Abstract
Objective
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.
Methods
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).
Results
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.
Significance
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.
NOV