To assess the effects of treatment with lurasidone on risk for metabolic syndrome (MetS) in patients with schizophrenia.

Rates of metabolic syndrome during treatment with lurasidone (40-160 mg/d) were analyzed using pooled, short-term data from three randomized, double-blind, placebo-controlled studies (vs olanzapine and quetiapine XR); long-term data from two active-comparator-controlled studies (vs risperidone and quetiapine XR); and data from two open-label studies in which patients were switched from olanzapine or risperidone to lurasidone.

MetS was defined based on the National Cholesterol Education Program criteria. In short-term studies, the odds of meeting criteria for MetS at week 6 LOCF (adjusted for baseline metabolic syndrome status) was similar for the lurasidone and placebo groups (OR = 1.18; [95% CI, 0.81-1.71]; P = .39), but the odds (vs placebo) were significantly greater for olanzapine (OR = 2.81; [95% CI, 1.53-5.15]; P < .001) and quetiapine (OR = 3.49; [95% CI, 1.93-6.29]; P < .0001). No dose effect was observed for lurasidone across the dose range of 40-160 mg/d. In long-term studies, the odds of MetS after 12 months of treatment was significantly higher for risperidone compared with lurasidone (OR = 2.12; 95% CI, 1.15-3.90; P = .016) and for quetiapine XR compared with lurasidone (OR = 3.92; 95% CI, 1.15-13.40; P = .029). In open-label extension studies, the rate of MetS decreased in patients switched to lurasidone after 6 weeks of treatment with olanzapine or 12 months of treatment with risperidone.

In this analysis of lurasidone clinical trials, the odds of developing metabolic syndrome were minimal during short- and long-term treatment with lurasidone (40-160 mg/d).

Depression is considered to be the most difficult to treat phase of bipolar disorder as patients experience residual symptoms causing long-term disability. This work aims to explore the role of add-on stimulant and stimulant-like medication in resistant bipolar depression patients.

Systematic review of add-on stimulants and stimulant-like drugs in resistant bipolar depression by following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Analysis was performed using the random-effects models. Heterogeneity was evaluated with Cochran’s Q and I2 statistics.

Six randomized controlled trials of add-on modafinil, armodafinil, and lisdexamphetamine (LDX) (n = 813) vs placebo (n = 815) in the treatment of resistant bipolar depression were included. These drugs were more likely to induce remission from an episode of resistant bipolar depression (relative risk [RR] = 1.37; 95% confidence interval [CI]: 1.06-1.77; number needed to treat for an additional beneficial outcome = 16). Moreover, they did not induce more dropouts than placebo (RR = 1.04; 95% CI: 0.91-1.18), nor did they increase the risk of adverse effects (53/772 vs 41/771) at the end of treatment (RR = 1.30; 95% CI: 0.81-2.10; number needed to treat for an additional harmful outcome = 62). Suicidality and manic switch were not affected by active treatment. Heterogeneity was low (Cochran’s Q: P > .05), but sometimes with a large CI.

LDX, modafinil, and armodafinil seem to offer a reasonably well-tolerated and safe treatment in resistant bipolar depression. Treatment guidelines should, therefore, be revised to include these medications earlier in the therapeutic algorithm for resistant acute bipolar depression. Further research is, however, necessary for the elucidation of the clinical usefulness of these and other similar compounds.

Little is known about the relationship between autistic traits and addictive behaviors such as problem gambling. Thus, the present study examined clinical characteristics and multiple facets of cognition in young adults who gamble and have autistic traits.

A total of 102 young adults who gamble were recruited from two Mid-Western university communities in the United States using media advertisements. Autistic traits were examined using the brief Autism-Spectrum Quotient (AQ-10). Clinician rating scales, questionnaires, and cognitive tests were completed. Relationships between AQ10 scores and demographic, gambling symptom, and neurocognitive measures were evaluated.

Autistic traits were correlated with disordered gambling symptoms, attention-deficit/hyperactivity disorder (ADHD) symptoms, trait impulsivity, and some types of obsessive–compulsive symptoms. In regression, ADHD no longer significantly related to autistic traits once disordered gambling symptoms were accounted for; whereas the link between autistic traits and disordered gambling symptoms was robust even controlling for ADHD.

These data suggest a particularly strong relationship between autistic traits and problem gambling symptoms, as well as certain aspects of impulsivity and compulsivity. The link between ADHD and autistic traits in some prior studies may have been attributable to disordered gambling symptoms, which was likely not screened for, and since individuals may endorse ADHD instruments due to other impulsive/compulsive symptom types (eg, gambling). The contribution of autistic traits to the emergence and chronicity of disordered gambling now requires further scrutiny, not only in community samples (such as this) but also in clinical settings.

This study examined the proximate causes of psychotic patients’ aggression upon the admission to the psychiatric wards of a university and two state hospitals.

The authors used a semistructured interview to elicit proximate causes of assaults from the assailants and victims. The treating psychiatrists and nurses provided additional information. Based on this interview, aggressive episodes were categorized as psychotic, impulsive and planned.

A total of 820 assaults committed by 289 newly admitted violent psychotic inpatients were evaluated. The interview ratings indicated that 76.71% of the assaults were directly driven by psychotic symptoms and 22.32% of all attacks were labeled as impulsive. Only 0.98% of assaults were categorized as planned.

These findings indicate that assaultive behavior among recently admitted acute psychiatric inpatients with untreated or undertreated psychosis is primarily driven by psychotic symptoms and disordered impulse control. Because each type of assault requires a different management, identifying the type of assault is crucial in determining treatment interventions.

Although problematic pornography use (PPU) will soon be diagnosable through the International Classification for Diseases, 11th revision, its clinical profile remains contentious. The current study assessed whether PPU may be characterized by various symptoms sometimes observed among online recovery forums that currently lack empirical assessment, such as heightened cognitive-affective issues following pornography use and sexual dysfunction with partners as a result of escalating use.

Cross-sectional surveys were completed by male PPUs (N = 138, mean age = 31.75 years, standard deviation = 10.72) recruited via online recovery communities and Amazon Mechanical Turk. Multiple regression analysis was performed using the Problematic Pornography Use Scale as the dependent variable and variables of interest (Arizona Sexual Experiences Scales modified for partnered sex and pornography use, Brunel Mood Scale, Social Interaction Anxiety Scale, and the Tolerance subscale from the Problematic Pornography Consumption Scale) and potential confounders (eg, comorbid psychopathology) as independent variables.

Current levels of pornography use, indicators of tolerance and escalation, greater sexual functioning with pornography, and psychological distress were uniquely associated with PPU severity, while cognitive-affective issues after pornography use, impulsivity and compulsivity were not. Although sexual dysfunction did not predict PPU severity, nearly half the sample indicated sexual dysfunction with intimate partners.

The present findings suggest that PPU may be characterized by tolerance and escalation (as per substance addiction models), greater sexual responsivity toward pornography, and psychological distress. Meanwhile, the high rate of partnered sexual dysfunction observed suggests that PPU might be somewhat separable from other forms of compulsive sexual behavior.

The present study aimed to determine whether the number of hospitalizations in schizophrenia patients is associated with reduced cognitive performance, which may in turn imply that recurrences indirectly lead to a worsening in the disorder’s progression.

Cognitive performance in stable schizophrenia patients was assessed using the Brief Assessment of Cognition in Schizophrenia, Japanese-language version, on 30 patients who had not experienced any hospitalizations (G0), 57 patients who had experienced only one hospitalization (G1), 47 patients with two hospitalizations (G2), and 59 patients with three or more hospitalizations (G3).

Significant differences in motor function and attention and processing speed were found between patients with G0 and those with G1. Significant differences in working memory and verbal fluency were found between patients with G1 and those with G2. Patients with G3 performed even more poorly in comparison with those with G1, showing deficits in verbal memory, working memory, executive function, and composite score. The patients with G3 displayed a greater range of impairment and demonstrated deficits in executive function compared with patients with G2. Finally, G2 and G3 performed more poorly than G0, with deficits in the various cognitive areas.

The number of hospitalizations predicted cognitive performance, which suggests that relapse or recurrence may have a long-term neuropsychological impact. Prospective follow-up studies must be completed to explore this effect further because better treatment adherence may have a protective effect on neurocognitive function.

Clinicians who recognize functional neurological disorders (FND) may not share that diagnosis with patients. Poor communication delays treatment and contributes to substantial disability in FND. Diagnostic (ICD-10) coding, one form of medical communication, offers an insight into clinicians’ face-to-face communication. Therefore, quantifying the phenomenon of noncoding, and identifying beliefs and practice habits that reduce coding, may suggest routes to improve medical communication in FND.

We reviewed all pediatric neurology consultations in our hospital from 2017 to 2020, selecting those in which neurologists explicitly stated an FND-related diagnosis (N = 57). We identified the neurological symptoms and ICD-10 codes assigned for each consultation. In parallel, we reviewed all encounters that utilized FND-related codes to determine whether insurers paid for this care. Finally, we assessed beliefs and practices that influence FND-related coding through a nationwide survey of pediatric neurologists (N = 460).

After diagnosing FND, neurologists selected FND-related ICD-10 codes in only 22.8% of consultations. 96.2% of neurologists estimated that they would code for non-epileptic seizure when substantiated by electroencephalography; in practice, they coded for 36.7% of such consultations. For other FND manifestations, neurologists coded in only 13.3% of cases. When presented with FND and non-FND scenarios with equal levels of information, neurologists coded for FND 41% less often. The strongest predictor of noncoding was the outdated belief that FND is a diagnosis of exclusion. Coding for FND never resulted in insurance nonpayment.

Noncoding for FND is common. Most factors that amplify noncoding also hinder face-to-face communication. Research based on ICD-10 coding (eg, prevalence and cost) may underestimate the impact of FND by >fourfold.