Parasympathetic and sympathetic activity are associated with individual differences in neural indices of selective attention in adults

Multiple theoretical frameworks posit that interactions between the autonomic nervous system and higher‐order neural networks are crucial for cognitive and emotion regulation. However, few studies have directly examined the relationship between measures of autonomic physiology and brain activity during cognitive tasks, and fewer studies have examined both the parasympathetic and sympathetic autonomic branches when doing so. Here, 93 adults completed an ERP auditory selective attention task concurrently with measures of parasympathetic activity (high‐frequency heart rate variability; HF‐HRV) and sympathetic activity (preejection period; PEP). We focus on the well‐studied N1 ERP component to test for associations with baseline values of HF‐HRV and PEP. Individuals with higher resting HF‐HRV and shorter resting PEP showed larger effects of selective attention on their ERPs. Follow‐up regression models demonstrated that HF‐HRV and PEP accounted for unique variance in selective attention effects on N1 mean amplitude. These results are consistent with the neurovisceral integration model, such that greater parasympathetic activity is a marker of increased selective attention, as well as other theoretical models that emphasize the role of heightened sympathetic activity in more efficient attention‐related processing. The present findings highlight the importance of autonomic physiology in the study of individual differences in neurocognitive function and, given the foundational role of selective attention across cognitive domains, suggest that both parasympathetic and sympathetic activity may be key to understanding variability in brain function across a variety of cognitive tasks.     

双相障碍抑郁发作患者氧化应激水平

目的:探讨自由基、抗氧化酶在双相障碍抑郁发作病理机制中的作用。方法:采用病例-对照研究设计,对56例符合美国精神障碍诊断与统计手册第4版诊断标准的门诊及住院双相障碍抑郁发作患者(包括双相Ⅰ型组23例及双相Ⅱ型组33例)以汉密尔顿抑郁量表(Hamilton Depression Scale,HAMD)评定抑郁症状,并检测血浆丙二醛(malondialdehyde,MDA)、超氧化物歧化酶(superoxide dismutase,SOD)、过氧化氢酶(catalase,CAT)以及谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)含量,选择32名正常健康人作为对照(对照组),使用单因素方差分析以及多元线性回归分析比较各参数在组间差异及其与HAMD评分之间的关系。结果:双相Ⅰ型和Ⅱ型组MDA水平均高于对照组,SOD、CAT及GSH-Px水平低于对照组,差异均有统计学意义;多因素分析显示,在控制身高、体质量指数和年龄等因素后HAMD评分与血浆MDA水平呈正相关(β=0.46,P<0.05),与SOD(β=-0.27,P<0.05)、CAT(β=-0.41,P<0.05)和GSH-PX(β=-0.34,P<0.05)水平呈负相关。结论:氧化应激反应可能参与双相障碍抑郁发作的发生过程,疾病严重程度可能与氧化应激反应失衡有关。     

Mood disorder service genetic database: Morbidity risks for mood disorders in 3,942 first-degree relatives of 671 index cases with single depression,recurrent depression,bipolar I,or bipolar II

There is increasing evidence that genetic factors play a role in the etiology of mood disorders. As a result, relatives of affected individuals are more often asking about their own risks to develop a mood disorder. From 1988 to 1990, all consecutive, unrelated inpatients and outpatients (index cases) presenting to the Mood Disorders Service, Department of Psychiatry, University of British Columbia, had detailed family histories taken, thus creating the Mood Disorders Service Genetic Database. Diagnoses for index cases and their first-degree relatives were made according to Research Diagnostic Criteria and Family History Research Diagnostic Criteria respectively. Morbidity risks for mood disorders were calculated for first-degree relatives (parents, siblings, children—aged 10 and above) of all index cases with a diagnosis of single depression, recurrent depression, bipolar I, or bipolar II disorder. Morbidity risks were calculated using the maximum likelihood approach. Morbidity risk data are presented according to the sex and diagnosis for the index case in an easy reference format for risk counselling. The risks are presented twice, including and excluding data for “high-risk” families whose genetic pedigree is suggestive of “autosomal dominant” inheritance. © 1994 Wiley-Liss, Inc.     

Meditation for treating adults with bipolar disorder II: A multi‐city study

There is a need to generate evidence on whether meditation's core aspect of building and nurturing calm and peace serves as a mood stabilizer for current and recurrent episodes of depression through the acute and maintenance phases of treating bipolar disorder II affected patients. A 2‐year longitudinal multi‐city randomized controlled trial experiment was conducted comprising 311 bipolar disorder II affected patients in the intervention and control group respectively across eight African and Asian cities. The Bipolar Depression Rating Scale (BDRS) was administered with the intervention and control groups that were equal at baseline. Meditation had a positive impact on the intervention group. Post intervention BDRS scores were significantly lower for patients from Asian cities, men, Hindus and Buddhists, middle class, and married patients as well as those who attended all the meditation rounds and regularly self‐practiced. Within the BDRS outcome measure, depressive symptoms were impacted the most as compared with mixed symptoms. Meditation helped alleviate guilt, depressed mood, and helplessness–hopelessness. The meditation programme can be used as a combination therapy along with pharmacological treatment to treat mood instability and depression among patients with bipolar disorder II.     

Schizotypal traits are associated with sleep spindles and rapid eye movement in adolescence

Research suggests an association between schizophrenia and a decrease in sleep spindle activity, as well as a change in sleep architecture. It is unknown how the continuum of psychotic symptoms relates to different features in the sleep electroencephalogram. We set out to examine how sleep architecture and stage 2 spindle activity are associated with schizotypy in a healthy adolescent population. The participants in our study (n = 176, 61% girls) came from a community‐based cohort. Schizotypal traits were evaluated using the Schizotypal Personality Scale (STA) in early adolescence (mean age 12.3 years, SD = 0.5) and the participants underwent ambulatory overnight polysomnography at mean age 16.9 years (SD = 0.1). Sleep was scored in 30‐s epochs into stages 1, 2, 3 and rapid eye movement (REM) sleep. Stage 2 spindles were detected using an automated algorithm. Spindle analyses from central and frontal derivations included spindle duration and density for slow (10–13 Hz) and fast (13–16 Hz) ranges. Covariates included sex and age. Those with the highest STA scores had a higher percentage of REM (B = 2.07 [95% CI, 0.17, 4.0]; p = .03) than those with the lowest scores. Those with the highest scores had shorter spindle duration, as derived from the frontal regions, and a slower oscillation range (B = ?0.04 [95% CI, ?0.07, ?0.01]; p = .023) than those with the lowest scores. We conclude that high levels of schizotypy characteristics measured in early adolescence may be associated with distinguished features of sleep architecture, namely with spindle morphology and a higher proportion of REM sleep.     

Fluoxetine treatment induces dose dependent alterations in depression associated behavior and neural plasticity in female mice

Antidepressant-induced increases in neurogenesis and neurotrophin mobilization in rodents and primates are proposed to be necessary for behavioral efficacy. The current study examines the relationship between the effects of fluoxetine treatment on behavior, cell proliferation and the neurotrophin BDNF in females. Female MRL/MpJ mice were treated acutely (5 and 10 mg/kg) or chronically (2.5, 5 and 10 mg/kg b.i.d.) with fluoxetine and tested in the tail suspension test (TST) and or novelty-induced hypophagia test (NIH), respectively. Mice treated chronically with fluoxetine received 4 (100 mg/kg) injections of 5-bromo-2′-deoxyuridine (BrdU) on the last 4 days of treatment to measure DNA synthesis. The other half of the hippocampus and the frontal cortex was removed and examined for BDNF levels. Fluoxetine treatment decreased immobility in the TST and latency to eat in the NIH test, but only the highest dose of fluoxetine significantly altered behavior in both tests. Chronic treatment with 5 and 10 mg/kg of fluoxetine significantly increased cell proliferation and BDNF levels in the hippocampus. Only chronic treatment with the highest of fluoxetine increased BDNF levels in the frontal cortex. Behavioral measures in the NIH test correlated with BDNF levels in the frontal cortex but not in the hippocampus or with cell proliferation in the hippocampus. These data suggest that females require high doses of fluoxetine for behavioral efficacy regardless of elevations of neurogenesis and BDNF mobilization in the hippocampus. Elevations in BDNF levels in the frontal cortex are related to the behavioral efficacy of fluoxetine.     

Psychological Treatment and Medication for the Mood and Anxiety Disorders: Moderators, Mediators, and Domains of Outcome

Studies that combine pharmacotherapy with psychological treatment for the mood and anxiety disorders must consider the role of moderators (pretreatment variables that specify the conditions under which treatments are effective) and mediators (change mechanisms in the causal pathways between treatments and outcomes) in explaining the impact of experimental treatments. This article gives examples of the kinds of moderators and mediators—both psychosocial and biological—that are important to examine in combination treatment studies. It conceptualizes outcome as involving multiple domains, including mood and anxiety symptoms, life functioning, and illness costs. Research should also examine the appropriate sequencing of pharmacological and psycho-social interventions and how this sequencing may vary from disorder to disorder.     

Attribution retraining group therapy for outpatients with major depression disorder, generalized anxiety disorder, and obsessive-compulsive disorder: a pilot study

The aim of this present study is to examine the efficacy of attribution retraining group therapy (ARGT) and to compare the responses of outpatients with major depression disorder (MDD),generalized anxiety disorder (GAD) and obsessive-compulsive disorder (OCD).We carried out a prospective uncontrolled intervention study with a 8-weeks of ARGT on sixty three outpatients with MDD,GAD or OCD.Hamilton rating scale for depression,Hamilton rating scale for anxiety,Yale-Brown obsessive-compulsive scale,attribution style questionnaire,self-esteem scale,index of well-being,and social disability screening schedule were administered before and after treatment.Significant improvement in symptoms and psychological and social functions from pre-to posttreatment occurred for all participants.The changes favored MDD patients.Our study suggested that ARGT may improve the symptoms and psychological-social functions of MDD,GAD,and OCD patients.MDD patients showed the best response.     

Polymorphisms of BDNF and CACNA1C are not associated with cognitive functioning in bipolar disorder or healthy controls

Introduction: The cause of cognitive dysfunction in bipolar disorder (BD) is not well understood. BDNF and CACNA1C are two susceptibility genes for the disorder that have also been reported to be associated with cognitive deficits in the disorder, but the studies have been small and with conflicting results. We therefore attempted to replicate an association between cognitive dysfunction with the most commonly studied single nucleotide polymorphisms rs6265 and rs1006737.

Methods: Regression models with five aggregated cognitive domains derived from a comprehensive test battery and IQ score were run using directly genotyped risk variants of SNPs rs6265 and rs1006737 as predictors with covariates as appropriate. Models were performed in a clinical sample of Swedish patients with BD (N?=?114) and sex- and age-matched population controls (N?=?104).

Results: No significant associations (regardless of correction for multiple testing) between the BDNF and CACNA1C risk variants and cognitive functioning were found in either patients or controls.

Conclusions: Our results do not support that the common genetic risk variants in rs6265 and rs1006737 are associated with cognitive dysfunction.     

Rest–activity rhythm and sleep characteristics associated with depression symptom severity in strained dementia caregivers

Depression is associated with disturbances to sleep and the 24‐h sleep–wake pattern (known as the rest–activity rhythm: RAR). However, there remains a need to identify the specific sleep/RAR correlates of depression symptom severity in population subgroups, such as strained dementia caregivers, who are at elevated risk for major depressive disorder. We assessed the cross‐sectional associations of sleep/RARs with non‐sleep depression symptom severity among 57 (mean age: 74 years, standard deviation: 7.4) strained dementia caregivers who were currently without clinical depression. We derived sleep measures from polysomnography and actigraphy, modelled RARs using a sigmoidally transformed cosine curve and measured non‐sleep depression symptom severity using the Hamilton Depression Rating Scale (HRDS) with sleep items removed. The following sleep–wake measures were associated with greater depression symptom severity (absolute Spearman's correlations ranged from 0.23 to 0.32): more time awake after sleep onset (WASO), higher RAR middle level (mesor), relatively shorter active periods (alpha), earlier evening settling time (down‐mesor) and less steep RARs (beta). In multivariable analysis, high WASO and low RAR beta were associated independently with depression symptom severity. Predicted non‐sleep HDRS means (95% confidence intervals) in caregivers with and without these characteristics were: normal WASO/beta = 3.7 (2.3–5.0), high WASO/normal beta = 5.5 (3.5–7.6), normal WASO/low beta = 6.3 (3.6–8.9) and high WASO/low beta = 8.1 (5.3–10.9). Thus, in our sample of strained caregivers, greater sleep fragmentation (WASO) and less sustained/sharply segregated resting and active periods (low RAR beta) correlate uniquely with depression symptom severity. Longitudinal studies are needed to establish whether these independent sleep–wake correlates of depression symptoms explain heightened depression risk in dementia caregivers.     

Serotonin‐2C and serotonin‐1A receptor genes are not associated with psychotic symptomatology of mood disorders

The serotonergic system is involved in both pathophysiology and treatment of mood disorders. In the present study we investigated the possible influence of the polymorphisms of the serotonin‐1A and 2C receptor genes on the symptomatology of mood disorders. Eighty‐four inpatients affected by mood disorders (72 bipolar and 12 major depressive disorder) were assessed by the Operational Criteria Checklist for Psychotic Illness to score their lifetime psychotic symptomatology. The subjects were also typed for 5HT1A and 5HT2C variants using polymerase chain reaction techniques. No association was found between 5HT2C and psychopathology as defined by the four symptomatologic factors used as phenotype definition (mania, depression, delusion, and disorganization) even when bipolar subjects were analyzed separately. Only one subject with the 5HT1A variant was observed. Genetic variation at the 5HT1A and 5HT2C receptor genes does not, therefore, play a major role in the pathogenesis of mood disorders symptomatology. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:161–166, 2000. © 2000 Wiley‐Liss, Inc.     

Psychostimulants for managing unipolar and bipolar treatment-resistant melancholic depression: A medium-term evaluation of cost benefits

Background

We earlier reported an open study of 50 unipolar and bipolar treatment resistant depressed patients indicating that psychostimulants may have differential superiority for the melancholic depressive sub-type. We designed an extension study to examine cost benefits of psychostimulants more closely for those only with melancholic depression.

Method

The sample comprised patients clinically diagnosed with melancholic depression who had failed to respond to and/or experienced significant side-effects with at least two antidepressants. Data were collected for 61 unipolar and 51 bipolar II patients receiving a psyschostimulant for a mean interval of 69 weeks. Benefits and side-effects were assessed.

Results

Effectiveness ratings were similar across unipolar and bipolar sub-sets. Psychostimulants were judged as ‘very’ effective for 20% of patients and ‘somewhat’ effective for 50%. Forty percent judged the psychostimulant as being ‘as effective’ or as ‘superior’ to previously prescribed antidepressants, and worthy of being maintained. Significant side-effects were experienced by 40% of patients, requiring medication to be ceased in 12%. Twenty percent of the bipolar patients experienced a worsening of highs.

Limitations

The study was uncontrolled and retrospective, no formal rater-completed or patient-completed interval measures of severity were completed, while diagnostic judgments about melancholic depression and bipolar disorder were clinically judged.

Conclusions

This open study suggests that psychostimulants may be efficacious antidepressant options for managing unipolar and bipolar melancholia, often seemingly having very rapid onset and generally requiring only low doses, and arguing the need for controlled studies in melancholic patients.     

Combined Psychotherapy and Pharmacotherapy for Mood and Anxiety Disorders in Adults: Review and Analysis

Studies suggest a complex relationship between cognitive-behavior therapy (CBT) and pharmacotherapy for the combined treatment of mood disorders and anxiety disorders. Combined treatment for depression may have beneficial effects when applied to patients with chronic depression and in cases to prevent relapse. In bipolar disorder there is evidence for a strong effect of psychosocial treatment on the course of the disorder. In the anxiety disorders, there are some benefits in the short term, but combined treatment may limit the maintenance of treatment gains offered by CBT alone. Combined treatment should not be considered the default treatment for mood and anxiety disorders, with the possible exception of bipolar disorder. Instead, decisions whether combined treatment is worth the added cost and effort should be made in relation to the disorder under treatment, the level of severity or chronicity, and the stage of treatment (e.g., acute vs. relapse prevention).     

Different familial transmission patterns in bipolar I disorder with onset before and after age 25

Gene identification in common disorders such as Alzheimer disease and breast cancer has greatly profited from the use of age of onset as criterion to delineate subgroups of disease characterized by different inheritance patterns. In bipolar affective disorder, where the majority of linkage studies have produced conflicting results, studies reporting clinical characteristics and familial occurrence of disease have suggested that age of onset might serve as an indicator for identifying more homogeneous subgroups of disease. Our study was the first to examine this hypothesis by the means of segregation analysis. We investigated a sample of 177 bipolar I probands recruited from consecutive admissions and their first‐ and second‐degree relatives (2,407 subjects). Probands were subdivided into an early‐onset (n = 107) and a late‐onset group (n = 70) using an age of onset of 25 as a cut‐off point. This age was chosen because the observed age of onset distribution was bimodal with a cut‐off of 25 years. Morbid risks for affective disorder were found significantly higher (P = 0.01) in relatives of probands with an early onset than in probands with late onset of disease. The segregation analysis showed that the disease is transmitted differently in early‐ and late‐onset groups. In the early‐onset group, a non‐Mendelian major gene with a polygenic component was favored while the data in the late‐onset group were compatible with a multifactorial model. This result may have important implications for future molecular studies aiming at the identification of disease‐associated genes. © 2001 Wiley‐Liss, Inc.     

Parental anxiety and depression associated with caring for a child newly diagnosed with type 1 diabetes: opportunities for education and counseling

Objective

To examine demographic and clinical characteristics, such as pediatric parenting stress and self-efficacy for diabetes care, of parents of children newly diagnosed with type 1 diabetes that are associated with parental anxiety and depression.

Methods

102 parents reported on their levels of depression (CESD), state anxiety (STAI), pediatric parenting stress (PIP), and self-efficacy for diabetes care (SED) within 4 weeks of their child's diagnosis with type 1 diabetes. Data were analyzed using hierarchical multiple regression.

Results

Parents’ scores in the clinical range for depression and anxiety were associated with increased frequency and difficulty of pediatric parenting stress, and there was a trend for depression to be related to lower self-efficacy for diabetes care. The association of female gender with anxiety and depression was partially mediated by more frequent pediatric parenting stress.

Conclusion

Parents of children newly diagnosed with type 1 diabetes are at risk for experiencing anxiety and depression, related, in part, to their experiences of pediatric parenting stress.

Practice implications

Providers and educators should be aware of the risk for depression and anxiety in parents and should work to decrease pediatric parenting stress, increase self-efficacy, and refer parents who are experiencing significant anxiety or depression following their child's diagnosis to a mental health specialist.