Relapse Of Depressive Symptoms Research Articles

Relationship of Subjective Cognitive Impairment with Psychosocial Function and Relapse of Depressive Symptoms in Patients with Major Depressive Disorder: Analysis of Longitudinal Data from PERFORM-J.

BackgroundAccumulating evidence suggests the presence of cognitive impairment in patients with major depressive disorder (MDD), which affects their psychosocial function and quality of life (QoL). PERFORM-J (Prospective Epidemiological Research on Functioning Outcomes Related to MDD in Japan) is an observational, multicenter study to assess longitudinal changes in depressive symptoms, psychomotor speed, subjective cognitive function, and psychosocial function.MethodsFive hundred and eighteen Japanese outpatients with MDD initiating new antidepressant monotherapy (first-line or switch from previous drug) as part of their routine medical care participated in this study. Assessments at baseline and over the 6-month observation period included physician-rated depression severity (Montgomery–Åsberg Depression Rating Scale), psychomotor speed (Digit Symbol Substitution Test; DSST), subjective cognition (Perceived Deficits Questionnaire–Depression), psychosocial function (Sheehan Disability Scale), and QoL (EuroQol-5 Dimension-5 Level).ResultsAntidepressant treatment for 6 months improved depressive symptoms and subjective cognitive impairment (cognitive complaints), whereas psychomotor speed remained impaired (ie, DSST total score was >1 standard deviation below the norm) in 35.6% of patients at 6 months. Impairment of subjective cognition, but not psychomotor speed at month 2 was associated with poor psychosocial function and QoL at 6 months. There was a trend for higher relapse rates at 6 months in patients with greater subjective cognitive impairment at 2 months.ConclusionThese findings highlight the importance of evaluating cognitive difficulties to predict long-term outcomes in patients with MDD. Early intervention for cognitive complaints may decrease the relapse rate, which warrants further study.

Single and repeated ketamine infusions for reduction of suicidal ideation in treatment-resistant depression.

Repeated administration of subanesthetic intravenous ketamine may prolong the rapid decrease in suicidal ideation (SI) elicited by single infusions. The purpose of this secondary analysis was to evaluate reduction in SI with a single ketamine infusion compared with an active control, and prolonged suppression of SI with repeated and maintenance infusions. Thirty-seven participants with treatment-resistant depression (TRD) and baseline SI first received a single ketamine infusion during a randomized, double-blind crossover with midazolam. Following relapse of depressive symptoms, participants received six open-label ketamine infusions administered thrice-weekly over 2 weeks. Antidepressant responders (≥50% decrease in Montgomery-Åsberg Depression Rating Scale [MADRS] scores) received four further open-label infusions administered once-weekly. Changes in SI were assessed with the suicide items on the MADRS (item 10, MADRS-SI) and the Quick Inventory of Depressive Symptomatology-Self Report (item 12, QIDS-SI). Linear mixed models revealed that compared with midazolam, a single ketamine infusion elicited larger reduction in SI (P = 0.01), with maximal effects measured at 7 days postinfusion (P < 0.001, Cohen's d = 0.83). Participants had cumulative reductions in MADRS-SI scores with repeated infusions (P < 0.001), and no further change with maintenance infusions (P = 0.94). QIDS-SI results were consistent with MADRS-SI. Overall, 69% of participants had a complete alleviation of SI following repeated infusions. In TRD, single and repeated ketamine infusions resulted in decreases in SI which were maintained with once-weekly maintenance infusions. This study adds to the growing body of research suggesting ketamine as a possible novel treatment strategy for SI in mood disorders.

Single, Repeated, and Maintenance Ketamine Infusions for Treatment-Resistant Depression: A Randomized Controlled Trial.

Subanesthetic ketamine doses have been shown to have rapid yet transient antidepressant effects in patients with treatment-resistant depression, which may be prolonged by repeated administration. The purpose of this study was to evaluate the antidepressant effects of a single ketamine infusion, a series of repeated ketamine infusions, and prolongation of response with maintenance infusions. Forty-one participants with treatment-resistant depression completed a single-site randomized double-blind crossover comparison of single infusions of ketamine and midazolam (an active placebo control). After relapse of depressive symptoms, participants received a course of six open-label ketamine infusions administered thrice weekly over 2 weeks. Responders, classified as those participants who had a ≥50% decrease in their scores on the Montgomery-Åsberg Depression Rating Scale (MADRS), received four additional infusions administered once weekly (maintenance phase). Compared with midazolam, a single ketamine infusion elicited a significantly greater reduction in depressive symptoms at the primary efficacy endpoint (24 hours postinfusion). Linear mixed models revealed cumulative antidepressant effects with repeated infusions and doubling of the antidepressant response rate. Fifty-nine percent of participants met response criteria after repeated infusions, with a median of three infusions required before achieving response. Participants had no further change in MADRS scores during weekly maintenance infusions. Repeated ketamine infusions have cumulative and sustained antidepressant effects. Reductions in depressive symptoms were maintained among responders through once-weekly infusions. These findings provide novel data on efficacious administration strategies for ketamine in patients with treatment-resistant depression. Future studies should further expand on optimizing administration to better translate the use of ketamine into clinical settings.

934. Cortical and Subcortical Morphometry Predicts Relapse of Depressive Symptoms following Electroconvulsive Therapy

934. Cortical and Subcortical Morphometry Predicts Relapse of Depressive Symptoms following Electroconvulsive Therapy

Antidepressants and sexual dysfunction: study with vortioxetina

IntroductionAntidepressant treatment, although it is effective to improve the manifestations of major depression, may also induce or exacerbate some symptoms of sexual dysfunction. Symptoms such as decreased libido, anorgasmia, delayed ejaculation, erection difficulty or dyspareunia, affect the quality of life of the subject who suffers and the self-esteem, can lead to lack of adherence to treatment and in accordingly, the relapse of depressive symptoms. Serotonergic antidepressants are frequently associated with the onset of sexual dysfunction in sexually active patients exceeding 70%. Clinicians underestimate the actual incidence of dysfunction as the technical specifications of drugs show lower levels than 25% and spontaneous reports of patients do not exceed 20-40%.AimsVortioxetina is a reuptake inhibitor of serotonin (5-HT) and is also an agonist of the 5-HT1A partial agonist 5-HT1B and an antagonist of 5-HT3, 5-HT1D and 5-HT7. Apparently, this molecule at doses of between 5 and 15 mg is safe and effective and does not cause sexual dysfunction. It is a well-tolerated and safe, with low incidence of sexual dysfunction.MethodsTo evaluate the action we have evaluated sexual dysfunction in patients with major depression before receiving treatment vortioxetina (whether state or not previously treated with other antidepressants) and at 2, 6 and 12 months after starting treatment with the drug. So we’ve used the SALSex scale (Scale for measuring sexual dysfunction secondary to psychotropic drugs).ResultsThe results of this study are still being analyzed.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Trazodone Addition to Paroxetine and Mirtazapine in a Patient with Treatment-Resistant Depression: The Pros and Cons of Combining Three Antidepressants.

Dual antidepressant combination for treatment-resistant depression is a strategy well supported by literature and accepted in clinical practice. Rather, the usefulness of the combination of more than two antidepressants is controversial. This may be related to the possibility of higher side-effect burden and to doubts about its pharmacological effectiveness and therapeutic advantage compared to other standard treatment options. We report a relapse of moderate-to-severe depressive symptoms with insomnia that successfully remitted after the addition of trazodone to a dual combination of paroxetine and mirtazapine (in standard effective doses) in a patient with treatment-resistant depression. We also review the literature and discuss the utility of triple antidepressant combination in treatment-resistant depression. This clinical case highlights the utility of combining trazodone as a third antidepressant for the relapse of depressive symptoms after the failure of a dual antidepressant combination. Trazodone may be advantageous in patients presenting recurrence of moderate-to-severe depressive symptoms that include sleep problems and/or insomnia and may be particularly useful when benzodiazepines are not recommended. Although its use may be controversial and associated with higher risk of side-effects, more investigation is needed to determine the efficacy and safety for triple antidepressant combinations as reliable strategies for treatment-resistant depression in clinical practice.

Transcranial Magnetic Stimulation Maintenance as a Substitute for Maintenance Electroconvulsive Therapy

Transcranial magnetic stimulation (TMS) is an efficacious, well-tolerated, noninvasive brain stimulation treatment for major depressive disorder. Electroconvulsive therapy (ECT) is an effective maintenance treatment for depression but is not tolerated by some patients and declined by others. We evaluated the effectiveness of TMS as a substitution strategy for successful maintenance ECT. A consecutive clinical case series (n = 6) of maintenance ECT patients were transitioned to maintenance TMS because of adverse effects from ECT or because of specific patient request and preference. Patients were in either full remission or had clinical response to ECT at the time of transition. Primary outcome was the change in the Beck Depression Inventory (BDI) score from initiation of TMS maintenance sessions to the last observation time point. Relapse of depressive symptoms was also documented. Mean age of patients was 64 years, and most were female (n = 5). The majority (5 of 6) were diagnosed with major depressive disorder. Reasons for transition from ECT to TMS were, in order of frequency, cognitive adverse effects, fear of general anesthesia, time burden, lack of remission with ECT, and stigma associated with ECT. The mean frequency of TMS sessions was 1 every 3.5 weeks. Based on BDI scores, all patients maintained or improved their clinical status achieved with ECT at 3 and 6 months of TMS treatment. At last observation (range, 7-23 months), 4 patients maintained or improved their clinical status (total BDI score remained constant or decreased by 1-8 points). Two patients had a relapse after 8 and 9 months. Stimulation was well tolerated with adverse effects limited to headache and scalp discomfort. In this case series, TMS was effective and safe when used as a substitution strategy for successful maintenance ECT.

The Subjective and Cognitive Effects of Acute Phenylalanine and Tyrosine Depletion in Patients Recovered from Depression

Although there is evidence for the involvement of dopamine (DA) in unipolar depression, no published study has yet used the technique of acute phenylalanine and tyrosine depletion (APTD), a dietary intervention that selectively lowers DA synthesis, in order to investigate the role of DA in mood disturbance. Tyrosine and phenylalanine depleted and placebo amino acid drinks were administered to 20 patients recovered from depression in a double-blind, placebo-controlled, crossover design. Measures included subjective effects, Hamilton Depression Rating Scale scores, and a comprehensive battery of well-validated computerized cognitive tests. APTD induced a substantial reduction in the ratio of plasma tyrosine and phenylalanine to large neutral amino acids. However, relapse of depressive symptoms was not seen. Although performance on most cognitive tests was unaffected, there was a selective effect on decision-making, with APTD causing participants to bet significantly less. In conclusion, These results suggest a specific role for the involvement of DA in reward/punishment processing in humans. While APTD did not induce relapse in any participant, it did cause patients recovered from depression to show lowered sensitivity to reward in a gambling game. It is hypothesized that tests involving reward/punishment processing are preferentially affected by DA depletion, and that a more complete account of depression is likely to result from considering the roles played by serotonin, noradrenaline, and DA in mediating the various cognitive and clinical symptoms, including anhedonia.