1 Research and Academic Affairs Service Line, W.G. "Bill" Hefner VA Medical Center , Salisbury, North Carolina.
2 Mid Atlantic Mental Illness Research Education and Clinical Center , Durham, North Carolina.
Brain Connect. 2018 May;8(4):205-211. doi: 10.1089/brain.2017.0556. Epub 2018 Apr 20.
Cross-sectional and longitudinal studies in active duty and veteran cohorts have both demonstrated that deployment-acquired traumatic brain injury (TBI) is an independent risk factor for developing post-traumatic stress disorder (PTSD), beyond confounds such as combat exposure, physical injury, predeployment TBI, and pre-deployment psychiatric symptoms. This study investigated how resting-state brain networks differ between individuals who developed PTSD and those who did not following deployment-acquired TBI. Participants included postdeployment veterans with deployment-acquired TBI history both with and without current PTSD diagnosis. Graph metrics, including small-worldness, clustering coefficient, and modularity, were calculated from individually constructed whole-brain networks based on 5-min eyes-open resting-state magnetoencephalography (MEG) recordings. Analyses were adjusted for age and premorbid IQ. Results demonstrated that participants with current PTSD displayed higher levels of small-worldness, F(1,12) = 5.364, p < 0.039, partial eta squared = 0.309, and Cohen's d = 0.972, and clustering coefficient, F(1, 12) = 12.204, p < 0.004, partial eta squared = 0.504, and Cohen's d = 0.905, than participants without current PTSD. There were no between-group differences in modularity or the number of modules present. These findings are consistent with a hyperconnectivity hypothesis of the effect of TBI history on functional networks rather than a disconnection hypothesis, demonstrating increased levels of clustering coefficient rather than a decrease as might be expected; however, these results do not account for potential changes in brain structure. These results demonstrate the potential pathological sequelae of changes in functional brain networks following deployment-acquired TBI and represent potential neurobiological changes associated with deployment-acquired TBI that may increase the risk of subsequently developing PTSD.
横断面和纵向研究表明，现役和退伍军人队列中的部署性创伤性脑损伤（TBI）是导致创伤后应激障碍（PTSD）的独立风险因素，除了战斗暴露、身体损伤、部署前 TBI 和部署前精神症状等混杂因素外。这项研究调查了在经历过部署性 TBI 后出现 PTSD 和未出现 PTSD 的个体之间，静息态脑网络有何不同。参与者包括有部署性 TBI 病史的退伍军人，这些人都经历过部署，有些患有 PTSD，有些则没有。从小世界特性、聚类系数和模块性等图形指标，基于个体构建的整个大脑网络，来自 5 分钟睁眼静息状态脑磁图（MEG）记录。分析调整了年龄和发病前智商。结果表明，目前患有 PTSD 的参与者具有更高的小世界特性，F(1,12) = 5.364，p < 0.039，偏 eta 平方 = 0.309，Cohen's d = 0.972，聚类系数，F(1,12) = 12.204，p < 0.004，偏 eta 平方 = 0.504，Cohen's d = 0.905，高于没有目前 PTSD 的参与者。模块性或存在模块的数量在两组之间没有差异。这些发现与 TBI 病史对功能网络的影响的超连接假说一致，而不是断开连接假说，表明聚类系数水平升高，而不是预期的降低；然而，这些结果没有考虑到大脑结构的潜在变化。这些结果表明，经历过部署性 TBI 后，功能脑网络的变化可能导致潜在的病理后果，这代表了与部署性 TBI 相关的潜在神经生物学变化，可能会增加随后发展为 PTSD 的风险。
