How long should a trial of escitalopram treatment be in patients with major depressive disorder, generalised anxiety disorder or social anxiety disorder? An exploration of the randomised controlled trial database

Baldwin, David S.; Stein, Dan J.; Dolberg, Ornah T.; Bandelow, Borwin

doi:10.1002/hup.1019

Cited by 54 publications

(17 citation statements)

References 41 publications

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“…Similarly, greater episode severity was found to predict a greater likelihood of attaining remission of depression following treatment with the SNRI duloxetine (Thase et al 2007), and the SNRI venlafaxine (Schmitt et al 2009) than SSRIs in MDD. In addition to episode severity, an early change (reduction) in depressive symptomatology has also been found to serve as both a predictor (temporally preceding outcome) and mediator (indicating a relationship between change in value during the course of therapy and outcome at endpoint) of outcome (Baldwin et al 2009 ;Nierenberg et al 1995Nierenberg et al , 2000Stassen et al 1996 ;Taylor et al 2006a, b).…”

Section: Clinical and Demographic Factorsmentioning

confidence: 93%

Surrogate markers of treatment outcome in major depressive disorder

Papakostas

2011

Int. J. Neuropsychopharm.

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Major depressive disorder (MDD) is a common medical illness affecting millions worldwide. Despite their widespread use since the 1950s and 1960s, the 'downstream' mechanism by which antidepressants ultimately exert their therapeutic effects remains elusive. In addition, except for a few exceptions such as episode severity and the presence of comorbid Axis-I or Axis-III disorders, biological or clinical characteristics which can accurately quantify the risk of poor treatment outcome are lacking, as are factors which could help patients and clinicians select treatment options that would result in superior outcome. The identification of such markers, termed 'surrogate' markers, could help shed further insights into what constitutes illness and recovery, help identify molecular targets for the development of future antidepressants, and lead the way to the design and refinement of a personalized medicine treatment model for MDD. In the following text, several major areas ('leads') where evidence exists regarding the presence of surrogate markers of efficacy outcome in MDD will be briefly reviewed. Leads include evidence from the role of demographic and clinical factors as surrogate markers, to the role of various biological markers including genotype, brain functional imaging, electroencephalography, dichotic listening, and molecular biology and immunology. The purpose of this work is to focus selectively on areas where there have been findings, as opposed to conducting an exhaustive literature review of studies which have failed to yield any significant breakthrough in our knowledge.

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Section: Clinical and Demographic Factorsmentioning

confidence: 93%

Surrogate markers of treatment outcome in major depressive disorder

Papakostas

2011

Int. J. Neuropsychopharm.

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“…A post hoc analysis of the clinical trial database with paroxetine indicates that many non-responders to treatment at 8 weeks become responders with a further 4 weeks of double-blind treatment [56]; however, a post hoc analysis of the clinical trial database for escitalopram suggests that a response is unlikely if there is no onset of clinical effect within the first 4 weeks of treatment [57]. The findings of randomized placebo-controlled relapse-prevention studies in patients who have responded to previous acute treatment show there is a significant advantage for staying on active medication (clonazepam, escitalopram, paroxetine, pregabalin, sertraline) for up to 6 months [31].…”

Section: Longer-term Treatmentmentioning

confidence: 97%

Pharmacological Treatment of Social Anxiety Disorder

Masdrakis

Turic²,

Baldwin³

2013

Modern Trends in Psychiatry

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Social anxiety disorder (social phobia) is a common and typically long-standing medical condition, characterized by an excessive fear of being observed or evaluated negatively in social or performance situations. Efficacious interventions in acute treatment include cognitive behavioural therapy and a range of medications including many antidepressants, some benzodiazepines and anticonvulsants, and the antipsychotic olanzapine. Most studies report no significant differences in overall efficacy or tolerability between active compounds. Responders to previous acute treatment benefit from continuing active medication for 6 months. Evidence of a dose-response relationship with antidepressant drugs is inconsistent, though only higher doses of pregabalin are efficacious. Switching between treatments with proven efficacy may be helpful. Augmentation of a selective serotonin reuptake inhibitor with buspirone or clonazepam can be beneficial. It is unlikely that combining pharmacotherapy with psychotherapy results in greater overall efficacy compared to either treatment given alone. Proof-of-concept and other preliminary studies suggest the efficacy of psychotherapy can be enhanced through prior administration of D-cycloserine, cannabidiol, or oxytocin.

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“…The primary pharmacological action of SSRIs is to block the serotonin transporter (5-HTT), the mechanism for clearing extracellular serotonin, putatively increasing central serotonin levels (Nutt et al, 1999). The clinical response to SSRI treatment typically emerges 2-3 weeks after treatment onset, at which point response is significantly predictive of long-term treatment response (Baldwin et al, 2009). This time frame coincides with hypothesized molecular mediators of antidepressant response including serotonin 1A autoreceptor desensitization and downregulation of 5-HTT (Benmansour et al, 2002;Blier and de Montigny, 1999;Richardson-Jones et al, 2010).…”

Section: Introductionmentioning

confidence: 94%

Fluctuations in [11C]SB207145 PET Binding Associated with Change in Threat-Related Amygdala Reactivity in Humans

Fisher

Haahr

Jensen

et al. 2015

Neuropsychopharmacol

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Serotonin critically affects the neural processing of emotionally salient stimuli, including indices of threat; however, how alterations in serotonin signaling contribute to changes in brain function is not well understood. Recently, we showed in a placebo-controlled study of 32 healthy males that brain serotonin 4 receptor (5-HT4) binding, assessed with [(11)C]SB207145 PET, was sensitive to a 3-week intervention with the selective serotonin reuptake inhibitor fluoxetine, supporting it as an in vivo model for fluctuations in central serotonin levels. Participants also underwent functional magnetic resonance imaging while performing a gender discrimination task of fearful, angry, and neutral faces. This offered a unique opportunity to evaluate whether individual fluctuations in central serotonin levels, indexed by change in [(11)C]SB207145 binding, predicted changes in threat-related reactivity (ie, fear and angry vs neutral faces) within a corticolimbic circuit including the amygdala and medial prefrontal and anterior cingulate cortex. We observed a significant association such that decreased brain-wide [(11)C]SB207145 binding (ie, increased brain serotonin levels) was associated with lower threat-related amygdala reactivity, whereas intervention group status did not predict change in corticolimbic reactivity. This suggests that in the healthy brain, interindividual responses to pharmacologically induced and spontaneously occurring fluctuations in [(11)C]SB207145 binding, a putative marker of brain serotonin levels, affect amygdala reactivity to threat. Our finding also supports that change in brain [(11)C]SB207145 binding may be a relevant marker for evaluating neurobiological mechanisms underlying sensitivity to threat and serotonin signaling.

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How long should a trial of escitalopram treatment be in patients with major depressive disorder, generalised anxiety disorder or social anxiety disorder? An exploration of the randomised controlled trial database

Abstract: The pattern of response in these RCTs suggests that in patients with MDD, GAD or SAD in wider clinical practice, a period of at least 4 weeks is worthwhile before considering further intervention.

Cited by 54 publications

References 41 publications

Surrogate markers of treatment outcome in major depressive disorder

Surrogate markers of treatment outcome in major depressive disorder

Pharmacological Treatment of Social Anxiety Disorder

Fluctuations in [11C]SB207145 PET Binding Associated with Change in Threat-Related Amygdala Reactivity in Humans

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