BACKGROUND: Psychotic depression (PD) is characterized by the co-occurrence of emotional dysfunction and psychotic symptoms such as delusions and hallucinations with poor clinical outcomes. TSH may involve in the development of PD. This study aims to explore relationship between TSH and PD.
METHODS: A total of 1718 outpatients diagnosed as FEDN MDD were recruited in this study. The relationship between PD and TSH was evaluated using multivariable binary logistic regression analysis. To assess the presence of non-linear associations, a two-piecewise linear regression model was employed. Furthermore, interaction and stratified analyses were conducted with respect to sex, education, marital status, comorbid anxiety, and suicide attempt.
RESULTS: Multivariable logistic regression analysis revealed that TSH was positively associated with the risk of PD after adjusting for confounders (OR = 1.26, 95% CI: 1.11 to 1.43; p < 0.05). Smoothing plots showed a nonlinear relationship between TSH and PD, with the inflection point of TSH being 4.94 mIU/L. On the right of the inflection point, for each unit increase in serum TSH level on the right side of the inflection point, the probability of PD increased substantially by 47% (OR = 1.47, 95% CI: 1.25 to 1.73, p < 0.001), while no significant association was observed on the left side of the inflection point (OR = 0.87, 95% CI: 0.67 to 1.14, p = 0.32).
CONCLUSIONS: Our investigation showed a nonlinear TSH-PD relationship in FEDN MDD patients, thus contributing to effective intervention strategies for psychotic symptoms in depression patients.

UNASSIGNED: The basic objective of any civilization is to preserve a happy family. The quality of one\'s sexual encounters is crucial to a happy marriage. Couples\' dissatisfaction in this area may be the cause of several social, psychological, and medical issues. The way reality is interpreted, which shapes behaviors and emotions, is established by beliefs. These beliefs, which are among the most frequent causes of male sexual problems, include those relating to high performance, women\'s sexual enjoyment, and sexual conservatism.
UNASSIGNED: To identify the misconceptions about sexuality among psychiatry patients. Method This cross-sectional study was carried out at the School of Medical Sciences and Research, Sharda University. We enrolled 200 samples and it is assessed through Sexual Beliefs Questionnaire (Male version).
UNASSIGNED: Sexual beliefs were assessed in different domains as well as overall sexual belief score was also estimated. The different domains in which the sexual beliefs were scored were sexual conservatism, female sexual power, macho belief, beliefs about women\'s sexual satisfaction, restrictive attitude toward sex, and sex as an abuse of men\'s power.
UNASSIGNED: The development of both psychiatric and sexological care will benefit from the early identification of the intricate relationships between psychopathology, the adverse effects of antipsychotic medicines, and sexuality. However, longitudinal studies are needed to anticipate the relationship more accurately between sexual dysfunction and sexual beliefs at a larger sample size. Sexual beliefs are significant contributors to sexual dysfunction.

Brain imaging-derived structural correlates of alcohol involvement have largely been speculated to arise as a consequence of alcohol exposure. However, they may also reflect predispositional risk. In substance naïve children of European ancestry who completed the baseline session of the Adolescent Brain Cognitive Development (ABCD) Study (n = 3013), mixed-effects models estimated whether polygenic risk scores (PRS) for problematic alcohol use (PAU-PRS) and drinks per week (DPW-PRS) are associated with magnetic resonance imaging-derived brain structure phenotypes (i.e., total and regional: cortical thickness, surface area and volume; subcortical volume; white matter volume, fractional anisotropy, mean diffusivity). Follow-up analyses evaluated whether any identified regions were also associated with polygenic risk among substance naïve children of African ancestry (n = 898). After adjustment for multiple testing correction, polygenic risk for PAU was associated with lower volume of the left frontal pole and greater cortical thickness of the right supramarginal gyrus (|βs| > 0.009; ps < 0.001; psfdr  < 0.046; r2 s < 0.004). PAU PRS and DPW PRS showed nominally significant associations with a host of other regional brain structure phenotypes (e.g., insula surface area and volume). None of these regions showed any, even nominal association among children of African ancestry. Genomic liability to alcohol involvement may manifest as variability in brain structure during middle childhood prior to alcohol use initiation. Broadly, alcohol-related variability in brain morphometry may partially reflect predisposing genomic influence. Larger discovery genome-wide association studies and target samples of diverse ancestries are needed to determine whether observed associations may generalize across ancestral origins.

Anxiety symptoms are common in Parkinson\'s disease (PD). A link between anxiety and cognitive impairment in PD has been demonstrated.
Using resting-state functional magnetic resonance imaging, we investigated intrinsic brain network connectivity correlates of anxiety symptoms in a cohort of drug-naive, cognitively unimpaired patients with PD.
The intrinsic functional brain connectivity of 25 drug-naive, cognitively unimpaired PD patients with anxiety, 25 without anxiety, and 20 matched healthy controls was compared. All patients underwent a detailed behavioral and neuropsychological evaluation. Anxiety presence and severity were assessed using the Parkinson\'s Disease Anxiety Scale. Single-subject and group-level independent component analyses were used to investigate functional connectivity differences within and between the major resting-state networks.
Decreased connectivity within the default-mode and sensorimotor networks (SMN), increased connectivity within the executive-control network (ECN), and divergent connectivity measures within salience and frontoparietal networks (SN and FPN) were detected in PD patients with anxiety compared with those without anxiety. Moreover, patients with anxiety showed a disrupted inter-network connectivity between SN and SMN, ECN, and FPN. Anxiety severity was correlated with functional abnormalities within these networks.
Our findings demonstrated that an abnormal intrinsic connectivity within and between the most reported large-scale networks may represent a potential neural correlate of anxiety symptoms in drug-naive PD patients even in the absence of clinically relevant cognitive impairment. We hypothesize that these specific cognitive and limbic network architecture changes may represent a potential biomarker of treatment response in clinical trials. © 2020 International Parkinson and Movement Disorder Society.

The objective of this study was to investigate the effects of levodopa on functional brain networks in Parkinson\'s disease.
We acquired resting state functional magnetic resonance imaging in 30 drug-naïve participants with Parkinson\'s disease and 20 age-matched healthy controls. Each participant was studied following administration of a single oral dose of either levodopa or placebo in a randomized, double-blind, crossover design.
The greatest observed differences in functional connectivity were between Parkinson\'s disease versus control participants, independent of pharmacologic intervention. By contrast, the effects of levodopa were much smaller and detectable only in the Parkinson\'s disease group. Moreover, although levodopa administration in the Parkinson\'s disease group measurably improved motor performance, it did not increase the similarity of functional connectivity in Parkinson\'s disease to the control group.
We found that a single, small dose of levodopa did not normalize functional connectivity in drug-naïve Parkinson\'s disease. © 2019 International Parkinson and Movement Disorder Society.

Patients with genetic generalized epilepsy (GGE) have subtle morphologic abnormalities of the brain revealed with magnetic resonance imaging (MRI), particularly in the thalamus. However, it is unclear whether morphologic abnormalities of the brain in GGE are a consequence of repeated seizures over the duration of the disease, or are a consequence of treatment with antiepileptic drugs (AEDs), or are independent of these factors. Therefore, we measured brain morphometry in a cohort of AED-naive patients with GGE at disease onset. We hypothesize that drug-naive patients at disease onset have gray matter changes compared to age-matched healthy controls.
We performed quantitative measures of gray matter volume in the thalamus, putamen, caudate, pallidum, hippocampus, precuneus, prefrontal cortex, precentral cortex, and cingulate in 29 AED-naive patients with new-onset GGE and compared them to 32 age-matched healthy controls. We subsequently compared the shape of any brain structures found to differ in gray matter volume between the groups.
The thalamus was the only structure to show reduced gray matter volume in AED-naive patients with new-onset GGE compared to healthy controls. Shape analysis revealed that the thalamus showed deflation, which was not uniformly distributed, but particularly affected a circumferential strip involving anterior, superior, posterior, and inferior regions with sparing of medial and lateral regions.
Structural abnormalities in the thalamus are present at the initial onset of GGE in AED-naive patients, suggesting that thalamic structural abnormality is an intrinsic feature of GGE and not a consequence of AEDs or disease duration.

BACKGROUND: Impulse control disorders can be triggered by dopamine replacement therapies in patients with PD. Using resting-state functional MRI, we investigated the intrinsic brain network connectivity at baseline in a cohort of drug-naive PD patients who successively developed impulse control disorders over a 36-month follow-up period compared with patients who did not.
METHODS: Baseline 3-Tesla MRI images of 30 drug-naive PD patients and 20 matched healthy controls were analyzed. The impulse control disorders\' presence and severity at follow-up were assessed by the Questionnaire for Impulsive-Compulsive Disorders in Parkinson\'s Disease Rating Scale. Single-subject and group-level independent component analysis was used to investigate functional connectivity differences within the major resting-state networks. We also compared internetwork connectivity between patients. Finally, a multivariate Cox regression model was used to investigate baseline predictors of impulse control disorder development.
RESULTS: At baseline, decreased connectivity in the default-mode and right central executive networks and increased connectivity in the salience network were detected in PD patients with impulse control disorders at follow-up compared with those without. Increased default-mode/central executive internetwork connectivity was significantly associated with impulse control disorders development (P < 0.05).
CONCLUSIONS: Our findings demonstrated that abnormal brain connectivity in the three large-scale networks characterizes drug-naive PD patients who will eventually develop impulse control disorders while on dopaminergic treatment. We hypothesize that these divergent cognitive and limbic network connectivity changes could represent a potential biomarker and an additional risk factor for the emergence of impulse control disorders. © 2017 International Parkinson and Movement Disorder Society.

BACKGROUND: Studies on the blood pressure lowering effect of renal denervation (RDN) in resistant hypertensive patients have produced conflicting results. Change in medication usage during the studies may be responsible for this inconsistency. To eliminate the effect of medication usage on blood pressure we focused on unmedicated hypertensive patients who underwent RDN.
RESULTS: Our study reports on a cohort of patients, who were not on blood pressure lowering drugs at baseline and during follow-up, from eight tertiary centers. Data of patients were used when they were treated with RDN and had a baseline office systolic blood pressure (SBP) ≥140 mmHg and/or 24-h ambulatory SBP ≥130 mmHg. Our primary outcome was defined as change in office and 24-h SBP at 12 months after RDN, compared to baseline. Fifty-three patients were included. There were three different reasons for not using blood pressure lowering drugs: (1) documented intolerance or allergic reaction (57 %); (2) temporary cessation of medication for study purposes (28 %); and (3) reluctance to take antihypertensive drugs (15 %). Mean change in 24-h SBP was -5.7 mmHg [95 % confidence interval (CI) -11.0 to -0.4; p = 0.04]. Mean change in office SBP was -13.1 mmHg (95 % CI -20.4 to -5.7; p = 0.001). No changes were observed in other variables, such as eGFR, body-mass-index and urinary sodium excretion.
CONCLUSIONS: This explorative study in hypertensive patients, who are not on blood pressure lowering drugs, suggests that at least in some patients RDN lowers blood pressure.

The etiology of schizophrenia continues to be confounding and elusive. Some knowledge gaps exist in the neurodegenerative theory of schizophrenia. Oxidative DNA damage and repair deficits are relevant to the mechanisms of neurodegeneration but have not been studied in drug naïve schizophrenia. The present study used the comet assay technique to study the extent of DNA damage in circulating peripheral lymphocytes of patients with drug naïve schizophrenia (n = 40) along with an age and gender matched control group (n = 40). We also assessed the DNA repair efficiency in cases following incubation in a nutrient medium. All the assayed comet parameters demonstrated significantly greater baseline DNA damage in cases in comparison to the controls except for head diameter (p < 0.001 for all significant results, p = 0.32 for head diameter). Gender, age and duration of illness (p = 0.21, 0.69 and 0.12 respectively for tail length) did not influence any of the parameters significantly. Significant decrease was noted in the comet tail length and percentage of DNA in comet tail (p < 0.001 for both) in cases following incubation suggesting that the DNA repair machinery was preserved. No difference in DNA repair efficiency was noted between the genders (p = 0.23 for tail length). Our findings confirm the presence of significant baseline DNA damage in schizophrenia even prior to the initiation of anti-psychotic treatment. Additionally, intact genomic repair efficiency was noted in this group as a whole. These results provide some evidence for oxidative DNA damage as molecular link underpinning neurodegeneration in drug naïve schizophrenia.

OBJECTIVE: We tested the hypothesis that metabolic disturbances in people with schizophrenia exist as a part of the schizophrenic syndrome, even when the antipsychotic drug effect is eliminated. We aimed to determine the prevalence of metabolic syndrome among patients with schizophrenia who were antipsychotic drug-naive or drug-free and their siblings for comparison with healthy controls.
METHODS: One-hundred-two patients with schizophrenia (drug-naïve or drug-free), 64 siblings and 70 age-matched healthy subjects were recruited for this case-control study. Metabolic syndrome was assessed based on Adult Treatment Panel (ATP) III, adapted ATP III and International Diabetes Federation criteria. Student\'s t-tests, chi-squared tests, Kruskal-Wallis tests and Bonferroni corrections were used as appropriate.
RESULTS: The diagnoses of metabolic syndrome and metabolic disturbances as a subsyndromal state were found to be significantly more frequent in patients and their siblings than in the controls. Low levels of high-density lipoprotein cholesterol and disturbances in blood pressure put the patient group at risk for metabolic syndrome even before they were exposed to antipsychotic drugs.
CONCLUSIONS: Although antipsychotic drugs have consistently been related to disturbances of glucose and lipid metabolism in patients with schizophrenia, this study showed that patients with schizophrenia and their siblings are already at a high risk for metabolic syndrome independent of any antipsychotic effects. These individuals should be monitored regularly following a diagnosis of schizophrenia.