Department of Neurology, UAB Epilepsy Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Departments of Neurobiology and Psychology, University of Alabama at Birmingham, Birmingham, AL, USA.
Epilepsia. 2021 Jan;62(1):107-119. doi: 10.1111/epi.16758. Epub 2020 Nov 25.
To utilize traumatic brain injury (TBI) as a model for investigating functioning during acute stress experiences in psychogenic nonepileptic seizures (PNES) and to identify neural mechanisms underlying the link between changes in processing of stressful experiences and mental health symptoms in PNES.
We recruited 94 participants: 50 with TBI only (TBI-only) and 44 with TBI and PNES (TBI + PNES). Participants completed mood (Beck Depression Inventory-II), anxiety (Beck Anxiety Inventory), and posttraumatic stress disorder (PTSD) symptom (PTSD Checklist-Specific Event) assessments before undergoing functional magnetic resonance imaging during an acute psychosocial stress task. Linear mixed-effects analyses identified clusters of significant interactions between group and neural responses to stressful math performance and stressful auditory feedback conditions within limbic brain regions (volume-corrected α = .05). Spearman rank correlation tests compared mean cluster signals to symptom assessments (false discovery rate-corrected α = .05).
Demographic and TBI-related measures were similar between groups; TBI + PNES demonstrated worse clinical symptom severity compared to TBI-only. Stressful math performance induced relatively greater reactivity within dorsomedial prefrontal cortex (PFC) and right hippocampal regions and relatively reduced reactivity within left hippocampal and dorsolateral PFC regions for TBI + PNES compared to TBI-only. Stressful auditory feedback induced relatively reduced reactivity within ventral PFC, cingulate, hippocampal, and amygdala regions for TBI + PNES compared to TBI-only. Changes in responses to stressful math within hippocampal and dorsal PFC regions were correlated with increased mood, anxiety, and PTSD symptom severity.
Corticolimbic functions underlying processing of stressful experiences differ between patients with TBI + PNES and those with TBI-only. Relationships between these neural responses and symptom assessments suggest potential pathophysiologic mechanisms in PNES.
利用创伤性脑损伤（TBI）作为模型，研究心理生理性非癫痫性发作（PNES）中急性应激体验期间的功能，并确定处理应激体验变化与 PNES 中心理健康症状之间关联的神经机制。
我们招募了 94 名参与者：50 名仅患有 TBI（TBI-only）和 44 名患有 TBI 和 PNES（TBI+PNES）。参与者在经历急性心理社会应激任务期间进行功能磁共振成像之前，完成了情绪（贝克抑郁量表-II）、焦虑（贝克焦虑量表）和创伤后应激障碍（PTSD）症状（PTSD 清单-特定事件）评估。线性混合效应分析确定了在边缘脑区（体积校正 α=.05）内，组间和对压力数学表现和压力听觉反馈条件的神经反应之间存在显著相互作用的聚类。Spearman 秩相关检验比较了平均聚类信号与症状评估（错误发现率校正 α=.05）。
两组间的人口统计学和 TBI 相关测量相似；TBI+PNES 与 TBI-only 相比，临床症状严重程度更差。与 TBI-only 相比，压力数学表现引起 TBI+PNES 背内侧前额叶皮质（PFC）和右侧海马区域的反应性相对较高，而左侧海马和背外侧 PFC 区域的反应性相对较低。与 TBI-only 相比，压力听觉反馈引起 TBI+PNES 腹侧 PFC、扣带回、海马和杏仁核区域的反应性相对较低。与压力数学表现相关的海马和背侧 PFC 区域的反应变化与情绪、焦虑和 PTSD 症状严重程度的增加相关。
处理应激体验的皮质边缘功能在 TBI+PNES 患者和 TBI-only 患者之间存在差异。这些神经反应与症状评估之间的关系表明了 PNES 中的潜在病理生理机制。
