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Women diagnosed with premenstrual dysphoric disorder (PMDD) report significant symptom relief when treated with selective serotonin reuptake inhibitors, but few studies have addressed the possibility of capturing this effect in behavioral, laboratory-based tests. This study examined the effects of intermittent treatment with escitalopram (vs. placebo) on a behavioral measure of impulsivity and inattentiveness in women reporting high levels of premenstrual irritability and anger. Participants (  = 27) rated cardinal PMDD mood symptoms over three menstrual cycles using Visual Analogue Scales. In Cycles 2 and 3, participants displaying cyclicity with respect to the irritability/anger item received escitalopram (20 mg) or placebo in a randomized, single-blind, crossover design. The participants completed the Conners Continuous Performance Test (CPT 3) in the luteal phase of the intervention cycles. Additionally, they filled out the UPPS Impulsive Behavior Scale, once in the luteal phase and once in the follicular phase of the placebo cycle. In line with previous reports, escitalopram caused a significant reduction in self-rated irritability and anger in the luteal phase. When on escitalopram, the participants demonstrated a lower frequency of anticipatory responses and greater consistency in response speed in the CPT 3. With respect to self-reported impulsivity, participants reported higher levels of urgency and lower levels of sensation seeking in the luteal placebo phase versus the follicular phase. The finding that escitalopram impacted the outcome of the CPT 3 test in women with premenstrual irritability highlights the possible role of impulsivity in this condition.

This is the first prospective study aiming to quantify the effectiveness and safety of escitalopram monotherapy initiation where therapeutic drug monitoring (TDM) was used to achieve the therapeutic reference range (TRR) of plasma concentration. PsyCise-E (NCT05210140) was a hospital-based study conducted in Belgrade, Serbia, involving 92 outpatients with a baseline Hamilton Rating Scale for Depression (HAM-D) score higher than 13. The primary endpoint was the relative reduction in HAM-D score from baseline to week eight, with dose personalization based on TDM four weeks after treatment initiation. Patients were categorized into groups: (1) unadjusted (they achieved TRR at 10 mg/day), (2) adjusted (their dose was adjusted to achieve TRR) and (3) inadequate (they did not reach TRR). Safety was assessed by the occurrence of adverse drug reactions (ADRs) and QTc interval prolongation. Most patients required a dose escalation beyond 10 mg/day (71/92), and most patients achieved TRR after eight weeks (79/92). The 55% (95% CI: 47–64) reduction in HAM-D scores did not correlate with escitalopram plasma concentrations and did not differ between groups; however, response and remission rates were significantly higher in patients who achieved TRR by week four. The incidence of ADRs (47/92) increased by 3.2% (0.1–6.3) per ng/ml escitalopram, with no significant differences between the groups. QTc prolongation of 5.5 ms (1.8–9.3) did not correlate with plasma concentration and did not differ between groups. While TDM-guided dosing likely only marginally improved escitalopram effectiveness, it increased treatment safety as TDM-guided dose escalation did not lead to ADRs or QTc prolongation.

Background Obsessive-Compulsive Disorder (OCD) involves persistent, intrusive thoughts and repetitive behaviors. While SSRIs like escitalopram are common treatments, some patients do not respond adequately. This study aims to assess memantine’s effectiveness as an adjunct therapy to enhance executive function in OCD patients. Methods This study was a 16-week, randomized, double-blind, placebo-controlled clinical trial to evaluate if adding memantine to escitalopram helps treat OCD. A total of 60 participants were recruited from Namazi Hospital and Ibn Sina Polyclinic in Shiraz, Iran. Participants were randomly divided into two groups: the control group received escitalopram plus placebo, and the intervention group received escitalopram plus memantine. The main outcome, the severity of OCD symptoms, was measured using the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), and executive function was assessed using the Barkley Deficits in Executive Functioning Scale (BDEFS). Safety was checked weekly using the Drug Adverse Event Questionnaire. Data were analyzed using SPSS, with a significance level set at p  < 0.05. Results All sixty participants completed the 16 weeks of the study. Thirty participants per group (Placebo, Memantine) showed no significant differences in age, gender, or education ( P  > 0.05) at baseline. Both groups showed significant reductions in Y-BOCS scores ( P  < 0.001), with the Placebo group decreasing from 32.83 (SD = 4.04) to 5.30 (SD = 3.18) and the Memantine group from 31.60 (SD = 2.62) to 5.20 (SD = 2.62) without difference between groups ( P  = 0.12). Notebale Improvements in executive function were observed, particularly in time management, where Memantine outperformed Placebo ( P  = 0.03). Other domains showed no significant differences. Adverse events were minimal; gastrointestinal symptoms were rare, with Memantine showing a higher incidence but not statistically significant. Conclusion The study found that while both treatment regimens significantly alleviated OCD symptoms, memantine did not provide notable advantages over escitalopram alone, except in time management. Further research is needed to assess long-term effects and mechanisms of this combination therapy. Trial registration IRCT20211118053093N5, 25/06/2025.

AbstractObjectiveTo evaluate the comparative effectiveness and acceptability of oral monotherapy using psychedelics and escitalopram in patients with depressive symptoms, considering the potential for overestimated effectiveness due to unsuccessful blinding.DesignSystematic review and Bayesian network meta-analysis.Data sourcesMedline, Cochrane Central Register of Controlled Trials, Embase, PsycINFO, ClinicalTrial.gov, and World Health Organization’s International Clinical Trials Registry Platform from database inception to 12 October 2023.Eligibility criteria for selecting studiesRandomised controlled trials on psychedelics or escitalopram in adults with depressive symptoms. Eligible randomised controlled trials of psychedelics (3,4-methylenedioxymethamphetamine (known as MDMA), lysergic acid diethylamide (known as LSD), psilocybin, or ayahuasca) required oral monotherapy with no concomitant use of antidepressants.Data extraction and synthesisThe primary outcome was change in depression, measured by the 17-item Hamilton depression rating scale. The secondary outcomes were all cause discontinuation and severe adverse events. Severe adverse events were those resulting in any of a list of negative health outcomes including, death, admission to hospital, significant or persistent incapacity, congenital birth defect or abnormality, and suicide attempt. Data were pooled using a random effects model within a Bayesian framework. To avoid estimation bias, placebo responses were distinguished between psychedelic and antidepressant trials.ResultsPlacebo response in psychedelic trials was lower than that in antidepression trials of escitalopram (mean difference −3.90 (95% credible interval −7.10 to −0.96)). Although most psychedelics were better than placebo in psychedelic trials, only high dose psilocybin was better than placebo in antidepression trials of escitalopram (mean difference 6.45 (3.19 to 9.41)). However, the effect size (standardised mean difference) of high dose psilocybin decreased from large (0.88) to small (0.31) when the reference arm changed from placebo response in the psychedelic trials to antidepressant trials. The relative effect of high dose psilocybin was larger than escitalopram at 10 mg (4.66 (95% credible interval 1.36 to 7.74)) and 20 mg (4.69 (1.64 to 7.54)). None of the interventions was associated with higher all cause discontinuation or severe adverse events than the placebo.ConclusionsOf the available psychedelic treatments for depressive symptoms, patients treated with high dose psilocybin showed better responses than those treated with placebo in the antidepressant trials, but the effect size was small.Systematic review registrationPROSPERO, CRD42023469014.

To evaluate the synergistic effect of the Shugan Jieyu Capsule combined with Escitalopram in the treatment of senile depression. The study protocol has been registered in PROSPERO with registration number CRD42023440270. Eight databases, including PubMed, Embase, Cochrane Library, Web of Science, China National Knowledge Network (CNKI), China Biomedical Literature Database (CBM), VIP database, and Wanfang Database, were searched, respectively. Randomized controlled trial (RCTs) of the Shugan Jieyu Capsule combined with Escitalopram in the treatment of senile depression was included. The search time was from the listing of Shugan Jieyu Capsule (2009) to January 1, 2025. Outcome measures included Total effective rate, Hamilton Depression Scale (HAMD) score, Hamilton Anxiety Scale (HAMA) score, serum 5-hydroxytryptamine (5-HT), serum norepinephrine (NE), and Incidence of adverse reactions. The treatment period should be at least 6 weeks. Data extraction and methodological quality evaluation were carried out for the included literature, and statistical analysis was performed using RevMan 5.3 software. Finally, the Grading of Recommendations Assessment, Development and Evaluation (GRADE ) system was used to assess the quality of the evidence. A total of 8 RCTs were included in the study, with a total of 765 patients. The results of this meta-analysis showed that the combination of Shugan Jieyu Capsule and Escitalopram could improve Total effective rate [OR = 4.25, 95%CI(2.53, 7.14), P <0.00001] and reduce HAMD score in terms of clinical symptom indicators [SMD=-1.26, 95%CI(-1.45, -1.08), P <0.00001], and decrease HAMA score [SMD=-0.82, 95%CI(-1.05, -0.59), P <0.00001]. In terms of laboratory indexes, serum 5-HT levels could be increased in the combined group [MD = 31.92, 95%CI(28.34, 35.50), P  < 0.00001]. In terms of safety, no serious adverse reactions were observed in both group, and the incidence of adverse reactions was lower in the combined group [OR = 0.62, 95%CI(0.42, 0.92), P  = 0.02]. During the treatment period of 12 weeks, Shugan Jieyu Capsule combined with Escitalopram had a good effect in the treatment of senile depression, which could significantly reduce HAMD and HAMA scores of senile depression. In addition, the combined application of the two drugs can help to increase the level of serum 5-HT, without increasing the occurrence of adverse events, and has a good application prospect.

IntroductionMajor depressive disorder (MDD) is the most prevalent mental illness. Antidepressants with rapid efficacy and acceptable tolerance have been investigated for many years. A preclinical study performed by our group revealed that the dysregulation of extracellular ATP is related to the pathophysiology of depression and that the medial prefrontal cortex-lateral habenula pathway is a potential cellular and neural circuit target for ATP involvement in depression-like behaviour. Moreover, through small-sample clinical trials, the group has preliminarily discovered the antidepressant effect of ATP. However, the antidepressant effects of and neural circuit mechanisms underlying ATP in depressed patients remain largely unexplored. This study pioneers the intravenous use of escitalopram in combination with oral escitalopram for the treatment of MDD, thus representing a new direction in antidepressant research.Methods and analysisThis clinical study is a single-centre, randomised, double-blind, placebo-controlled, superiority trial involving 120 MDD patients evenly divided into two groups. The experimental group will receive an intravenous injection of 10 mL ATP in 100 mL normal saline (NS) two times per day (BD) for 2 weeks, whereas the control group will receive 110 mL NS BD for 2 weeks. All of the participants will take 10 mg of oral escitalopram daily for 4 weeks, with flexible adjustment thereafter based on clinical response. Our primary outcome will be the change in the Hamilton Depression Rating Scale 24 (HAMD-24) score from baseline to 2 and 4 weeks. The secondary outcomes assessment (at 1, 2, 4, 12 and 24 weeks) will be done by the Montgomery-Asberg Depression Rating Scale, HAMD-24, Hamilton Anxiety Scale, Beck Depression Inventory, Snaith-Hamilton Pleasure Scale, Clinical Global Impression, Insomnia Severity Index, Columbia-Suicide Severity Rating Scale, Side Effect Rating Scale of Asberg, MRI, cognitive function and cytokine level analyses.Ethics and disseminationThe study protocol and all of the related materials were approved by the Institutional Ethics Committee of Nanfang Hospital, Southern Medical University (No. NFEC-2024-070, NFEC-2020-153, Guangzhou, China). Results will be disseminated through peer-reviewed publications and conference presentations.Trial registration numberNCT06266715.

Aims To explore the efficacy of Femoston plus escitalopram for perimenopausal women with chronic insomnia and the relevant biomarkers. Methods A total of 166 patients randomly received: escitalopram plus placebo (Escitalopram Group), Femoston plus placebo (Hormone Group), and Femoston plus escitalopram (Combined Group) for 3 months and followed for 2, 4, 8, and 12 weeks. The primary efficacy endpoint was changes in Pittsburgh Sleep Quality Index Scale (PSQI), Insomnia Severity Index Scale (ISI), and Epworth Sleepiness Scale (ESS) scores at week 12 from baseline. Secondary endpoints included changes in the Modified Kupperman Menopausal Index Scale (KMI) scores, blood 5‐HT neurotransmitters and their receptor, and blood sex hormone levels during the treatment. Results Compared with baseline levels, all groups displayed increased serum 5‐HT levels and decreased serum FSH levels, with more significant changes in the combined group. Compared with the other two groups, the combined group reported a gradual increase in serum E2 levels and a gradual decrease in serum LH levels, and the lowest KMI, ESS, ISI, and PSQI scores at weeks 4 and 12. The PSQI score was negatively correlated with serum 5‐HT and E2 and positively correlated with serum FSH and LH levels, respectively. Conclusion Femoston plus escitalopram improves chronic insomnia in perimenopausal women. Serum levels of 5‐HT, E2, FSH, and LH may objectively indicate the clinical severity of chronic insomnia in this population. Compared with hormone or escitalopram alone, a combined therapy of Femoston with escitalopram may be more effective in the treatment of perimenopausal chronic insomnia. Serum levels of 5‐HT, E2, FSH, and LH may serve as objective indicators to assess the disease severity in perimenopausal women.

This study aims to evaluate the predictive performance of the published population pharmacokinetic (PopPK) model of escitalopram in Chinese patients using an external validation method. PubMed, Embase, and Web of Science databases were searched to identify PopPK models. Clinical data collected from Chinese patients treated with escitalopram were used to evaluate these models. The predictive performance of the models was evaluated using both prediction-based diagnostic methods and simulation-based diagnostic methods. Ten published PopPK models were included in the external validation. A total of 241 serum concentration samples were collected from 193 Chinese patient. Among all evaluated models, the Poweleit 2023 model exhibited the optimal predictive performance, with the PE of -2.14% and the RMSE of 22.27% at the individual level, and corresponding values of 14.13% and 104.19% at the population level, followed the model by Liu 2022. While the predictive performance of the other models was unsatisfactory. Published PopPK models of escitalopram showed wide variations in predictive performance among our patient cohort. External models should be accurately evaluated before their application in clinical practice.

Recent clinical trial data suggests that ratings on depression scales are lowered after psilocybin therapy compared to placebo, though it is unclear what neuropsychological mechanisms underpin these effects. This study compared psilocybin, with an established antidepressant, escitalopram, to investigate whether there are shared or distinct effects on emotional information processing. Patients with long-standing moderate-to-severe depression were randomly and double-blindly assigned in a 1:1 ratio to receive either 1) two doses of 25 mg of psilocybin, 3-weeks apart, plus 6-weeks of daily placebo (psilocybin group N = 30); or 2) two doses of 1 mg of psilocybin 3-weeks apart plus 6-weeks of daily oral escitalopram (escitalopram group N = 29); all patients received the same psychological support. Behavioural measures of affective bias as well as subjective measures of depression were collected at baseline and at the primary 6-week endpoint, using an established computerised task (Facial Emotion Recognition Task) and Quick Inventory of Depressive Symptomatology, respectively. Change in affective bias was further correlated with change in depression scores measured concurrently as well as at 1-month post-trial follow-up (week-10), corrected for baseline depression severity. Negative bias in facial expression recognition decreased after both treatments to a comparable level. Concurrently, change in negative affective bias was not associated with change in depression. Longitudinally, a decrease in the misclassification of positive faces as negative was associated with a decrease in depression scores at week-10 for the escitalopram group only. Therefore, a more positive behavioural bias in emotional processing was seen following psilocybin and citalopram compared to baseline. This highlights the potential for at least some overlap in cognitive mechanisms across two distinct treatments, which is noteworthy given the short dosing regimen with psilocybin.

Reinforcement learning is a fundamental aspect of adaptive behaviour, since it involves the acquisition and updating of associations between actions and their outcomes based on the rewarding or punishing consequences. Acute experimental manipulations of serotonin have provided compelling evidence for its role in reinforcement learning. However, it remains unknown how more chronic manipulation of serotonin, which holds greater clinical relevance, affects reinforcement learning and the underlying neural mechanisms. Consequently, we aimed to investigate the effect of a three-week administration of the SSRI, escitalopram, on a reinforcement learning paradigm during functional magnetic resonance imaging. The study used a double-blind, placebo-controlled design with 64 healthy volunteers. Participants were semi-randomised, ensuring matched groups for age, sex and intelligence quotient (IQ), to receive either 20 mg of escitalopram ( n  = 32) or placebo ( n  = 32) for at least 21 days. We analysed group differences in reinforcement learning using both analysis of covariance as well as innovative hierarchical Bayesian modelling of the reinforcement learning task. Escitalopram reduced learning from punishment during punishment trials. A key novel finding was that there was decreased activation of the intraparietal sulcus in the escitalopram group when compared to the placebo group during reward trials. The involvement of the intraparietal sulcus suggests that escitalopram affects the encoding of value outcome, which may lead to reduced reinforcement sensitivity, and thereby impacting adaptive learning from feedback. Understanding these mechanisms may help to optimize SSRI treatment to mitigate clinical symptoms and improve quality of life for neuropsychiatric patients, by elucidating serotonin’s effects on affect, cognition, and behaviour.