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1 randomized to sertraline, venlafaxine-XR, or escitalopram).
2 or bupropion to 0.83 [95% CI, 0.67-0.98] for escitalopram).
3 ponse to sertraline and venlafaxine, but not escitalopram.
4 nt selection in depression, particularly for escitalopram.
5 serotonin reuptake inhibitors fluoxetine and escitalopram.
6 s after 8 weeks of open-label treatment with escitalopram.
7 measures of executive function more than the escitalopram.
8 3 points higher with nortriptyline than with escitalopram.
9 ctions than historical controls treated with escitalopram.
10 ive behavior therapy, and 6 nonresponders to escitalopram.
11 reuptake inhibitors (SSRIs), sertraline and escitalopram.
12 a double-blind, randomized clinical trial of escitalopram.
13 by 1.35 (1.06) for MBSR and 1.43 (1.17) for escitalopram.
14 pression (CANBIND-1) RCT, which administered escitalopram.
15 in healthy humans following daily intake of escitalopram.
16 difference in the scores with placebo versus escitalopram.
17 ign with 8 wk of standardized treatment with escitalopram.
18 ed 8 wk of standardized pharmacotherapy with escitalopram.
19 r the selective serotonin reuptake inhibitor escitalopram.
20 subjects who completed phase 1 responded to escitalopram.
21 D-1) protocol received 8 weeks of open-label escitalopram.
22 s after 8 weeks of open-label treatment with escitalopram.
23 atin (40 mg per day) or placebo as add-on to escitalopram (10 mg for the first 2 weeks, then increase
27 igned to one of four conditions: 16 weeks of escitalopram (10-20 mg/day) plus modular CBT, followed b
28 ual likelihood to 12 weeks of treatment with escitalopram (10-20 mg/day), duloxetine (30-60 mg/day),
31 lop depression than individuals who received escitalopram (11 major and 2 minor cases of depression [
34 we examined the effect of 3-5 weeks of SSRI escitalopram (20 mg daily) on brain response to angry, f
35 ompare nCCR-GD to a gold-standard treatment (escitalopram: 20 mg per 12 weeks) in 11 treatment-resist
36 At the end of 6 weeks, more patients taking escitalopram (34.2% [95% CI, 25.4%-43.0%]) had absence o
37 , 51 given amitriptyline (53%), and 37 given escitalopram (38%) (P = .05, after treatment, adjusted f
39 ADS-A (exercise, -4.0; 95% CI, -4.7 to -3.2; escitalopram, -5.7; 95% CI, -6.4 to -5.0) compared with
40 occurred for 110 participants randomized to escitalopram (78.6%) and 21 participants randomized to M
41 cognitive behavior therapy, 11 remitters to escitalopram, 9 nonresponders to cognitive behavior ther
43 lammation, predicts differential response to escitalopram (a serotonin reuptake inhibitor) and nortri
44 n this study, we investigated the effects of escitalopram, a selective serotonin reuptake inhibitor (
45 essive disorder, we compared psilocybin with escitalopram, a selective serotonin-reuptake inhibitor,
48 wed by 28 weeks of maintenance escitalopram; escitalopram alone, followed by maintenance escitalopram
52 MDD patients were treated with citalopram or escitalopram and blood was drawn at baseline, 4 and 8 we
55 py (CBT) and two antidepressant medications (escitalopram and duloxetine) in patients with major depr
57 cell states, which may enable repurposing of escitalopram and other drugs to limit cardiac remodeling
58 nce in mean cumulative response rate between escitalopram and placebo (57%; 95% CI, 46%-67%; vs 45%;
60 rmetabolism was associated with remission to escitalopram and poor response to cognitive behavior the
61 ith AG compared to brand-name initiation for escitalopram and sertraline (HR [95% CI]: 1.06 [0.98-1.1
62 the selective serotonin reuptake inhibitors escitalopram and sertraline and the serotonin-norepineph
64 the selective serotonin reuptake inhibitors escitalopram and sertraline than did A allele carriers.
69 Participants received 12 weeks of open-label escitalopram and were then randomly assigned to one of f
70 ric hospitalization rate (for sertraline and escitalopram), and insulin initiation (for glipizide) be
71 thiazines, fluoxetine, citalopram (including escitalopram), and methadone were significantly more fre
72 fluoxetine and cognitive behavioral therapy, escitalopram, and collaborative care demonstrated benefi
73 talopram than those treated with placebo and escitalopram, and median time to onset of anxiolytic res
77 inicians need to be cautious in recommending escitalopram as an alternative to citalopram for this co
78 nt scores were improved with eszopiclone and escitalopram at every point (P < .02), while CGI of Seve
79 ask was correlated with clinical response to escitalopram at week 8. Early (baseline to week 2) incre
81 wed the noninferiority of MBSR compared with escitalopram based on the improvement in CGI-S score.
82 tional enrichment analysis demonstrates that escitalopram-based remission associates to functions rel
83 d the serotonin selective reuptake inhibitor escitalopram both effectively restored DNIC after TBI in
84 s a randomized double-blind 12-week trial of escitalopram, bupropion, or the combination of the two i
85 med significantly above chance in a combined escitalopram-buproprion treatment group in COMED (n=134;
88 y outcomes generally favored psilocybin over escitalopram, but the analyses of these outcomes lacked
89 y outcomes generally favored psilocybin over escitalopram, but the analyses were not corrected for mu
90 atments including psychotherapy, sertraline, escitalopram, citalopram, mirtazapine, duloxetine, trazo
93 and depression, 18 months of treatment with escitalopram compared with placebo did not significantly
95 heart disease and baseline MSIMI, 6 weeks of escitalopram, compared with placebo, resulted in a lower
96 , open-label nonrandomized clinical trial of escitalopram conducted at an outpatient geriatric psychi
97 whether pretreatment with the antidepressant escitalopram could reduce IL-2-induced neuroendocrine, i
98 CAN-BIND-1, patients received 10 to 20 mg of escitalopram daily; nonresponders at 8 weeks received ar
103 e difference in the decrease for tDCS versus escitalopram (difference, -2.3 points; 95% confidence in
104 participants were randomized 1:1 to receive escitalopram (dose began at 5 mg/d, with titration to 20
105 ession who were randomly assigned to receive escitalopram, duloxetine, or CBT monotherapy and complet
106 l to achieve remission as a result of CBT or escitalopram, either alone or in combination, have a dis
108 placebo or the serotonin reuptake inhibitor, escitalopram (ESC) 10-20 mg/day, 2 weeks before, and dur
109 ersely, early exposure to the antidepressant escitalopram (ESC; Lexapro) results in decreased anxiety
110 bin 3 weeks apart plus 6 weeks of daily oral escitalopram (escitalopram group); all the patients rece
111 lar CBT, followed by 28 weeks of maintenance escitalopram; escitalopram alone, followed by maintenanc
112 escitalopram alone, followed by maintenance escitalopram; escitalopram plus CBT, followed by pill pl
115 n adults: bupropion, citalopram, duloxetine, escitalopram, fluoxetine, fluvoxamine, milnacipran, mirt
116 pram, clomipramine, desipramine, duloxetine, escitalopram, fluoxetine, imipramine, mirtazapine, nefaz
117 onin reuptake inhibitors (SSRIs; citalopram, escitalopram, fluoxetine, paroxetine, and sertraline), v
119 body dysmorphic disorder received open-label escitalopram for 14 weeks (phase 1); 58 responders were
121 proaches such as citalopram, desvenlafaxine, escitalopram, gabapentin, paroxetine, and venlafaxine ar
122 ividuals treated with citalopram (STAR*D) or escitalopram (GENDEP) identified an intergenic region on
123 ity scores were significantly greater in the escitalopram group (-0.52; 95% CI, -0.64 to -0.40 vs -0.
124 chemia were slightly lower at 6 weeks in the escitalopram group (45.8% [95% CI, 36.6%-55.0%]) than in
125 cantly among those whose mothers were in the escitalopram group (compared with those whose mothers we
126 pation time of 18.4 months (n = 185) for the escitalopram group and 18.7 months (n = 187) for the pla
127 n was diagnosed in 8% of the patients in the escitalopram group and 19% in the placebo group (absolut
128 20.2 at baseline to 11.2 at 12 weeks in the escitalopram group and from 21.4 to 12.5 in the placebo
129 tarted treatment, 10 (8%) dropped out of the escitalopram group and none from the MBSR group due to a
130 4.93; P = .01) and greater reductions in the escitalopram group compared with the exercise group (F1,
131 greater reductions in the exercise group and escitalopram group compared with the placebo group (F1,1
132 (95% CI, 21% to 43%) of the patients in the escitalopram group developed a MADRS score of 13 or high
133 ) for the MBSR group and 4.51 (0.78) for the escitalopram group in the per-protocol sample and 4.49 (
135 ee weeks after treatment ended, women in the escitalopram group reported a mean 1.59 (95% CI, 0.55-2.
136 cipants randomized to the exercise group and escitalopram group reported greater reductions in HADS-A
137 nges in parental functioning: Mothers in the escitalopram group reported significantly greater improv
140 art plus 6 weeks of daily oral escitalopram (escitalopram group); all the patients received psycholog
141 ore (P < .01, adjusted mean change in score: escitalopram group, 10.0; nonescitalopram group, 3.1) an
142 ore (P < .01, adjusted mean change in score: escitalopram group, 11.3; nonescitalopram group, 2.5).
144 e from baseline was 11.3+/-6.5 points in the escitalopram group, 9.0+/-7.1 points in the tDCS group,
145 eduction of response to fearful faces in the escitalopram group, but lesser effects for the psilocybi
146 psilocybin group and in 48% of those in the escitalopram group, for a between-group difference of 22
147 all types were significantly reduced in the escitalopram group, with no change or a slight increase
154 ases showed that patients with depression on escitalopram have a lower incidence of cardiac hypertrop
155 s previously reported to predict response to escitalopram in a sample different from the current stud
158 These findings do not support the use of escitalopram in patients with chronic systolic heart fai
159 rial, we assessed the efficacy and safety of escitalopram in treating agitation in AD after failure o
160 r example, high-dose duloxetine outperformed escitalopram in treating core emotional symptoms (effect
164 Baseline amygdala-vmPFC connectivity and escitalopram-induced increased amygdala-angular gyrus co
165 ake inhibitors (SSRIs) such as fluoxetine or escitalopram inhibit SERT and are currently the principa
167 itors of monoamine transporters (reboxetine, escitalopram, JHW-007) whereas its effects on the length
168 ental cardiovascular effects than sertraline/escitalopram (large ES); antidepressants were neutral on
169 xine (MD -2.69, 95% CrI -3.50 to -1.89), and escitalopram (MD -2.45, 95% CrI -3.27 to -1.63) were mor
170 lower than that in antidepression trials of escitalopram (mean difference -3.90 (95% credible interv
171 ter than placebo in antidepression trials of escitalopram (mean difference 6.45 (3.19 to 9.41)).
173 Remitters to escitalopram compared with escitalopram/memantine combination treatment display uni
174 placebo-controlled trial of escitalopram or escitalopram/memantine in late-life depression with subj
177 data analysis sample received treatment with escitalopram (n = 22) or duloxetine (n = 14) for 10 week
178 ouble-blind placebo-controlled comparison of escitalopram (n = 43) with placebo (n = 45), and a nonbl
179 ouble-blind placebo-controlled comparison of escitalopram (n = 59) with placebo (n = 58), and a nonbl
180 Of 127 participants randomized to receive escitalopram (n = 64) or placebo (n = 63), 112 (88.2%) c
183 n ancestry treated for major depression with escitalopram (N=394) or nortriptyline (N=312) over a 12-
184 gness was associated with poorer efficacy of escitalopram (odds ratio [OR] = 1.04; 95% CI, 1.02 to 1.
185 80% (from 78.6% for odansetron to 93.9% for escitalopram) of study drug new-use prescriptions occurr
188 Here, we investigate the effects of the SSRI escitalopram on presynaptic density as a proxy for synap
189 investigate the chronic effect of the SSRI, escitalopram, on measures of 'cold' cognition (including
191 with a 2-way analysis of variance treatment (escitalopram or cognitive behavior therapy) x outcome (r
192 ressive disorder and were assigned to either escitalopram or cognitive behavioral therapy based on fl
193 ssigned to 12 weeks of treatment with either escitalopram or cognitive-behavioral therapy (CBT).
194 - and male-identifying patients treated with escitalopram or desvenlafaxine and assessed for treatmen
195 ind, randomized, placebo-controlled trial of escitalopram or escitalopram/memantine in late-life depr
196 ived randomized 8-week treatment with either escitalopram or mindfulness-based stress reduction.
197 ssociated with the outcome of treatment with escitalopram or nortriptyline at suggestive levels of si
198 iagnosis of GAD randomized to receive either escitalopram or placebo and conducted between January 20
199 ssed patients with recent stroke, the use of escitalopram or problem-solving therapy resulted in a si
200 umulate within lipid membranes by >=18-fold (escitalopram) or 180-fold (fluoxetine), and possibly by
201 ent with cognitive behavioral therapy (CBT), escitalopram, or duloxetine for major depressive disorde
204 of depression did not show noninferiority to escitalopram over a 10-week period and was associated wi
205 ignment to 12 weeks of treatment with either escitalopram oxalate (10-20 mg/d) or 16 sessions of manu
206 % CI, 1.28-1.44; 23 studies; 1492 patients), escitalopram oxalate (CYP2C19 PM vs NM, RoM, 2.63; 95% C
207 y prior to treatment randomization to either escitalopram oxalate or cognitive behavior therapy for 1
208 pram hydrobromide, duloxetine hydrochloride, escitalopram oxalate, fluoxetine hydrochloride, mirtazap
209 ted with the FDA-approved drugs tramadol and escitalopram oxalate, they release or uptake serotonin i
211 flashes per day at week 8 among women taking escitalopram (P < .001), with mean reductions of 4.60 (9
214 pression after an 8-week open-label trial of escitalopram (phase 1), randomly assigned in a 1:1 ratio
215 alone, followed by maintenance escitalopram; escitalopram plus CBT, followed by pill placebo; and esc
218 us ziprasidone, N=71) or adjunctive placebo (escitalopram plus placebo, N=68), with 8 weekly follow-u
219 =21; 6 women and 15 men) received 6 weeks of escitalopram plus two dosing sessions with a nonpsychoac
223 1:1 ratio to receive adjunctive ziprasidone (escitalopram plus ziprasidone, N=71) or adjunctive place
224 reuptake inhibitors (SSRIs), citalopram and escitalopram prolong the QT interval to the greatest ext
228 ects then received 8 weeks of treatment with escitalopram; remission was defined as a posttreatment 2
229 o -2.4; P = .03); participants randomized to escitalopram reported less anxiety compared with those r
231 escitalopram, treatment with eszopiclone and escitalopram resulted in significantly improved sleep an
232 enzofuran-5-carboni trile), and its eutomer, escitalopram (S-(+)-1) are selective serotonin reuptake
234 Participants were randomized to 1 of 3 arms: escitalopram, sertraline (serotonin-specific reuptake in
235 eks of randomized open-label treatment ADMs: escitalopram, sertraline or venlafaxine-extended release
237 mes for three commonly used antidepressants (escitalopram, sertraline, and extended-release venlafaxi
238 ndomly assigned to 8 weeks of treatment with escitalopram, sertraline, or extended-release venlafaxin
239 whom 576 completed 8 weeks of treatment with escitalopram, sertraline, or extended-release venlafaxin
240 the selective serotonin reuptake inhibitors escitalopram, sertraline, or fluoxetine may be prescribe
241 ive disorder (n = 124) randomized to receive escitalopram, sertraline, or venlafaxine (8 weeks) and h
242 1:1:1 ratio to antidepressant treatment with escitalopram, sertraline, or venlafaxine extended-releas
243 ment with one of three antidepressant drugs (escitalopram, sertraline, or venlafaxine extended-releas
244 pressed participants were then randomized to escitalopram, sertraline, or venlafaxine-extended releas
246 olving Therapy, stroke patients who received escitalopram showed improvement in global cognitive func
247 iority margin of -2.75 (50% of placebo minus escitalopram), so noninferiority could not be claimed.
248 Mental Stress-Induced Myocardial Ischemia to Escitalopram) study underwent psychometric assessments,
249 rial (Treatments for Anxiety: Meditation and Escitalopram [TAME]) included a noninferiority design wi
250 her in patients treated with eszopiclone and escitalopram than those treated with placebo and escital
252 ime to relapse was significantly longer with escitalopram than with placebo treatment (hazard ratio=2
254 h the selective serotonin reuptake inhibitor escitalopram; this is consistent with data from a separa
255 2-week washout period, participants received escitalopram titrated to a target of 20 mg/d for 12 week
256 S-induced histamine increase, the ability of escitalopram to augment extracellular serotonin is impai
257 in histamine synthesis boosts the ability of escitalopram to increase extracellular serotonin levels
259 owing acute response; more than one-third of escitalopram-treated subjects experienced further improv
260 italopram delayed time to relapse, and fewer escitalopram-treated subjects relapsed than did placebo-
262 ants received an 8-week treatment regimen of escitalopram treatment (10-20 mg), and EMBARC participan
264 antly improved during 6 additional months of escitalopram treatment following acute response; more th
265 We externally validated the model in the escitalopram treatment group (n=151) of an independent c
266 The model was externally validated in the escitalopram treatment group (N=151) of COMED (accuracy
268 nfounders, there was a significant effect of escitalopram treatment on the change in RBANS total scor
270 Compared with treatment with placebo and escitalopram, treatment with eszopiclone and escitalopra
273 total, 173 participants were randomized (84 escitalopram versus 89 placebo; mean +/- s.d. age = 78.4
274 to double-blind continuation treatment with escitalopram versus switch to placebo for 6 months (phas
275 for prolonging the QT interval (citalopram, escitalopram) versus the risk among those initiating SSR
276 f dropout, mean cumulative response rate for escitalopram was 69% (95% confidence interval [CI], 58%-
277 ents who did not achieve remission with CBT, escitalopram was added (CBT plus medication group) to th
282 e level, but an association with response to escitalopram was detected in the interleukin-6 gene, whi
283 Prophylactic antidepressant treatment with escitalopram was effective in reducing the incidence and
286 randomized sample was smaller than planned, escitalopram was not effective in treating agitation in
287 8 weeks, 95% CI, 1.6 to 3.1; P < .001), but escitalopram was not significantly different from placeb
289 rolling for prior history of mood disorders, escitalopram was superior to placebo (23.1% vs 34.5%; ad
292 5-HT levels before and after treatment with escitalopram were dose-dependent and variable across pat
293 nausea, and adverse effects associated with escitalopram were not significantly different between th
294 thcognitive behavior therapy, duloxetine, or escitalopram were prospectively monitored for up to 21 m
295 els of hippocampal 5HT; however responses to escitalopram were significantly impaired in the hippocam
296 humans given a single dose of an SSRI (20 mg escitalopram), which can decrease post-synaptic serotoni
297 nitive behavior therapy and poor response to escitalopram, while insula hypermetabolism was associate
299 We hypothesized that patients who received escitalopram would show improved performance in neuropsy
300 xercise z score = 0.05; 95% CI, -0.2 to 0.3; escitalopram z score = -0.24; 95% CI, -0.4 to 0; placebo