ABSTRACT
Abstract Objective To conduct a systematic review of literature on use and efficacy of cognitive-behavioral therapy (CBT) for treatment of treatment-resistant depression in adults and adolescents. Methods We performed a systematic review according to the Prisma Guidelines of literature indexed on the PubMed, SciELO, Psychiatry Online, Scopus, PsycArticles, Science Direct and the Journal of Medical Case Reports databases. Randomized controlled trials, open studies and case reports were included in the review. Results The searches returned a total of 1,580 articles, published from 1985 to 2017. After applying the inclusion criteria, 17 articles were selected, their complete texts were read and 8 were included in this review. Four of these studies were randomized controlled trials with adults, one of which covered a post-study follow-up period; two were randomized controlled trials with adolescents, one of which presented follow-up data; one was an open study; and one was a case report. The studies provide good quality and robust evidence on the topic addressed. Conclusions A combination of CBT with pharmacotherapy for treatment-resistant patients shows a decrease in depressive symptoms. CBT can be an effective type of therapy for adults and adolescents with treatment-resistant depression.
Resumo Objetivos Realizar uma revisão sistemática sobre o uso da terapia cognitivo-comportamental (TCC) e sua eficácia no tratamento da depressão resistente ao tratamento em adultos e adolescentes. Métodos Realizamos uma revisão sistemática utilizando os critérios do Prisma Guidelines, nos seguintes bancos de dados: PubMed, SciELO, Psychiatry Online, Scopus, PsycArticles, Science Direct e Journal of Medical Case Reports. Estudos controlados randomizados, estudos abertos e relatos de casos foram incluídos neste estudo. Resultados A pesquisa retornou um total de 1.580 artigos, publicados de 1985 até 2017. Após aplicarmos os critérios de inclusão, 17 artigos foram selecionados, seus textos completos foram lidos e 8 foram incluídos nesta revisão. Do total, quatro eram estudos controlados randomizados com adultos, tendo um incluído um período de seguimento pós-estudo; dois eram estudos controlados randomizados com adolescentes, tendo um apresentado dados de seguimento; um era um estudo aberto; e o último era um relato de caso. Os estudos apresentaram boa qualidade e evidências robustas sobre o tópico abordado. Conclusões A combinação de TCC com tratamento medicamentoso para pacientes resistentes ao tratamento mostra uma diminuição dos sintomas depressivos. A TCC pode ser um tipo eficaz de terapia para adultos e adolescentes com depressão resistente ao tratamento.
Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Young Adult , Cognitive Behavioral Therapy , Depressive Disorder, Major/therapy , Depressive Disorder, Treatment-Resistant/therapyABSTRACT
Baclofen is a gamma-aminobutyric acid type B receptor agonist used as an anti-craving agent for treatment of alcohol dependence. It has gained popularity in the recent times because it is well tolerated even in patients with hepatic impairments. Herein we are summarizing the latest literature about baclofen induced hypomania and are reporting a case of baclofen abuse because of its mood elevating property in a patient of alcohol dependence with comorbid major depressive disorder. Literature review and case study of a 36-year-old male with alcohol dependence with comorbid major depressive disorder was prescribed with tablet baclofen as an anti-craving agent along with antidepressant medicines. The patients who did not improve with conventional antidepressant therapy started feeling better in terms of his mood symptoms on taking tablet baclofen. Owing to the mood elevating property he started abusing baclofen. Despite its safety profile in hepatic impairment, one must be very cautious in prescribing baclofen because of its mood altering property which may account for its abuse potentiality.
Subject(s)
Adult , Humans , Male , Alcoholism , Baclofen , Depressive Disorder, Major , Depressive Disorder, Treatment-Resistant , gamma-Aminobutyric AcidABSTRACT
The light therapy has been known to be effective to non-seasonal affective disorder as well as seasonal affective disorder. Although the mechanism of action of light therapy for depressive disorder has not been verified yet, its clinical application revealed similar effects like antidepressants and relatively smaller side effects. However, it is not common to apply the light therapy for treatment resistant depressive disorder. This case report indicates a robust efficacy of light therapy and its clinical usefulness, illustrating the complete remission in a treatment resistant patient with major depressive disorder after bright light therapy.
Subject(s)
Humans , Antidepressive Agents , Depressive Disorder , Depressive Disorder, Major , Mood Disorders , Phototherapy , Seasonal Affective DisorderABSTRACT
OBJECTIVE: This study examined the association between the brain-derived neurotrophic factor (BDNF) (Val66Met) polymorphism and the response to the addition of an atypical antipsychotic drug to a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) in treatment-refractory depression. METHODS: The study enrolled 64 patients meeting the Diagnostic and Statistical Manual of Mental Disorders-IV criteria for major depressive disorder who were treated with at least two courses of a single antidepressant, but who had Hamilton Depression Rating Scale (HAMD-17) scores > or =15 points that were reduced less than 50% over at least a 4-week treatment period. There were 24 males and 40 females (age range 27-68 years; mean+/-SD, 48+/-13 years). The patients' clinical improvement was evaluated using the HAMD-17. Patients with at least a 50% decrease in the HAMD-17 score were defined as responders. Serum BDNF levels were assayed using enzyme-linked immunosorbent assays and the presence of the BDNF (Val66Met) polymorphism was determined using the TaqMan genotyping assay. RESULTS: No correlation was found between the BDNF (Val66Met) polymorphism and a positive response to adding an atypical antipsychotic drug. No differences were observed in the changes in the serum BDNF levels and HAMD-17 scores between Val66Val and Met-carriers. In addition, in patients who experienced remission, the atypical antipsychotic drug was discontinued after at least 3 months of treatment and the patients were then followed for 1 year; 14 of 27 patients (52%) relapsed within 1 year. CONCLUSION: These results suggest that the BDNF (Val66Met) polymorphism is not associated with the response to the augmentation of a SSRI or SNRI with an atypical antipsychotic drug, and that the combination of an atypical antipsychotic drug and a SSRI or SNRI should be continued for 3 months or more in refractory depressed patients in the Japanese population.