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Objective : To compare the prevalence of Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) mania symptoms in a prepubertal and early adolescent bipolar disorder phenotype(PEA-BP) to those with attention deficit hyperactivity disorder (ADHD) and normal community controls (CC). Methods : To optimize generalizeability, subjects with PEA-BP and ADHD were consecutively ascertained from outpatient pediatric and psychiatric sites, and CC subjects were obtained from a random survey. All 268 subjects (93 with PEA-BP, 81 with ADHD, and 94 CC) received comprehensive, blind, baseline research assessments of mothers about their children and of children about themselves. PEA-BP was defined by DSM-IV mania with elation and/or grandiosity as one criterion to ensure that subjects had one of the two cardinal symptoms of mania and to avoid diagnosing mania only by criteria that overlapped with those for ADHD. Results : Five symptoms (i.e., elation, grandiosity, flight of ideas/racing thoughts, decreased need for sleep, and hypersexuality) provided the best discrimination of PEA-BP subjects from ADHD and CC controls. These five symptoms are also mania-specific in DSM-IV (i.e., they do not overlap with DSM-IV symptoms for ADHD). Irritability, hyperactivity, accelerated speech, and distractibility were very frequent in both PEA-BP and ADHD groups and therefore were not useful for differential diagnosis. Concurrent elation and irritability occurred in 87.1% of subjects with PEA-BP. Data on suicidality, psychosis, mixed mania, and continuous rapid cycling were also provided. Conclusion : Unlike late teenage/adult onset bipolar disorder, even subjects with PEA-BP selected for DSM-IV mania with cardinal symptoms have high rates of comorbid DSM-IV ADHD. High rates of concurrent elation and irritability were similar to those in adult mania.

A large body of research has focused on identifying the optimal number of dimensions – or spectra – to model individual differences in psychopathology. Recently, it has become increasingly clear that ostensibly competing models with varying numbers of spectra can be synthesized in empirically derived hierarchical structures. We examined the convergence between top-down (bass-ackwards or sequential principal components analysis) and bottom-up (hierarchical agglomerative cluster analysis) statistical methods for elucidating hierarchies to explicate the joint hierarchical structure of clinical and personality disorders. Analyses examined 24 clinical and personality disorders based on semi-structured clinical interviews in an outpatient psychiatric sample (n=2900). The two methods of hierarchical analysis converged on a three-tier joint hierarchy of psychopathology. At the lowest tier, there were seven spectra – disinhibition, antagonism, core thought disorder, detachment, core internalizing, somatoform, and compulsivity – that emerged in both methods. These spectra were nested under the same three higher-order superspectra in both methods: externalizing, broad thought dysfunction, and broad internalizing. In turn, these three superspectra were nested under a single general psychopathology spectrum, which represented the top tier of the hierarchical structure. The hierarchical structure mirrors and extends upon past research, with the inclusion of a novel compulsivity spectrum, and the finding that psychopathology is organized in three superordinate domains. This hierarchy can thus be used as a flexible and integrative framework to facilitate psychopathology research with varying levels of specificity (i.e., focusing on the optimal level of detailed information, rather than the optimal number of factors).

The extant major psychiatric classifications DSM-IV, and ICD-10, are atheoretical and largely descriptive. Although this achieves good reliability, the validity of a medical diagnosis would be greatly enhanced by an understanding of risk factors and clinical manifestations. In an effort to group mental disorders on the basis of aetiology, five clusters have been proposed. This paper considers the validity of the fourth cluster, emotional disorders, within that proposal. We reviewed the literature in relation to 11 validating criteria proposed by a Study Group of the DSM-V Task Force, as applied to the cluster of emotional disorders. An emotional cluster of disorders identified using the 11 validators is feasible. Negative affectivity is the defining feature of the emotional cluster. Although there are differences between disorders in the remaining validating criteria, there are similarities that support the feasibility of an emotional cluster. Strong intra-cluster co-morbidity may reflect the action of common risk factors and also shared higher-order symptom dimensions in these emotional disorders. Emotional disorders meet many of the salient criteria proposed by the Study Group of the DSM-V Task Force to suggest a classification cluster.

Most mental illnesses emerge during adolescence and early adulthood, with considerable associated distress and functional decline appearing during this critical developmental phase. Our current diagnostic system lacks therapeutic validity, particularly for the early stages of mental disorders when symptoms are still emerging and intensifying and have not yet stabilized sufficiently to fit the existing syndromal criteria. While this is, in part, due to the difficulty of distinguishing transient developmental or normative changes from the early symptoms of persistent and disabling mental illness, these factors have contributed to a growing movement for the reform of our current diagnostic system to more adequately inform the choice of therapeutic strategy, particularly in the early stages of a mental illness. The clinical staging model, which defines not only the extent of progression of a disorder at a particular point in time but also where a person lies currently along the continuum of the course of an illness, is particularly useful as it differentiates early, milder clinical phenomena from those that accompany illness progression and chronicity. This will not only enable clinicians to select treatments relevant to earlier stages of an illness, where such interventions are likely to be more effective and less harmful than treatments delivered later in the course of illness, but also allow a more efficient integration of our rapidly expanding knowledge of the biological, social, and psychological vulnerability factors involved in the development of mental illness into a useful diagnostic framework.

Bipolar II disorder (recurrent depressive and hypomanic episodes) and related disorders (united in the bipolar spectrum) are understudied, despite a prevalence of about 5% in the community and about 50% in depressed outpatients. The apparent increase in prevalence of the bipolar spectrum is related to several changes in diagnostic criteria, including improved probing for history of hypomania (focused more on overactivity than on mood change), lower minimum duration of hypomania, and inclusion of unipolar depressions with bipolar signs (eg, family history of bipolar disorder, mixed depression). Prevalence of mixed depression, a combination of depression and manic or hypomanic symptoms, is high in patients with bipolar disorders. Controlled studies are needed to investigate treatment of mixed depression; antidepressants can worsen manic and hypomanic symptoms, and mood stabilising agents might be necessary.

Neuropsychological research in patients with affective disorders shows heterogeneous results with regard to the severity and profile of cognitive impairments. In this paper we hypothesize that the investigation of clinical (subtypes, comorbidity, traumatization, personality, severity, diurnal swings, course, duration, age of onset, biased processing, rumination, motivation, experience of failure, sleep, suicidal tendencies, computer attitudes), demographic (age, education, gender) and neurobiological factors (structural and functional brain changes, glucocorticoids, medication, ECT) that are related to cognitive performance has specified the understanding of severity and profile of neuropsychological impairments. We reviewed the literature pertaining to clinical, demographic and neurobiological factors following Pubmed and PsychInfo databases using different combinations of general key-terms including “Affective Disorder,” “Depression,” “Mania,” “Neuropsychological,” “Neurobiological,” “Moderator,” and “Review” as well as more specific demographic, clinical and neurobiological search terms. Findings from the literature show that the consideration of these factors has improved knowledge about the severity of neuropsychological impairments in patients with affective disorders whereas the neuropsychological profile is still poorly understood. Despite limited understanding, however, the existent results provide promising suggestions for the development of treatment programs.

In the classification of mood disorders, major depressive disorder is separate from bipolar disorders whereas mania is not. Studies on pure mania are therefore rare. Our paper reviews the evidence for distinguishing pure mania (M) and mania with mild depression (Md) from bipolar disorder. Two large epidemiological studies found a prevalence of 1.7–1.8 % of M/Md in adolescents and adults. Several clinical follow-up studies demonstrated good stability of the diagnosis after a previous history of three manic episodes. Compared to bipolar disorder, manic disorder is characterised by a weaker family history for depression, an earlier onset, fewer recurrences and better remission, and is less comorbid with anxiety disorders. In addition, mania is strongly associated with a hyperthymic temperament, manifests more psychotic symptoms and is more often treated with antipsychotics. Twin and family studies find mania to be more heritable than depression and show no significant transmission from depression to mania or from mania to depression. Cardiovascular mortality is elevated among patients with mood disorders generally and is highest among those with mania. In non-Western countries, mania and the manic episodes in bipolar disorder are reported to occur more frequently than in Western countries.

Over the past two decades, immune–inflammatory dysregulation has emerged as a central paradigm in the biology of mood disorders. Patients with major depression (MDD) and bipolar disorder (BD) frequently display low-grade systemic inflammation. Elevated C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) identify clinically relevant subgroups of patients characterized by greater severity, cognitive impairment, and poor treatment response. Changes in the gut microbiota and disruptions of the blood–brain barrier (BBB) act as important gateways through which systemic immune activity can influence the brain. At the intracellular level, pattern-recognition receptors activate convergent hubs including NF-κB, JAK/STAT, and MAPK cascades, while the NLRP3 inflammasome integrates mitochondrial dysfunction and oxidative stress with IL-1β release and pyroptosis. These pathways converge on glial dysregulation, impaired BDNF/TrkB signaling, and kynurenine pathway (KP) alterations, fostering excitotoxicity and synaptic deficits. Translational studies demonstrate that elevated CRP and IL-6 predict poor antidepressant outcomes. Anti-inflammatory agents such as infliximab and celecoxib show efficacy in specific subgroups of patients. Emerging multi-omics approaches identify immuno-metabolic biotypes, supporting the rationale for biomarker-guided stratification. These findings define an ‘inflammatory biotype’ of mood disorders and highlight the need for biomarkers and precision-based trials to guide treatment.

The extant major psychiatric classifications, DSM-IV and ICD-10, are purportedly atheoretical and largely descriptive. Although this achieves good reliability, the validity of a medical diagnosis is greatly enhanced by an understanding of both risk factors and clinical history. In an effort to group mental disorders on the basis of risk factors and clinical manifestations, five clusters have been proposed. The purpose of this paper is to consider the position of bipolar disorder (BPD), which could be either with the psychoses, or with emotional disorders, or in a separate cluster. We reviewed the literature on BPD, unipolar depression (UPD) and schizophrenia in relation to 11 validating criteria proposed by the DSM-V Task Force Study Group, and then summarized similarities and differences between BPD and schizophrenia on the one hand, and UPD on the other. There are differences, often substantial and never trivial, for 10 of the 11 validators between BPD and UPD. There are also important differences between BPD and schizophrenia. BPD has previously been classified together with UPD, but this is the least justifiable place for it. If it is to be recruited to a 'psychotic cluster', there are several important respects in which it differs from schizophrenia, so the cluster would have a division within it. The alternative would be to allow it to be in an intermediate position in a cluster of its own.

ABSTRACTBackgroundAnxiety and depression symptoms change over the lifespan and older adults use different terms to describe their mental health, contributing to under identification of anxiety and depression in older adults. To date, research has not examined these differences in younger and older samples with comorbid anxiety and depression. MethodsOne hundred and seven treatment-seeking participants (47 older, 60% female, and 60 younger, 50% female) with anxiety and mood disorders completed the Anxiety Disorders Interview Schedule and a symptom checklist to examine differences in symptom severity, symptom profiles and terms used to describe anxiety and mood. ResultsThe findings indicated several key differences between the presentation and description of anxiety and depression in younger and older adults. Older adults with Social Phobia reported fearing a narrower range of social situations and less distress and interference. Older adults with Generalized Anxiety Disorder (GAD) reported less worry about interpersonal relationships and work/school than younger adults, however, there were no differences between age groups for behavioral symptoms endorsed. Further older adults reported phobia of lifts/small spaces more frequently than younger adults. Depressed older depressed adults also reported more anhedonia compared to younger adults, but no differences in terms of reported sadness were found. Finally, older and younger adults differed in their descriptions of symptoms with older adults describing anxiety as feeling stressed and tense, while younger adults described anxiety as feeling anxious, worried or nervous. ConclusionsClinicians need to assess symptoms broadly to avoid missing the presence of anxiety and mood disorders especially in older adults.