Psilocybin Therapy (PT) is being increasingly studied as a psychiatric intervention. Personality relates to mental health and can be used to probe the nature of PT's therapeutic action.

In a phase 2, double-blind, randomized, active comparator controlled trial involving patients with moderate-to-severe major depressive disorder, we compared psilocybin with escitalopram, over a core 6-week trial period. Five-Factor model personality domains, Big Five Aspect Scale Openness aspects, Absorption, and Impulsivity were measured at Baseline, Week 6, and Month 6 follow-up.

PT was associated with decreases in neuroticism (B = −0.63), introversion (B = −0.38), disagreeableness (B = −0.47), impulsivity (B = −0.40), and increases in absorption (B = 0.32), conscientiousness (B = 0.30), and openness (B = 0.23) at week 6, with neuroticism (B = −0.47) and disagreeableness (B = −0.41) remaining decreased at month 6. Escitalopram Treatment (ET) was associated with decreases in neuroticism (B = −0.38), disagreeableness (B = −0.26), impulsivity (B = −0.35), and increases in openness (B = 0.28) at week 6, with neuroticism (B = −0.46) remaining decreased at month 6. No significant between-condition differences were observed.

Personality changes across both conditions were in a direction consistent with improved mental health. With the possible exception of trait absorption, there were no compelling between-condition differences warranting conclusions regarding a selective action of PT (v. ET) on personality; however, post-ET changes in personality were significantly moderated by pre-trial positive expectancy for escitalopram, whereas expectancy did not moderate response to PT.

This study is about the clinical uses of three antidepressants( escitalopram, desvenlafaxine, vortioxetine) in the treatment of anxioun depression.

The purpose of this study was to compare the efficacy and safety of escitalopram, desvenlafaxine, vortioxetine, and aripiprazole augmentation with escitalopram in the acute treatment of anxious depression.

Patients (n=189) with DSM5 major depression and high levels of anxiety were evenly randomized to escitalopram, desvenlafaxine, vortioxetine, and aripiprazole augmentation with escitalopram in a six-week, randomized, rater-blinded, head to head comparative trial. Changes in overall depressive and anxiety symptoms were assessed.

Patients demonstrated similar baseline-to-endpoint improvement in HAMD and HAMA total scores. Patients also demonstrated similar response rate and remission rate in HAMD and HAMA. In analysis of individual HAMD and HAMA items, desvenlafaxine had greatly reduced scores for anxiety somatic (p=0.013), hypochondriasis (p=0.014), cardiovascular symptoms (p=0.005), respiratory symptoms (p=0.013) compared to escitalopram or vortioxetine. Each treatment were well tolerated with no significant differences.

These results showed no significant differences in efficacy and tolerability of escitalopram, desvenlafaxine, vortioxetine, and aripiprazole augmentation with escitalopram in this subtype of patients with anxious depression during the acute phase treatment.

No significant relationships.

Serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants thanks to the overall safety and tolerability spectrum. However, they can cause different side effects that not all of them are well identified.

We intend to clarify the clinical presentation of mydriasis caused by Escitalopram.

Reporting the case of a patient suffering a major depressive disorder, that presented a mydriasis after adjusting her antidepressant medication. Then, we conducted a literature review using “PubMed” database and keywords “Mydriasis”, “escitalopram”, “SSRI”,” side effects”.

A 29-year-old female with no past clinical history, presented in May 2021 a severe depression requiring an antidepressant treatment. Under 10 mg per day of escitalopram there was a partial remission of the symptoms, leading to increase the dose by another 10 mg. One month after taking 20 mg/day, she consults before the appointment suffering from a blurry vision and photophobia. Ophthalmologic examination showed a bilateral reactive half-mydriasis, eye pressure was 14 mmHg and fundus examination was normal. Iatrogenic origin of mydriasis was suspected. A gradual interruption of the medication lead to disappearance of the latter. A pharmacological investigation concluded to the suspension of escitalopram and to be vigilant if antidepressant medication would be needed.

Mydriasis is an uncommon side effect caused by SSRI that needs to be kept in mind by clinicians. Therapeutic patient education can help to detect abnormal side effects and treat them if needed.

No significant relationships.

Psoriasis is a chronic skin disease, affecting up to 2-4% of population. The majority of investigations agree that this disease appears to be a result of confluence of genetic, allergenic and emotional factors. There is usually more than one trigger that leads to the manifestation or exacerbation of symptoms. Psychogenic factors are clearly in a pattern here. Some personality traits may lead to instability of the emotional sphere that can act alternately as a cause, then as an aftereffect of exacerbation of the chronic process, forming a so called “vicious circle” of psychosomatic disease.

To discover the impact of escitalopram on the symptoms of psoriasis.

14 patients were diagnosed with psoriasis. All patients underwent psychiatric interviewing and psychological testing (STAI and HADS). The results revealed increased trait anxiety levels among 8 of them with moderate severity of the process according to SCORAD index. 3 cases demonstrated symptoms of clinically expressed and 4 subclinical levels of depression. Escitalopram (10 to 20 mg. daily) was administered along with common dermatologic therapy in these patients.

Patients treated with escitalopram showed a reduction of anxiety and depression tests scores as well as the values some dermatological symptoms such as pruritus.

These preliminary results of 3 months study gives us a hope of successful psychopharmacological treatment of psoriasis in cooperation with dermatologists. Finding intercommunications in pathogenesis of skin and emotional disorders could optimize the treatment and improve patient’s quality of life. The publication was prepared with the support of the “RUDN University Program 5-100”.

Poststroke depression (PD) occurs in approximately one third of the patients within first two years of a cerebrovascular event. However, no definite consensus has been reached on the best treatment option. The aim was to determine the efficacy and safety escitalopram, a selective serotonin reuptake inhibitor, in PSD treatment.

Patients with symptoms of depression within 6 months of a cerebrovascular event were included. Patients with Hamilton depression (HAM-D) score of < 13, mini mental standardized test score of < 23, schizophrenia, behavioral disorders, substance abuse, history of alcoholism, current use of antidepressants, and history of stroke or major depression within the last one year were excluded. Patients were administered escitalopram 10 mg/day for 3 months. HAM-D scores, stroke severity and extent of functional impairment were assessed and side effects were recorded; the relationship between HAM-D scores and sociodemographic variables and stroke localization was investigated.

Totaly,35 patients (60% female; mean age, 67± 6) were included. Depression was diagnosed 3±1.2 months after the stroke. HAM-D scores decreased significantly in all visits (days 15, 30, 45 and 90). The mean HAM-D score decreased from 27.5±4.7 to 4.65±2.47 at day 90 (p< 0.0001). No significant correlation was found between HAM-D scores and cerebrovascular event localization, sociodemographic variables and medical history (p>0.05). Escitalopram was well tolerated. A total of 9 patients reported nausea, anxiety, drowsiness and dyspepsia.

In this open-label study escitalopram was found to be safe and effective for use in poststroke depression patients.

To examine the relationship between different intervention approaches and subsequent real-life outcomes in patients changing treatment from escitalopram 10mg.

This was a retrospective cohort study of patients starting antidepressant treatment between 2002 and 2004. Data were extracted from a US health-insurance reimbursement claims database. Eligible patients started escitalopram 10mg and changed within 3 months to: escitalopram ≥20mg; another antidepressant; or a combination of escitalopram with another antidepressant. Medication persistence and healthcare costs over 3 months were compared between the treatment groups.

Overall, 37,791 patients started escitalopram 10mg. Of the 12,830 patients (34%) who changed treatment, 56% increased escitalopram dose, 26% switched antidepressant and 18% combined escitalopram with another antidepressant. Patients in the switch and combination groups had significantly higher rates of non-persistence (56% and 91%, respectively) vs the dose-increase group (39%; both P<0.001). Combination-group patients incurred significantly greater costs vs the dose-increase group ($2805 vs $1767, respectively; P<0.001).

Results suggest that increasing escitalopram dose in patients responding inadequately to 10mg is associated with higher persistence rates vs the other treatment approaches. Receiving an increased dose of escitalopram was associated with significantly lower costs than combining escitalopram 10mg with another antidepressant.

Geriatric depression often presents with memory and cognitive complaints that are associated with increased risk for Alzheimer’s disease (AD). In a parent clinical trial of escitalopram combined with memantine or placebo for geriatric depression and subjective memory complaints, we found that memantine improved executive function and delayed recall performance at 12 months (NCT01902004). In this report, we used positron emission tomography (PET) to assess the relationship between in-vivo amyloid and tau brain biomarkers and clinical and cognitive treatment response.

In a randomized double-blind placebo-controlled trial, we measured 2-(1-{6-[(2-[F18]fluoroethyl)(methyl)amino]-2-naphthyl}ethylidene) malononitrile ([18F]FDDNP) binding at baseline and assessed mood and cognitive performance at baseline, posttreatment (6 months), and naturalistic follow-up (12 months).

Twenty-two older adults with major depressive disorder and subjective memory complaints completed PET scans and were included in this report.

Across both treatment groups, higher frontal lobe [18F]FDDNP binding at baseline was associated with improvement in executive function at 6 months (corrected p = .045). This effect was no longer significant at 12 months (corrected p = .12). There was no association of regional [18F]FDDNP binding with change in mood symptoms (corrected p = .2).

[18F]FDDNP binding may predict cognitive response to antidepressant treatment. Larger trials are required to further test the value of [18F]FDDNP binding as a biomarker for cognitive improvement with antidepressant treatment in geriatric depression.

The objective of this work was to describe treatment-emergent sexual dysfunction (TESD) and tolerability following a switch from selective serotonin reuptake inhibitor (SSRI: citalopram, paroxetine, or sertraline) monotherapy to vortioxetine or escitalopram monotherapy in adults with well-treated major depressive disorder (MDD) and SSRI-induced sexual dysfunction.

Data were analyzed from the primary study, an 8-week, randomized, double-blind, head-to-head study in which participants with well-treated depressive symptoms but experiencing TESD with SSRIs were directly switched to flexible doses (10/20 mg) of vortioxetine or escitalopram. Sexual functioning was assessed by the Changes in Sexual Functioning Questionnaire-14 (CSFQ-14), efficacy by the Montgomery–Åsberg Depression Rating Scale scores (MADRS) and Clinicians Global Impression of Severity/Improvement (CGI-S/CGI-I), and tolerability by adverse events. Efficacy and tolerability were assessed by pre-switch SSRI therapy where possible, and by participant characteristics.

Greater improvements in TESD were seen in the vortioxetine compared with escitalopram groups based on: participant demographics (≤45 years, women; P = 0.045), prior SSRI treatment (P = 0.044), number of prior major depressive episodes (MDEs) (1–3; P = 0.001), and duration of prior SSRI therapy (>1 year; P = 0.001). Prior SSRI treatment did not appear to influence the incidence or severity of TEAEs, except for nausea. Regardless of prior SSRI, both treatments maintained antidepressant efficacy after 8 weeks.

Results suggest that vortioxetine is a safe and effective switch therapy for treating SSRI-induced sexual dysfunction in adults with well-treated MDD. Also, improvement in sexual dysfunction with vortioxetine or escitalopram may be influenced by prior SSRI usage, sex, age, and history of MDEs.

Genetic and environmental factors interact in the development of major depressive disorder (MDD). While neurobiological correlates have only partially been elucidated, altered levels of calcitonin gene-related peptide (CGRP)-like immunoreactivity (LI) in animal models and in the cerebrospinal fluid of depressed patients were reported, suggesting that CGRP may be involved in the pathophysiology and/or be a trait marker of MDD. However, changes in CGRP brain levels resulting from interactions between genetic and environmental risk factors and the response to antidepressant treatment have not been explored.

We therefore superimposed maternal separation (MS) onto a genetic rat model (Flinders-sensitive and -resistant lines, FSL/FRL) of depression, treated these rats with antidepressants (escitalopram and nortriptyline) and measured CGRP-LI in selected brain regions.

CGRP was elevated in the frontal cortex, hippocampus and amygdala (but not in the hypothalamus) of FSL rats. However, MS did not significantly alter levels of this peptide. Likewise, there were no significant interactions between the genetic and environmental factors. Most importantly, neither escitalopram nor nortriptyline significantly altered brain CGRP levels.

Our data demonstrate that increased brain levels of CGRP are present in a well-established rat model of depression. Given that antidepressants have virtually no effect on the brain level of this peptide, our study indicates that further research is needed to evaluate the functional role of CGRP in the FSL model for depression.

Persisting symptoms after treatment for major depressive disorder (MDD) contribute to ongoing impairment and relapse risk. Whether cognitive behavior therapy (CBT) or antidepressant medications result in different profiles of residual symptoms after treatment is largely unknown.

Three hundred fifteen adults with MDD randomized to treatment with either CBT or antidepressant medication in the Predictors of Remission in Depression to Individual and Combined Treatments (PReDICT) study were analyzed for the frequency of residual symptoms using the Montgomery Asberg Depression Rating Scale (MADRS) item scores at the end of the 12-week treatment period. Separate comparisons were made for treatment responders and non-responders.

Among treatment completers (n = 250) who responded to CBT or antidepressant medication, there were no significant differences in the persistence of residual MADRS symptoms. However, non-responders treated with medication were significantly less likely to endorse suicidal ideation (SI) at week 12 compared with those treated with CBT (non-responders to medication: 0/54, 0%, non-responders to CBT: 8/30, 26.7%; p = .001). Among patients who terminated the trial early (n = 65), residual MADRS item scores did not significantly differ between the CBT- and medication-treated groups.

Depressed adults who respond to CBT or antidepressant medication have similar residual symptom profiles. Antidepressant medications reduce SI, even among patients for whom the medication provides little overall benefit.

The present study investigated alteration of brain resting-state activity induced by antidepressant treatment and attempted to investigate whether treatment efficacy can be predicted at an early stage of pharmacological treatment.

Forty-eight first-episode medication-free patients diagnosed with major depression received treatment with escitalopram. Resting-state functional magnetic resonance imaging was administered prior to treatment, 5 h after the first dose, during the course of pharmacological treatment (week 4) and at endpoint (week 8). Resting-state activity was evaluated in the course of the 8-week treatment and in relation to clinical improvement.

Escitalopram dynamically modified resting-state activity in depression during the treatment. After 5 h the antidepressant induced a significant decrease in the signal in the occipital cortex and an increase in the dorsolateral and dorsomedial prefrontal cortices and middle cingulate cortex. Furthermore, while remitters demonstrated more obvious changes following treatment, these were more modest in non-responders suggesting possible tonic and dynamic differences in the serotonergic system. Changes after 5 h in the caudate, occipital and temporal cortices were the best predictor of clinical remission at endpoint.

This study revealed the possibility of using the measurement of resting-state neural changes a few hours after acute administration of antidepressant to identify individuals likely to remit after a few weeks of treatment.

Brain-derived neurotrophic factor (BDNF) seems to play an important role in the course of depression including the response to antidepressants in patients with depression. We aimed to study the effect of an antidepressant intervention on peripheral BDNF in healthy individuals with a family history of depression.

We measured changes in BDNF messenger RNA (mRNA) expression and whole-blood BDNF levels in 80 healthy first-degree relatives of patients with depression randomly allocated to receive daily tablets of escitalopram 10 mg versus placebo for 4 weeks.

We found no statistically significant difference between the escitalopram and the placebo group in the change in BDNF mRNA expression and whole-blood BDNF levels. Post hoc analyses showed a statistically significant negative correlation between plasma escitalopram concentration and change in whole-blood BDNF levels in the escitalopram-treated group.

The results of this randomised trial suggest that escitalopram 10 mg has no effect on peripheral BDNF levels in healthy individuals.

While oral antidepressants reach efficacy after weeks, single-dose intravenous (i.v.) ketamine has rapid, yet time-limited antidepressant effects. We aimed to determine the efficacy and safety of single-dose i.v. ketamine augmentation of escitalopram in major depressive disorder (MDD).

Thirty outpatients with severe MDD (17-item Hamilton Rating Scale for Depression total score ⩾24) were randomized to 4 weeks double-blind treatment with escitalopram 10 mg/day+single-dose i.v. ketamine (0.5 mg/kg over 40 min) or escitalopram 10 mg/day + placebo (0.9% i.v. saline). Depressive symptoms were measured using the Montgomery–Asberg Depression Rating Scale (MADRS) and the Quick Inventory of Depressive Symptomatology – Self-Report (QIDS-SR). Suicidal ideation was evaluated with the QIDS-SR item 12. Adverse psychopathological effects were measured with the Brief Psychiatric Rating Scale (BPRS)-positive symptoms, Young Mania Rating Scale (YMRS) and Clinician Administered Dissociative States Scale (CADSS). Patients were assessed at baseline, 1, 2, 4, 24 and 72 h and 7, 14, 21 and 28 days. Time to response (⩾50% MADRS score reduction) was the primary outcome.

By 4 weeks, more escitalopram + ketamine-treated than escitalopram + placebo-treated patients responded (92.3% v. 57.1%, p = 0.04) and remitted (76.9% v. 14.3%, p = 0.001), with significantly shorter time to response [hazard ratio (HR) 0.04, 95% confidence interval (CI) 0.01–0.22, p < 0.001] and remission (HR 0.11, 95% CI 0.02–0.63, p = 0.01). Compared to escitalopram + placebo, escitalopram + ketamine was associated with significantly lower MADRS scores from 2 h to 2 weeks [(peak = 3 days–2 weeks; effect size (ES) = 1.08–1.18)], QIDS-SR scores from 2 h to 2 weeks (maximum ES = 1.27), and QIDS-SR suicidality from 2 to 72 h (maximum ES = 2.24). Only YMRS scores increased significantly with ketamine augmentation (1 and 2 h), without significant BPRS or CADSS elevation.

Single-dose i.v. ketamine augmentation of escitalopram was safe and effective in severe MDD, holding promise for speeding up early oral antidepressant efficacy.

Objective: Considering that mitochondria may be drug targets and some characteristics of drug–mitochondria interactions may still be misjudged because of the difficulty in foreseeing and understanding all possible implications of the complex pathophysiology of mitochondria, our study aimed to investigate the effect of escitalopram on the activity of enzymes of mitochondrial energy metabolism.

Methods: Animals received daily administration of escitalopram dissolved in saline [10 mg/kg, intraperitoneal (IP)] at 1.0 ml/kg volume for 14 days. Control rats received an equivalent volume of saline, 1.0 ml/kg (IP), for the same treatment period. Twelve hours after last injection, rats were killed by decapitation and brain areas were rapidly isolated. The samples were homogenised and the activities of mitochondrial respiratory chain complexes, some enzymes of Krebs cycle (citrate synthase, malate dehydrogenase and succinate dehydrogenase) and creatine kinase were measured.

Results: We verified that chronic administration of escitalopram decreased the activities of complexes I and II–III in cerebellum, hippocampus, striatum and posterior cortex whereas prefrontal cortex was not affected. Complex II activity was decreased only in striatum without affecting prefrontal cortex, hippocampus, cerebellum and posterior cortex. However, chronic administration of escitalopram did not affect complex IV and enzymes of Krebs cycle activities as well as creatine kinase.

Conclusion: In this study we showed a decrease in the activities of complexes I and II–III in most of the brain structures analysed and complex II activity was decreased only in striatum. However, it remains to be determined if mitochondrial dysfunction is rather a causal or a consequential event of abnormal signalling.

Healthy first-degree relatives of patients with major depression (rMD+) show brain structure and functional response anomalies and have elevated risk for developing depression, a disorder linked to abnormal serotonergic neurotransmission and reward processing.

In a two-step functional magnetic resonance imaging (fMRI) investigation, we first evaluated whether positive and negative monetary outcomes were differentially processed by rMD+ individuals compared to healthy first-degree relatives of control probands (rMD−). Second, in a double-blinded placebo-controlled randomized trial we investigated whether a 4-week intervention with the selective serotonergic reuptake inhibitor (SSRI) escitalopram had a normalizing effect on behavior and brain responses of the rMD+ individuals.

Negative outcomes increased the probability of risk-averse choices in the subsequent trial in rMD+ but not in rMD− individuals. The orbitofrontal cortex (OFC) displayed a stronger neural response when subjects missed a large reward after a low-risk choice in the rMD+ group compared to the rMD− group. The enhanced orbitofrontal response to negative outcomes was reversed following escitalopram intervention compared to placebo. Conversely, for positive outcomes, the left hippocampus showed attenuated response to high wins in the rMD+ compared to the rMD− group. The SSRI intervention reinforced the hippocampal response to large wins. A subsequent structural analysis revealed that the abnormal neural responses were not accounted for by changes in gray matter density in rMD+ individuals.

Our study in first-degree relatives of depressive patients showed abnormal brain responses to aversive and rewarding outcomes in regions known to be dysfunctional in depression. We further confirmed the reversal of these aberrant activations with SSRI intervention.

A pooled-analysis on the long-term outcome in four head-to-head studies: agomelatine versus fluoxetine, sertraline, and (twice) escitalopram.

A meta-analytic approach was used. Hamilton Depression Rating Scale (HAM-D) scores, response and remission rates, Clinical Global Impression of Improvement (CGI-I) scores, response and remission rates, and completion rates/discontinuation rates due to adverse events were analyzed.

At the last post-baseline assessment on the 24-week treatment period, the final HAM-D-17 score was significantly lower in patients treated with agomelatine than in patients treated with selective serotonin reuptake inhibitors (SSRIs), as well in the total group of patients with severe depression (P = 0.014 and 0.040, respectively). HAM-D response rates at the end of 24 weeks were significantly higher in patients treated with agomelatine than in patients treated with SSRIs, as well in the total group of patients with severe depression (P = 0.031 and 0.048, respectively). HAM-D remission rates at the end of 24 weeks were numerically but not significantly higher in patients treated with agomelatine than in patients treated with SSRIs. Final CGI-I scores were significantly lower for agomelatine. CGI-I response as well as remission rates were numerically higher in patients treated with agomelatine, without statistical significance. The percentage of patients with at least one emergent adverse event leading to treatment discontinuation was 9.4% in patients treated with SSRIs and 6.6% in patients treated with agomelatine (P = 0.065).

The present pooled analysis shows that, from a clinical point of view, agomelatine is at least as efficacious as the investigated SSRIs with a trend to fewer discontinuations due to adverse events.