Treatment of atypical depression: Post-hoc analysis of a randomized controlled study testing the efficacy of sertraline and cognitive behavioural therapy in mildly depressed outpatients
ABSTRACT Atypical features are common among depressed primary care patients, but clinical trials testing the efficacy of psychopharmacological and/or psychotherapeutic treatment are lacking. This paper examines the efficacy of sertraline and cognitive behavioural therapy (CBT) among depressed patients with atypical features.
Analyses involve a double-blind comparison of sertraline versus placebo (N=47) and a single-blind comparison between CBT versus a guided self-help group (GSG) (N=48), with primary efficacy endpoints being the Inventory of Depressive Symptomatology (IDS(C)) and Hamilton Depression Scale (HAMD-17).
In intent-to-treat (ITT) analyses, the decrease on the IDS(C) scale (and HAMD-17) was greater after CBT compared to GSG: p=0.01 (HAMD-17: p=0.01). The difference between selective serotonin reuptake inhibitors (SSRI) versus placebo was not significant: p=0.22 (HAMD-17: p=0.36).
The number of cases in each treatment group was small, thereby limiting statistical power. Patients medicated with sertraline were 10 to 15 years younger than those included in the other groups of treatment.
CBT may be an effective alternative to GSG for mildly depressed patients with atypical features. Although SSRI were not superior to placebo, it would be premature to rule out SSRI as efficacious in atypical depression.
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ABSTRACT: Objective This paper examines whether atypical depression is still a valid entity as a diagnosis subtype in the light of publications with most recent antidepressants. Method First, we present the origins of the diagnosis sub-specification of atypical depression, which is based on a different drug response to tricyclic antidepressants and mono amino oxydase inhibitors. Secondly, we discuss the different definitions that can be found for the terms of atypical depression. We present more specifically the definition of atypical depression as it is described in the DSM-IV, with its most important criterion: mood reactivity. Then we present a review of scientific publications questioning atypical depression validity as a clinical syndrome (based on medline researches). We will see whether this diagnosis is still relevant with the latest drugs used to treat mood disorders. A special focus is made on the link between atypical depression and bipolar disorder, based on Benazzi's work. Results Most of publications confirm that atypical depression is a valid syndrome regarding first antidepressants clinical trials. Nevertheless, more studies with the latest antidepressants and atypical antipsychotics are needed to confirm this hypothesis. The link between atypical depression and bipolar disorders seems to be quite strong although it requires further investigations. Discussion There are very few double-blind drug trials focusing on atypical depressions and results need to be confirmed by trials with new drugs. Moreover, we regret that there are no studies including cerebral imagery. More studies are also needed on neurobiology and psychotherapy specificity. Conclusion Atypical depression is still a useful concept, because of its specific clinical presentation, evolution and treatments, even if more studies should be done. Atypical depression could also be useful to diagnose more easily some bipolar disorders and should help clinicians to focus more on suicidal risks and addiction evaluation for these patients, considering the mood reactivity and the link with bipolar disorder. To conclude, we propose that atypical depression should still figure in the future DSM-V for these different reasons.L Encéphale 09/2013; 39(4):258–264. DOI:10.1016/j.encep.2012.08.008 · 0.70 Impact Factor
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ABSTRACT: Objective: Clinical significance determines whether an intervention makes a real difference in the everyday life of a client. One of the most recommended approaches for conducting group-level analyses of clinical significance is to evaluate whether the treated clinical group is equivalent to a normal comparison group (normative comparisons). The purpose of this study was to demonstrate the analytical and practical power of assessing clinical significance using normative comparisons that are robust to violations of normality and homogeneity of variance assumptions. Method: Six datasets were gleaned from published intervention studies for depression. Results: We found that normative comparisons using a robust Schuirmann-Yuen test determined equivalency for 11% fewer clinical samples compared to original normative comparisons that use a Schuirmann test of equivalence. Conclusions: We recommend that researchers conducting normative comparisons utilize the Schuirmann-Yuen procedure as it provides the most reliable method available for determining if a treated clinical group is equivalent to a normative comparison group.Psychotherapy Research 02/2014; 25(2). DOI:10.1080/10503307.2014.889329 · 1.75 Impact Factor
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ABSTRACT: According to the recently proposed vigilance model of affective disorders (vigilance in the sense of "brain arousal"), manic behaviour is partly interpreted as an autoregulatory attempt to stabilise vigilance by creating a stimulating environment, and the sensation avoidance and withdrawal in Major Depressive Disorder (MDD) is seen as an autoregulatory reaction to tonically increased vigilance. Indeed, using a newly developed EEG-based algorithm, hyperstable vigilance was found in MDD, and the contrary, with rapid drops to sleep stages, in mania. Furthermore, destabilising vigilance (e.g. by sleep deprivation) triggers (hypo)mania and improves depression, whereas stabilising vigilance, e.g. by prolonged sleep, improves mania. ADHD and mania have common symptoms, and the unstable vigilance might be a common pathophysiology. There is even evidence that psychostimulants might ameliorate both ADHD and mania. Hyperactivity of the noradrenergic system could explain both the high vigilance level in MDD and, as recently argued, anhedonia and behavioural inhibition. Interestingly, antidepressants and electroconvulsions decrease the firing rate of neurons in the noradrenergic locus coeruleus, whereas many antimanic drugs have opposite effects.Neuroscience & Biobehavioral Reviews 07/2014; 44:45-57. DOI:10.1016/j.neubiorev.2012.10.008 · 8.80 Impact Factor