Rapid onset of true antidepressant action

Taylor, Matthew

doi:10.1007/s11920-007-0064-0

Cited by 16 publications

(11 citation statements)

References 15 publications

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“…In addition to the neural changes described above, 7 days' treatment with escitalopram was associated with some reduction in HAM-D scores, and this was numerically greater in later clinical responders. This raises the possibility that the change in neural activity found in the second scan in subsequent treatment responders might be secondary to this early improvement, 32 rather than the neural changes leading to the subsequent clinical response. However, when this initial change in HAM-D score was accounted for in our statistical model, the early changes in neural response were still predictive of the therapeutic outcome.…”

Section: Discussionmentioning

confidence: 99%

Early changes in emotional processing as a marker of clinical response to SSRI treatment in depression

et al. 2016

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Antidepressant treatment reduces behavioural and neural markers of negative emotional bias early in treatment and has been proposed as a mechanism of antidepressant drug action. Here, we provide a critical test of this hypothesis by assessing whether neural markers of early emotional processing changes predict later clinical response in depression. Thirty-five unmedicated patients with major depression took the selective serotonin re-uptake inhibitor (SSRI), escitalopram (10 mg), over 6 weeks, and were classified as responders (22 patients) versus non-responders (13 patients), based on at least a 50% reduction in symptoms by the end of treatment. The neural response to fearful and happy emotional facial expressions was assessed before and after 7 days of treatment using functional magnetic resonance imaging. Changes in the neural response to these facial cues after 7 days of escitalopram were compared in patients as a function of later clinical response. A sample of healthy controls was also assessed. At baseline, depressed patients showed greater activation to fear versus happy faces than controls in the insula and dorsal anterior cingulate. Depressed patients who went on to respond to the SSRI had a greater reduction in neural activity to fearful versus happy facial expressions after just 7 days of escitalopram across a network of regions including the anterior cingulate, insula, amygdala and thalamus. Mediation analysis confirmed that the direct effect of neural change on symptom response was not mediated by initial changes in depressive symptoms. These results support the hypothesis that early changes in emotional processing with antidepressant treatment are the basis of later clinical improvement. As such, early correction of negative bias may be a key mechanism of antidepressant drug action and a potentially useful predictor of therapeutic response.

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Section: Discussionmentioning

confidence: 99%

Early changes in emotional processing as a marker of clinical response to SSRI treatment in depression

et al. 2016

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“…Considering the range of serotonergic manifestations evident in ADS, especially those of a neuropsychiatric nature such as anxiety, irritability and sleep disturbances (Table ; Coupland et al ., ), postsynaptic 5‐HT 1A/2C receptors are very likely one of the central receptor systems responsible for ADS. Somatodendritic 5‐HT 1A receptors are down‐regulated following chronic antidepressant use and are central to successful remission of the illness (Taylor, ; Stahl, ). Following abrupt discontinuation of the antidepressant, the ensuing decrease in presynaptic 5‐HT concentrations in the vicinity of the cell body (Figure ), and the down‐regulated state of 5‐HT 1A autoreceptors, will evoke a disinhibition of 5‐HT release and a relative increase in 5‐HT release in distal projection regions of the 5‐HT neuron (Figure ), including activation of postsynaptic 5‐HT 1A and 5‐HT 2C receptors, which will drive circadian rhythm disturbances and other neuropsychiatric changes leading to the typical symptoms of ADS (Table ).…”

Section: Antidepressant Discontinuation Syndrome: An Inseparable Linkmentioning

confidence: 99%

New insights on the antidepressant discontinuation syndrome

Harvey

Slabbert

2014

Human Psychopharmacology

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“…Faster expected time to onset, efficacy in comorbid conditions (such as anxiety), and persistence of treatment response are characteristics that may be associated with specific mechanisms of action. [2][3][4] Since many patients do not achieve remission following initial treatment 5 and most patients have residual symptoms, which are associated with lower quality of life and greater risk for relapse, 6 antidepressant options are essential.…”

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confidence: 99%

Efficacy and Safety of Vilazodone in Major Depressive Disorder

Croft¹,

Pomara²,

Gommoll³

et al. 2014

J. Clin. Psychiatry

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Introduction:Vilazodone is a potent serotonin (5-HT) reuptake inhibitor and 5-HT 1A receptor partial agonist approved by the US Food and Drug Administration for the treatment of major depressive disorder (MDD) in adults. This study evaluated the efficacy and tolerability of vilazodone in the treatment of MDD.Method: This 8-week, randomized (1:1), doubleblind, placebo-controlled, parallel-group, fixed-dose study conducted from January 2012 to February 2013 compared vilazodone 40 mg/d with placebo in outpatients with DSM-IV-TR-diagnosed MDD. The primary efficacy measure was Montgomery-Asberg Depression Rating Scale (MADRS) total score change from baseline to week 8 analyzed by a mixed-effects model for repeated measures on the intent-to-treat population (placebo = 252, vilazodone = 253). Secondary efficacy outcomes were Clinical Global ImpressionsSeverity of Illness (CGI-S) Scale score change from baseline and MADRS sustained response rate (total score ≤ 12 for at least the last 2 consecutive double-blind visits).Results: Approximately 83% of patients completed the study. Least squares mean differences (95% CI) were statistically significant for vilazodone versus placebo on MADRS (−5.117 [−6.886 to −3.347], P < .00001) and CGI-S (−0.622 [−0.845 to −0.399], P < .00001) change from baseline; statistically significant improvements versus placebo occurred at week 2 and persisted for the study duration. The MADRS sustained response rate was 17% for placebo and 27% for vilazodone (P < .01). Patients taking vilazodone versus placebo had higher rates of diarrhea and nausea; most incidences were mild in severity. Weight increase and sexual dysfunction adverse events were low in both groups. Conclusions:A large and significant treatment effect on the MADRS and statistically significant improvement on the CGI-S demonstrated meaningful depressive symptom improvements. Vilazodone was generally well tolerated.Trial Registration: ClinicalTrials.gov identifier: NCT01473394

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Rapid onset of true antidepressant action

Cited by 16 publications

References 15 publications

Early changes in emotional processing as a marker of clinical response to SSRI treatment in depression

Early changes in emotional processing as a marker of clinical response to SSRI treatment in depression

New insights on the antidepressant discontinuation syndrome

Efficacy and Safety of Vilazodone in Major Depressive Disorder

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