Personalized Mobile Health-Enhanced Cognitive Behavioral Intervention for Maternal Distress: Examining the Moderating Role of Adverse Childhood Experiences.

BACKGROUND: Maternal history of trauma is a risk factor for distress during pregnancy. The purpose of this paper was to examine the theorized differential impact of a cognitive behavioral intervention (Mothers and Babies Personalized; MB-P) on maternal distress and emotional regulation for those with ≥ 1 adverse childhood experiences (ACEs; vs no ACEs) from pregnancy to 3 months postpartum. METHODS: Between August 2019 and August 2021, eligible pregnant individuals aged ≥ 18 years, < 22 weeks' gestation, and English-speaking were recruited from 6 university-affiliated prenatal clinics. Participants (N = 100) were randomized to MB-P (n = 49) or control (n = 51). Analyzable data were collected for 95 participants. Analyses tested progression of change (slope) and at individual timepoints (panel analysis) for perinatal mental health outcomes. RESULTS: The majority of participants (n = 68, 71%) reported experiencing > 1 ACE (median = 1, range: 0-11). Participants demonstrated significant differential effects for depressive symptoms in absence of ACEs (standardized mean differences [SMD] = 0.82; 95% confidence interval [CI] = [0.13-1.51]) vs in presence of ACEs (SMD = 0.39; 95% CI = [-0.20 to 0.97]) and perceived stress in absence of ACEs (SMD = 0.92; 95% CI = [0.23-1.62]) vs in presence of ACEs (SMD = -0.05; 95% CI = [-0.63 to 0.53]). A panel analysis showed significantly reduced depressive symptoms postintervention and increased negative mood regulation at 3 months postpartum for individuals with ACEs. CONCLUSIONS: Findings support effectiveness of the MB-P intervention to reduce prenatal distress for all pregnant individuals. Preliminary exploration suggests the possibility that individuals with ACEs may benefit from enhanced trauma-informed content to optimize the effects of a perinatal intervention.

Cerebral cortical thickness and cognitive decline in Parkinson's disease.

In Parkinson's disease (PD), reduced cerebral cortical thickness may reflect network-based degeneration. This study performed cognitive assessment and brain MRI in 30 PD participants and 41 controls at baseline and 18 months later. We hypothesized that cerebral cortical thickness and volume, as well as change in these metrics, would differ between PD participants who remained cognitively stable and those who experienced cognitive decline. Dividing the participant sample into PD-stable, PD-decline, and control-stable groups, we compared mean cortical thickness and volume within segments that comprise the prefrontal cognitive-control, memory, dorsal spatial, and ventral object-based networks at baseline. We then compared the rate of change in cortical thickness and volume between the same groups using a vertex-wise approach. We found that the PD-decline group had lower cortical thickness within all 4 cognitive networks in comparison with controls, as well as lower cortical thickness within the prefrontal and medial temporal networks in comparison with the PD-stable group. The PD-decline group also experienced a greater rate of volume loss in the lateral temporal cortices in comparison with the control group. This study suggests that lower thickness and volume in prefrontal, medial, and lateral temporal regions may portend cognitive decline in PD.

Cross-sectional and longitudinal associations between total and regional white matter hyperintensity volume and cognitive and motor function in Parkinson's disease.

BACKGROUND: White matter hyperintensities (WMH) are frequently observed on T2-weighted brain magnetic resonance imaging studies of healthy older adults and have been linked with impairments in balance, gait, and cognition. Nonetheless, few studies have investigated the longitudinal effects of comorbid WMH on cognition and motor function in Parkinson's disease. METHODS: The Lesion Segmentation Tool for Statistical Parametric Mapping was used to obtain total lesion volume and map regional WMH probabilities in 29 PD and 42 control participants at two study visits 18 months apart. Both cross-sectional and longitudinal comparisons were made between composite scores in the domains of executive function, memory, and language, and Unified Parkinson's Disease Rating Scale (UPDRS) scores. RESULTS: We found no difference between disease and control groups in total WMH volume or progression during the study. Greater regional and global WMH at baseline was more strongly associated with lower executive function in PD subjects than in controls. Increased regional WMH was also more strongly associated with impaired memory performance in PD relative to controls. Longitudinally, no associations between cognitive change and total or regional WMH progression were detected in either group. A positive relationship between baseline regional WMH and total UPDRS scores was present in the control group, but not PD. However, greater WMH increase was associated with a greater increase in UPDRS motor sub-scores in PD. CONCLUSIONS: These findings suggest that although PD patients do not experience greater mean WMH load than normal aged adults, comorbid WMH do exacerbate cognitive and motor symptoms in PD.

Longitudinal white matter microstructural change in Parkinson's disease.

Postmortem studies of Parkinson's disease (PD) suggest that Lewy body pathology accumulates in a predictable topographical sequence, beginning in the olfactory bulb, followed by caudal brainstem, substantia nigra, limbic cortex, and neocortex. Diffusion-weighted imaging (DWI) is sensitive, if not specific, to early disease-related white matter (WM) change in a variety of traumatic and degenerative brain diseases. Although numerous cross-sectional studies have reported DWI differences in cerebral WM in PD, only a few longitudinal studies have investigated whether DWI change exceeds that of normal aging or coincides with regional Lewy body accumulation. This study mapped regional differences in the rate of DWI-based microstructural change between 29 PD patients and 43 age-matched controls over 18 months. Iterative within- and between-subject tensor-based registration was completed on motion- and eddy current-corrected DWI images, then baseline versus follow-up difference maps of fractional anisotropy, mean, radial, and axial diffusivity were analyzed in the Biological Parametric Mapping toolbox for MATLAB. This analysis showed that PD patients had a greater decline in WM integrity in the rostral brainstem, caudal subcortical WM, and cerebellar peduncles, compared with controls. In addition, patients with unilateral clinical signs at baseline experienced a greater rate of WM change over the 18-month study than patients with bilateral signs. These findings suggest that rate of WM microstructural change in PD exceeds that of normal aging and is maximal during early stage disease. In addition, the neuroanatomic locations (rostral brainstem and subcortical WM) of accelerated WM change fit with current theories of topographic disease progression.