Contributions of Sensorimotor Processing To Traumatic Memory Retrieval in Post-traumatic Stress Disorder
Abstract
Traumatic re-experiencing, a hallmark symptom of post-traumatic stress disorder (PTSD), involves vividly reliving traumatic events and is often accompanied by sensory detail, motoric re-enactment, perceptual disorientation, involuntary memory retrieval, and/or intense emotional and physiological reactions. This suggests that traumatic events may be stored as a unique memory representation, herein termed traumatic memory. Chapter 1 presents a rationale for investigating lesser-explored sensorimotor contributions to the neurobiological representation of traumatic memory, highlighting its sensorimotor-rich characteristics. Chapter 2 employs independent component analysis to explore functional connectivity between the sensorimotor network (SMN) and posterior default mode network (pDMN), a network involved in typical autobiographical memory, in individuals with moral injury-related PTSD and trauma-exposed controls during script-driven memory retrieval. Hyperconnectivity between the SMN and pDMN emerge during traumatic (but not neutral) memory retrieval. From a dimensional perspective, those with higher dissociative symptoms additionally show greater de-coupling of the anterior and posterior DMN during traumatic memory retrieval. Chapter 3 leverages a whole-brain region of interest (ROI) to ROI approach to further examine the same sample as Chapter 2, with additional subgroup delineation into PTSD and its dissociative subtype (PTSD+DS). This analysis reveals reduced functional connectivity between the cerebellum and the thalamus, basal ganglia, and frontal cortex in both PTSD and PTSD+DS. Notably, PTSD+DS is characterized by distinct patterns of occipital-basal ganglia and occipital-thalamic hypoconnectivity alongside brainstem-cerebellar hyperconnectivity. Chapter 4 examines the effectiveness of Deep Brain Reorienting (DBR), a sensorimotor-based psychotherapy, for treating core PTSD symptoms through a randomized controlled trial. Those who received DBR show significant re-experiencing and overall symptom reduction, whereas no significant symptom reductions emerge for those on a Waitlist. Chapter 5 replicates the methodology of Chapter 2 to demonstrate that DBR-related clinical improvements align with a reduction of SMN-pDMN functional connectivity, as well as an increase in within-DMN coherence, during traumatic memory provocation. We propose that a unique neurobiological representation of traumatic memory may arise from a disrupted encoding process, where sensorimotor-based representations fail to fully integrate into past-contextualized memory networks. DBR may promote this integration, transforming a fragmented traumatic memory into a past-contextualized narrative and alleviating core PTSD symptoms.