Systematic review exploring the relationship between sexual abuse and lower urinary tract symptoms.

INTRODUCTION AND HYPOTHESIS: Patients presenting with lower urinary tract symptoms (LUTS) may report a history of sexual abuse (SA), and survivors of SA may report LUTS; however, the nature of the relationship is poorly understood. The aim of this review is to systematically evaluate studies that explore LUT dysfunction in survivors of SA. METHODS: A systematic literature search of six databases, Cochrane Database of Systematic Reviews, MEDLINE, EMBASE, CINAHL, AMED, and PsycINFO, was performed. The last search date was June 2021 (PROSPERO CRD42019122080). Studies reporting the prevalence and symptoms of LUTS in patients who have experienced SA were included. The literature was appraised according to the PRISMA statement. The quality of the studies was assessed. RESULTS: Out of 272 papers retrieved, 18 publications met the inclusion criteria: studies exploring LUTS in SA survivors (n=2), SA in patients attending clinics for their LUTs (n=8), and cross-sectional studies (n=8). SA prevalence ranged between 1.3% and 49.6%. A history of SA was associated with psychosocial stressors, depression, and anxiety. LUTS included urinary storage symptoms, voiding difficulties, voluntary holding of urine and urinary tract infections. Most studies were of moderate quality. Assessment of SA and LUTS lacked standardisation. CONCLUSIONS: The review highlights the need for a holistic assessment of patients presenting with LUTS. Although most of the studies were rated as being of 'moderate' quality, the evidence suggests the need to provide a "safe space" in clinic for patients to share sensitive information about trauma. Any such disclosure should be followed up with further assessment.

Prevalence of autistic traits in functional neurological disorder and relationship to alexithymia and psychiatric comorbidity.

INTRODUCTION: In a cohort of adults with Functional Neurological Disorder (FND), we aim to: METHODS: 91 patients participating in a FND 5-week outpatient program completed baseline self-report questionnaires for total phobia, somatic symptom severity, attention deficit hyperactivity disorder (ADHD) and dyslexia. Patients were grouped by Autism Spectrum Quotient (AQ-10) score of <6 or ≥ 6 and compared for significant differences in tested variables. This analysis was repeated with patients grouped by alexithymia status. Simple effects were tested using pairwise comparisons. Multistep regression models tested direct relationships between autistic traits and psychiatric comorbidity scores, and mediation by alexithymia. RESULTS: 36 patients (40%) were AQ-10 positive (scoring ≥6 on AQ-10). A further 36 patients (across AQ-10 positive and AQ-10 negative groups) (40%) screened positive for alexithymia. AQ-10 positive patients scored significantly higher for alexithymia, depression, generalised anxiety, social phobia, ADHD, and dyslexia. Alexithymia positive patients scored significantly higher for generalised anxiety, depression, somatic symptoms severity, social phobia, and dyslexia. Alexithymia score was found to mediate the relationship between autistic trait and depression scores. CONCLUSION: We demonstrate a high proportion of autistic and alexithymic traits, in adults with FND. A higher prevalence of autistic traits may highlight a need for specialised communication approaches in FND management. Mechanistic conclusions are limited. Future research could explore links with interoceptive data.

A framework for focal and connectomic mapping of transiently disrupted brain function.

The distributed nature of the neural substrate, and the difficulty of establishing necessity from correlative data, combine to render the mapping of brain function a far harder task than it seems. Methods capable of combining connective anatomical information with focal disruption of function are needed to disambiguate local from global neural dependence, and critical from merely coincidental activity. Here we present a comprehensive framework for focal and connective spatial inference based on sparse disruptive data, and demonstrate its application in the context of transient direct electrical stimulation of the human medial frontal wall during the pre-surgical evaluation of patients with focal epilepsy. Our framework formalizes voxel-wise mass-univariate inference on sparsely sampled data within the statistical parametric mapping framework, encompassing the analysis of distributed maps defined by any criterion of connectivity. Applied to the medial frontal wall, this transient dysconnectome approach reveals marked discrepancies between local and distributed associations of major categories of motor and sensory behaviour, revealing differentiation by remote connectivity to which purely local analysis is blind. Our framework enables disruptive mapping of the human brain based on sparsely sampled data with minimal spatial assumptions, good statistical efficiency, flexible model formulation, and explicit comparison of local and distributed effects.

Progressive alterations in white matter microstructure across the timecourse of Huntington's disease.

BACKGROUND: Whole-brain longitudinal diffusion studies are crucial to examine changes in structural connectivity in neurodegeneration. Here, we investigated the longitudinal alterations in white matter (WM) microstructure across the timecourse of Huntington's disease (HD). METHODS: We examined changes in WM microstructure from premanifest to early manifest disease, using data from two cohorts with different disease burden. The TrackOn-HD study included 67 controls, 67 premanifest, and 10 early manifest HD (baseline and 24-month data); the PADDINGTON study included 33 controls and 49 early manifest HD (baseline and 15-month data). Longitudinal changes in fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity, and radial diffusivity from baseline to last study visit were investigated for each cohort using tract-based spatial statistics. An optimized pipeline was employed to generate participant-specific templates to which diffusion tensor imaging maps were registered and change maps were calculated. We examined longitudinal differences between HD expansion-carriers and controls, and correlations with clinical scores, including the composite UHDRS (cUHDRS). RESULTS: HD expansion-carriers from TrackOn-HD, with lower disease burden, showed a significant longitudinal decline in FA in the left superior longitudinal fasciculus and an increase in MD across subcortical WM tracts compared to controls, while in manifest HD participants from PADDINGTON, there were significant widespread longitudinal increases in diffusivity compared to controls. Baseline scores in clinical scales including the cUHDRS predicted WM microstructural change in HD expansion-carriers. CONCLUSION: The present study showed significant longitudinal changes in WM microstructure across the HD timecourse. Changes were evident in larger WM areas and across more metrics as the disease advanced, suggesting a progressive alteration of WM microstructure with disease evolution.