scholarly journals Differentiating Recurrent Unipolar Depressive Disorder from Bipolar Affective Disorder as a diagnostic code within the Coventry IPU 3-8 (Affective Disorders).

2017 ◽  
Vol 8 ◽  
Author(s):  
Sazgar Hamad
2007 ◽  
Vol 190 (1) ◽  
pp. 6-10 ◽  
Author(s):  
Sanne G. H. A. Swinnen ◽  
Jean-Paul Selten

BackgroundMigration is a risk factor for the development of schizophrenia.AimsTo examine whether migration is also a risk factor for bipolar affective disorder, unipolar depressive disorder and mood disorders in general.MethodMedline was searched for population-based incidence studies concerning mood disorders among migrants and mean relative risks were computed using a mixed-effects statistical model.ResultsOnly a few studies of unipolar depressive disorder were retrieved. The mean relative risk of developing bipolar affective disorder among migrants was 2.47 (95% C11.33–4.59). However, after excluding people of African-Caribbean origin in the UK this risk was no longer significantly increased. The mean relative risk of mood disorders of unspecified polarity was 1.25 (95% CI 1.04–1.49) and that of any mood disorder was 1.38 (95% CI 1.17–1.62).ConclusionsThere is no conclusive evidence for a large increase in the risk of mood disorders associated with migration.


Author(s):  
Pierre Oswald ◽  
Daniel Souery ◽  
Julien Mendlewicz

Advances towards the understanding of the etiological mechanisms involved in mood disorders provide interesting yet diverse hypotheses and promising models. In this context, molecular genetics has now been widely incorporated into genetic epidemiological research in psychiatry. Affective disorders and, in particular, bipolar affective disorder (BPAD) have been examined in many molecular genetic studies which have covered a large part of the genome, specific hypotheses such as mutations have also been studied. Most recent studies indicate that several chromosomal regions may be involved in the aetiology of BPAD. Other studies have reported the presence of anticipation in BPAD and in unipolar affective disorder (UPAD). In parallel to these new developments in molecular genetics, the classical genetic epidemiology, represented by twin, adoption and family studies, provided additional evidence in favour of the genetic hypothesis in mood disorders. Moreover, these methods have been improved through models to test the gene-environment interactions. In addition to genetic approaches, psychiatric research has focused on the role of psychosocial factors in the emergence of mood disorders. In this approach, psychosocial factors refer to the patient's social life context as well as to personality dimensions. Abnormalities in the social behavior such as impairment in social relationships have been observed during episode of affective disorders, and implicated in the etiology of affective disorders. Further, gender and socio-economic status also emerged as having a possible impact on the development of affective disorders. Finally, the onset and outcome of affective disorders could also be explained by interactions between the social life context and the individual's temperament and personality. The importance of temperament and personality characteristics in the etiology of depression has been emphasized in various theories, although disagreement exists with regard to terminology and the etiology. While significant advances have been done in these two major fields of research, it appears that integrative models, taking into account the interactions between biological (genetic) factors and social (psychosocial environment) variables offer the most reliable way to approach the complex mechanisms involved in the etiology and outcome of mood disorders. This chapter will review some of the most promising genetic and psychosocial hypotheses in mood disorders that can be integrated in interactive models.


2019 ◽  
Vol 64 ◽  
pp. S130-S131
Author(s):  
Y. Liao ◽  
J. Benson ◽  
S. Higgins ◽  
P. Drakatos ◽  
J.S. Kaler ◽  
...  

1997 ◽  
Vol 12 (S2) ◽  
pp. 63s-69s ◽  
Author(s):  
D Souery ◽  
O Lipp ◽  
B Mahieu ◽  
J Mendlewicz

SummaryThe present article reviews the recent molecular genetic findings in affective disorders. Results of linkage and association studies are discussed in regard to the main limitations of these approaches in psychiatric disorders. On the whole, linkage and association studies contributed to the localisation of some potential vulnerability genes for Bipolar affective disorder on chromosomes 18, 5, 11, 4, 21 and X. The hypothesis of anticipation in affective disorders is also considered in light of interesting results with trinucleotide repeat mutations.


Author(s):  
S. A. Yaroslavtsev

362 patients with cognitive impairment in depressive disorders were examined: 123 patients with recurrent depressive disorder (RDD), 141 patients with bipolar affective disorder (BAD) and 98 people with prolonged depressive reaction (PDR). It was found that cognitive dysfunctions were less pronounced in patients with PDR, than in patients with RDD and BAR (p<0,035). Cognitive dysfunctions in depressive disorders was underlined by the presence of disorders in the mental sphere, in the sphere of attention, executive, visual-spatial and linguistic functions. The differential features of cognitive impairment in patients with RDD, BAR and PDR are highlighted and it should be taken during conducting differential diagnosis of cognitive impairment in depressive disorders. Keywords: patients with cognitive impairment, depressive disorders, cognitive dysfunctions, recurrent depressive disorder, bipolar depressive disorder, prolonged depressive reaction.


Author(s):  
Oliver D. Howes ◽  
Michael E. Thase ◽  
Toby Pillinger

AbstractTreatment resistance affects 20–60% of patients with psychiatric disorders; and is associated with increased healthcare burden and costs up to ten-fold higher relative to patients in general. Whilst there has been a recent increase in the proportion of psychiatric research focussing on treatment resistance (R2 = 0.71, p < 0.0001), in absolute terms this is less than 1% of the total output and grossly out of proportion to its prevalence and impact. Here, we provide an overview of treatment resistance, considering its conceptualisation, assessment, epidemiology, impact, and common neurobiological models. We also review new treatments in development and future directions. We identify 23 consensus guidelines on its definition, covering schizophrenia, major depressive disorder, bipolar affective disorder, and obsessive compulsive disorder (OCD). This shows three core components to its definition, but also identifies heterogeneity and lack of criteria for a number of disorders, including panic disorder, post-traumatic stress disorder, and substance dependence. We provide a reporting check-list to aid comparisons across studies. We consider the concept of pseudo-resistance, linked to poor adherence or other factors, and provide an algorithm for the clinical assessment of treatment resistance. We identify nine drugs and a number of non-pharmacological approaches being developed for treatment resistance across schizophrenia, major depressive disorder, bipolar affective disorder, and OCD. Key outstanding issues for treatment resistance include heterogeneity and absence of consensus criteria, poor understanding of neurobiology, under-investment, and lack of treatments. We make recommendations to address these issues, including harmonisation of definitions, and research into the mechanisms and novel interventions to enable targeted and personalised therapeutic approaches.


Author(s):  
Serhii Yaroslavtsev

362 patients with cognitive impairment in depressive disorders were examined: 123 patients with recurrent depressive disorder (RDD), 141 patients with bipolar affective disorder (BAD) and 98 patients with prolonged depressive reaction (PDR). A set of research methods was used: clinical-psychopathological and statistical. As a result of the study, the clinical and psychopathological features of affective disorders in different types of depressive disorders were identified: a predominance of apathy, emotional lability, hypothymia, anxiety, feelings of dissatisfaction, despair and anhedonia were identified in patients with RDD; a low mood, apathy, emotional coldness, hypothymia, ambivalence of emotions, dysphoria, dissatisfaction, feelings of sadness and annoyance were identified in patients with BAD; a feelings of despair, anxiety, dissatisfaction, hypothymia, fear, sadness, feelings of horror and fear, emotional lability, feelings of anger, hostility and shame and sensitivity were dominated in patients with PDR.


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