Cyclothymia reloaded: A reappraisal of the most misconceived affective disorder.

Data emerging from both academic centers and from public and private outpatient facilities indicate that from 20% to 50% of all subjects that seek help for mood, anxiety, impulsive and addictive disorders turn out, after careful screening, to be affected by cyclothymia. The proportion of patients who can be classified as cyclothymic rises significantly if the diagnostic rules proposed by the DSM-5 are reconsidered and a broader approach is adopted. Unlike the DSM-5 definition based on the recurrence of low-grade hypomanic and depressive symptoms, cyclothymia is best identified as an exaggeration of cyclothymic temperament (basic mood and emotional instability) with early onset and extreme mood reactivity linked with interpersonal and separation sensitivity, frequent mixed features during depressive states, the dark side of hypomanic symptoms, multiple comorbidities, and a high risk of impulsive and suicidal behavior. Epidemiological and clinical research have shown the high prevalence of cyclothymia and the validity of the concept that it should be seen as a distinct form of bipolarity, not simply as a softer form. Misdiagnosis and consequent mistreatment are associated with a high risk of transforming cyclothymia into severe complex borderline-like bipolarity, especially with chronic and repetitive exposure to antidepressants and sedatives. The early detection and treatment of cyclothymia can guarantee a significant change in the long-term prognosis, when appropriate mood-stabilizing pharmacotherapy and specific psychological approaches and psychoeducation are adopted. The authors present and discuss clinical research in the field and their own expertise in the understanding and medical management of cyclothymia and its complex comorbidities.

A case series on the hypothesized connection between dementia and bipolar spectrum disorders: bipolar type VI?

BACKGROUND: The concept of bipolar spectrum disorders has opened therapeutic opportunities for patients with atypical and complex affective conditions. The literature has recently described several commonalities in pathophysiological processes of bipolar disorders and dementia. However, this connection has been insufficiently appreciated at the clinical level, in part because affective dysregulation in the elderly and, particularly in the dementia setting, is typically attributed either to secondary depressive states or otherwise relegated to a neurologically understandable behavioral complication resulting from cerebral disease. METHODS: We selected a case series of 10 elderly patients with late-onset mood and related behavioral symptomatology and cognitive decline without past history of clear-cut bipolar disorder. Clinical features, temperament, cognition, family history and pharmacological response were assessed to identify prototypical patients to illustrate the complexities of the dementia-bipolar interface. RESULTS: Mixed and depressive mood symptoms were most commonly observed and all patients had been premorbidly of hyperthymic, cyclothymic and/or irritable temperaments. Most patients had a family history of bipolar disorder or disorders related to the bipolar diathesis. Symptoms were often refractory to or aggravated by antidepressants and acetylcholinesterase inhibitors, whereas mood stabilizers and/or atypical antipsychotics were beneficial, promoting behavioral improvement in all treated patients and marked cognitive recovery in five. LIMITATIONS: Case series with retrospective methodology. CONCLUSION AND CLINICAL IMPLICATIONS: Patients with cognitive decline and frequent mood lability might be manifesting a late-onset bipolar spectrum disorder, which we posit as type VI. We further posit that dementia and/or other biopsychosocial challenges associated with aging might release latent bipolarity in such individuals. Antidepressants, even drugs targeting dementia, might aggravate the behavioral dysregulation in these patients. Evaluation of premorbid temperament and/or family history of bipolarity and related disorders might help in broadening the clinical and biological understanding of such patients, providing a rationale for better customized treatment along the lines of mood stabilization and avoidance of antidepressants.

Toward an integrative model of the spectrum of mood, behavioral and personality disorders based on fear and anger traits: I. Clinical implications.

Current formal psychiatric approaches to nosology are plagued by an unwieldy degree of heterogeneity with insufficient appreciation of the commonalities of emotional, personality, behavioral, and addictive disorders. We address this challenge by building a spectrum model that integrates the advantages of Cloninger's and Akiskalian approaches to personality and temperament while avoiding some of their limitations. We specifically propose that "fear" and "anger" traits--used in a broader connotation than in the conventional literature--provide an optimum basis for understanding how the spectra of anxiety, depressive, bipolar, ADHD, alcohol, substance use and other impulse-control, as well as cluster B and C personality disorders arise and relate to one another. By erecting a bidimensional approach, we attempt to resolve the paradox that apparently polar conditions (e.g. depression and mania, compulsivity and impulsivity, internalizing and externalizing disorders) can coexist without cancelling one another. The combination of excessive or deficient fear and anger traits produces 4 main quadrants corresponding to the main temperament types of hyperthymic, depressive, cyclothymic and labile individuals, which roughly correspond to bipolar I, unipolar depression, bipolar II and ADHD, respectively. Other affective temperaments resulting from excess or deficiency of only fear or anger include irritable, anxious, apathetic and hyperactive. Our model does not consider schizophrenia. We propose that "healthy" or euthymic individuals would have average or moderate fear and anger traits. We further propose that family history, course and comorbidity patterns can also be understood based on fear and anger traits. We finally discuss the implications of the new derived model for clinical diagnosis of the common psychiatric disorders, and for subtyping depression and anxiety as well as cognitive and behavioral styles. We submit this proposed schema represented herein as a heuristic attempt to build bridges between basic and clinical science.