The various major American and European guidelines for the treatment of depression provide similar basic principles of treatment, which include individualizing the treatment plan, preparing the patient for potential long-term treatment, providing measurement-based care, and treating to remission. While the guidelines are all evidence-based, certain factors can influence differences in specific recommendations, such as the consensus group's composition, underlying mandates, and cultural attitudes. The similarities and differences among 6 sets of guidelines from Europe and the Americas published in the past decade are reviewed here (American Psychiatric Association, British Association for Psychopharmacology, Canadian Network for Mood and Anxiety Treatments, National Institute for Health and Clinical Excellence, Texas Medication Algorithm Project, and World Federation of Societies of Biological Psychiatry). In the guidelines, mild depression has the most variance in treatment recommendations; some, but not all, guidelines suggest that it may resolve with exercise or watchful waiting, but psychotherapy or antidepressants could be used if initial efforts fail. Moderate and severe major depression carry broadly similar recommendations among the guidelines. First-line treatment recommendations for moderate major depressive disorder include antidepressant monotherapy, psychotherapy, and the combination of both. Severe depression may require the combination of an antidepressant and an antipsychotic, electroconvulsive therapy, or the combination of an antidepressant and psychotherapy. Benzodiazepines play a very limited role in the treatment of depression; if the patient has catatonic depression, acutely suicidal depression, or depression with symptoms of anxiety, agitation, or insomnia, benzodiazepines are recommended by some guidelines for short-term treatment only.
"Depression is one of the most common mental disorders in current Western societies. At present, it continues to grow in numbers and is one of the main causes of disability around the world, particularly in high-income regions (e.g., Davidson, 2010; McKenna, Michaud, Murray, & Marks, 2005; World Health Organization [WHO], 2005). To deal with this relevant health and social problem, there are several efficient interventions such as use of antidepressant drugs (ADs; Geddes et al., 2003; Perestelo-Pérez et al., 2010) and psychological treatments, particularly those derived from a cognitive-behavioural approach (Aguilera, Garza, & Muñoz, 2010; Kaltenthaler et al., 2006; Merry, McDowell, Hetrick, Bir, & Muller, 2004). "
[Show abstract][Hide abstract] ABSTRACT: The objective of this research study was to assess pharmacological, somatic and/or
psychological treatments in adults with a diagnosis of major depressive disorder who have not
responded to at least one course of antidepressant medication. We conducted a systematic
review to identify systematic scientific reviews and meta-analyses on treatment-resistant
depression (TRD) published until February 2012. Of the sixty studies selected, sixteen met the
inclusion criteria and were therefore included in the review. We considered eight main themes,
including the definition of TRD, long-term results, and different treatment strategies, including
so-called somatic therapies. Based on the review, the definition of TRD should be standardized
in order to achieve a shared conceptualization of this disorder. This would allow a better
understanding among clinicians and researchers in the field, promoting a homogeneous research
methodology and thus leading to more reliable and comparable results. This essential conceptual
clarification would also have a positive impact on patients with TRD, their families, and social
and health systems.
International Journal of Clinical and Health Psychology 05/2014; 14(2):145-153. DOI:10.1016/S1697-2600(14)70048-1 · 2.79 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The primary mechanism by which amphetamine exerts its neurobehavioral effects is through an enhancement of synaptic monoamine levels, which is mediated by interactions with monoamine transporters, storage, and metabolism. However, preclinical data are now emerging that support more widespread neurobiologic effects for amphetamine. This review describes preclinical evidence suggesting that direct interactions of amphetamine with monoamine systems, which results in increased synaptic monoamine availability, has downstream effects on nonmonoaminergic systems, including glutamate, endogenous opioid, endocannabinoid, and acetylcholine systems. Furthermore, evidence suggests that amphetamine can modulate synaptic plasticity through modulation of glutamatergic systems, intracellular signaling cascades, and neurotrophic factor activity. Functional activity of these systems is implicated in the regulation of neurobehavioral processes that include cognition, mood, motivated behavior/hedonic processes/addiction, and arousal. As such, the ability of amphetamine to influence the function of systems that mediate these processes suggests amphetamine-based agents may have utility in the treatment of psychiatric disorders in which these systems and processes are dysfunctional. Amphetamine-based agents are currently approved by the US Food and Drug Administration only for the treatment of attention-deficit/hyperactivity disorder and narcolepsy. Preclinical and clinical research for amphetamine-based pharmacotherapy for other psychiatric disease states is examined. This should encourage further research on the preclinical pharmacology of amphetamine and its implications for the treatment of neuropsychiatric disorders.
"Many groups have previously found that use of antipsychotic medication is a likely risk factor for MetS, obesity and diabetes in schizophrenia (Smith et al. 2008) and bipolar disorder (Vancampfort et al. 2013). Adjunctive treatment with antipsychotic medications has been endorsed for treatment-resistant depression by several clinical practice guidelines (Davidson, 2010) and was supported by a recent meta-analysis (Farahani & Correll, 2012). It is also clear that different antipsychotics differ in their cardiometabolic risk profile (Correll et al. 2011; De Hert et al. 2011c). "
[Show abstract][Hide abstract] ABSTRACT: Individuals with depression have an elevated risk of cardiovascular disease (CVD) and metabolic syndrome (MetS) is an important risk factor for CVD. We aimed to clarify the prevalence and correlates of MetS in persons with robustly defined major depressive disorder (MDD).
We searched Medline, PsycINFO, EMBASE and CINAHL up until June 2013 for studies reporting MetS prevalences in individuals with MDD. Medical subject headings 'metabolic' OR 'diabetes' or 'cardiovascular' or 'blood pressure' or 'glucose' or 'lipid' AND 'depression' OR 'depressive' were used in the title, abstract or index term fields. Manual searches were conducted using reference lists from identified articles.
The initial electronic database search resulted in 91 valid hits. From candidate publications following exclusions, our search generated 18 studies with interview-defined depression (n = 5531, 38.9% male, mean age = 45.5 years). The overall proportion with MetS was 30.5% [95% confidence interval (CI) 26.3-35.1] using any standardized MetS criteria. Compared with age- and gender-matched control groups, individuals with MDD had a higher MetS prevalence [odds ratio (OR) 1.54, 95% CI 1.21-1.97, p = 0.001]. They also had a higher risk for hyperglycemia (OR 1.33, 95% CI 1.03-1.73, p = 0.03) and hypertriglyceridemia (OR 1.17, 95% CI 1.04-1.30, p = 0.008). Antipsychotic use (p < 0.05) significantly explained higher MetS prevalence estimates in MDD. Differences in MetS prevalences were not moderated by age, gender, geographical area, smoking, antidepressant use, presence of psychiatric co-morbidity, and median year of data collection.
The present findings strongly indicate that persons with MDD are a high-risk group for MetS and related cardiovascular morbidity and mortality. MetS risk may be highest in those prescribed antipsychotics.
Psychological Medicine 11/2013; 44(10):1-12. DOI:10.1017/S0033291713002778 · 5.94 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.