scholarly journals Mixed Depression: A Survey on Psychopathological, Diagnostic, and Therapeutic Approaches among a Sample of Italian Psychiatrists

2021 ◽  
Vol 17 (1) ◽  
pp. 331-341
Author(s):  
Ludovico Mineo ◽  
Alessandro Rodolico ◽  
Carmen Concerto ◽  
Antimo Natale ◽  
Manuela Pennisi ◽  
...  

Background: The Diagnostic and Statistical Manual for Mental Disorders (5th edition) introduced the specifier “with Mixed Features” to the diagnosis of Major Depressive Episode to designate the presence of (hypo) manic symptoms as part of the clinical presentation. This change has led to renewed attention on the operational definition, diagnosis, and treatment of Mixed Depression. Objective: To investigate the diagnostic and therapeutic approaches towards Mixed Depression among a representative sample of Italian psychiatrists. Methods: Between March and April 2021, 342 psychiatrists working in Italian adult mental health services were invited to participate in an anonymous online survey comprising 32 questions designed to investigate clinical and psychopathological approaches regarding the management of mixed depression in daily psychiatric practice. Results: 83.74% of participants reported having performed a diagnosis of mixed depression in the last five years, with the majority of respondents affirming that they had not used any diagnostic tool. Only 7,5% of the surveyed psychiatrists considered the DSM-5 criteria to be fully adequate in the description of this clinical entity. The most used pharmacological approach was combined therapy, in particular antipsychotics plus mood stabilizers. For monotherapy, the preferred drugs were Valproate and Quetiapine. Regarding the conceptualization of mood disorders, 199 of the participants chose the Kraepelinian unitary spectrum view; meanwhile, 101 expressed their preference for the binary model. Conclusion: Our results suggest a prominent position of mixed depression in the context of mood disorders. Univocal operational criteria and additional research on pharmacological treatment are also needed to ensure the correct recognition and management of mixed depression.

CNS Spectrums ◽  
2016 ◽  
Vol 22 (2) ◽  
pp. 177-185 ◽  
Author(s):  
Minoru Takeshima

The DSM–5 incorporates a broad concept of mixed states and captured ≥3 nonoverlapping symptoms of the opposite polarity using a “with mixed features” specifier to be applied to manic/hypomanic and major depressive episodes. Pharmacotherapy of mixed states is challenging because of the necessity to treat both manic/hypomanic and depressive symptoms concurrently. High-potency antipsychotics used to treat manic symptoms and antidepressants can potentially deteriorate symptoms of the opposite polarity. This review aimed to provide a synthesis of the current evidence for pharmacotherapy of mixed states with an emphasis on mixed mania/hypomania. A PubMed search was conducted for randomized controlled trials (RCTs) that were at least moderately sized, included a placebo arm, and contained information on acute-phase and maintenance treatments of adult patients with mixed episodes or mania/hypomania with significant depressive symptoms. Most studies were post-hoc subgroup and pooled analyses of the data from RCTs for acute manic and mixed episodes of bipolar I disorder; only two prospectively examined efficacy for mixed mania/hypomania specifically. Aripiprazole, asenapine, carbamazepine, olanzapine, and ziprasidone showed the strongest evidence of efficacy in acute-phase treatment. Quetiapine and divalproex/valproate were also efficacious. Combination therapies with these atypical antipsychotics and mood stabilizers can be considered in severe cases. Olanzapine and quetiapine (alone or in combination with lithium/divalproex) showed the strongest evidence of efficacy in maintenance treatment. Lithium and lamotrigine may be beneficial given their preventive effects on suicide and depressive relapse. Further prospective studies primarily focusing on mixed states are needed.


CNS Spectrums ◽  
2017 ◽  
Vol 22 (2) ◽  
pp. 196-202 ◽  
Author(s):  
Mark Zimmerman

During the past two decades, a number of studies have found that depressed patients frequently have manic symptoms intermixed with depressive symptoms. While the frequency of mixed syndromes are more common in bipolar than in unipolar depressives, mixed states are also common in patients with major depressive disorder. The admixture of symptoms may be evident when depressed patients present for treatment, or they may emerge during ongoing treatment. In some patients, treatment with antidepressant medication might precipitate the emergence of mixed states. It would therefore be useful to systematically inquire into the presence of manic/hypomanic symptoms in depressed patients. We can anticipate that increased attention will likely be given to mixed depression because of changes in the DSM–5. In the present article, I review instruments that have been utilized to assess the presence and severity of manic symptoms and therefore could be potentially used to identify the DSM–5 mixed-features specifier in depressed patients and to evaluate the course and outcome of treatment. In choosing which measure to use, clinicians and researchers should consider whether the measure assesses both depression and mania/hypomania, assesses all or only some of the DSM–5 criteria for the mixed-features specifier, or assesses manic/hypomanic symptoms that are not part of the DSM–5 definition. Feasibility, more so than reliability and validity, will likely determine whether these measures are incorporated into routine clinical practice.


2009 ◽  
Vol 2 (2) ◽  
pp. 92-105 ◽  
Author(s):  
Ueli Kramer ◽  
Guy Bodenmann ◽  
Martin Drapeau

AbstractThe construct of cognitive errors is clinically relevant for cognitive therapy of mood disorders. Beck's universality hypothesis postulates the relevance of negative cognitions in all subtypes of mood disorders, as well as positive cognitions for manic states. This hypothesis has rarely been empirically addressed for patients presenting bipolar affective disorder (BD). In-patients (n= 30) presenting with BD were interviewed, as were 30 participants of a matched control group. Valid and reliable observer-rater methodology for cognitive errors was applied to the session transcripts. Overall, patients make more cognitive errors than controls. When manic and depressive patients were compared, parts of the universality hypothesis were confirmed. Manic symptoms are related to positive and negative cognitive errors. These results are discussed with regard to the main assumptions of the cognitive model for depression; thus adding an argument for extending it to the BD diagnostic group, taking into consideration specificities in terms of cognitive errors. Clinical implications for cognitive therapy of BD are suggested.


2007 ◽  
Vol 7 (4) ◽  
pp. 203-210 ◽  
Author(s):  
Russ Curtis ◽  
Phyllis Robertson ◽  
Amy Forst ◽  
Caroline Bradford
Keyword(s):  

2019 ◽  
pp. S3-S15 ◽  
Author(s):  
M. ĽUPTÁK ◽  
J. HROUDOVÁ

Mitochondria primarily serve as source of cellular energy through the Krebs cycle and β-oxidation to generate substrates for oxidative phosphorylation. Redox reactions are used to transfer electrons through a gradient to their final acceptor, oxygen, and to pump hydrogen protons into the intermembrane space. Then, ATP synthase uses the electrochemical gradient to generate adenosine triphosphate (ATP). During these processes, reactive oxygen species (ROS) are generated. ROS are highly reactive molecules with important physiological functions in cellular signaling. Mitochondria play a crucial role in intracellular calcium homeostasis and serve as transient calcium stores. High levels of both, ROS and free cytosolic calcium, can damage mitochondrial and cellular structures and trigger apoptosis. Impaired mitochondrial function has been described in many psychiatric diseases, including mood disorders, in terms of lowered mitochondrial membrane potential, suppressed ATP formation, imbalanced Ca2+ levels and increased ROS levels. In vitro models have indicated that mood stabilizers affect mitochondrial respiratory chain complexes, ROS production, ATP formation, Ca2+ buffering and the antioxidant system. Most studies support the hypothesis that mitochondrial dysfunction is a primary feature of mood disorders. The precise mechanism of action of mood stabilizers remains unknown, but new mitochondrial targets have been proposed for use as mood stabilizers and mitochondrial biomarkers in the evaluation of therapy effectiveness.


2017 ◽  
Author(s):  
Hasan A Baloch ◽  
Jair C. Soares

Affective disorders are among the most common disorders in psychiatry. They are generally classified according to the persistence and extent of symptoms and by the polarity of these symptoms. The two poles of the affective spectrum are mania and depression. Bipolar disorder is characterized by the presence of the mania or hypomania and often depression. Unipolar depression is defined by depression in the absence of a lifetime history of mania or hypomania. These differences are not merely categorical but have important implications for the prognosis and treatment of these conditions. Bipolar disorder, for example, is better treated using mood-stabilizing medication, whereas unipolar depression responds optimally to antidepressant medications. In addition, prognostically, unipolar depression may sometimes be limited to one episode in a lifetime, whereas bipolar disorder is typically a lifelong condition. The course of both conditions, however, is often chronic, and frequently patients can present with unipolar depression only to later develop manic symptoms. A thorough understanding of both conditions is therefore required to treat patients presenting with affective symptomatology. This chapter discusses the epidemiology, etiology and genetics, pathogenesis, diagnosis, and treatment of unipolar depression and bipolar disorder. Figures illustrate gray matter differences with lithium use and the bipolar spectrum. Tables list the pharmacokinetics of commonly used antidepressants and medications commonly used in the treatment of bipolar disorder. This review contains 2 figures, 2 tables, and 136 references.


Author(s):  
Daniel R. Strunk ◽  
Katherine Sasso

In this chapter, we provide an overview of the phenomenology of the mood disorders, including attention to both symptoms and functional impairment. Our overview emphasizes the heterogeneity among those with these disorders, as well as the most influential approaches to describing this variability across and within bipolar and depressive disorders. We discuss the degree of overlap between bipolar and depressive disorders, paying special attention to the clinical significance of low levels of manic symptoms. We also review several influential symptom-based specifiers, including those that refer to melancholic, atypical, anxious, and psychotic features. Having considered variability in the symptoms of these disorders, we then consider the course of these disorders. We survey the remarkable variability in course as well as current approaches to characterizing these differences. We conclude with a discussion of future directions.


CNS Spectrums ◽  
2013 ◽  
Vol 18 (5) ◽  
pp. 272-284 ◽  
Author(s):  
Gonzalo Laje

Pharmacogenetics brought the promise of matching individuals with treatments that would be efficacious while minimizing adverse events. This has been long needed in psychiatry, where treatment options have been empirical and treatment choices have been made largely based on clinical judgment. The efficacy and tolerability of antidepressants, the most common drugs used in mood disorders, have been widely studied in pharmacogenetics. Genetic association studies have been reported for pharmacokinetic genes such as the CYP450 isoenzymes or MDR1, and pharmacodynamic genes such as the serotonin transporter (SLC6A4) or the serotonin 2A receptor (HTR2A). However, despite the large number of reports, clinically useful predictors are still scarce for antidepressant monotherapy. Pharmacogenetic predictors of efficacy for mood stabilizers such as lithium and anticonvulsants have not had a dissimilar fate, and clinically meaningful markers are yet to emerge. The lack of consistent results may be in part due to small samples of heterogeneous populations and lack of consensus on phenotype definitions. Current pharmacogenetic recommendations include testing for HLA-B*1502 when using carbamazepine in Asian ancestry populations to prevent Stevens–Johnson syndrome, CYP2D6 genotypes when using pimozide, and CYP2D6 in polypharmacy to minimize drug interactions. This review, which is aimed at clinicians, lays the basis for understanding strengths and weaknesses of pharmacogenetic studies and outlines current clinical uses of these biomarkers.


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