Manic Phase Research Articles

Study of 45 candidate genes suggests CACNG2 may be associated with lithium response in bipolar disorder

BackgroundBipolar disorder is a neuropsychiatric disorder that is characterized by fluctuations between manic and depressive phases. Lithium is the original and best mood stabilizing treatment for bipolar disorder. While its mechanism is not well understood, it is believed to have a strong genetic component, as several studies suggest that lithium responsiveness, in bipolar disorder, is heritable. In this study we aimed to identify genetic variants that are associated with lithium responsiveness in bipolar disorder. MethodsHere we present two cohorts; a retrospective cohort in which patients were surveyed about their response to lithium, and a prospective cohort, in which patients were placed on a lithium monotherapy and monitored for their response to lithium. In both cohorts, patients were stratified into two categories in terms of lithium response; good responders and poor responders. 45 genes were selected based on previous associations with lithium pathways or bipolar disorder and 684 SNPs within these genes were selected to test for association with lithium response. ResultsWhile no single SNP was significant after correcting for multiple comparisons, there were several that were nominally significant (p < 0.05). Of these nominally significant SNPs, the most highly significant SNP in both the prospective and retrospective cohorts were found to be in CACNG2, or Stargazin. The second best association with lithium response was several SNPs in NRG1, a gene that has previously been associated with schizophrenia. ConclusionsEvidence for the association of lithium response with SNPs in CACNG2 is consistent with previous findings that have identified CACNG2 as associated with both bipolar disorder and lithium responsiveness.

Using Lithium in Older Age Bipolar Disorder: Special Considerations.

Lithium is the gold-standard treatment for bipolar disorder, and is effective in the management of manic, depressive, and maintenance phases of bipolar disorder treatment. Despite this, the implications of lithium use in the older population remain less understood. This critical narrative review aims to better understand the impact of lithium in older age bipolar disorder (OABD), including tolerability and efficacy, based on up-to-date evidence. Relevant studies of efficacy, effectiveness, and tolerability published any time prior to May 2018 were identified using the PubMed keyword search "lithium older adult bipolar disorder" and references from recent international bipolar disorder guidelines. One randomized controlled trial was identified, the GERI-BD (Acute Pharmacotherapy in Late-Life Mania) study. This study found lithium to be effective in late-life mania and hypomania. The remaining literature examining lithium in OABD was reviewed, comprising of a number of small open-label and retrospective studies, with special considerations highlighted. In summary, there is a small yet increasing geriatric evidence base that lithium is effective in OABD. Although there can be adverse effects with lithium, it is generally well tolerated, and there are methods to minimize these risks. Further research would strengthen the evidence base for lithium therapy in OABD. In the meantime, lithium remains the gold-standard treatment for OABD.

Effect size of lithium, carbamazepine, and sodium valproate in child and adolescent bipolar 1 disorder during manic phase: A prospective open-label study.

Aim:The aim was to evaluate the “effect size (ES),” tolerability, and acceptability of lithium, carbamazepine, and sodium valproate in the acute phase treatment of pediatric Bipolar 1 disorder patients during manic phase.Materials and Methods:This hospital-based, prospective, open-label study included 67 patients in manic phase of bipolar I disorder, aged 6–17 years, after informed consent by the caregivers. The patients were randomly assigned to the lithium group (n = 30), carbamazepine group (n = 20), and sodium valproate group (n = 17). They were assessed with the Schedule for Affective Disorders for School Age Children’s-Present and Life time version administered to the parent and child separately, Conner’s Abbreviated Rating Scale, and Cassidy Scale for Manic States (CSMS). Lithium was started in the dose of 30 mg per kg of body weight, carbamazepine in the dose of 10–20 mg/kg/day, and sodium valproate in the dose of 10–20 mg/kg body weight. Antipsychotic (chlorpromazine [CPZ] 100–500 mg per day or haloperidol up to 750 mg of CPZ equivalent) was allowed in the study. Injection haloperidol 10 mg and injection promethazine 50 mg intramuscular were allowed for initial 3–5 days to combat acute agitation. Rescue medication such as injection lorazepam 2–4 mg intramuscular was allowed throughout the study duration. The patients were rated weekly on CSMS, Bipolar Clinical Global Impression, Udvalg for kliniske Undersogelser Side Effect Rating Scale, and side effect checklist for lithium, sodium valproate, and carbamazepine, respectively. The serum level of concerned drug was obtained at weekly intervals and dose hiked, if needed to get target serum level.Results:The response rate was 90% in lithium group, 70% in carbamazepine group, and 88% in sodium valproate group on the basis of ≥33% reduction from baseline CSMS. The effects of change of CSMS over the 6 weeks across the three treatment group were found to be highly statistically significant.Conclusions:In the acute phase treatment of pediatric bipolar 1 disorder patients during manic phase, the ES for lithium was 0.85, for carbamazepine 0.71, and for sodium valproate 0.84. These agents are well tolerated in treating bipolar disorder in children.

Serum BICC1 levels are significantly different in various mood disorders.

PurposeMood disorders are recurrent chronic disorders with fluctuating mood states and energy, and misdiagnosis is common when based solely on clinical interviews because of overlapping symptoms. Because misdiagnosis may lead to inappropriate treatment and poor prognosis, finding an easily implemented objective tool for the discrimination of different mood disorders is very necessary and urgent. However, there has been no accepted objective tool until now. Recently, BICC1 has been identified as a candidate gene relating to major depressive disorder (MDD). Therefore, the aim of this study is to evaluate the ability of serum BICC1 to discriminate between various mood disorders, including MDD and the manic and depressive phases of bipolar disorder, namely bipolar mania (BM) and bipolar depression (BD).Patients and methodsSerum BICC1 levels in drug-free patients with MDD (n=30), BM (n=30), and BD (n=13), and well-matched healthy controls (HC, n=30) were measured with ELISA kits. Pearson correlation analyses were used to analyze the correlations between serum BICC1 levels and clinical information. Receiver operating characteristic (ROC) curve analysis was used to analyze the differential discriminative potential of BICC1 for different mood disorders.ResultsOne-way ANOVA indicated that serum BICC1 levels were significantly increased in all patient groups compared with the HC group and significantly different between each pair of patient groups. Correlation analyses found no relationship between serum BICC1 levels and any clinical variables in any study group. ROC curve analysis showed that serum BICC1 could discriminate among all three mood disorders from each other accurately with fair-to-excellent discriminatory capacity (area under the ROC curve from 0.787 to 1.0).ConclusionThe findings of this preliminary study indicated significant differences in serum BICC1 levels in patients with different mood disorders. This study provides preliminary evidence that serum BICC1 may be regarded as a promising, objective, easy-to-use tool for diagnosing different mood disorders.

Bipolar Disorder: Its Etiology and How to Model in Rodents.

Characterized by the switch of manic and depressive phases, bipolar disorder was described as early as the fifth century BC. Nevertheless up to date, the underlying neurobiology is still largely unclear, assuming a multifactor genesis with both biological-genetic and psychosocial factors. Significant process has been achieved in recent years in researching the causes of bipolar disorder with modern molecular biological (e.g., genetic and epigenetic studies) and imaging techniques (e.g., positron emission tomography (PET) and functional magnetic resonance imaging (fMRI)). In this chapter we will first summarize our recent knowledge on the etiology of bipolar disorder. We then discuss how several factors observed to contribute to bipolar disorder in human patients can be manipulated to generate rodent models for bipolar disorder. Finally, we will give an overview on behavioral test that can be used to assess bipolar-disorder-like behavior in rodents.

Lithium therapy in bipolar disorder is associated with higher in-vivo cortical neurite density

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.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 .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.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.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.

Gene expression pattern of CCL2, CCL3, and CXCL8 in patients with bipolar disorder.

Background:Bipolar disorder (BD) is one of the most important psychiatric disorders in the world. There is evidence suggesting the role of inflammatory mediators such as chemokines in the etiology of BD. The objective of the current study was to evaluate the gene expression of CCL2, CCL3, and CXCL8 in patients with BD and compare them to healthy controls.Materials and Methods:A total of 48 patients with confirmed BD and 48 healthy controls enrolled in this study. All patients were recruited from April to August 2016 at Ibn-Sina Psychiatric Hospital, Mashhad University of Medical Sciences, Mashhad, Iran. RNA was extracted from the whole blood samples and then cDNA was synthesized. Gene expression of CCL2, CCL3, and CXCL8 was measured using SYBR® Green real-time polymerase chain reaction. The difference of delta-CT values between patients and healthy controls was compared with the independent samples t-tests.Results:CCL2 and CXCL8 genes expressed at higher levels in patients with BD as compared to healthy controls, but not significant. On the contrary, we found lower expression levels for CCL3 gene in our patients compared to healthy controls, but the difference was not statistically significant.Conclusion:Our findings do not show an association between the gene expression of CCL2, CCL3 and CXCL8 and BD. Increasing the sample size and evaluation on the gene expression of other chemokines in depression and mania phases of BD might be helpful to get a better conclusion.

Executive Functions in Bipolar Affective Disorder During Remission Phase of Mania

Background: Executive function is one of the important part of cognitive abilities that regulate our decision making and problem solving process. Generally it waxes and wanes in concert with the clinical symptoms of bipolar disorder. Though, it is still unclear that improvement in executive functions simply legs behind normalization of mood. Purpose: Present study was conducted to expend the limited knowledge base regarding executive function in bipolar affective disorder (mania) to reveal the controversial issue in bipolar affective disorder so that a new dimension could be added while making a prognosis of the illness and a management plan. Methods: Executive function was assessed to 80 adult bipolar affective disorder patients with current episode of mania during remission phase equally included by gender. Only those patients were included fulfilling less than five years of illness and had two to three episodes. All they were assessed on Wisconsin Card Sorting Test and compared to normal control. Result: Findings suggested impairment in domains of executive function. 41.3% patients performed poorer to normal control. They significantly performed poorer in all dimension of WCST except in non-perseverative errors, percent non-perseverative errors and failure to maintain set variable. But when compared on different dysfunction categories patients group did not significantly differ to each other on variables non-perseverative errors, percent non-perseverative errors, conceptual level responses, percent conceptual level responses, and failure to maintain set. Further, age, sex and education were to be found significantly influencing the performance on some variables of WCST. Conclusion: Undoubtedly, ample number of patients of bipolar affective disorder with manic episode does not reach to optimum level of their executive abilities during normal or remission phase of the illness and need consideration while managing them.

Predominant polarity in bipolar I and II disorders: A five-year follow-up study.

Patients with bipolar disorder (BD) differ in their relative predominance of types of episodes, yielding predominant polarity, which has important treatment implications. However, few prospective studies of predominant polarity exist. In the Jorvi Bipolar Study (JoBS), a regionally representative cohort of 191 BD I and BD II in- and outpatients was followed for five years using life-chart methodology. Differences between depressive (DP), manic (MP), and no predominant polarity (NP) groups were examined regarding time ill, incidence of suicide attempts, and comorbidity. At baseline, 16% of patients had MP, 36% DP, and 48% NP. During the follow-up the MP group spent significantly more time euthymic, less time in major depressive episodes, and more time in manic states than the DP and NP groups. The MP group had significantly lower incidence of suicide attempts than the DP and NP group, lower prevalence of comorbid anxiety disorders but more psychotic symptoms lifetime and more often (hypo)manic first phase of the illness than the DP group. Classification of predominant polarity was influenced by the timeframe used. The retrospective counting of former phases is vulnerable to recall bias. Assignment of dominant polarity may necessitate a sufficient number of illness phases. Predominant polarity has predictive value in predicting group differences in course of illness, but individual patients' classification may change over time. Patients with manic polarity may represent a more distinct subgroup than the two others regarding illness course, suicide attempts, and psychiatric comorbidity.

Mental Capacity and Decision Making in Bipolar Disorder

Bipolar disorder is a chronic, recurrent and potentially debilitating illness characterised by fluctuations in mood state and energy, which is associated with significant impairments in cognitive, social and everyday functioning. Difficulties appear especially in the manic or depressive phase, but this disorder allows more than half of these patients to have a normal life and make their own decisions when no severe symptoms appear, which is in these patients for most of their life.

An Interesting Case of Carbamazepine-Induced Stevens-Johnson Syndrome.

A 29-year-old Black female patient was admitted to a psychiatric ward with symptoms of major depressive disorder with psychosis. The patient was started on amitriptyline 50 mg/day and haloperidol 10 mg/day. On day 4 post-admission, the preferred first-line antidepressant, fluoxetine, became available and the patient was switched from amitriptyline to fluoxetine 20 mg/day. On the same day, the dose of haloperidol was reduced to 5 mg/day. Thirteen days post-initiation of these medications the patient became talkative, associated with emotional lability, an expansive mood, irritability and restlessness. The working diagnosis was changed to bipolar affective disorder in the manic phase. Fluoxetine was discontinued and carbamazepine 600 mg/day was added to the patient’s treatment regimen. Her manic symptoms started to resolve; however, 14 days post-initiation of carbamazepine, the patient had a fever; itchy, discharging eyes; respiratory distress; generalised symmetrical erythematosus rash; buccal ulceration; and conjunctival injection with difficulty opening her eyes. Carbamazepine was immediately discontinued and the patient received intravenous fluid resuscitation. The patient recovered considerably after 12 days of symptomatic and supportive management, and was transferred back to the psychiatric ward for the continuation of bipolar disorder management. Lithium therapy was instituted and the patient was subsequently discharged. Using the Algorithm of Drug causality for Epidermal Necrolysis (ALDEN) Stevens–Johnson Syndrome/toxic epidermal necrolysis (SJS/TEN) drug causality scoring system, carbamazepine and fluoxetine were evaluated as ‘very probable’ and ‘possible’ causes of SJS, respectively, in this patient. Fluoxetine-induced SJS was considered on account of previous case reports, however no evidence of causality was found in this patient. Consecutive administration with a potential increase in carbamazepine due to inhibition of cytochrome P450 (CYP) 3A4 metabolism by fluoxetine was also not ruled out. A diagnosis of carbamazepine-induced SJS was made and was considered an idiosyncratic adverse drug reaction.

The metabolic basis of psychosis in bipolar disorder: A positron emission tomography study.

Psychotic symptoms are a common feature in bipolar disorder (BD), especially during manic phases, and are associated with a more severe course of illness. However, not all bipolar subjects experience psychosis during the course of their illness, and this difference often guides assessment and pharmacological treatment. The aim of the present study is to elucidate, for the first time, the FDG uptake dysfunctions associated with psychosis in BD patients with and without a history of past psychotic symptoms, through a positron emission tomography (PET) approach. Fifty BD patients with lifetime psychotic symptoms, 40 BD patients without lifetime psychotic symptoms and 27 healthy controls (HC) were recruited and underwent an 18F-FDG-PET session. Compared to HC, BD subjects shared common FDG uptake deficits in several brain areas, including insula, inferior temporal gyrus and middle occipital gyrus. Moreover, we found that BD patients with a history of past psychotic symptoms had a unique FDG uptake alteration in the right fusiform gyrus compared to both BD patients without lifetime psychotic symptoms and HC (all P<0.01, cFWE corrected). Overall, our results suggest that FDG uptake alterations in brain regions involved in emotion regulation are a key feature of BD, regardless the presence of past psychosis. Finally, we demonstrated that the FDG uptake reduction in fusiform gyrus is associated with the presence of past psychotic symptoms in BD, ultimately leading towards the idea that the fusiform gyrus might be considered a putative biomarker of psychosis.

Altered amygdala circuits underlying valence processing among manic and depressed phases in bipolar adults

BackgroundDisruptions 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. MethodsThe 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 . ResultsBeta-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. LimitationsAs 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. ConclusionsThese 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.

Opposing patterns of neuronal variability in the sensorimotor network mediate cyclothymic and depressive temperaments.

Affective temperaments have been described since the early 20th century and may play a central role in psychiatric illnesses, such as bipolar disorder (BD). However, the neuronal basis of temperament is still unclear. We investigated the relationship of temperament with neuronal variability in the resting state signal-measured by fractional standard deviation (fSD) of Blood-Oxygen-Level Dependent signal-of the different large-scale networks, that is, sensorimotor network (SMN), along with default-mode, salience and central executive networks, in standard frequency band (SFB) and its sub-frequencies slow4 and slow5, in a large sample of healthy subject (HC, n = 109), as well as in the various temperamental subgroups (i.e., cyclothymic, hyperthymic, depressive, and irritable). A replication study on an independent dataset of 121 HC was then performed. SMN fSD positively correlated with cyclothymic z-score and was significantly increased in the cyclothymic temperament compared to the depressive temperament subgroups, in both SFB and slow4. We replicated our findings in the independent dataset. A relationship between cyclothymic temperament and neuronal variability, an index of intrinsic neuronal activity, in the SMN was found. Cyclothymic and depressive temperaments were associated with opposite changes in the SMN variability, resembling changes previously described in manic and depressive phases of BD. These findings shed a novel light on the neural basis of affective temperament and also carry important implications for the understanding of a potential dimensional continuum between affective temperaments and BD, on both psychological and neuronal levels.

Auditory–Visual Speech Integration in Bipolar Disorder: A Preliminary Study

This study aimed to investigate how individuals with bipolar disorder integrate auditory and visual speech information compared to healthy individuals. Furthermore, we wanted to see whether there were any differences between manic and depressive episode bipolar disorder patients with respect to auditory and visual speech integration. It was hypothesized that the bipolar group’s auditory–visual speech integration would be weaker than that of the control group. Further, it was predicted that those in the manic phase of bipolar disorder would integrate visual speech information more robustly than their depressive phase counterparts. To examine these predictions, a McGurk effect paradigm with an identification task was used with typical auditory–visual (AV) speech stimuli. Additionally, auditory-only (AO) and visual-only (VO, lip-reading) speech perceptions were also tested. The dependent variable for the AV stimuli was the amount of visual speech influence. The dependent variables for AO and VO stimuli were accurate modality-based responses. Results showed that the disordered and control groups did not differ in AV speech integration and AO speech perception. However, there was a striking difference in favour of the healthy group with respect to the VO stimuli. The results suggest the need for further research whereby both behavioural and physiological data are collected simultaneously. This will help us understand the full dynamics of how auditory and visual speech information are integrated in people with bipolar disorder.

Exploring mania-associated white matter injury by comparison with multiple sclerosis: a diffusion tensor imaging study

Bipolar disorder (BD), especially in its active phases, has shown some neuroimaging and immunological similarities with multiple sclerosis (MS). The objective of this study was to compare white matter (WM) alterations in BD patients in manic phase (M-BD) and MS patients at early stage of disease and with low lesion burden. We compared diffusion tensor imaging (DTI)-derived fractional anisotropy (FA), mean diffusivity (MD) and radial diffusivity (RD) in a priori selected WM regions (i.e., corpus callosum and cingulum) betwixt 23 M-BD, 23 MS patients and 46 healthy controls. Both M-BD and MS showed WM changes in the corpus callosum, which, however, showed a greater impairment in MS patients. However, considering the different sub-regions of corpus callosum separately (i.e., genu, body, splenium), M-BD and MS presented an opposite pattern in spatial distribution of WM microstructure alterations, with a greater impairment in the anterior region in M-BD and in the posterior region in MS. Common features as well as divergent patterns in DTI changes are detected in M-BD and early MS, prompting a deeper investigation of analogies and differences in WM and immunological alterations of these disorders.

NEUROEPIGENETICS OF BIPOLAR DIATHESIS: FROM THE SYNDROME OF MENTAL IMMUNE PROFICIENCY TO THE SYNDROME OF MENTAL IMMUNE DEFICIENCY

The aim of the article is the conceptual and methodological substantiation of epigenetic dysfunctions of mental immunity in the development of bipolar diathesis, represented by pre-nosological states and syndromes of mental immune proficiency (SMIP) and deficiency (SMID). In the onset of bipolar disorder (BD), these syndromes evolve into the manic phase (MPh) and/or depressive phase (DPh) of the disease. The allocated syndromes transgenerationally accumulate epigenetic labels of future possible BD and other mental diseases. Their pre-nosological functional diagnostics allows for screening and early prevention of mental disorders. These syndromes are the initial dysfunctional link in the development of the mental epidemiological cascade: mental epidemics - destructive mental epidemics - the pandemic of mental immune deficiency. Pandemic of mental immune deficiency is manifested by an increase in the prevalence of all mental and psychosomatic disorders, requiring a shift in the focus of preventive-corrective efforts to early pre-nosological fractals of the disease development. The clinical model of BD shows the pathoplastics and pathokinetics of mental immunity dysfunctions in the development of the disease. Mental immunity as an identity matrix predetermines the lateral mental constitution of the personality and the resources of its mental resilience. It is suggested to consider the clinic of mixed forms of BD as a manifestation of the ambidextral mental constitution. In the development of the BD, three pre-nosological fractals are distinguished: 1) predisposition - a bipolar family; 2) latent - bipolar diathesis (SMIP/SMID); 3) initial - the onset of the BD; and three nosological: 4) the full-scale clinical picture of BD (MPh and/or DPh); 5) chronization - the types and forms of the course; 6) outcome - somatopsychic and socio-moral complications.

Thiol/disulphide homeostasis in manic episode and remission phases of bipolar disorder

Purpose: Bipolar disorder (BD) is a chronical psychiatric disorder of which pathophysiology was demonstrated to be related with oxidative stress. Thiol–disulphide homeostasis is an indicator of oxidative balance. This study aims to investigate thiol–disulphide homeostasis in BD.Materials and methods: 27 patients in manic episode (MA), 29 patients in remission (RE) and 60 healthy participants (HC) were included to the study. Serum native thiol and total thiol levels were measured with a novel colorimetric, automated method. The disulphide levels and disulphide/native thiol ratios were also calculated from these measured parameters.Results: Native thiol levels and total thiol levels of both MA and RE groups were lower than HC. No significant difference detected between MA and RE in terms of native thiol levels and total thiol levels. Disulphide levels and disulphide/native thiol ratio was detected statistically similar between three groups.Conclusion: Our results support the oxidative imbalance theory in pathophysiology of BD. Further studies with larger sample sizes are needed for being able to understand these pathways in detail and use them as a target of treatment.

Increased Serum C3 and Decreased UA in Patients of Bipolar Disorder in Chinese Han Population.

The aim of this study is to explore the changes and clinical significance of serum C3, C4, hypersensitive C-reactive protein (hsCRP) and uric acid (UA) in patients of bipolar disorder (BD). In this case-control study, we recruited 141 BD patients from The Second Xiangya Hospital, Central South University, and 151 age and gender matched healthy controls (HC) from the health management central of The Second Xiangya Hospital. These patients were divided into two subgroups based on medicines use: 91 patients were treated with psychiatric drugs and 50 patients were drugs free, or four subgroups based on mood states: 54 patients in manic/hypomanic phase, 30 patients in depressive phase, 52 patients in euthymic phase and 5 patients in mixed phase. Serum levels of C3, C4, hsCRP and UA were measured in all subjects. The serum C3 levels in BD patients (0.9981 ± 0.1849 g/L) were significantly lower than that in HC group (1.0637 ± 0.2186 g/L), especially the drugs free subgroup and the euthymic subgroup (0.975 ± 0.153 and 0.983 ± 0.182 g/L), while the serum UA levels were significantly higher (354.6 ± 90.4 vs. 332.9 ± 88.7 μmol/L), especially the drug-treated subgroup and manic/hypomanic subgroup (361.56 ± 93.20 and 376.70 ± 88.89 μmol/L), and rates of hyperuricaemia (31.91 vs. 17.88%) were significantly higher in BD patients than in HC group. The serum C4 and hsCRP levels in HC group showed no significant difference with BD patients in whole or those subgroups. These findings suggested that the complement and purinergic systems of BD patients might be disrupted, the UA levels could be a potential marker in manic phase and the C3 might be the marker of therapeutic evaluation of BD patients.

Assessment of Behavioral Approach and Behavioral Inhibition Systems in Mood Disorders.

Introduction:Psychiatric disorders could be evaluated in terms of behavioral activation and inhibition systems. Dysregulation of these systems may lead to development of manic or depressive episodes in patients with mood disorders. This study aimed to identify Behavioral Approach System (BAS) and Behavioral Inhibition System (BIS) hypersensitivity as the functional brain system behaviors in patients with major depressive disorder and bipolar mood disorder I, compared to healthy individuals.Methods:This case-control study was conducted in Razi Psychiatric Hospital, a mental health referral center in Northwest of Iran. The study consisted of two groups of patients, one with major depressive and the other with bipolar mood disorders and one healthy group. Each group had 40 patients (20 men and 20 women). The study data were collected through BIS and BAS questionnaire, Beck Depression Inventory (BDI-II), Young Mania Rating Scale (YMRS). The obtained data were analyzed by SPSS version 18.Results:The findings showed a significant negative correlation between BIS, BAS and BAS subscales with the severity of depression and positive correlation with mania symptoms (P<0.05).Conclusion:BAS and BIS dysregulations may predispose people to mood disorder symptoms. BAS is hyperactive during manic phase and may predict the symptom severity of bipolar mood disorder.