的健康对照来自阿尔茨海默病神经影像学倡议(ADNI)、国家心理健康研究所(NIMH)内部健康志愿者数据集、帕金森病进展标志物倡议(PPMI)和自闭症脑成像数据交换(ABIDE)。TBI受试者的MRI图像在受伤后14 - 32天内获得。MRI数据使用FreeSurfer的recon - all管道和海马亚区分割模块进行预处理和分割。
TBI患者的平均海马体积明显小于对照组(β = -191.0,p = 8.33e - 04,FDR p = 1.47e - 03,Cohen's d = -0.36),特别是在左右CA1头部区域。总体而言,TBI +和TBI -患者之间未发现显著的海马体积差异。在60岁以上的患者中,TBI +患者右侧CA1头部的体积明显大于TBI -患者(β = 57.43,p = 0.0300,FDR p = 0.040;Cohen's d = 1.06)。
海马萎缩在TBI患者中很明显,但在大多数年龄组中与PTE的发生没有直接联系。在60岁以上的患者中,右侧CA1头部的肥大可能与PTE有关,表明年龄和海马区域变化会影响TBI后的癫痫风险。这些发现突出了海马在PTE中的参与复杂性,并提示与阿尔茨海默病等神经退行性疾病可能存在共同机制。