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To investigate whether mood instability (MI) qualify as a trait marker for bipolar disorder (BD) we investigated: 1) differences in smartphone-based self-reported MI between three groups: patients with newly diagnosed BD, unaffected first-degree relatives (UR), and healthy control individuals (HC); 2) the correlation between MI and functioning, stress, and duration of illness, respectively; and 3) the validity of smartphone-based self-evaluated mood ratings as compared to observer-based ratings of depressed and manic mood.203 patients with newly diagnosed BD, 54 UR and 109 HC were included as part of the longitudinal Bipolar Illness Onset study. Participants completed daily smartphone-based mood ratings for a period of up to two years and were clinically assessed with ratings of depression, mania and functioning.Mood instability scores were statistically significantly higher in patients with BD compared with HC (mean=1.18, 95%CI: 1.12;1.24 vs 1.05, 95%CI: 0.98;1.13, p = 0.007) and did not differ between patients with BD and UR (mean=1.17, 95%CI: 1.07;1.28, p = 0.91). For patients, increased MI scores correlated positively with impaired functioning (p0.001), increased stress level (p0.001) and increasing number of prior mood episodes (p0.001). Smartphone-based mood ratings correlated with ratings of mood according to sub-item 1 on the Hamilton Depression Rating Scale 17-items and the Young Mania Rating Scale, respectively (p´s0.001).The study had a smaller number of UR than planned.Mood instability is increased in patients with newly diagnosed BD and unaffected relatives and associated with decreased functioning. The findings highlight MI as a potential trait marker for BD.

Purpose The BDSx (Bipolar Disorder Symptom Scale) is a brief self-report instrument designed for repeated measurement of bipolar disorder (BD) symptoms over time. Previous research indicates that the BDSx measures two depression (cognitive and somatic symptoms) and two hypo/mania factors (affrontive symptoms and elation/loss of insight). The purpose of this study was to validate BDSx responses relative to diagnoses of BD mood episodes. Methods Sixty BD outpatients attending routine clinic appointments completed the BDSx, the Hamilton Rating Scale for Depression, the Altman Self-Rating Mania Scale, and the Satisfaction with Life Scale. Blind to scale responses by patients, a clinic psychiatrist determined if patients were currently symptomatic. Results BDSx depression and hypo/mania subscales showed good construct validity vis-a-vis clinical diagnoses, and concurrent/discriminant validity with other self-report scales. And though not designed as a screening measure, sensitivity for the depression subscale is high at 88% (6+, 76% specificity), yet lower at 57% for the hypo/mania subscale (5+, 90% specificity). Conclusions The results of this study indicate that BDSx responses distinguish patients experiencing depressive and hypo/manic mood episodes. Findings support the psychometric properties of the Hebrew version of this scale. The BDSx enables those with bipolar disorder to monitor their symptoms, gauge symptom variability, and identify factors that proceed and sustain BD symptoms over time.

Objective: Abnormalities in spontaneous brain activity, measured with resting-state functional magnetic resonance imaging (rs-fMRI), may be key biomarkers for bipolar disorders. This systematic review compares rs-fMRI findings in people experiencing a bipolar depressive or (hypo)manic episode to bipolar euthymia and/or healthy participants. Methods: Medline, Web of Science and Embase were searched up until April 2021. Studies without control group, or including minors, neurological co-morbidities or mixed episodes, were excluded. Qualitative synthesis was used to report results and risk of bias was assessed using the National Heart, Lung and Blood Institute tool for case-control studies. Results: Seventy-one studies were included (3167 bipolar depressed/706 (hypo)manic). In bipolar depression, studies demonstrated default-mode (DMN) and frontoparietal network (FPN) dysfunction, altered baseline activity in the precuneus, insula, striatum, cingulate, frontal and temporal cortex, and disturbed regional homogeneity in parietal, temporal and pericentral areas. Functional connectivity was altered in thalamocortical circuits and between the cingulate cortex and precuneus. In (hypo)mania, studies reported altered functional connectivity in the amygdala, frontal and cingulate cortex. Finally, rs-fMRI disturbances in the insula and putamen correlate with depressive symptoms, cerebellar resting-state alterations could evolve with disease progression and altered amygdala connectivity might mediate lithium effects. Conclusions: Our results suggest DMN and FPN dysfunction in bipolar depression, whereas local rs-fMRI alterations might differentiate mood states. Future studies should consider controlling rs-fMRI findings for potential clinical confounding factors such as medication. Considerable heterogeneity of methodology between studies limits conclusions. Standardised clinical reporting and consistent analysis approaches would increase coherence in this promising field.

Background: An emotional intelligence (EI) deficit has been noticed in euthymic bipolar spectrum disorder (BD) patients. However, whether this deficit is affected by mood or subtype is unclear.Objectives:The aim of this study was to investigate whether an EI deficit is mood-dependent, and which mood symptoms have more impact on EI in BD.Methods: Two hundred and thirty participants aged between 18 and 65 years old were recruited [130 BD patients (51 bipolar I disorder (BDI) and 79 bipolar II disorder (BDII): 39.2% males; 91 healthy controls (HCs): 48.4% males)]. The Mayer–Salovey–Caruso Emotional Intelligence Test (MSCEIT), which contains experiential and strategic EI ratings, was used to assess social cognition. The Hamilton Depression Rating Scale (HDRS) and the Young's Mania Rating Scale (YMRS) were used for evaluating the severity [HAMD and YMRS scores ≦7 were euthymic (BDeut) and HAMD YMRS sores ≧8 were episodic (BDepi)]. Analyses of covariance (ANCOVA) were performed, with adjustment for background information between the BD patients and HCs.Results: The results showed that, compared to the HCs, the BDeut patients showed no difference in any MSCEIT measures, while the BDepi patients showed lower scores in all MSCEIT measures, except for perceiving emotions. In addition, a main effect of mood state instead of BD subtype was found for the managing emotions branch (p < 0.0007). Regression analyses showed that the duration of illness and HDRS scores were correlated with the scores in the strategic area of the MSCEIT, while age and YMRS scores were more relevant to the scores in the experiential area of the MSCEIT.Conclusion: The results confirm that an EI deficit is mood-dependent in BD patients. In addition, a depressive mood is more related to the strategic EI area, while a manic mood is correlated with the experiential EI area. Understanding the different domains of EI deficits in BD patients may be helpful for developing interventions for BD.

Bipolar disorder (BD) is a serious neuropsychiatric disorder characterized by alternating periods of mania, depression, and euthymia. Abnormal spontaneous brain activity within the cortical-striatal neural circuits has been observed in patients with BD. However, whether the abnormality appears in patients with BD while not in a manic mood state is unclear.This study collected resting-state fMRI data from 65 patients with BD who were not in a manic mood state and 85 matched healthy controls. First, we examined differences in amplitude of low-frequency fluctuations (ALFF) between the patients with BD and the healthy controls to identify regions that show abnormal local spontaneous activity in the patients. Based on the ALFF results, we conducted seed-based resting-state functional connectivity (rsFC) analysis to identify the changes in brain networks that are centered on the regions showing abnormal local spontaneous activity in the patients. Finally, we repeated these analyses in a sub-sample comprising euthymic BD patients (N = 37) and between the euthymic BD patients and all the other patients who had at least mild depressive symptoms.BD patients exhibited increased ALFF in the right caudate/putamen and increased rsFC in the right caudate/putamen with the right inferior parietal lobe (cluster-level FWE p 0.05). Further analyses showed that the euthymic BD patients showed similar abnormalities in ALFF and rsFC maps as found in all patients with BD. And the euthymic BD patients were comparable with all the other patients who had at least mild depressive symptoms in ALFF values.Our results indicated the important role of the right striatum in the baseline brain function of BD patients and suggested that the abnormality of spontaneous brain activity in the cortical-striatal neural circuits may be a trait-like variant in patients with BD. The results deepen our understanding of the neurobiological mechanisms associated with BD etiology.

Background Disruptions in affective processing characterize mood disorders, yet the neural mechanisms underlying internal state dependency in affective processes are not well understood. The present work presents a pilot investigation into state dependency among neural circuits known to be involved in processing affective information, by examining acute manic and depressive mood phases in adults with bipolar disorder and major depressive disorder. Methods The present study probed affective processes with a well-validated passive picture-viewing task amongst acutely manic (n = 8) or acutely depressed (bipolar depression: n = 11; major depression: n = 15) mood-disordered adults during functional magnetic resonance imaging . Results Beta-series correlation analyses seeded from the amygdala revealed distinct neural circuits distinguished across current mood state rather than diagnostic boundaries. We delineated an amygdala-striatum pathway that distinguished depressed from manic mood phase, rather than between diagnostic boundaries, in processing valenced information. Specifically, we found differences in this neural response to negative, but not positive, images across clinical mood states. Limitations As a preliminary investigation of state-dependent affective processes, the current investigation is predominantly limited by the small sample size. While it provides direction and generates hypotheses for further work, future studies need to replicate and expand the reported effects with larger samples. Conclusions These findings demonstrate the conditions under which mood state-dependent affective processes cut cross traditional diagnostic boundaries, speaking to recent advances in transdiagnostic disease mechanisms, and can guide future work examining the neural mechanisms driving symptomatology in affective disorders.

Background The amplified emotionality characteristics of bipolar disorder (BD) may interfere with goal pursuit in the recovery process. This is the first study to test the coping flexibility model empirically among people with BD. Finding ways to cope with goal-striving life events should shed light on managing elevated mood states. Methods Using a 12-month longitudinal follow-up design, this study examined the stability in coping flexibility with experimentally-devised Behavioral Approach System (BAS) activating life events and mood states at 6- and 12-month time points for individuals with BD (n = 83) and healthy controls (n = 89). Hierarchical linear modeling tested the individual growth model by studying the longitudinal data. Results The findings showed fluctuations in different components of coping flexibility and mood states across time. They confirmed the amplified emotionality characteristics of BD. Moreover, coping flexibility took precedence over BAS sensitivity and psychosocial functioning levels in predicting mood states. Limitations Measurements of BAS sensitivity may focus on trait nature only and prone to subjective bias. The assessment of mood or coping flexibility may not accurately capture actual experience in daily life. Lack of respective data on bipolar subtypes and significant differences in some dimensions between the BD and control groups are further limitations of the study. Conclusions The study's findings have implications for coping with amplified emotionality within the personal recovery process for people with BD. Judicious application of coping strategies and adjustment of perceived controllability are crucial for individuals to reach goals pertinent to personal recovery and manage potential manic mood symptoms.

Objectives Network analyses of psychopathology examine the relationships between individual symptoms in an attempt to establish the causal interactions between symptoms that may give rise to episodes of psychiatric disorders. We conducted a network analysis of mood symptoms in adolescents with or at risk for bipolar spectrum disorders. Methods The sample consisted of 272 treatment-seeking adolescents with or at high risk for bipolar disorder who had at least subsyndromal depressive or (hypo)manic symptoms. Based on symptom scores assessed via semi-structured interviews, we constructed the network of depressive and manic symptoms and identified the most central symptoms and symptom communities within the network. We used bootstrapping analyses to determine the reliability of network parameters. Results Symptoms within the depressive and manic mood poles were more related to each other than to symptoms of the opposing mood pole. Four communities were identified, including a depressive symptom community and three manic symptom communities. Fatigue and depressed mood were the strongest individual symptoms within the overall network (ie the most highly correlated with other symptoms), followed by motor hyperactivity. Mood lability and irritability were found to be "bridge" symptoms that connected the two mood poles. Conclusions Symptoms of activity/energy (ie fatigue and hyperactivity) and depressed mood are the most prominent mood symptoms among youth with bipolar spectrum disorders. Mood lability and irritability represent potential warning signs of emergent episodes of either polarity. Targeting these central and bridge symptoms would lead to more efficient assessments and therapeutic interventions for bipolar disorder.

Ketosis is a metabolic state in which the body uses ketones derived from breakdown of fatty acids as the primary mitochondrial fuel source instead of glucose. In recent years an accumulation of evidence for the beneficial effects of the ketotic state on the brain have heightened interest in its potential for use in neurological conditions. The ketogenic diet (KD) induces ketosis and is an effective treatment for medically resistant epilepsy. There is significant comorbidity between epilepsy and bipolar disorder (BD) and both conditions are treated by anti-convulsant drugs. In addition, reports on bipolar disease online fora have highlighted subjective mood stabilization effects associated with the KD. These KD reported effects could be explained if there was a disorder in the conversion of pyruvate into Acetyl-CoA (and subsequent impairment of oxidative phosphorylation) which was bypassed by ketones providing an alternative substrate for oxidative phosphorylation. This is consistent with growing evidence that mitochondrial dysfunction plays a causal role in BD and explains the reported TCA cycle dysfunction and elevated pyruvate levels in BD. Reduced levels of ATP affects the normal operation of the Na, K-ATPase in the brain with differing levels of reduction either leading to reduced neuronal action potential and inhibition of neurotransmitter release (consistent with the depressed state in BD) or increased neuronal resting potential and hyper-excitability (consistent with a [hypo]manic mood state). We hypothesize that the mitochondrial dysfunction is due to a disorder of the Pyruvate Dehydrogenase Complex (PDC) and/or Mitochondrial Carrier Protein (MCP) shuttle which moves intracellular pyruvate into mitochondria. The resultant reduction in ATP generation could explain mood instability and cycling in BD (through mechanisms such as those delineated by Mallakh and Peters). This proposed novel causal pathway could explain mood de-stabilization in BD and the reported positive effects of KD. If true, this hypothesis would suggest that there should be increased research attention to PDC (and in particular the E1 alpha subunit) as potential therapeutic targets and further study of a possible role of KD in BD to improve mood stability. Experimental approaches, such as through a clinical trial of KD on mood stabilization in BD, are required to further investigate this hypothesis.

Background Chronic pain is highly prevalent among individuals with mood disorders. While much is known about the relationship between pain and unipolar depression, little is known about pain experiences among people with bipolar disorder. This pilot study addresses this gap by examining pain and its relationship to mood and functioning in a sample of US military veterans with bipolar disorder. Methods Qualitative interviews were conducted with 15 veterans with bipolar disorder and chronic pain who were recruited from outpatient services within a Veterans Affairs medical center. Results Veterans reported a bidirectional relationship between pain and bipolar depression. When discussing manic episodes, individuals’ experiences varied between notable reductions in pain (usually in euphoric states), increases in pain (usually in angry/irritable states), and feeling disconnected from pain. Many reported that increased activity when manic contributed to worse pain after an episode. Veterans clearly articulated how these connections negatively affected their functioning and quality of life. Limitations This was a small, retrospective study that included a non-random sample of veteran participants from one VA medical center. All veterans were engaged in outpatient mental health care, so the majority reported that their mood has been well-stabilized through medications and/or psychotherapy. Conclusions Chronic pain experiences appear to be related to depressive and manic mood states and significantly affects functioning and quality of life in Veterans with bipolar disorder. This study highlights the need to assess chronic pain among veterans with bipolar disorder, as changes in mood could have significant implications for functioning and pain management.

Objectives To examine the differential impact of depressive and manic mood states on alcohol craving in patients with bipolar disorder and comorbid alcoholism. Methods Forty-four men and women, ages 18-65, with DSM-IV-TR comorbid diagnoses of bipolar I disorder and alcohol dependence were assessed over a three-month period to examine the extent to which their depressive and manic symptoms were associated with alcohol cravings (i.e., desire to use and not to use alcohol) at each assessment point, controlling for age, ethnicity, socio-economic status, baseline alcohol use, and number of assessments. Results Both manic and depressive symptoms were associated with greater desire to use alcohol. Only depressive symptomatology was associated with reduced desire not to use alcohol, and desire not to use alcohol declined over the course of the three-month treatment period. Conclusion Whereas enhanced desire to drink alcohol may be a conditioned reaction to both manic and depressed mood states, desire not to drink alcohol may be more of an indicator of treatment motivation, which is negatively affected by depressed mood. Depressive symptoms may warrant prioritization and aggressive targeting early in treatment given that desire to refrain from alcohol use was only influenced by depressive symptoms and declined over the course of treatment.

The aim of this study was to conduct a systematic review of literature to retrieve all randomized controlled trials that evaluated the efficacy of tamoxifen on manic mood episodes and meta-analyze their quantitative results.Four electronic databases were systematically searched from their inception to March 2014: PubMed, Cochrane Library (Cochrane Central Register of Controlled Trials), Scopus, and PsychINFO. Pooled difference in means of changes in mania scores and pooled odds ratio of treatment response (for tamoxifen monotherapy) were calculated as the main effect size. A random effects model was used to pool the data across studies. Quantitative syntheses were expressed by forest plots.Five randomized controlled trials (3 adjunct trials and 2 monotherapy trials) were included. Regarding adjunct tamoxifen, the standardized difference in mean of mania score changes in tamoxifen arm as compared with control arm was 0.669 (95% confidence interval [CI], 0.15-1.189; P = 0.012). Regarding monotherapy, the pooled difference in means of mania score changes in the tamoxifen arm as compared with the placebo arm was 22.09 (95% CI, 20.98-23.192; P0.000000001). Pooled odds ratio of response to treatment was 15.36 (95% CI, 2.99-78.73; P = 0.001) in the tamoxifen group as compared with the placebo group.Tamoxifen can be considered an effective treatment for manic bipolar patients. Making a conclusion regarding the efficacy and safety for longer periods warrants further studies with a larger sample size and longer follow-up duration.

Bipolar disorder (BD) is a unique disorder where the same patient exhibits depression and mania, states with polar opposite mood symptoms. Lithium is an alkali metal that is widely used for the treatment of BD. However, it is largely unknown why lithium can stabilize mood. Lithium is known to inhibit glycogen synthase kinase-3β (GSK3 β). Interestingly, both in the glutamatergic system and GABAergic system, active GSK3 β decreases neuronal excitability, whereas inhibition of GSK3 β increases neuronal excitability, suggesting that activation of GSK3 β leads to depressive mood, and inhibition of GSK3 β leads to manic mood. The activity of GSK3β is regulated by many kinases and a phosphatase, and they are further controlled by several neurotransmitters and signaling molecules. Thus, these complicated control systems might make the swing of GSK3β activity, the swing of GSK3β activity makes the swing of neuronal excitability and finally resulting in the intrinsic swing of mood, usually observed in healthy human. BD is considered that the amplitude of the mood swing is enhanced by many factors. Lithium can dose-dependently decrease the amplitude of the swing of GSK3β activity. In addition, lithium also inhibits K+ channel activation, leading to the elongation of refractory period, resulting in the inhibition of neuronal excitability. Therefore, in depressive mood, lithium can increase neuronal activity via the inhibition of neuronal GSK3beta activity, and in manic mood, lithium can inhibit neuronal excitability via inhibiting K+ channel activation, therefore the amplitude of the mood swing is decreased, i.e. alleviating the depressive state and the manic state, resulting in the normalization of the mood swing.

Background: Recently, more evidence has been presented regarding the role of behavioral activation/inhibition systems as predictors of substance use disorders. In fact, these systems are regarded as potentially important factors in the development of this complex psychiatric problem. Objectives: This study aimed to determine how behavioral activation/inhibition systems, namely behavioral activation, behavioral inhibition, and fight-flight freezing systems, affect substance abuse in bipolar patients. Methods: A total of 79 patients with bipolar disorder were selected among hospitalized patients in the psychiatric ward of Kamkar-Arabnia Hospital in Qom, Iran. The participants completed the Gray-Wilson personality questionnaire, Hamilton Rating Scale for Depression, Mood Disorder Questionnaire, and a sociodemographic questionnaire. Results: Behavioral activation and behavioral inhibition systems emerged as significant predictors of substance abuse in bipolar patients (χ2 = 52.511; df = 3; P < 0.0005). Gender and type of bipolar disorder (I or II) showed no significant association with the scores of behavioral activation, behavioral inhibition, or fight-flight freezing systems. Also, the behavioral inhibition system scores could predict manic mood (χ2 = 7.067; df = 3; P < 0.070). Conclusions: The findings of the current study provide further evidence regarding the role of behavioral activation and inhibition systems as predictors of substance abuse in bipolar patients.

Background While mood elevation and euphoria are the most commonly described phenotypic descriptors of hypo/mania, irritability and anger may dominate. This study was designed to pursue possible determinants of such differing states. Methods Patients with bipolar I or II disorder were assigned to an ‘irritable/snappy’ or ‘euphoric/happy’ sub-set on the basis of their dominant hypo/manic symptoms. Group differences were examined across clinical, personality, lifestyle and illness impact measures. Results The two sub-sets did not differ on age of depression onset, family history of mood disorders, or depression severity and impairment. The snappy sub-set reported higher levels of irritability in depressed phases and were more likely to have a comorbid anxiety disorder. Their hypo/manic episodes were shorter and they were more likely to be hospitalized at such times. On a temperament measure they scored as more irritable and self-focussed and as less cooperative and effective – indicative of higher levels of disordered personality functioning. Limitations Some comparison analyses were undertaken on a reduced sample size, giving rise to power issues. Our bipolar I and II diagnoses deviated to some extent from DSM-5 criteria in not imposing duration criteria for hypo/manic episodes. Conclusions Findings support a spectrum model for the bipolar disorders linking temperament to bipolar symptomatic state and which may have treatment implications.

OBJECTIVES Quantitative mapping of T1 relaxation in the rotating frame (T1ρ) is a magnetic resonance imaging technique sensitive to pH and other cellular and microstructural factors, and is a potentially valuable tool for identifying brain alterations in bipolar disorder. Recently, this technique identified differences in the cerebellum and cerebral white matter of euthymic patients vs healthy controls that were consistent with reduced pH in these regions, suggesting an underlying metabolic abnormality. The current study built upon this prior work to investigate brain T1ρ differences across euthymic, depressed, and manic mood states of bipolar disorder. METHODS Forty participants with bipolar I disorder and 29 healthy control participants matched for age and gender were enrolled. Participants with bipolar disorder were imaged in one or more mood states, yielding 27, 12, and 13 imaging sessions in euthymic, depressed, and manic mood states, respectively. Three-dimensional, whole-brain anatomical images and T1ρ maps were acquired for all participants, enabling voxel-wise evaluation of T1ρ differences between bipolar mood state and healthy control groups. RESULTS All three mood state groups had increased T1ρ relaxation times in the cerebellum compared to the healthy control group. Additionally, the depressed and manic groups had reduced T1ρ relaxation times in and around the basal ganglia compared to the control and euthymic groups. CONCLUSIONS The study implicated the cerebellum and basal ganglia in the pathophysiology of bipolar disorder and its mood states, the roles of which are relatively unexplored. These findings motivate further investigation of the underlying cause of the abnormalities, and the potential role of altered metabolic activity in these regions.

Seasonal variation of manic and depressive symptoms is a controversial topic in bipolar disorder research. Several studies report seasonal patterns of hospital admissions for depression and mania and variation in symptoms that appear to follow a seasonal pattern, whereas others fail to report such patterns. Differences in research methodologies, data analysis strategies, and temporal resolution of data may partly explain the variation in findings between studies. The current study adds a novel perspective to the literature by investigating specific meteorological factors such as atmospheric pressure, hours of sunshine, relative humidity, and daily maximum and minimum temperatures as more proximal predictors of self-reported daily mood change in people diagnosed with bipolar disorder. The results showed that daily maximum temperature was the only meteorological variable to predict clinically-relevant mood change, with increases in temperature associated with greater odds of a transition into manic mood states. The mediating effects of sleep and activity were also investigated and suggest at least partial influence on the prospective relationship between maximum temperature and mood. Limitations include the small sample size and the fact that the number and valence of social interactions and exposure to natural light were not investigated as potentially important mediators of relationships between meteorological factors and mood. The current data make an important contribution to the literature, serving to clarify the specific meteorological factors that influence mood change in bipolar disorder. From a clinical perspective, greater understanding of seasonal patterns of symptoms in bipolar disorder will help mood episode prophylaxis in vulnerable individuals.

Bipolar disorder is a chronic, recurrent mental illness characterized by extreme episodes of depressed and manic mood, interspersed with less severe but highly variable mood fluctuations. Here, we develop a novel mathematical approach for exploring the dynamics of bipolar disorder. We investigate how the dynamics of subjective experience of mood in bipolar disorder can be understood using a relaxation oscillator (RO) framework and test the model against mood time-series fluctuations from a set of individuals with bipolar disorder. We show that variable mood fluctuations in individuals diagnosed with bipolar disorder can be driven by the coupled effects of deterministic dynamics (captured by ROs) and noise. Using a statistical likelihood-based approach, we show that, in general, mood dynamics are described by two independent ROs with differing levels of endogenous variability among individuals. We suggest that this sort of nonlinear approach to bipolar disorder has neurobiological, cognitive and clinical implications for understanding this mental illness through a mechacognitive framework.

Objectives: Olfactory dysfunction is described in several neuropsychiatric disorders but there is little research on olfactory processing in bipolar disorder. Methods: We assessed odor detection threshold (sensitivity) and smell identification test scores, along with symptoms, cognition, and social function in 20 DSM-IV bipolar disorder patients and 44 control subjects. Results: The patient and control groups had similar demographic measures, intelligence, and mean olfaction scores, but significantly differed in social domains, including adjustment, function, and anxiety. Odor detection sensitivity showed significantly opposite correlations for the depressive and manic mood domains in bipolar disorder (r to z = 2.83, p = 0.005). Depressive symptoms were related to increased sensitivity (the ability to detect odors at a lower concentration) and mania symptoms were related to decreased sensitivity for odor detection. Increased sensitivity for odor detection also predicted significantly better employment (r = -0.642, p = 0.024), whereas less sensitivity was associated with social avoidance (r = 0.702, p = 0.024) and social fear (r = 0.610, p = 0.046). Conclusions: Diminished odor detection sensitivity predicted mania and social avoidance, whereas more sensitive odor detection predicted more depressive symptoms but better employment functioning in bipolar disorder patients. Odor acuity may be an illness state marker of mood syndromes in bipolar disorder. Alternatively, differences in odor acuity may identify heterogeneous subgroups within the bipolar spectrum. Longitudinal assessments in a large, sex-stratified sample are needed to understand the implications of odor sensitivity in patients with bipolar disorder. Language: en

Lex C, Hautzinger M, Meyer TD. Cognitive styles in hypomanic episodes of bipolar I disorder. Bipolar Disord 2011: 13: 355–364. © 2011 The Authors. Journal compilation © 2011 John Wiley & Sons A/S. Objectives: Cognitive vulnerability-stress theories have recently been extended to bipolar disorder by suggesting that an activation of negative cognition might lead to depressive mood episodes and an activation of positive cognition might lead to manic mood episodes. Alternatively, the manic defense hypothesis claims that hypomanic and manic states are not the opposite of depression but rather contain similar underlying negative cognitions. The objective of this study was to further evaluate these theories by examining the cognitive patterns in bipolar I hypomania. Methods: We compared 15 hypomanic bipolar I disorder patients, 26 remitted bipolar I disorder patients, and 21 healthy individuals in a cross-sectional study. All participants completed the Dysfunctional Attitude Scale, the Attributional Style Questionnaire, the Emotional Stroop Task, and the Emotional Auditory Verbal Learning Test. Results: Hypomanic bipolar disorder individuals showed cognitions associated with depressive states as well as cognitions associated with manic states. The results for the remitted bipolar disorder patients paralleled those for the control group. Conclusion: Dysfunctional cognition in bipolar disorder seems to relate to state rather than to trait. Hypomania includes depression-related as well as mania-related cognitions and can therefore not be considered as the mere opposite of depression.

Dysphoric mania is a common and often difficult to treat subset of bipolar mania that is associated with significant depressive symptoms.This post hoc analysis was designed to evaluate the efficacy of ziprasidone in the treatment of depressive and other symptoms in a cohort of patients with dysphoric mania.Pooled data were examined from two similarly designed, 3-week placebo-controlled trials in acute bipolar mania. Patients scoring/=2 on at least two items of the extracted Hamilton Rating Scale for Depression (HAM-D) met criteria for dysphoric mania and were included in the post hoc analysis. Changes from baseline in symptom scores were evaluated by a mixed-model analysis of covariance.179 patients with dysphoric mania were included in the post hoc analysis (ziprasidone, n=124; placebo, n=55). Beginning at day 4, HAM-D scores were significantly lower at all visits in patients treated with ziprasidone compared with those treated with placebo (p0.05). Ziprasidone-treated patients also demonstrated significant improvements on the Mania Rating Scale and all secondary efficacy measures, and had significantly higher response and remission rates compared with placebo.The main limitations are the use of a post hoc analysis and the pooling of two studies with slightly different designs.In this analysis, ziprasidone significantly improved both depressive and manic mood symptoms in patients with dysphoric mania, suggesting that it might be a useful treatment option in this patient population. Further prospective controlled trials are needed to confirm these findings.

Objective To explore sex differences in pediatric bipolar disorder in terms of subtype and severity of depressive and manic symptomatology. Method Participants were 760 youth (aged 5-17 years) and their legal guardians. Participants were part of a larger outpatient assessment protocol enriched for bipolar disorder. Youth were assessed for DSM-IV diagnoses using the Schedule for Affective Disorders and Schizophrenia for School-Age Children-Epidemiologic Version. Their presenting mood state was determined using the Young Mania Rating Scale and the Children's Depression Rating Scale-Revised. The study was conducted from January 1996 to February 2003. Results 387 youth (51%) met DSM-IV criteria for diagnoses of bipolar spectrum disorders. Results showed no sex differences in rates of bipolar spectrum disorders or any of the bipolar subtypes. Sex differences were found with regard to presenting mood states: boys presented with higher rates of manic mood, and girls presented with higher rates of depressed mood. Older children were also more likely than younger children to exhibit higher levels of depressed mood. There were no age differences in levels of manic mood. Conclusion This study highlights how bipolar disorder can manifest itself differently among girls and boys despite equivalent rates of diagnosis. It is important for clinicians to consider the full range of mood states in order to accurately diagnose and treat children. Future research is needed to assess the roles that genetics, puberty, cognitive styles, and environmental factors play in the expression of mania and depression in girls and boys over the course of their development.

A number of studies have reported mood-congruent biases in processing facial expressions of emotion in depression and mania. Most of them have failed to establish that mood reliably affects relevant more than irrelevant expressions, or that the effect is specifically mood-related rather than due to resource or task difficulty artefacts. The aim was to examine, using appropriate statistical methods, whether depressed mood in bipolar patients decreases and manic mood increases sensitivity to facial expressions of happiness and vice versa for facial expressions of negative emotion.Sensitivity to facial expression of six basic emotions in bipolar patients when depressed and when manic was compared to closely matched controls.Mood-related biases in sensitivity to facial expressions of happiness and of negative affect in general operate in persons with bipolar disorder when depressed. There is little evidence of similar biases in persons with bipolar disorder when manic.These data show a mood-congruent bias in sensitivity to facial expressions in bipolar depressed patients.

Background. Demonstrating differences between euthymic bipolar subjects and healthy controls in response to positive (happy) mood induction may help elucidate how mania evolves. This pilot study evaluates the Go task in a reward paradigm as a method for inducing a happy mood state and compares the response of euthymic bipolar subjects and healthy controls.Method. The Sense of Hyperpositive Self Scale, the Tellegen positive and negative adjectives, the Global-Local task and a visual analogue scale for measuring positive affect were administered to 15 euthymic bipolar subjects and 19 age-and-sex-matched healthy control subjects before and after they had performed the Go task in a reward paradigm.Results. Significant differences were found between subjects and controls on several measures at each time-point but there were no differences across the groups across time except for the visual analogue scales, where subjects had a more sustained duration in self-reported happiness compared with controls.Conclusions. This pilot study has shown that a positive affect can be induced in bipolar subjects and controls which can be demonstrated by changes in scores on several tasks. However, only the visual analogue scales showed a significant difference between cases and controls over time. Such tests may prove valuable in furthering understanding about the evolution of manic mood states.

Objectives: Manic patients exhibit impaired verbal learning and memory, particularly following longstanding illness. However, it is unclear whether recognition and recall performance are differentially influenced by a manic mood state. Methods: To examine this issue, we administered the California Verbal Learning Test and symptom-rating scales to inpatients with pure or mixed mania, euthymic outpatients, and healthy comparison subjects. Results: An overall performance difference was identified between groups. Manic and euthymic patients performed more poorly than healthy subjects on recall. However, manic patients performed more poorly than euthymic patients and healthy subjects on recognition. Conclusions: These results suggest that verbal retrieval deficits are stable vulnerability indicators in bipolar disorder, whereas verbal encoding deficits are manic episode indicators. The known subcortical dysfunction in this disorder may produce stable retrieval deficits while acute mood symptoms attenuate encoding during affective episodes only.

The Hypomanic Personality Scale (HPS) was designed to measure a predispositional personality style to bipolar disorder. Its properties have largely been assessed in non-clinical samples. We undertook a number of analyses to determine if it is likely to be a measure of actual personality style or is confounded by items capturing hypomanic/manic mood symptoms. A total of 112 bipolar and 164 unipolar patients completed the measure. Several principal components analyses were undertaken and associations were examined between HPS items and scores on a measure designed to identify bipolar disorder--the Mood Swings Questionnaire (MSQ). Principal components analyses generated a similar set of four factors in both the unipolar and bipolar sample sub-sets and congruent with previous analyses undertaken in non-clinical samples, suggesting identification of normative dimensions that underpin hypomanic and manic mood states. A number of HPS items correlated highly with the MSQ. Results suggest that HPS is unlikely to simply be a measure of personality style and appears strongly confounded by hypomanic/manic mood symptoms. The measure may therefore--in its current form--be inappropriate for at-risk research seeking to determine the capacity of personality style to predict onset of a bipolar disorder.

Over the course of 1 year, a patient with a rapid cycling bipolar affective disorder was followed at weekly intervals to examine whether plasma hormones and urinary catecholamines could predict current or future mood. Higher cortisol levels were found to predict depressed mood 3 days after blood sampling, higher urinary dopamine predicted a manic mood 3 days after blood sampling, urinary norepinephrine was associated with severity of current mood and prolactin was lower with concurrent depressed mood. In multivariate analyses of mood against cortisol, prolactin and three urinary catecholamines, > 50% of the variance in mood state in 3 days was explained by combinations of these biologic measures, especially cortisol and urinary dopamine, while all five biologic variables contributed to explaining 50% of the variance in current mood state. Based on the interrelationships between urinary dopamine, norepinephrine and mood, we postulate the existence of an overcompensating mechanism which is reflected in opposing correlations between urinary dopamine and norepinephrine with mood, despite the two urinary catecholamines being positively correlated.

IntroductionBehavioral disturbances are common in psychiatric patients. This symptom may be caused by several disorders and clinical status.Case reportWe report the case of a 40 year-old male who was diagnosed of nonspecific psychotic disorder, alcohol dependence, cannabis abuse and intellectual disability. The patient was admitted into a long-stay psychiatric unit because of behavioral disturbances consisted in aggressive in the context of a chronic psychosis consisted in delusions of reference and auditory pseudohallucinations. During his admission the patient received the diagnosis of bipolar disorder type 1, presenting more severe behavioral disturbances during these mood episodes. It was necessary to make diverse pharmacological changes to stabilize the mood of the patient. Finally, the treatment was modified and it was prescribed clozapine (25 mg/24 h), clotiapine (40 mg/8 h), levomepromazine (200 mg/24 h), topiramate (125 mg/12 h), clomipramine (150 mg/24 h) and clorazepate dipotassium (50 mg/24 h). With this treatment, the patient showed a considerable improvement of symptoms, presenting euthymic and without behavioral disturbances.DiscussionIn this case report, we present a patient with severe behavioral disturbances. The inclusion of bipolar disorder in the diagnosis of the patient was very important for the correct treatment and management, because of depressive and manic mood episodes the behavioral disturbances were exacerbated.ConclusionsPatients with behavioral disturbances could present psychotic and affective symptoms as cause of them. It is necessary to explore these symptoms and try different treatments to improve them.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Whether responses to antidepressants differ in bipolar and unipolar depression remains unresolved.We analyzed patient characteristics and outcomes of antidepressant treatment of 1036 depressed patients with bipolar-I or bipolar-II disorder, or unipolar major depression, using bivariate and multivariate methods and survival analysis, testing the hypothesis that responses would be superior in unipolar depression.Antidepressants were given to 84.8% (878/1036) of depressed patients: 58.9% of 93 bipolar-I, 80.1% of 117 bipolar-II, and 91.3% of 668 unipolar disorder cases. The 158 not given antidepressants had more manias/year, spent more months in mania and depression, and were far more likely to receive mood stabilizers or antipsychotics long term. Improvement of HDRS21 depression ratings ranked: bipolar-II (69.6%)bipolar-I (62.9%)unipolar (57.9%; P0.0001), independent of initial illness severity. Responder rates (≥50% improved without switching) ranked: bipolar-II (77.0%)bipolar-I (71.6%)unipolar (61.7%; P0.0001). Remission rates (final HDRS7) ranked: 54.0%, 50.6%, and 40.8% respectively (P = 0.02); 67.5% remitted within 12 weeks of treatment. Survival-computed median time to remission (15.0 weeks, overall) was shortest for bipolar-II patients (10.7 weeks). The 3-month risk of switching into mania-hypomania ranked: bipolar-II (15.8%)bipolar-I (8.60%)unipolar (0.56%). Multivariate modeling found bipolar diagnosis, shorter latency to remission, more recent trial year, and fewer weeks depressed before treatment to be associated with greater percent improvement of HDRS ratings.Selective use of antidepressants with or without mood stabilizers in non-agitated, depressed bipolar disorder patients for short periods was effective with moderate risk of potentially dangerous, manic mood elevation.

OBJECTIVE: The aim of this study was to translate the Structured Clinical Interview for Mood Spectrum into Brazilian Portuguese, measuring its reliability, validity, and defining scores for bipolar disorders. METHOD: Questionnaire was translated (into Brazilian Portuguese) and back-translated into English. Sample consisted of 47 subjects with bipolar disorder, 47 with major depressive disorder, 18 with schizophrenia and 22 controls. Inter-rater reliability was tested in 20 subjects with bipolar disorder and MDD. Internal consistency was measured using the Kuder Richardson formula. Forward stepwise discriminant analysis was performed. Scores were compared between groups; manic (M), depressive (D) and total (T) threshold scores were calculated through receiver operating characteristic (ROC) curves. RESULTS: Kuder Richardson coefficients were between 0.86 and 0.94. Intraclass correlation coefficient was 0.96 (CI 95 % 0.93-0.97). Subjects with bipolar disorder had higher M and T, and similar D scores, when compared to major depressive disorder (ANOVA, p < 0.001). The sub-domains that best discriminated unipolar and bipolar subjects were manic energy and manic mood. M had the best area under the curve (0.909), and values of M equal to or greater than 30 yielded 91.5% sensitivity and 74.5% specificity. CONCLUSION: Structured Clinical Interview for Mood Spectrum has good reliability and validity. Cut-off of 30 best differentiates subjects with bipolar disorder vs. unipolar depression. A cutoff score of 30 or higher in the mania sub-domain is appropriate to help make a distinction between subjects with bipolar disorder and those with unipolar depression. OBJETIVO: Traduzir e validar para o português a Entrevista Clínica Estruturada para Distúrbios do Humor, mensurando sua validade, confiabilidade, bem como definindo os escores para transtornos bipolares. MÉTODO: A entrevista foi traduzida (para o português) e novamente traduzida para o inglês. A amostra incluiu 47 indivíduos com transtornos bipolares, 47 com transtorno depressivo maior, 18 com esquizofrenia e 22 controles. A confiabilidade entre avaliadores foi testada em 20 indivíduos com transtornos bipolares e transtorno depressivo maior. A consistência interna foi mensurada por meio da fórmula de Kuder Richardson. Análise discriminante foi realizada. Escores dos diversos grupos foram comparados; limiares para mania (M), depressão (D) e valores totais foram calculados usando curvas de "receiver operating characteristic" (ROC). RESULTADOS: Coeficientes de Kuder Richardson ficaram entre 0,86 e 0,94. O coeficiente de correlação intraclasse foi de 0,96 (IC 95% 0,93-0,97). Participantes com transtornos bipolares apresentaram escores M e T aumentados, e escores D semelhantes aos do grupo transtorno depressivo maior (ANOVA, p < 0,001). Os subdomínios que melhor discriminaram indivíduos com doença uni ou bipolar foram energia maníaca e humor maníaco. M apresentou a melhor área sob a curva (0,909); valores de M igual ou superiores a 30 associaram-se a sensibilidade de 91,5% e especificidade de 74,5%. CONCLUSÃO: Entrevista Clínica Estruturada para Distúrbios do Humor apresenta boa validade e reliabilidade. Escore de mania igual ou superior a 30 adequadamente diferencia transtornos bipolares de depressão unipolar.

Indices of agreement of six definitions of mania and four definitions of schizoaffective mania were calculated in a series of 81 manically disturbed patients. In particular, the concordance of the manic triad definition of overactivity, pressure of speech, and manic mood with stricter definitions was measured. The agreement among criteria was generally low for mania and even lower for schizoaffective mania. Although the manic triad definition diagnoses a wider range of patients, its coverage is less than might be expected from the small number of symptoms included in the definition. Tighter constructs of mania generally do not seem much more valid.

Patients suffering from mania are overactive, intrusive, excited, and belligerent. They may believe that they have special powers, are related to public figures, and can read the minds of others. They spend money lavishly. Voices on the radio or television are sometimes understood as personal communications. They speak rapidly, with illogical and confused thoughts, move constantly, and write page after page of nonsense. They typically sleep and eat poorly, have little interest in work, friends, or family, and often require restraint or seclusion. Suicide is a perpetual threat. Some manic patients are likable, while others are angry and frightening. Psychosis is a frequent feature. Manic patients believe that their parents are not their real parents, asserting that they have royal blood. They believe that they can predict the future. They know that others are watching or talking about them, and they hear voices when no one is present. Delusional mania requires more intensive treatment and almost always hospital care. In older classifications of psychiatric illnesses, these patients were considered to be suffering from a manic-depressive illness. In modern classification, this term has been discarded and the illness is now conceived as bipolar disorder for patients with manic and depressive features and major depression for those with depressive symptoms only. Bipolar disorders, ranging from mild to severe, are divided into numerous subtypes. The variety of symptoms that admit the diagnosis of bipolar disorder has led to a virtual epidemic of diagnoses of the condition. Many patients so labeled do not exhibit the sleep difficulty, loss of appetite, and loss of weight, or the severity of illness, that were the criteria for manic-depressive illness. In manic-depressive illness, the manic episode persists for hours, days, weeks, or months and interferes with normal living. Once the episode resolves, it may suddenly recur; or manic episodes may alternate with periods of depression, or occur as simultaneous mixed episodes of depression and mania. When the shift in mood from mania to depression takes place within one or a few days, the condition is labeled rapid cycling, a particularly malignant form of the illness. In manic-depressive illness, the manic episode persists for hours, days, weeks, or months and interferes with normal living.

Objective This article is one of the series of review articles aiming to present a convenient guideline for practicing clinicians in their selection of scales for clinical and research purposes. This article focuses on assessment scales for mood (depression, mania). Methods After reviewing the basic principles of clinical psychometrics, we present a selective review of representative scales measuring depressed or manic mood. Results We reviewed and reported on reliability, validity, interpretability, and feasibility of the following rating scales: Patient Health Questionnaire-9 (PHQ-9), K6, Beck Depression Inventory II (BDI-II), and Quick Inventory of Depressive Symptomatology Self-Report (QIDS-SR) as self-report scales for depressed mood; Hamilton Rating Scale for Depression (HAM-D) and Montgomery–Asberg Depression Rating Scale (MADRS) as clinician-administered measure for depression; and Young Mania Rating Scale (YMRS) as a clinician-administered instrument for mania. Conclusion Although the rating scales for mood represent a well-trodden terrain, this brief review of the most frequently used scales in the literature revealed there is still some room for improvement and for further research, especially with regard to their clinical interpretability.

Summary Computerized evaluation of pauses between spoken words can be conducted in the medical office or over the telephone. Frequency and duration of long speech hesitation pauses (LP = > 1 sec.) can be correlated with coronary-risk and mood. Pauses of 100 + msec are sorted into many fluency levels. Peak fluency of LP irrespective of pause-time, and at maximal pause-time, are behavioral correlates of mood. At intermediate fluency they are explained by left-hemisphere, right-hemisphere and interhemispheric transit, respectively. Short pauses (SP = < 1 sec.) sorted at these fluency nodes monitor competence of asymmetric and interhemispheric brain functions. Diurnal mood variation is monitored by comparing the morning and evening frequency and duration of the patient's pauses. The frequency of pauses within < 1.16 second may diagnose manic mood modulated by the basal region of the right temporal lobe. LP and SP may monitor interrelationships among mood and thought disorders subserved by the left dorsal pref...

In order to determine whether epigenetic changes specific to the manic mood state can be detected in peripheral blood samples we assayed DNA methylation levels genome-wide in serum samples obtained from 20 patients hospitalized for mania and 20 unaffected controls using the Illumina 450K methylation arrays. We identified a methylation locus in the CYP11A1 gene, which is regulated by corticotropin, that is hypo-methylated in individuals hospitalized for mania compared with unaffected controls. DNA methylation levels at this locus appear to be state related as levels in follow-up samples collected from mania patients six months after hospitalization were similar to those observed in controls. In addition, we found that methylation levels at the CYP11A1 locus were significantly correlated with three inflammatory markers in serum in acute mania cases but not in unaffected controls. We conclude that mania is associated with alterations in levels of DNA methylation and inflammatory markers. Since epigenetic markers are potentially malleable, a better understanding of the role of epigenetics may lead to new methods for the prevention and treatment of mood disorders.

In the present study, we report seven cases,two with manic mood syndrome with evidence of organicity, and five of bipolar disorder, manic displaying transient grasp reflex, magnet reaction and palmomental reflex

Background Bipolar disorder is characterized by depressive and manic mood episodes. Despite an overall high heritability, environmental factors play a critical role in bipolar disorder. Stress negatively influences the clinical course bipolar disorder and may trigger mood episodes. Surprisingly, the study of stress reactivity in bipolar patients has remained relatively unexplored. Moreover, it is unknown whether altered stress reactivity may be a trait marker in unaffected siblings of bipolar disorder patients who possess an increased genetic risk for this disorder. Methods Male and female euthymic bipolar disorder patients (N=49), unaffected siblings (N=27) and healthy controls (N=48) were exposed to a validated social stress test. The endocrine stress response was measured using saliva cortisol levels, whereas salivary alpha-amylase (sAA) were determined as an index for the adrenergic stress response. Results Exposure to stress resulted in a differential endocrine and adrenergic stress reactivity between bipolar disorder patients and their unaffected sibling. Importantly, bipolar disorder patients displayed a blunted endocrine but exaggerated adrenergic response. Conclusions Our findings illustrate the importance of measuring stress reactivity in bipolar disorder. These results provide insight into stress system functionality of euthymic bipolar disorder and enable a direct comparison with unaffected siblings who display an increased risk but have not developed bipolar disorder.

Considerable evidence implicates the neurotransmitter gamma-aminobutyric acid (GABA) in the biochemical pathophysiology of mood disorders. Animal models of depression show regional brain GABA deficits and GABA agonists have antidepressant activity in these models. Somatic treatments for depression and mania upregulate the GABAB receptor, similar to the effect of GABA agonists. Clinical data indicate that decreased GABA function accompanies depressed or manic mood states. GABA agonists are effective antidepressant and antimanic agents. Low GABA levels are found in brain, cerebrospinal fluid and plasma of patients with depression and in plasma of patients with mania. Plasma GABA levels, which reflect brain GABA, are not normalized with treatment and clinical remission in depression, suggesting low GABA is not a marker for mood state. Some somatic treatments, including valproic acid and electroconvulsive shock, reduced plasma GABA and response to these correlates with higher levels of baseline plasma GABA. From these data, a GABA hypothesis for mood disorders is formulated. Low GABA function is proposed to be an inherited biological marker of vulnerability for development of mood disorders. Environmental factors, including stress and excessive alcohol use, may increase GABA, causing symptoms of depression or mania. Treatment, or the passage of time, then returns GABA to its presymptomatic baseline as the symptoms remit. This hypothesis, applicable to a subset of mood disordered persons, is testable.

Catatonia was delineated only as a type of schizophrenia in the many American Psychiatric Association DSM classifications and revisions from 1952 until 1994 when “catatonia secondary to a medical condition” was added. Since the 1970s the diagnosis of catatonia has been clarified as a syndrome of rigidity, posturing, mutism, negativism, and other motor signs of acute onset. It is found in about 10% of psychiatric hospital admissions, in patients with depressed and manic mood states and in toxic states. It is quickly treatable to remission by benzodiazepines and by ECT. The DSM-V revision proposes catatonia in two major diagnostic classes, specifiers for 10 principal diagnoses, and deletion of the designation of schizophrenia, catatonic type. This complex recommendation serves no clinical or research purpose and confuses treatment options. Catatonia is best considered in the proposed ICD revision as a unique syndrome of multiple forms warranting a single unique defined class similar to that of delirium.

Background. Previous work suggests that subthreshold depression and Subthreshold (hypo)mania are common, although little is known about the prognosis in terms of transition to clinical disorder. This paper presents data on the temporal relationship between subthreshold and clinical expression of mood phenotypes. Method. In a random general population sample of 7076 individuals, symptoms of depression and (hypo)mania were measured with the Composite International Diagnostic Interview (CIDI) at baseline, after 1 year, and 2 years later. Results. At baseline, the lifetime prevalences of depressive and (hypo)manic symptoms were 17(.)2% and 1(.)2% respectively. Predictive values of mood symptoms for a DSM-III-R mood disorder ranged from 14(.)3% to 50%. (Hypo)manic mood symptoms had much higher predictive values than unipolar manifestations, not only for bipolar disorder but also for major depression. Conclusions. The subthreshold expressions of depression and (hypo)mania are prevalent and continuous with more severe clinical states. The cross-prediction of mood symptoms may Support a continuum from depressive to (hypo)manic symptoms. The high predictive value of (hypo)manic symptoms for mood disorders suggests that the experience of (hypo)manic symptoms is a stronger indicator of vulnerability for mood dysregulation than the experience of depressive symptoms.

• We measured motor activity with a self-contained monitoring device worn on the wrists of affectively ill patients and volunteer normal control subjects. Decreases in the daytime motor activity level were observed in depressed patients, compared with their improved (euthymic) or manic mood states. Moreover, affectively ill patients, even during euthymic periods, showed lower daytime motor activity levels than the control group housed in the same ward. These data provide objective evidence for decreases in motor activity that occur concomitantly with the depressive phase of illness in patients with affective disorder, and fluctuate in patients in euthymic or manic phases.