Dose Of Escitalopram Research Articles

Temporomandibular dislocation due to aripiprazole induced dystonia

We wish to report the case of a patient who developed temporomandibular joint dislocation due to dystonia following a single dose of aripiprazole. Our patient was a 23-year-old woman presenting with persistent low mood, fatiguability, insomnia and suicidal ideation. There was no past history of psychiatric morbidity. There was family history of depressive episode and deliberate self harm in her husband who was her paternal cousin. She was given 10 mg escitalopram and 0.5 mg clonazepam for insomnia on a diagnosis of a moderate depressive episode and improved over the next 3 weeks. However she developed irritability and agitation while on the above medications for which she was given a single dose of aripiprazole 10 mg at night by another psychiatrist not attached to our institution, which was not appropriate for her condition. The patient had taken 10 mg escitalopram in the morning. There was no history of intake of any over the counter drugs or herbal preparations. Twelve hours after the first dose she developed sedation and salivation and her care givers withheld subsequent doses of aripiprazole, escitalopram and clonazepam. Twenty hours after the first dose, she developed painful spasms of the muscles of her neck on the right side. She also had forced opening and deviation of jaw, both to the left and right. This was followed by persistent deviation of the jaw to the left and pain in the left temporomandibular joint. She was unable to close her mouth, swallow or talk for which she was brought to the emergency department of our hospital. A left-sided temporomandibular dislocation was diagnosed and a manual reduction was performed, after which the pain subsided. The next morning she was examined by us and seen to have forced mouth opening, excessive salivation and bilateral hand tremors. There were no other dystonic reactions. The dystonia and temporomandibular joint dislocation could not be part of the somatic symptoms of depression. We gave her 50 mg promethazine intramuscularly on suspicion of an aripiprazole induced dystonia. Two hours later, the dystonic movements subsided and the patient was sent home on oral promethazine. She did not have dystonic movements on follow-up the next morning. A rechallenge with aripiprazole could not be done for ethical reasons. The dystonia was rated as possibly due to aripiprozole according to the Naranjo adverse drug reaction probability scale [1]. She was restarted on escitalopram and clonazepam. A 1 month follow-up did not reveal any dystonic reactions. The adverse drug reaction was reported to the regional pharmacovigilance reporting centre. Aripiprazole is a second generation anti-psychotic which has a low propensity to cause extra-pyramidal side effects [2]. There are reports of acute dystonia induced by aripiprazole in drug-naive [3], and cocaine dependent patients [4] and in a patient on sertraline [5]. It has been proposed that aripiprazole caused dystonia because it lacked a protective anti-cholinergic action unlike other second generation anti-psychotics like clozapine [3]. Temporomandibular joint dislocations have been reported with conventional neuroleptics [6, 7] but no case has been reported with aripiprazole. Aripiprazole has been found to have no meaningful effect on the pharmacokinetics of escitalopram [8].We propose that our patient developed temporomandibular dislocation due to a dystonic reaction to aripiprazole possibly mediated through a pharmacodynamic synergism with escitalopram as selective serotonin re-uptake inhibitors can cause extrapyramidal side effects including dystonias through serotonergically mediated inhibition of the dopaminergic system [9]. From our case report we recommend a lower starting dose of aripiprazole especially in drug naive non psychotic patients and close monitoring of such patients.

Increasing escitalopram dose is associated with fewer discontinuations than switch or combination approaches in patients initially on escitalopram 10 mg

PurposeTo examine the relationship between different intervention approaches and subsequent real-life outcomes in patients changing treatment from escitalopram 10mg. MethodThis 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. ResultsOverall, 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). ConclusionResults 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.

A single high dose of escitalopram disrupts sensory gating and habituation, but not sensorimotor gating in healthy volunteers

Early mechanisms to limit the input of sensory information to higher brain areas are important for a healthy individual. In previous studies, we found that a low dose of 10mg escitalopram (SSRI) disrupts habituation, without affecting sensory and sensorimotor gating in healthy volunteers. In the current study a higher dose of 15mg was used. The hypothesis was that this higher dose of escitalopram would not only disrupt habituation, but also sensory and sensorimotor gating. Twenty healthy male volunteers received either placebo or 15mg escitalopram, after which they were tested in a P50 suppression, and a habituation and prepulse inhibition (PPI) of the startle reflex paradigm. Escitalopram significantly decreased P50 suppression and habituation, but had no effect on PPI. The results indicate that habituation and sensory gating are disrupted by increased serotonergic activity, while sensorimotor gating seems relatively insensitive to such a rise. Since the patients who are frequently treated with SSRIs (patients with schizophrenia and affective disorders) might already suffer from disrupted sensory gating and habituation, the current results call for caution in the determination of a proper dose.

Involvement of NMDA receptors and l-arginine-nitric oxide-cyclic guanosine monophosphate pathway in the antidepressant-like effects of escitalopram in the forced swimming test

Escitalopram is a serotonin reuptake inhibitor used in the treatment of depression and anxiety disorders. This study investigated the effect of escitalopram in forced swimming test (FST) and in the tail suspension test (TST) in mice, and tested the hypothesis that the inhibition of NMDA receptors and NO-cGMP synthesis is implicated in its mechanism of action in the FST. Escitalopram administered by i.p. route reduced the immobility time both in the FST (0.3–10 mg/kg) and in the TST (0.1–10 mg/kg). Administration of escitalopram by p.o route (0.3–10 mg/kg) also reduced the immobility time in the FST. The antidepressant-like effect of escitalopram (3 mg/kg, p.o.) in the FST was prevented by the pretreatment of mice with NMDA (0.1 pmol/site, i.c.v.), l-arginine (750 mg/kg, i.p., a substrate for nitric oxide synthase) or sildenafil (5 mg/kg, i.p., a phosphodiesterase 5 inhibitor). The administration of 7-nitroindazole (50 mg/kg, i.p., a neuronal nitric oxide synthase inhibitor), methylene blue (20 mg/kg, i.p., an inhibitor of both nitric oxide synthase and soluble guanylate cyclase) or ODQ (30 pmol/site i.c.v., a soluble guanylate cyclase inhibitor) in combination with a subeffective dose of escitalopram (0.1 mg/kg, p.o.) reduced the immobility time in the FST as compared with either drug alone. None of the drugs produced significant effects on the locomotor activity in the open-field test. Altogether, our data suggest that the antidepressant-like effect of escitalopram is dependent on inhibition of either NMDA receptors or NO-cGMP synthesis. The results contribute to the understanding of the mechanisms underlying the antidepressant-like effect of escitalopram and reinforce the role of NMDA receptors and l-arginine-NO-GMP pathway in the mechanism of action of antidepressant agents.

Escitalopram versus placebo in the treatment of dysthymic disorder

Numerous studies have assessed the acute efficacy of antidepressants, including selective serotonin reuptake inhibitors, in treating dysthymic disorder; however, escitalopram, the S-enantiomer of citalopram, has not been studied. Thirty-six outpatients with Structured Clinical Interview for DSM-III-R-diagnosed dysthymic disorder, aged 23-65 years (mean±SD=44.7±11 years), were randomly assigned to double-blind escitalopram (maximum dose 20 mg/day) versus placebo for 12 weeks. Inclusion criteria included age 18-65 years and Hamilton Depression Rating Scale (HDRS) score≥12. We hypothesized that escitalopram would be superior to placebo in the HDRS-24 item total score at week 12. We also hypothesized the superiority of escitalopram over placebo for secondary measures, including the percentage of participants classified as responders and remitters, as well as social functioning (Social Adjustment Scale), clinical global impression-improvement, Global Assessment of Functioning Scale. Participants' baseline HDRS-24 averaged 23.4±5.9. Final HDRS-24 scores at last observation carried forward did not differ significantly between escitalopram-treated (mean±SD=10.88±5.83) and placebo-treated individuals (mean±SD=16.4±6.34) (F=2.82, degrees of freedom=1,32, P=0.10). Significant differences favoring active medication were found on the Social Adjustment Scale and the Clinical Global Impression Severity and Global Assessment of Functioning Scale, but not in the percentages of responders or remitters. A larger study sample or higher escitalopram dose may show more significant placebo-medication differences.

An Open-Label Trial of Topiramate in the Treatment of Skin Picking in Pervasive Developmental Disorder Not Otherwise Specified

An Open-Label Trial of Topiramate in the Treatment of Skin Picking in Pervasive Developmental Disorder Not Otherwise Specified

Effect of escitalopram on the processing of emotional faces

Serotonin has been implicated in the neurobiology of depressive and anxiety disorders, but little is known about its role in the modulation of basic emotional processing. The aim of this study was to determine the effect of the selective serotonin reuptake inhibitor, escitalopram, on the perception of facial emotional expressions. Twelve healthy male volunteers completed two experimental sessions each, in a randomized, balanced order, double-blind design. A single oral dose of escitalopram (10 mg) or placebo was administered 3 h before the task. Participants were presented to a task composed of six basic emotions (anger, disgust, fear, happiness, sadness, and surprise) that were morphed between neutral and each standard emotion in 10% steps. Escitalopram facilitated the recognition of sadness and inhibited the recognition of happiness in male, but not female faces. No drug effect on subjective measures was detected. These results confirm that serotonin modulates the recognition of emotional faces, and suggest that the gender of the face can have a role in this modulation. Further studies including female volunteers are needed.

P03-377 - Escitalopram induced bradycardia, hypotonia and syncope

ObjectivesEscitalopram is considered to be more effective than citalopram and to have less side effects. Previous studies have found that common cardiac manifestations of escitalopram overdose are QT prolongation and bradycardia. Some case reports inform about bradycardia without ECG abnormalities with therapeutic doses of escitalopram.MethodsWe report of a 29-year-old female patient diagnosed with major depression, hospitalized for 2 weeks. She had no history of any treatment with antidepressive drugs. After administration of 5 mg/day escitalopram the patient's blood pressure and pulse rate were mildly reduced and we observed presyncopal episodes daily. After 1 week of treatment the dose of escitalopram was raised to 10 mg/day and she complained about dizziness. In this case we found that presyncopal episodes lasted longer and both hypotension and bradycardia increased. These symptoms disappeared within 24 hours after escitalopram treatment was discontinuated. Results from routine laboratory tests, ECG, EEG, brain CT were normal. No other farmacologic causes were supposed to induce the above mentioned vegetativ symptoms.ConclusionBradycardia and hypotonia have been previously reported with citalopram, but there are only a few case reports about these side effects induced by a therapeutic dose of escitalopram. Both central and - by directly inhibiting the entry of Ca into vascular smooth muscles resulting in vasodilatation - periferial effects of escitalopram are supposed to be responsible for these rare phenomena. This case report supports the importance of monitoring heart rate and blood pressure when escitalopram treatment is introduced, especially in cases of previously untreated depressive patients.

Open-label study of high (30 mg) and moderate (20 mg) dose escitalopram for the treatment of obsessive–compulsive disorder

This study sought to investigate the efficacy of escitalopram at different dosages for the treatment of obsessive-compulsive disorder (OCD). Thirty individuals were enrolled in a 16-week, open-label trial of escitalopram and randomly assigned to the 20 or 30 mg study arm. Study measures assessing OCD symptoms, anxiety, depression, and quality of life were administered at baseline and weeks 2, 4, 8, 12, and 16. For the 23 study completers, pretreatment and posttreatment analyses revealed significant improvements (P<0.05) on clinician-rated and self-rated measures of OCD symptoms, quality of life, anxiety, and depression. Approximately half of the sample (n = 12) satisfied full medication response criteria and less than one-quarter (n = 5) were partial medication responders. Intention-to-treat analyses showed similar improvements (P<0.05) on all study measures. At study completion, a superior responder rate and more improvement on the Yale-Brown Obsessive Compulsive Scale (P<0.05) was reported for those in the 30 versus 20 mg study arm. The difference between the two groups, however, disappeared when initial differences in baseline depression and anxiety scores were used as analysis covariates. These results suggest that the 30 mg (vs. 20 mg) dose of escitalopram may provide a superior reduction in OCD symptoms for those sufferers with comorbid depression and/or anxiety.

Acute Maniform Reaction to a Single Dose of Escitalopram in a Social Phobic Patient – An Atypical Jitteriness Syndrome?

We report an unusual acute mental side-effect [4] of the selective serotonin reuptake inhibitor (SSRI) escitalopram in a 23-year-old male student of mathematics, who has suffered from severe social fears and avoidance behaviour since kindergarten. He was diagnosed with social anxiety disorder (DSM-IV) and admitted for in-patient therapy. A structured diagnostic interview (SCID) revealed no psychiatric comorbidity, physical examination and laboratory work-up showed no peculiarities besides slight obesity. About one hour after the first dose of escitalopram (5 mg) he unexpectedly became giddy, chatty, kidding, vociferous, uncommonly gregarious, restless, incapable of controlling his thoughts and actions. After eight hours the symptoms subsided without any pharmacological intervention; escitalopram treatment was stopped. The patient abnegated intake of illegal drugs, no such substances could be detected in his blood or urine. One week later, when escitalopram was initiated a second time, only short-lived motor restlessness, trembling, fidgetiness and difficulty in concentrating emerged, but no maniform symptoms. Escitalopram was gradually increased to 15 mg/d without further side-effects during the following six weeks.

Specific effects of escitalopram on neuroendocrine response

Citalopram, a selective serotonin reuptake inhibitor, is used as a neuroendocrine probe in human subjects to assess serotonin function as reflected in prolactin and plasma cortisol release. Citalopram is a racemic mixture of equal proportions of the S(+) and R(-) enantiomers. Inhibition of serotonin reuptake and, consequently, antidepressant activity is associated, almost exclusively, with the S(+) enantiomer ("escitalopram"). Studies in animal models indicate that the presence of the R(-) isomer may interfere with the serotonin reuptake activity of escitalopram. The current study compared the neuroendocrine effects of citalopram and escitalopram in healthy human volunteers. Plasma cortisol and prolactin levels following a single oral dose of citalopram (40 mg) or escitalopram (20 mg) were compared in samples taken every 15-30 min over a period of 240 min. Plasma citalopram concentration was determined at the same intervals. Escitalopram and citalopram caused equivalent increases in plasma cortisol and prolactin. The administration of dexamethasone prior to the escitalopram challenge blocked the evoked increase in cortisol. This is the first study to prove that a single dose of escitalopram acts centrally and not peripherally, providing further support of the use of oral escitalopram as a probe for brain serotonergic function.

A single high dose of escitalopram increases mismatch negativity without affecting processing negativity or P300 amplitude in healthy volunteers

Information processing deficits are commonly found in psychiatric illnesses, while at the biochemical level serotonin seems to play a role in nearly all psychiatric disorders. Processing negativity (PN), mismatch negativity (MMN) and P300 amplitude are electrophysiological measures of information processing. The present study was designed to replicate and further extent the results of our initial study on the effects of a low dose of escitalopram (10 mg) on MMN, PN and P300 amplitude. In a randomised, double-blind, cross-over experiment, 20 healthy male volunteers received either a single, orally administered dose of 15 mg escitalopram (a highly selective serotonin reuptake inhibitor (SSRI)) or placebo, after which their PN, MMN and P300 amplitude were assessed. Similar to our initial study with 10 mg escitalopram, 15 mg escitalopram significantly increased MMN, while it did not affect P300 amplitude. In contrast to our initial study, however, the currently higher dose of escitalopram did not increase PN. Results support the view that a broad range of increased serotonergic activity enhances MMN, while the relationship between serotonin and PN seems more complex. The current study does not support a serotonergic involvement in P300 amplitude.

Escitalopram prolonged fear induced by simulated public speaking and released hypothalamic-pituitary-adrenal axis activation

Simulated public speaking (SPS) test is sensitive to drugs that interfere with serotonin-mediated neurotransmission and is supposed to recruit neural systems involved in panic disorder. The study was aimed at evaluating the effects of escitalopram, the most selective serotonin-selective reuptake inhibitor available, in SPS. Healthy males received, in a double-blind, randomized design, placebo (n = 12), 10 (n = 17) or 20 (n = 14) mg of escitalopram 2 hours before the test. Behavioural, autonomic and neuroendocrine measures were assessed. Both doses of escitalopram did not produce any effect before or during the speech but prolonged the fear induced by SPS. The test itself did not significantly change cortisol and prolactin levels but under the higher dose of escitalopram, cortisol and prolactin increased immediately after SPS. This fear-enhancing effect of escitalopram agrees with previously reported results with less selective serotonin reuptake inhibitors and the receptor antagonist ritanserin, indicating that serotonin inhibits the fear of speaking in public.

P02-229 Escitalopram prolonged fear induced by simulated public speaking and released hypothalamic-pituitary-adrenal axis activation

Simulated Public Speaking (SPS) test is sensitive to drugs that interfere with serotonin-mediated neurotransmission and is supposed to recruit neural systems involved in panic disorder. The study was aimed at evaluating the effects of escitalopram, the most selective serotonin selective reuptake inhibitor available, in SPS. Healthy males received, in a double-blind, randomized design, placebo (n=12), 10 (n=17) or 20 (n=14) mg of escitalopram two hours before the test. Behavioural, autonomic and neuroendocrine measures were assessed. Both doses of escitalopram did not produce any effect before or during the speech, but prolonged the fear induced by SPS. The test itself did not significantly change cortisol and prolactin levels, but under the higher dose of escitalopram, cortisol and prolactin increased immediately after SPS. This fear-enhancing effect of escitalopram agrees with previously reported results with less selective serotonin reuptake inhibitors and the receptor antagonist ritanserin, indicating that serotonin inhibits speaking fear.

An Open Pilot Study of the Combination of Escitalopram and Bupropion-SR for Outpatients with Major Depressive Disorder

Monotherapy with a selective serotonin reuptake inhibitor (SSRI) is the most common initial treatment for major depressive disorder (MDD), but this monotherapy leads to remission in fewer than a third of patients. The combination of the SSRI escitalopram and bupropion-SR is commonly used for treating patients with MDD who have had an inadequate response to antidepressant monotherapy. This pilot study was conducted to evaluate this combination in the treatment of MDD in patients with chronic or recurrent MDD to estimate safety, tolerability, and remission rates. In this study, 51 outpatients with chronic or recurrent non-psychotic MDD were treated with a combination of escitalopram and bupropion-SR for up to 12 weeks. Participants were started on escitalopram at 10 mg/day, and bupropion-SR was then added at week 1, starting at 150 mg/day. The maximum dose of escitalopram was 20 mg/day and the maximum dose of bupropion-SR was 400 mg/day. Rates of response (62%) and remission (50%) at study exit (based on participants for whom at least one post-baseline measure was collected) were significantly higher than is typical for SSRI monotherapy. The level of treatment emergent adverse events was low, and only 3 participants (6%) discontinued treatment due to side effects. The mean maximum dose of escitalopram was 18 mg/day, which was achieved by week 6, and the mean dose at study exit was also 18 mg/day. The mean maximum dose of bupropion-SR was 329 mg/day, which was achieved by week 8, and the mean dose at study exit was 327 mg/day. These results suggest that the combination of escitalopram and bupropion-SR is effective and well tolerated. Further controlled trials comparing this combination with monotherapy are needed.

P.4.a.005 An investigation of clinical factors influence the therapeutic response of paroxetine in patients with panic disorder

Background: The S-enantiomer of citalopram (escitalopram) is the active moiety linked to the anti-depressant effects associated with citalopram (the racemate). For escitalopram to be approved for the treatment of depression in Europe, findings from clinical trials of escitalopram are required to match previous results from studies of the racemate, citalopram.Objective: The aim of this study was to compare the efficacy and tolerability of escitalopram and citalopram in outpatients with major depressive disorder (MDD).Methods: This prospective, randomized, double-blind, active-controlled study was conducted at 8 psychiatric outpatient clinics in the Federation of Russia. Adult outpatients aged 25 to 45 years with MDD and a total score >25 on the Montgomery-Asberg Depression Rating Scale (MADRS) were eligible. Patients were randomly assigned to receive 6 weeks of treatment with fixed daily doses of escitalopram 10 rag, citalopram 10 rag, or citalopram 20 rag. Efficacy assessments were made at weeks 0 (baseline), 1, 4, and 6 (study end or last observation carried forward). The primary efficacy parameter was the change from baseline in MADRS total score. Secondary measures were the change from baseline in MADRS total score in a subgroup of severely depressed patients (baseline MADRS total score, >35), MADRS core depression subscale score, and Clinical Global Impression-Severity and Improvement (CGI-S and CGI-I) scores; and the proportions of patients classified as responders and remitters at study end. Tolerability was assessed using adverse events (AEs) recorded by the investigator.Results: Of 330 assessable randomized patients, 8 withdrew, including 7 who withdrew consent and 1 who withdrew due to recurrence of a preexisting event. Thus, 322 patients were included in the assessment (mean age, 35 years; 41.6% male; all white; escitalopram 10 rag, 108 patients; citalopram 10 rag, 106; citalopram 20 rag, 108). At study end, the mean (SE) change from baseline in MADRS total score was significantly greater in the escitalopram arm than in the 10- and 20-rag citalopram arms (-28.70 [0.78] vs -20.11 [0.80] and -25.19 [0.78]; both, P < 0.001). Improvements were more marked in the severely depressed subgroup (-30.33 [0.95] vs -20.87 [0.99] and -26.34 [0.91]). Changes in the CGI-S and CGI-I scores and the rates of response and remission were significantly greater in the escitalopram group compared with those in the citalopram 10- and 20-rag groups (CGI-S: -2.60 [0.10] vs -1.61 [0.10] and -2.05 [0.10]; CGI-I: +1.58 [0.09] vs +2.35 [0.10] and +1.80 [0.09]; response: 95.4% vs 44.3% and 83.3%; remission: 89.8% vs 25.5% and 50.9% [all, P < 0.001]). Mean (SE) changes from baseline in core depression subscale score were -19.00 (0.59), -13.00 (0.60), and -16.52 (0.58) with escitalopram, citalopram 10 rag, and citalopram 20 mg, respectively. The prevalence of AEs was significantly lower in the escitalopram group (7) compared with the citalopram groups (16 and 19 in the 10- and 20-mg groups, respectively; both, P < 0.05). Nausea (2 [1.9%], 5 [4.7%], and 7 [6.5%] patients in the escitalopram and citalopram 10- and 20-mg groups, respectively) and headache (1 [0.9%], 2 [1.9%], and 4 [3.7%]) were the most frequently reported AEs.Conclusions: The results from this study suggest that escitalopram 10 mg was more effective than citalopram 10 and 20 mg at 6 weeks in these adult outpatients with MDD. All treatments were well tolerated. (Clin Ther. 2007;29:2319-2332) Copyright © 2007 Excerpta Medica, Inc.

An Open-Label, Rater-Blinded, Flexible-Dose, 8-Week Trial of Escitalopram in Patients With Major Depressive Disorder With Atypical Features

Although selective serotonin reuptake inhibitors (SSRIs) have become the standard of care for the treatment of major depressive disorder (MDD), limited data exist to support their use in MDD with atypical features. The current study investigates the efficacy of the SSRI escitalopram in an 8-week, open-label, flexible-dose, rater-blinded trial. Seventeen DSM-IV MDD subjects aged from 18 through 65 years completed screening procedures, provided informed consent, and went through a minimum 2-week washout from preexisting antide-pressants except fluoxetine (a minimum 4-week wash-out). They subsequently received escitalopram (10-20 mg/day) for 8 weeks. The primary efficacy measure was a change in score from baseline to end of treatment on the Structured Interview Guide for the Hamilton Rating Scale for Depression-Seasonal Affective Disorder version (SIGH-SAD), which includes a set of items for atypical symptoms. Secondary efficacy measures were defined as changes from baseline to end of treatment in scores on the SIGH-SAD atypical symptoms subscale (consisting of 8 items specific to atypical features), Beck Depression Inventory-II, Beck Anxiety Inventory, Sheehan Disability Scale, and Epworth Sleepiness Questionnaire. The study was conducted from October 2005 to November 2006. The mean age was 43.9 years, and 70.6% of subjects were women. The dropout rate was 11.8% (N = 2/17). The mean dose of escitalopram was 18.3 mg/day. The total SIGH-SAD score (mean ± SD) reduced by 53.8% from baseline (33.3 ± 8.2) to end of treatment (15.4 ± 9.4) (t = 4.24, p < .001). The atypical symptoms subscale score reduced by 44.5% from baseline (11.0 ± 4.3) to end of treatment (6.1 ± 2.8) (t = 5.26, p = .001). Ten subjects (62.5%) were classified as responders at end of treatment as defined by ≥ 50% reduction in SIGH-SAD total score. Overall, escitalopram was well tolerated. Our preliminary study indicates that escitalopram may be beneficial in the treatment of MDD with atypical features. Adequately powered, randomized, double-blind, placebo-controlled trials are necessary to determine the efficacy of escitalopram in this disorder. clinicaltrials.gov Identifier: NCT00610506.

Escitalopram in painful polyneuropathy: A randomized, placebo-controlled, cross-over trial

Serotonin (5-HT) is involved in pain modulation via descending pathways in the central nervous system. The aim of this study was to test if escitalopram, a selective serotonin reuptake inhibitor (SSRI), would relieve pain in polyneuropathy. The study design was a randomized, double-blind, placebo-controlled cross-over trial. The daily dose of escitalopram was 20 mg once daily. During the two treatment periods of 5 weeks duration, patients rated pain relief (primary outcome variable) on a 6-point ordered nominal scale. Secondary outcome measures comprised total pain and different pain symptoms (touch- or pressure-evoked pain, lancinating pain, constant burning or deep aching pain) by the use of 0–10-point numeric rating scales. Changes in health-related quality of life and severity of depression were measured with the SF-36 and the Major Depression Inventory (MDI). Forty-one patients were included in the data analysis. Patients reported a better pain relief during treatment with escitalopram compared with placebo ( p = 0.001). Total pain and different pain symptoms were lower during escitalopram treatment ( p = 0.001–0.024). The Number needed to treat (NNT) to obtain one patient with good or complete pain relief was 6.8. Health-related quality of life and depressive symptoms were unaltered ( p = 0.086–1.0). Five patients (10.4%) discontinued the study because of adverse effects during escitalopram. This study found a pain-relieving effect of escitalopram in patients with painful polyneuropathy, but a clinically relevant effect was obtained in only few patients. Currently, the drug cannot be recommended as a standard treatment in neuropathic pain.

Comparative study of the efficacy of acute and continuation treatment with Escitalopram versus Duloxetine in patients with major depressive disorder

Purpose:This study evaluated the efficacy and tolerability of escitalopram and duloxetine in the treatment of major depressive disorder (MDD).Methods:Patients were randomised to 24 weeks of double-blind treatment with fixed doses of escitalopram (20mg) (n=144) or duloxetine (60mg) (n=151). The primary analysis of efficacy was an ANCOVA of change from baseline to endpoint (Week 24) in MADRS total score (last observation carried forward).Results:At Week 8, the mean change from baseline in total MADRS score was -19.5 for escitalopram-treated patients (n=143) and -17.4 for duloxetine-treated patients (n=151), a difference of 2.1 points (p<0.05). At Week 8, the proportion of responders (at least 50% decrease in MADRS) was 69% (escitalopram) and 58% (duloxetine) (p<0.05) and remission (MADRS<=12) rates were 56% (escitalopram) and 48% (duloxetine) (NS). For the primary endpoint, the mean change from baseline in total MADRS score at Week 24 was -23.4 for escitalopram-treated patients and -21.7 for duloxetine-treated patients, a difference of 1.7 points (p=0.055, one-sided). The difference in mean change from baseline in MADRS total score favoured escitalopram at Weeks 1, 2, 4, 8, 12, and 16 (p<0.05). The overall withdrawal rates were 22% (escitalopram) and 26% (duloxetine) (NS). The withdrawal rate due to adverse events was lower for escitalopram (9%) compared to duloxetine (17%) (p<0.05) and significantly more patients treated with duloxetine reported insomnia (12.6% versus 4.9%) and constipation (8.6% versus 2.8%).Conclusion:Escitalopram was superior to duloxetine in acute treatment, and at least as efficacious and better tolerated in long-term treatment of MDD.

Prevalence of depression, stress, and anxiety among tobacco-using male college students in Ranchi and the relationship with cotinine in the body

demic inpatient service and in urban outpatient private practices. Materials and methods: 42 DSM-IV MDD patients (23.8% males, 76.2% females), mean age 52.0± 11.2 years (range 24–75) were prescribed open-label escitalopram for 6 weeks after signing informed consent. 14 (33.3%) of the patients suffered from their first major depressive episode (fMDE), and 28 (66.7%) had severe depression (at least 28 points on MADRS). Escitalopram was started at 10 mg/day and could be increased once to 20 mg/day on Day 28 according to clinical estimate. No other antidepressants were allowed. Participants' depressive and anxiety symptoms were assessed on Days 0, 7, 14, 28, and 42 by MADRS and HAM-A. Spontaneously reported adverse events were recorded at each timepoint, as well as a detailed assessment of side effects by UKU scale was elicited. Results: Mean total intensity of depression was reduced by 46.9% by the end of Week 6. All individual symptoms and symptom factors underwent similar (equivalent) improvement. Notably, suicidal ideation was significantly and permanently diminished from Day 7 to the end of the study period. Symptoms of anxiety responded in unison to depressive symptoms with a final reduction by 50.6%. Mean daily dose of escitalopram used was 13.9± 4.9mg, and 59.5% of the sample did not need an increase of the initial dose. 12/14 fMDE patients responded to 10 mg/day. 38.1% of the sample did not need any additional treatments, while the rest received benzodiazepines or zolpidem for varying periods. 50.0% of the sample were considered responders (having reduced their baseline total MADRS scores by at least 50%) on Day 42. 30.9% of all patients achieved remission (12 or less points on MADRS) in six weeks. Only 4.8% of the sample did not respond favourably to escitalopram till the end of study period. Mean group blood pressure and heart rate did not display significant variations in time. Mean group body weight was insignificantly reduced (by 3.3%). No marked individual variations of body weight were recorded, and in 42.9% of the sample weight did not change throughout the study period. The most frequent adverse events were nausea (23.8%), asthenia (21.4%), and orthostatic hypotension (19%). All adverse events were mild and did not result in premature termination of treatment, except for a high level of anxiety/tension in one patient. 28.6% of the sample did not report any adverse experiences. Conclusion: The results of this small open-label naturalistic study are comparable to international experience and suggest that escitalopram is an effective and tolerable option for treating MDD of various severity in widely differing settings.