Social anxiety disorder (SAD) can accompany emotional symptoms as well as physical reactions. The assessment and real-time measurement of SAD is difficult in real-world.

This study aims to predict the severity of specific anxiety states and virtual reality (VR) sickness in SAD patients by a machine learning model based on only quantitative measuring of autonomic physiologic signals during VR therapy sessions.

In total, 32 individuals with SAD symptoms were enrolled in VR participatory sessions. We assessed patients’ specific anxiety symptoms through Internalized Shame Scale (ISS) and Post-Event Rumination Scale (PERS), and VR sickness through Simulator Sickness Questionnaire (SSQ). Specific anxiety symptoms and VR sickness were divided into severe and non-severe states based on the total score of each scale by K-means clustering. Logistic regression, Random Forest, Naïve Bayes classifier, and Support Vector Machine were used based on the physiological signal data to predict the severity group in subdomains of ISS, PERS, and SSQ.

Prediction performance (F1 score) for the severity of the ISS mistake anxiety subdomain was higher than other scales with 0.8421. For VR sickness, prediction performance for the severity of the physical subdomain was higher than the non-physical subdomain with 0.7692.

The study findings present that mistake anxiety and physical sickness could be predicted more accurately by only autonomic physiological signals, suggesting these features are probably associated with autonomic responses. Based on the present study results, we could provide the evidence for predicting the severity of specific anxiety or VR adverse effects only based on in-situ physiological signals.

No significant relationships.

Cerebral microbleeds (CMBs) may contribute to cognitive deficits in stroke. Cognitive impairment that does not meet the criteria for dementia (cognitive impairment no dementia [CIND]) is common in stroke, and patients with such impairment can revert to normal cognition.

To investigate the association of CMBs and remission of poststroke CIND.

To understand the evolution of poststroke cognitive impairment no dementia (CIND) is bi-directional.

143 patients with CIND at three months after stroke were recruited and followed up for one year. Remission of CIND was defined as a conversion of cognitive status from CIND to cognitively intact at follow-up. MRI variables in terms of infarction, cerebral microbleeds (CMBs), and white matter hyperintensities (WMHs) and hippocampal volume were analyzed. Logistic regression was performed to find the predictors of the remission of poststroke CIND.

30 (21.0%) out of the 143 patients converted to cognitive intact at follow-up. In univariate comparisons, subjects with remission of CIND had younger age (67.1 ± 9.5 vs.73.6 ± 7.6 years, p < 0.001) and higher education years (5.1 ± 4.0 vs.3.6 ± 4.0, p = 0.039). They also had lower WMHs volume (8.2 ± 8.2 vs. 18.6 ± 19.7 cm3, p < 0.001), lower frequency of CMBs (10.0% vs. 31.0%, p = 0.021) and lower volume of the lateral ventricle (33.3 ± 16.5 vs.42.6 ± 19.4 cm3, p = 0.017). In logistic regression, age (odds ratio [OR] = 0.913, 95%C.I. = 0.866–0.962, p = 0.001) and absence of CMBs (OR = 4.292, 95%C.I. = 1.174–15.625, p = 0.028) were significant predictors of remission of CIND.

Younger age and absence of CMBs predict the remission of poststroke CIND.

Longitudinal studies of predicting dementia conversion of poststroke cognitive impairment no dementia (CIND) are limited.

To investigate the clinical and imaging predictors of dementia conversion in poststroke patients with CIND.

To understand dementia conversion of CIND.

143 patients with CIND (defined as impairment in at least one cognitive domain without meeting the criteria of dementia) at three months after stroke were recruited and followed up for one year. Dementia was diagnosed using the criteria of Diagnostic and Statistical Manual of Mental Disorders (4th edition, DSM-IV). MRI measurements including infarction, microbleeds, white matter hyperintensities (WMHs) and hippocampal volume were conducted. Logistic regression was performed to find the predictors of dementia at follow-up.

16 (11.2%) out of the 143 patients developed dementia 15 months after stroke. In univariate comparisons, subjects with dementia at follow-up had older age (78.0 ± 5.3 vs.71.5 ± 8.5 years, p = 0.003) and higher NIHSS score (7.1 ± 3.5 vs.4.7 ± 3.3, p = 0.005) on admission. They also had higher frequency of old infarcts in the thalamus (31.3% vs. 11.0%, p = 0.025), larger volume of old infarcts (4.2 ± 11.2 vs. 0.7 ± 2.6 cm3, p < 0.001) and WMHs volume (33.2 ± 34.0 vs. 14.2 ± 14.1 cm3, p = 0.016). In logistic regression, age (odds ratio [OR] =1.203, 95%C.I.=1.054-1.373, p = 0.006), NIHSS score on admission (OR = 1.324, 95%C.I.=1.082-1.619, p = 0.006) and WMHs volume (OR = 1.045, 95%C.I.=1.007-1.084, p = 0.019) were significant predictors of dementia at follow-up.

WMHs volume predicts dementia in poststroke patients with CIND, suggesting subcortical ischemic vascular disease was an important origin of poststroke delayed dementia.

Prefrontal cortex and sex difference are involved in verbal fluency network described in normal participants. Stroke patients often have prefrontal cortex atrophy.

To investigate whether atrophy in subdivisions of prefrontal cortex and sex difference contribute to verbal fluency in non-aphasic stroke patients.

To understand the relationship between the atrophy of left dorsolateral prefrontal cortex and verbal performance in elderly poststroke women.

30 elderly (age> = 60 years old) women with non-aphasic ischemic stroke and 30 age-controlled stroke men recruited. Automatic segmentation methods were used to assess the volume of both sides of the whole prefrontal cortex, anterior cingulate cortex, orbital frontal cortex and dorsalateral prefrontal cortex (DLPFC), as well as white matter lesions (WMLs) volume. Mini-mental state examination (MMSE) and semantic verbal fluency test (VFT, category: foods and animals) were administered at 3 and 15 months after the index stroke.

The mean (s.d) age was 73.3 ± 7.2 in women and 72.1 ± 6.9 in men. Men had higher education years, less diabetes and higher MMSE scores (p < 0.05). At 3 months after stroke, volume of the left DLPFC was significantly correlated with VFT score in women rather than men, even after controlled by age, education years, neurological deficit, diabetes, WMLs volume and infarct location (partial r = 0.477, p = 0.018). At 15 months, this correlation remained significant (partial r = 0.548, p = 0.006) in women.

Sex difference may be present in the neuropsychological mechanism of verbal fluency impairment in patients with cerebrovascular disease.

The aims of this study were to examine whether different domains of quality of life (QOL) are differently affected by depressive disorders by comparing QOL of subjects with and without depressive disorders, and to examine the association of QOL with self-stigma, insight and adverse effects of medication among subjects with depressive disorders.

The QOL on the four domains of the WHOQOL-BREF Taiwan version were compared between the 229 subjects with depressive disorders and 106 control subjects without depressive disorder. Among the subjects in the depressive group, the association between the four QOL domains and subjects' self-stigma, insight, and adverse effects of medication were examined using multiple regression analyses by controlling for the influence of depression, socio-demographic and clinical characteristics and family function.

The results found that subjects with depressive disorders had poorer QOL on the physical, psychological and social relationship domains than the non-depressive control group. The depressive subjects who had more severe self-stigma had poorer QOL on all four domains. The depressive subjects who had higher levels of awareness of illness had poorer QOL on the physical and psychological domains. The depressive subjects who perceived more severe adverse effects from medication had poorer QOL on the physical, psychological and environmental domains.

The results of this study demonstrate that different domains of QOL are differently affected by depressive disorders, and that clinicians must consider the negative influences of self-stigma, insight and adverse effects from medication on QOL of subjects with depressive disorders.

Somatization is a common symptom of depression. Somatization is also related to sleep problem including insomnia.Depression is the one of the most common cuase of insomnia. Therefore, it would be needed to investigate the interaction between depression, insomnia and somatization.

To investigate the independent effects of major depressive disorder (MDD) and insomnia on somatization.

To compare somatization of primary insomnia, MDD with insomnia, MDD without insomnia, and normal controls.

A total of 181 participants without serious medical problem were recruited. Subjects were divided into 4 groups based on the SCID-IV and ICD-10 insomnia criteria:

1. 1) normal controls,

2. 2) primary insomnia,

3. 3) MDD without insomnia, and

4. 4) MDD with insomnia.

The somatization subscores of the SCL-90-R were completed by participants.

There were significant between-group differences in somatization (F=25.30, p< 0.001). MDD with insomnia showed higher somatization compared to normal controls (p< 0.001), primary insomnia (p=0.01), or MDD without insomnia (p< 0.001). Primary insomnia had higher somatization than normal controls (p< 0.01), while there was no significant difference between MDD without insomnia and normal controls. Presence of insomnia predicted higher somatization (beta=0.44, p< 0.001), while there was only non-significant association between MDD and somatization (beta=0.14, p=0.08).

In the current study, insomnia was associated with somatization independently from major depression. Subjects with primary insomnia showed higher somatization. Within MDD patients, presence of insomnia was related to higher somatization. Our finding suggests that insomnia may partly mediate the relationship between depression and somatization.

This study was conducted to examine sexual dimorphic effects of highly palatable food access during adolescence and youth on psychoemotional behaviors of rats and its underlying neural mechanism.

Male and female Sprague Dawley pups had free access to chocolate cookie rich in fat (highly palatable food) from postnatal day 28 in addition to ad libitum chow, and the control groups received chow only. The food conditions were continued though out the entire experimental period, and the neurochemical and behavioral measurements were performed during young adulthood. Corticosterone levels during 2 h of restraint stress were analyzed with radioimmunoassay, and ΔFosB and brain-derived neurotrophic factor (BDNF) expression in the nucleus accumbens (NAc) with western blot analysis.

Cookie access did not affect body weight gain and total caloric intake in both sexes; however, it increased retroperitoneal fat depot only in males. The time spent in open arms during elevated plus maze test was decreased and immobility during forced swim test was increased in cookie-fed males, but not in cookie-fed females. Main effect of food condition on the stress-induced corticosterone increase was observed in males, but not in females, and cookie access increased BDNF expression in the NAc only in males.

Increased BDNF expression in the NAc and fat depot, in addition to the HPA axis dysfunction, may play roles in the pathophysiology of depression- and/or anxiety-like behaviors induced by cookie access.

The authors have not supplied their declaration of competing interest.

Although a number of studies have examined the relationship between depression and obesity, it is still insufficient to establish the specific pattern of relationship between depression and body mass index (BMI) categories. Thus, this study was aimed to investigate the relationship between depression and BMI categories.

A cross-sectional study was conducted for a cohort of 159,390 Korean based on Kangbuk Samsung Health Study (KSHS). Study participants were classified into 5 groups by Asian-specific cut-off of BMI (18.5, 23, 25 and 30 kg/m2). The presence of depression was determined by Center for Epidemiologic Studies-Depression scales (CES-D) = 16 and = 25. The adjusted odd ratios (ORs) for depression were evaluated by multiple logistic regression analysis, in which independent variable was 5 categories of BMI and dependent variable was depression. Subgroup analysis was conducted by gender and age.

When normal group was set as a reference, the adjusted ORs for depression formed U-shaped pattern of relationship with BMI categories [underweight: 1.31 (1.14–1.50), overweight: 0.94 (0.85–1.04), obese group: 1.01 (0.91–1.12), severe obese group: 1.28 (1.05–1.54)]. This pattern of relationship was more prominent in female and young age group than male and elderly subgroup. BMI level with the lowest likelihood of depression was 18.5 kg/m2 to 25 kg/m2 in women and 23 kg/m2 to 25 kg/m2 in men.

There was a U-shaped relationship between depression and BMI categories. This finding suggests that both underweight and severe obesity are associated with the increased risk for depression.