Learning anxiety disorder detrimentally impacts both academic performance and the mental well-being of university students. This study aims to investigate whether the integration of electronic communication technology into teaching methods within universities can alleviate students’ learning anxiety and assess the efficacy of this approach.

Participants were selected from a university and divided into an experimental group and a control group. The experimental group underwent classroom teaching using electronic communication technology, encompassing online teaching platforms, virtual laboratories, and other relevant tools. In contrast, the control group received traditional face-to-face teaching. Anxiety questionnaires and academic performance metrics were employed as data collection instruments. Data were analyzed using Stata 8.0 statistical software.

The learning anxiety scores of students in the experimental group were notably lower compared to those in the control group. Specifically, the average anxiety score for the experimental group was 3.82, while the control group had an average anxiety score of 4.96. Statistical analysis utilizing appropriate methods confirmed a statistically significant difference between the two groups (P<0.05).

Empirical evidence from this study substantiates that the integration of electronic communication technology effectively mitigates symptoms of learning anxiety among students and enhances their learning outcomes. Utilizing online teaching platforms, virtual laboratories, and similar tools empowers students to engage in more self-directed and proactive learning, consequently reducing anxiety that may arise from face-to-face teaching scenarios.

The Philosophy and Social Science Research Project of Higher Education of Jiangsu Province (No. 2021SJA2140).

Few studies have examined treatment response in adolescents with schizophrenia who are treatment-naive; and there is no placebo-controlled study that we are aware of in first episode treatment-naive patients with schizophrenia. The aim of this analysis was to evaluate the long-term efficacy of lurasidone in antipsychotic-naive adolescents with schizophrenia.

Patients aged 13–17 years with schizophrenia, and a PANSS total score ≥70 and <120, were randomized to 6 weeks of double-blind (DB) treatment with lurasidone (40 or 80 mg/day) or placebo. Six-week completers were eligible to enroll in a 2-year open-label extension phase receiving lurasidone flexibly dosed from 20–80 mg/day. In a post-hoc analysis, efficacy was evaluated for 2 patient groups based on treatment status prior to entering the initial 6-week DB study (treatment naïve [TN] vs. treated previously [TP]). Treatment-naïve was defined as never having received antipsychotic treatment. Efficacy measures included the PANSS total score and the Clinical Global Impression, Severity (CGI-S) score. Level of functioning was assessed using the Children’s Global Assessment Scale (CGAS), with a score of 70 representing normative levels of functioning.

A total of 50 TN and 221 TP patients completed the 6-week DB study and entered the extension study; and 30 (60.0%) TN and 126 (57.0%) TP patients completed 104 weeks. During the initial 6 weeks of DB treatment, mean change in PANSS total score at endpoint was greater for lurasidone vs. placebo in both the TN group (−25.0 vs. −14.4; P<0.02; effect size, 0.75), and in the TP group (−17.3 vs. −10.0; P<0.001; effect size, 0.45). During OL extension phase treatment with lurasidone, mean change from DB baseline in the PANSS total score for TN and TP patients, at week 52 was −32.6 (n=38) and −28.1 (n=151), respectively; and at week 104 was −33.6 (n=30) and −29.2 (n=126), respectively. Mean change from DB baseline in CGI-S score at both weeks 52 and 104 was −1.8 for TN patients and −1.5 for TP patients. At DB baseline mean CGAS scores indicated significant functional impairment in both the TN and TP patients (CGAS=48 and 43, respectively). During OL treatment with lurasidone, mean change (from DB baseline) in the CGAS score at Weeks 52 and 104, respectively, was +22.0 and +22.9 in TN patients, and +21.1 and +22.9 in TP patients. During OL treatment with lurasidone, mean observed change from DB baseline in the weight (in kg,) at Weeks 52 and 104, respectively, was +4.2 and +4.8 in TN patients, and +4.0 and +5.0 in TP patients. These weight increases are consistent with expected weight gains in adolescents during a 2-year period (based on CDC growth charts).

In this post-hoc analysis of a 2-year study, adolescents with schizophrenia who had received no previous antipsychotic therapy showed greater improvement compared to previously treated patients during both short- and long-term treatment with lurasidone.

Sunovion Pharmaceuticals Inc.

Fibromyalgia (FM) is a chronic widespread pain syndrome. Although its mechanism remains relatively unknown, accelerated neurodegeneration in the brain has been reported in patients with FM. Sleep disturbance can increase the risk of neurocognitive disorders, which are associated with tau and beta-amyloid (Aβ) protein accumulation. We hypothesize neurodegeneration in patients with FM may be associated with sleep disturbance.

In this case-control study, we analyzed serum tau and Aβ levels and their association with symptom profiles for patients with FM, by recruiting 22 patients with FM and 22 age-matched healthy participants. The visual analog scale, Fibromyalgia Impact Questionnaire, pressure pain threshold test, Pittsburgh Sleep Quality Index (PSQI), Beck Depression Inventory-II, Beck Anxiety Inventory, and serum tau and beta-amyloid-42 (Aβ-42) levels were recorded. The Mann–Whitney test was conducted to compare questionnaire and protein level results between the groups. Pearson correlation test was conducted to investigate the correlation of questionnaire scores with tau and Aβ-42 levels in patients with FM. The significance level was set at P < .05.

Serum tau and Aβ-42 levels were significantly higher in patients with FM than in controls. A positive correlation between serum tau levels and PSQI scores was observed in patients with FM (r = 0.476, P = .025). We found that only sleep disturbance in patients with FM was significantly associated with higher serum tau levels among all symptom scores.

We suggest sleep disturbance may play a vital role in the pathomechanism of accelerated neurodegeneration in FM.

Optimizing TMS treatment for Depression - The 19 Minute Dash™ protocol

NeuroStar transcranial magnetic stimulation (TMS) is an effective treatment for patients with major depressive disorder. Due to the treatment session duration, a reduced treatment time would promote patients’ comfort and convenience. Also, shorter treatment sessions of retained efficacy and safety would increase access to treatment. This reduction could be accomplished by decreasing the time between TMS pulse sequences, the intertrain interval (ITI).

Meta-analysis of TMS delivered using varying treatment parameters, particularly the ratio of train duration (“on-time”) to ITI (“off-time”). PubMed and SCOPUS databases were searched through March 30, 2015 using the terms: “transcranial magnetic stimulation”, “TMS”, “rTMS”, “inter-train interval”, “inter-stimulus interval”, and “cortical spread”. Three hundred and one articles were identified comprising a total of 3359 patients. Clinical outcomes were reported as the proportion of patients achieving response defined as 50% reduction in baseline score on the primary outcome measure in each study. Treatment risk was assessed by the frequency of adverse events reported, and specifically considering the incidence of seizures.

This analysis confirms prior reports that the variables which impact treatment efficacy are the number of treatmentsessions, the number of pulses per session and the percent motor threshold. Varying the train duration/ITI (on-time/off-time) ratio over a broad range from 2.0 to 14 did not impact efficacy or safety.

Shortening the ITI to 11 seconds does not impact the safety and antidepressant effectiveness of the NeuroStar TMS and would result in shortening of each treatment session from approximately 37.5 to 19 minutes.

Neuronetics, Inc.

How the trajectory of response to medication (and placebo response) varies among selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), benzodiazepines and across anxiety disorders is unknown.

We performed a meta-analysis using weekly symptom severity data from randomized, parallel-group, placebo-controlled trials of SSRIs, SNRIs, and benzodiazepines in adults with anxiety disorders. Response was modeled for the standardized change in anxiety using Bayesian hierarchical models.

Across 122 trials (N=15,760), SSRIs, SNRIs, and benzodiazepines produced significant improvement in anxiety compared to placebo. Benzodiazepines produced faster improvement by the first week of treatment (p < 0.001). By week 8, the response for benzodiazepines and SSRIs (p = 0.103) and SNRIs (p = 0.911) did not differ nor did SSRIs and SNRIs differ (p = 0.057), although for patients with generalized anxiety disorder (GAD), the benzodiazepines produced greater improvement than SNRIs at week 8 (difference − 12.42, CrI: −25.05 to −0.78, p = 0.037). Medication response was similar across anxiety disorders except for benzodiazepines, which produced greater improvement over the first 4 weeks compared to SSRIs and SNRIs in panic disorder. For SSRIs and SNRIs, women improved more than men, and for benzodiazepines, older patients improved more compared to younger patients. Finally, placebo response plateaued by week 4 of treatment, and, at week 8, social anxiety disorder trials had lower placebo response compared to other anxiety disorders.

Benzodiazepines show early improvement compared to SSRIs and SNRIs. However, by week 8, all treatments yield similar results. Patient characteristics influence the improvement trajectory and magnitude, suggesting potential for personalized medication selection.

Serotonin norepinephrine reuptake inhibitors (SNRIs) have been postulated to afford benefits in alleviating anhedonia and amotivation. This post hoc pooled analysis evaluated the effect of venlafaxine XR, an SNRI, on these symptoms in patients with major depressive disorder (MDD).

Data was pooled from five short-term randomized, placebo-controlled studies of venlafaxine XR for the treatment of MDD, comprising 1087 (venlafaxine XR, n = 585; placebo, n = 502) adult subjects. The change from baseline score in the MADRS anhedonia factor (based on items 1 [apparent sadness], 2 [reported sadness], 6 [concentration difficulties], 7 [lassitude], and 8 [inability to feel]) for anhedonia, and in motivational deficits (based on 3 items of HAM-D17: involvement in work and activities, psychomotor retardation, and energy level [ie, general somatic symptoms]) for amotivation, were measured through 8 weeks. Mixed model repeated measures (MMRMs) were used to analyze changes over time and ANCOVA to analyze the change from baseline at week 8 with LOCF employed to handle missing data.

At the end of 8 weeks, the change from baseline was significantly greater in patients on venlafaxine XR in both anhedonia (mean, 95% CI: −2.73 [−3.63, −1.82], p < 0.0001) and amotivation scores (mean, 95% CI: −0.78 [−1.04, −0.52], p < 0.0001) than those on placebo. For both measures, the between-group separation from baseline was statistically significant starting from week 2 onwards, and it increased over time.

This analysis demonstrates that venlafaxine XR is effective in improving symptoms of anhedonia and motivational deficits in patients with MDD.

(1) To determine whether there are sleep variables specific for obsessive-compulsive disorder (OCD) that are identifiable on polysomnographic findings; (2) to determine the possible relationship of OCD to other psychopathological disorders, with special emphasis on major depressive disorder (MDD).

Eighteen patients suffering from OCD (five of whom had a comorbid depressive disorder) were assessed by means of a standardized sleep questionnaire, the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) for the assessment of severity of obsessive-compulsive symptoms, and overnight polysomnography. Results were compared with those from a control group of 18 age- and sex-matched controls with no history of psychiatric disorders.

We found a significant decrease in sleep efficiency index (SEI), REM percent, REM latency, and slow wave sleep latency among OCD patients, compared with controls. The presence of comorbid major depression had no effect on the severity of OCD and had no significant effect on the sleep measures.

Sleep changes recorded polysomnographically in patients with OCD can be primary in origin and are independent of an associated major depressive disorder.