Although sexual victimization during adolescence increases risk for later revictimization, mechanisms for increased risk among new college students have not been identified. Female undergraduates (N = 87) were assessed at the start and end of their first academic year. Those who reported initial sexual victimization at Time 1 were more likely than other women to report later college victimization at Time 2. Path analyses showed that self-blame and decreased sexual refusal assertiveness (SRA) explained this effect. Specifically, initial victimization was associated with increased self-blame; in turn, self-blame indirectly predicted later college victimization via decreased sexual refusal assertiveness. Prevention efforts focused on self-blame and other barriers to SRA may reduce risk for revictimization during women's transition to college.

An extensive electrophysiological literature has proposed a pathological “slowing” of neuronal activity in patients on the Alzheimer’s disease (AD) spectrum. Supported by numerous studies reporting increases in low frequency and decreases in high frequency neural oscillations, this pattern has been suggested as a stable biomarker with potential clinical utility. However, no spatially-resolved metric of such slowing exists, stymieing efforts to understand its relation to proteinopathy and clinical outcomes. Further, the assumption that this slowing is occurring in spatially overlapping populations of neurons has not been empirically validated. In the current study, we collected cross-sectional resting state measures of neuronal activity using magnetoencephalography (MEG) from 38 biomarker-confirmed patients on the AD spectrum and 20 cognitively-normal (CN) biomarker-negative older adults. From these data, we compute and validate a new metric of spatially resolved oscillatory deviations from healthy aging for each patient on the AD spectrum. Using this Pathological Oscillatory Slowing Index (POSI), we show that patients on the AD spectrum exhibit robust neuronal slowing across a network of temporal, parietal, cerebellar, and prefrontal cortices. This slowing effect is shown to be directly relevant to clinical outcomes, as oscillatory slowing in temporal and parietal cortices significantly predicted both general (i.e. MoCA scores) and domain-specific (i.e. attention, language, and processing speed) cognitive function. Further, regional amyloid-beta (Aβ) accumulation, as measured by quantitative 18F florbetapir PET, robustly predicted the strength of this pathological neural slowing effect, and the strength of this relationship between Aβ burden and neural slowing also predicted attentional impairments across patients. These findings provide empirical support for a spatially overlapping effect of oscillatory neural slowing in biomarker-confirmed patients on the AD spectrum, and link this effect to both regional proteinopathy and cognitive outcomes in a spatially resolved manner. The POSI also represents a novel metric that is of potentially high utility across a number of clinical neuroimaging applications, as oscillatory slowing has also been extensively documented in other patient populations, most notably Parkinson’s disease, with divergent spectral and spatial features.

Covictimized women experience both physical and sexual forms of abuse. The purpose of the present research was to compare covictimized women to those who experienced physical violence only or unwanted sexual activity only from dating partners. Data were collected from two samples of female undergraduates in heterosexual relationships. Covictimization was associated with less general satisfaction (Study 1) and sexual satisfaction (Study 2), more arguing (Study 1) and verbal conflict (Study 2), and more partner psychological aggression (Studies 1 and 2). Overall, findings suggest that dating partner covictimization may be a distinct type of interpersonal abuse that warrants further research.

Introduction Numerous studies have described aberrant patterns of rhythmic neural activity in patients along the Alzheimer's disease (AD) spectrum, yet the relationships between these pathological features and cognitive decline are uncertain. Methods We acquired magnetoencephalography (MEG) data from 38 amyloid‐PET biomarker‐confirmed patients on the AD spectrum and a comparison group of biomarker‐negative cognitively normal (CN) healthy adults, alongside an extensive neuropsychological battery. Results By modeling whole‐brain rhythmic neural activity with an extensive neuropsychological profile in patients on the AD spectrum, we show that the spectral and spatial features of deviations from healthy adults in neural population‐level activity inform their relevance to domain‐specific neurocognitive declines. Discussion Regional oscillatory activity represents a sensitive metric of neuronal pathology in patients on the AD spectrum. By considering not only the spatial, but also the spectral, definitions of cortical neuronal activity, we show that domain‐specific cognitive declines can be better modeled in these individuals.

Background Despite living a normal lifespan, at least 35% of persons with HIV (PWH) in resource-rich countries develop HIV-associated neurocognitive disorder (HAND). This high prevalence of cognitive decline may reflect accelerated ageing in PWH, but the evidence supporting an altered ageing phenotype in PWH has been mixed. Methods We examined the impact of ageing on the orienting of visual attention in PWH using dynamic functional mapping with magnetoencephalography (MEG) in 173 participants age 22–72 years-old (94 uninfected controls, 51 cognitively-unimpaired PWH, and 28 with HAND). All MEG data were imaged using a state-of-the-art beamforming approach and neural oscillatory responses during attentional orienting were examined for ageing, HIV, and cognitive status effects. Findings All participants responded slower during trials that required attentional reorienting. Our functional mapping results revealed HIV-by-age interactions in left prefrontal theta activity, alpha oscillations in the left parietal, right cuneus, and right frontal eye-fields, and left dorsolateral prefrontal beta activity ( p <.005). Critically, within PWH, we observed a cognitive status-by-age interaction, which revealed that ageing impacted the oscillatory gamma activity serving attentional reorienting differently in cognitively-normal PWH relative to those with HAND in the left temporoparietal, inferior frontal gyrus, and right prefrontal cortices ( p <.005). Interpretation This study provides key evidence supporting altered ageing trajectories across vital attention circuitry in PWH, and further suggests that those with HAND exhibit unique age-related changes in the oscillatory dynamics serving attention function. Additionally, our neural findings suggest that age-related changes in PWH may serve a compensatory function. Funding National Institutes of Health, USA.

Insomnia frequently occurs with trauma exposure and depression, but can ameliorate with improvements in depression. Insomnia was assessed by the insomnia subscale of the Hamilton Rating Scale for Depression in 106 women with childhood sexual abuse (CSA) and major depression receiving Interpersonal Psychotherapy in an uncontrolled pilot (n = 36) and an immediately subsequent randomized controlled trial (n = 70) comparing IPT to treatment as usual. Depression improved in each study and in both treatment conditions; insomnia had smaller, nonsignificant improvements. Overall, 95 women (90%) endorsed insomnia on the Structured Clinical Interview for DSM-IV at baseline and, of those, 90% endorsed insomnia following treatment. Despite improvements in depression, insomnia persists for most women with CSA.Trauma related to childhood sexual abuse (CSA) is associated with psychiatric and interpersonal difficulties during adulthood, including depression and anxiety (Kendler et al., 2000). Less attention has been focused on insomnia, the difficulty of initiating and maintaining sleep, in the context of CSA. In general, insomnia is strongly linked to depression (Pigeon & Perlis, 2007) with approximately 90% of individuals with major depressive disorder (MDD) also experiencing sleep disturbances (Riemann & Voderholzer, 2003).Insomnia symptoms tend to persist following various treatments for MDD including medication treatment (Menza, Marin, & Opper, 2003), cognitive behavior therapy (CBT;Carney, Segal, Edinger, & Krystal, 2007;Manber, et al., 2003), and stepped care depression management (Pigeon et al., 2008). This evidence suggests that insomnia may not reliably improve with these forms of depression treatment.Interpersonal psychotherapy (IPT) has recently been evaluated for the treatment of depression in CSA survivors, where it was found to decrease depression in an uncontrolled pilot study (Talbot et al., 2005) as well as in a subsequent randomized trial (RCT) comparing IPT to treatment as usual (TAU) (Talbot, Ward & Lu, 2008). The current study undertook secondary analyses of both sets of clinical trial data to specifically evaluate the effect of IPT on insomnia. The hypotheses were that there would be a significant effect of IPT treatment over time for insomnia, that insomnia would improve more with IPT than with TAU in the RCT, and that the effect sizes would be relatively smaller for insomnia than for depression. Method ParticipantsThe sample is derived from two closely related studies in depressed women with CSA presenting at a community mental health center. During intake assessments, 1,080 women were screened for eligibility, consisting of depressive symptoms and self-report of CSA. Of 163 eligible women, 133 agreed to be contacted for evaluation, of which 22 were excluded (8 with alcohol/substance abuse, 6 with active psychosis, 6 without MDD, and 2 without CSA), 4 did not complete the baseline evaluation, and 1 withdrew immediately. Thus, 106 participants with a history of CSA established through a structure...

Background: Alzheimer's disease (AD) is generally thought to spare primary sensory function; however, such interpretations have drawn from a literature that has rarely taken into account the variable cognitive declines seen in patients with AD. As these cognitive domains are now known to modulate cortical somatosensory processing, it remains possible that abnormalities in somatosensory function in patients with AD have been suppressed by neuropsychological variability in previous research. Methods: In this study, we combine magnetoencephalographic (MEG) brain imaging during a paired-pulse somatosensory gating task with an extensive battery of neuropsychological tests to investigate the influence of cognitive variability on estimated differences in somatosensory function between biomarker-confirmed patients on the AD spectrum and cognitively-normal older adults. Findings: We show that patients on the AD spectrum exhibit largely non-significant differences in somatosensory function when cognitive variability is not considered (p-value range: .020À.842). However, once attention and processing speed abilities are considered, robust differences in gamma-frequency somatosensory response amplitude (p < .001) and gating (p = .004) emerge, accompanied by significant statistical suppression effects. Interpretation: These findings suggest that patients with AD exhibit insults to functional somatosensory processing in primary sensory cortices, but these effects are masked by variability in cognitive decline across individuals.

HIV‐infection has been associated with widespread alterations in brain structure and function, although few studies have examined whether such aberrations are co‐localized and the degree to which clinical and cognitive metrics are related. We examine this question in the somatosensory system using high‐resolution structural MRI (sMRI) and magnetoencephalographic (MEG) imaging of neural oscillatory activity. Forty‐four participants with HIV (PWH) and 55 demographically‐matched uninfected controls completed a paired‐pulse somatosensory stimulation paradigm during MEG and underwent 3T sMRI. MEG data were transformed into the time‐frequency domain; significant sensor level responses were imaged using a beamformer. Virtual sensor time series were derived from the peak responses. These data were used to compute response amplitude, sensory gating metrics, and spontaneous cortical activity power. The T1‐weighted sMRI data were processed using morphological methods to derive cortical thickness values across the brain. From these, the cortical thickness of the tissue coinciding with the peak response was estimated. Our findings indicated both PWH and control exhibit somatosensory gating, and that spontaneous cortical activity was significantly stronger in PWH within the left postcentral gyrus. Interestingly, within the same tissue, PWH also had significantly reduced cortical thickness relative to controls. Follow‐up analyses indicated that the reduction in cortical thickness was significantly correlated with CD4 nadir and mediated the relationship between HIV and spontaneous cortical activity within the left postcentral gyrus. These data indicate that PWH have abnormally strong spontaneous cortical activity in the left postcentral gyrus and such elevated activity is driven by locally reduced cortical gray matter thickness.