The Age of Onset of Bipolar Disorders

2018 ◽  
pp. 75-110
Author(s):  
Jessica Dagani ◽  
Ross J. Baldessarini ◽  
Giulia Signorini ◽  
Olav Nielssen ◽  
Giovanni de Girolamo ◽  
...  
2020 ◽  
Vol 63 (6) ◽  
pp. 40-50
Author(s):  
Hugo Enrique Hernández-Martínez ◽  
Marta Georgina Ochoa-Madrigal

The diagnosis and treatment of bipolar disorders (BPD) in children is currently one of the biggest challenges and area of controversy in the field of child psychiatry. Bipolar disorders encompass several affective disorders that involve alterations in the degree of activity, content and form of thinking that are characterized by biphasic episodes of mood. This group of disorders affect approximately 1% of the world population and begin in youth (the average age of onset of ~20 years). However, in some studies a delay of 5 years has been observed since the presentation of symptoms at the beginning of the treatment. Currently, the diagnosis of TBP in children and adolescents should be based on the same set of symptoms applied to adults, as well as the general principles of the treatment. The research carried out around this disorder has resulted in changes in the conceptualization and approach of this pathology, now conceived as a group of disorders that share changes in mood and other cardinal symptoms, of a chronic and progressive nature that impacts in a negative way in those who suffer them. Key words: Bipolar disorder; childhood; mania; hypomania; depression.


2017 ◽  
Vol 41 (S1) ◽  
pp. S211-S211
Author(s):  
N. Smaoui ◽  
L. Zouari ◽  
N. Charfi ◽  
M. Maâlej-Bouali ◽  
N. Zouari ◽  
...  

IntroductionAge of onset of illness may be useful in explaining the heterogeneity among older bipolar patients.ObjectiveTo examine the relationship of age of onset with clinical, demographic and behavioral variables, in older patients with bipolar disorder.MethodsThis was a cross-sectional, descriptive and analytical study, including 24 patients suffering from bipolar disorders, aged 65 years or more and followed-up in outpatient psychiatry unit at Hedi Chaker university hospital in Sfax in Tunisia. We used a standardized questionnaire including socio-demographic, behavioral and clinical data. Age of onset was split at age 40 years into early-onset (< 40 years; n = 12) and late-onset (≥ 40 years; n = 12) groups.ResultsThe mean age for the entire sample was 68.95 years. The mean age of onset was 39.95 years. The majority (60%) of patients were diagnosed with bipolar I. Few meaningful differences emerged between early-onset and late-onset groups, except that tobacco use was significantly higher in the late-onset group (66.6% vs. 16.6%; P = 0.027). No significant differences between the early-onset and late-onset groups were seen on demographic variables, family history and number of medical diagnoses or presence of psychotic features.ConclusionOur study found few meaningful behavioral differences between early versus late age at onset in older adults with bipolar disorder.Disclosure of interestThe authors have not supplied their declaration of competing interest.


1993 ◽  
Vol 8 (3) ◽  
pp. 125-129 ◽  
Author(s):  
JM Menchon ◽  
C Gasto ◽  
J Vallejo ◽  
R Catalan ◽  
A Otero ◽  
...  

SummaryOne hundred and sixteen patients with RDC unipolar recurrent depressive disorder, melancholic subtype, were treated with imipramine or phenelzine and followed-up for six months. None of the patients had a first-degree relative with bipolar I disorder. Twenty-six patients (22.4%) presented an hypomanic episode (‘hypomanic group’). This group of patients, when depressed, had a significantly lower age of onset of the disorder and higher response to antidepressant therapy than patients who did not present an hypomanic episode. Significantly more patients (88%) of the ‘hypomanic group’ had at least one first-degree relative with a history of major depressive disorder. These patients displayed some of the typical features of bipolar II disorder. Overall results support the continuum in clinical phenomena between unipolar and bipolar disorders.


2018 ◽  
Vol 49 (2) ◽  
pp. 232-242 ◽  
Author(s):  
Osvaldo P. Almeida ◽  
Andrew H. Ford ◽  
Graeme J. Hankey ◽  
Bu B. Yeap ◽  
Jonathan Golledge ◽  
...  

AbstractBackgroundRecent research has identified several potentially modifiable risk factors for dementia, including mental disorders. Psychotic disorders, such as schizophrenia and delusional disorder, have also been associated with increased risk of cognitive impairment and dementia, but currently available data difficult to generalise because of bias and confounding. We designed the present study to investigate if the presence of a psychotic disorder increased the risk of incident dementia in later life.MethodsProspective cohort study of a community-representative sample of 37 770 men aged 65–85 years who were free of dementia at study entry. They were followed for up to 17.7 years using electronic health records. Clinical diagnoses followed the International Classification of Diseases guidelines. As psychotic disorders increase mortality, we considered death a competing risk.ResultsA total of 8068 (21.4%) men developed dementia and 23 999 (63.5%) died during follow up. The sub-hazard ratio of dementia associated with a psychotic disorder was 2.67 (95% CI 2.30–3.09), after statistical adjustments for age and prevalent cardiovascular, respiratory, gastrointestinal and renal diseases, cancer, as well as hearing loss, depressive and bipolar disorders, and alcohol use disorder. The association between psychotic disorder and dementia risk varied slightly according to the duration of the psychotic disorder (highest for those with the shortest illness duration), but not the age of onset. No information about the use of antipsychotics was available.ConclusionOlder men with a psychotic disorder have nearly three times greater risk of developing dementia than those without psychosis. The pathways linking psychotic disorders to dementia remain unclear but may involve mechanisms other than those associated with Alzheimer's disease and other common dementia syndromes.


2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
M. Preisig ◽  
F. Ferrero

Aims:The major aims of the present paper were to:1.assess associations between the course of bipolar-I disorder in probands and the presence and course characteristics of mood disorders in their relatives and2.assess associations between manic and depressive symptoms in probands and relatives.Methods:A family study including 125 bipolar-I patients and all available first-degree relatives has been conducted at two Swiss sites. All participants were evaluated using the Diagnostic Interview for Genetic Studies. Assessed course variables included the age of onset, the number of episodes and social functioning in terms of GAF scores. Among the 237 interviewed relatives of bipolar probands, 32 also exhibited bipolar disorder.Results:The occurrence of bipolar disorders in relatives was not associated with course variables in bipolar probands, whereas the occurrence of unipolar depression in relatives was associated with a more favorable course in probands in terms of higher lifetime GAF scores. Regarding the expression of symptoms during episodes, associations between disorders in probands and relatives were observed for dysphoric and psychotic rather than for typical manic symptom patterns.Conclusion:Our data did not provide support for a significant association between the course of bipolar disorder and the presence or the course characteristics of bipolar disorders in relatives. Surprisingly, the presence of unipolar depression in relatives was even associated with a better course of the bipolar disorder in probands. Nevertheless, bipolar disorder revealed some degree of similarity across family members, particularly regarding the expression of dysphoric and psychotic symptom patterns.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Richard McCarty ◽  
Travis Josephs ◽  
Oleg Kovtun ◽  
Sandra J. Rosenthal

AbstractBipolar disorders (BDs) exhibit high heritability and symptoms typically first occur during late adolescence or early adulthood. Affected individuals may experience alternating bouts of mania/hypomania and depression, with euthymic periods of varying lengths interspersed between these extremes of mood. Clinical research studies have consistently demonstrated that BD patients have disturbances in circadian and seasonal rhythms, even when they are free of symptoms. In addition, some BD patients display seasonal patterns in the occurrence of manic/hypomanic and depressive episodes as well as the time of year when symptoms initially occur. Finally, the age of onset of BD symptoms is strongly influenced by the distance one lives from the equator. With few exceptions, animal models useful in the study of BD have not capitalized on these clinical findings regarding seasonal patterns in BD to explore molecular mechanisms associated with the expression of mania- and depression-like behaviors in laboratory animals. In particular, animal models would be especially useful in studying how rates of change in photoperiod that occur during early spring and fall interact with risk genes to increase the occurrence of mania- and depression-like phenotypes, respectively. Another unanswered question relates to the ways in which seasonally relevant changes in photoperiod affect responses to acute and chronic stressors in animal models. Going forward, we suggest ways in which translational research with animal models of BD could be strengthened through carefully controlled manipulations of photoperiod to enhance our understanding of mechanisms underlying seasonal patterns of BD symptoms in humans. In addition, we emphasize the value of incorporating diurnal rodent species as more appropriate animal models to study the effects of seasonal changes in light on symptoms of depression and mania that are characteristic of BD in humans.


2004 ◽  
Vol 367 (2) ◽  
pp. 232-234 ◽  
Author(s):  
Sheue-Jane Hou ◽  
Feng-Chang Yen ◽  
Chih-Ya Cheng ◽  
Shih-Jen Tsai ◽  
Chen-Jee Hong

2000 ◽  
Vol 12 (3) ◽  
pp. 65-68 ◽  
Author(s):  
D. Souery ◽  
I. Massat ◽  
J. Mendlewicz

ABSTRACTAdvances 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. This phenomenon describes the increase in clinical severity and decrease in age of onset observed in successive generations. This mode of transmission correlates with the presence of specific mutations (Trinucleotide Repeat Sequences) and may represent a genetic factor involved in the transmission of the disorder. 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. While significant advances have been made in this major field 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.


2016 ◽  
Vol 33 (S1) ◽  
pp. S56-S56
Author(s):  
G. de Girolamo ◽  
M. Bani ◽  
J. Dagani ◽  
C. Ferrari ◽  
A. Pastore ◽  
...  

IntroductionAlthough the onset of bipolar disorder (BD) is usually estimated in early adulthood (Burke et al., 1990; Kessler et al., 1997), it is still not clear which age-specific triggering factors may contribute to the underlying vulnerability.Objectives/aimsThe present meta-analysis attempts to clarify the number of untreated years of BD, from first symptoms appearance, to first actions carried out by health services (first diagnosis, treatment and hospitalization).MethodsA literature search of three databases PubMed, Web of Science and Psychology and Behavioral Sciences Collection was performed, looking for peer-reviewed publications in English, French, German and Italian language that reported the AOO of BD; the search string adopted was “bipolar and onset”. Standardized mean differences were calculated between (i) mean AOO, operationally defined as onset of first symptoms/episodes, and (ii) mean AOO, operationally defined according to four criteria: first contact with services, date of the diagnosis, first pharmacological treatment, or first hospitalization.ResultsThe searches yielded 8710 articles; 2424 of these articles met the inclusion criteria. A final set of 19 studies presenting multiple definitions of AOO has been analyzed, revealing an overall effect size of 6.96 of untreated years (Cohen's d = 0.65)ConclusionTo our knowledge, this is the first meta-analysis that addresses the definition and the modulation of the AOO in bipolar disorder. Identifying the time-frame of untreated illness is very important for the best planning of timely interventions.Disclosure of interestThe authors have not supplied their declaration of competing interest.


Sign in / Sign up

Export Citation Format

Share Document