Mood Recovery Research Articles

A Meta-Analysis Evaluating the Effectiveness of Two Different Upper Limb Hemiparesis Interventions on Improving Health-Related Quality of Life Following Stroke

Purpose: The aim of this article is to quantitatively assess the efficacy of different upper limb interventions on health-related quality of life (QOL) in stroke patients. Method: Two botulinum type A injection (BTX-A) studies and 4 constraint-induced movement therapy (CIMT) studies were separately combined in a meta-analysis using a fixed effects model. QOL mean scores were extracted and transformed into weighted mean differences. Results: Combined, the BTX-A studies showed no significant improvements in overall health-related QOL. Similarly, a meta-analysis of 4 CIMT studies revealed nonsignificant findings for the domains of activities of daily living, communication, and hand function. A separate meta-analysis of 3 CIMT studies showed a significant increase in strength scores (P = .007); however, sensitivity analysis for this domain due to significant heterogeneity led to a newP value of .078, showing a nonsignificant increase in strength. Further results for memory, mobility, mood, participation, and overall recovery were all nonsignificant. Conclusion: This report did not show these types of upper limb interventions to be effective in improving health-related QOL in the poststroke population.

Attentional biases and the persistence of sad mood in major depressive disorder.

This study examined whether attentional biases for emotional information are associated with impaired mood recovery following a sad mood induction among individuals with and without major depressive disorder (MDD). Attentional biases were assessed with an exogenous cuing task using emotional facial expressions as cues among adults with (n = 48) and without (n = 224) current MDD. Mood reactivity and recovery were measured following a sad mood induction. Mood reactivity strongly predicted mood recovery; however, this relationship was moderated by attentional biases for negative emotional stimuli. Biases for sad and fear stimuli were associated with diminished mood recovery following mood induction across the sample. However, biases for sad stimuli were associated with significantly greater impairments in mood recovery among individuals with MDD than healthy controls. Furthermore, within the MDD group, impaired mood recovery was positively associated with depression severity. These results suggest that attentional biases maintain depression, in part, by facilitating the persistence of sad mood.

Serotonin transporter genotype modulates functional connectivity between amygdala and PCC/PCu during mood recovery.

The short (S) allele of the serotonin transporter-linked polymorphic region (5-HTTLPR) has been associated with increased susceptibility to depression. Previous neuroimaging studies have consistently showed increased amygdala activity during the presentation of negative stimuli or regulation of negative emotion in the homozygous short allele carriers, suggesting the key role of amygdala response in mediating increased risk for depression. The brain default mode network (DMN) has also been shown to modulate amygdala activity. However, it remains unclear whether 5-HTTLPR genetic variation modulates functional connectivity (FC) between the amygdala and regions of DMN. In this study, we re-analyzed our previous imaging dataset and examined the effects of 5-HTTLPR genetic variation on amygdala connectivity. A total of 15 homozygous short (S/S) and 15 homozygous long individuals (L/L) were scanned in functional magnetic resonance imaging (fMRI) during four blocks: baseline, sad mood, mood recovery, and return to baseline. The S/S and L/L groups showed a similar pattern of FC and no differences were found between the two groups during baseline and sad mood scans. However, during mood recovery, the S/S group showed significantly reduced anti-correlation between amygdala and posterior cingulate cortex/precuneus (PCC/PCu) compared to the L/L group. Moreover, PCC/PCu-amygdala connectivity correlated with amygdala activity in the S/S group but not the L/L group. These results suggest that 5-HTTLPR genetic variation modulates amygdala connectivity which subsequently affects its activity during mood regulation, providing an additional mechanism by which the S allele confers depression risk.

Qigong and mindfulness-based mood recovery: Exercise experiences from a single case

Sara, the participant in this single case study, had to leave work due to burnout. She is now recovered and working, but still complains of disturbed moods and worries about getting burned out again. The aim of this study was to, by way of Qigong and mindfulness exercise, increase the participant's positive mood to a functional level and to increase exercise experiences by combining mindfulness and Qigong practice. The professional practice intervention was planned to last twelve weeks, combining mindfulness practice and three different Qigong exercise techniques. Exercise behavior was noted daily, stress-energy and wellness were followed up weekly, and mindfulness was followed up after four, nine and 12 weeks. Sara feels that her moods (more energy, wellness and joy, as well as less stress and worry) have stabilized at a high level (good to very good), and her mindfulness score also improved to a high level (4.2 on a six-point scale). Sara also states that she enjoys life more: accepts stressful situations as they are, is less worried about becoming burned out again, and is more open to life. Exercise professionals may use mindfulness practice and Qigong exercise when recovering moods, probably even better in preventing burnout syndromes.

The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticity

Recent evidence suggests that neuronal plasticity plays an important role in the recovery from depression. Antidepressant drugs and electroconvulsive shock treatment increase the expression of several molecules, which are associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Furthermore, these treatments increase neurogenesis and synaptic numbers in several brain areas. Conversely, depression, at least in its severe form, is associated with reduced volumes of the hippocampus and prefrontal cortex and in at least some cases these neurodegenerative signs can be attenuated by successful treatment. Such observations suggest a central role for neuronal plasticity in depression and the antidepressant effect, and also implicate BDNF signaling as a mediator of this plasticity. The antidepressant fluoxetine can reactivate developmental-like neuronal plasticity in the adult visual cortex, which, under appropriate environmental guidance, leads to the rewiring of a developmentally dysfunctional neural network. These observations suggest that the simple form of the neurotrophic hypothesis of depression, namely, that deficient levels of neurotrophic support underlies mood disorders and increases in these neurotrophic factors to normal levels brings about mood recovery, may not sufficiently explain the complex process of recovery from depression. This review discusses recent data on the role of BDNF and its receptors in depression and the antidepressant response and suggests a model whereby the effects of antidepressant treatments could be explained by a reactivation of activity-dependent and BDNF-mediated cortical plasticity, which in turn leads to the adjustment of neuronal networks to better adapt to environmental challenges.

Serotonin transporter genotype modulates amygdala activity during mood regulation

Recent studies have implicated the short allele of the serotonin transporter-linked polymorphic region (5-HTTLPR) in depression vulnerability, particularly in the context of stress. Several neuroimaging studies have shown that 5-HTTLPR genotype predicts amygdala reactivity to negatively valenced stimuli, suggesting a mechanism whereby the short allele confers depression risk. The current study investigated whether 5-HTTLPR genotype similarly affects neural activity during an induced sad mood and during recovery from sad mood. Participants were 15 homozygous short (S) and 15 homozygous long (L) individuals. Regional cerebral blood flow was measured with perfusion functional magnetic resonance imaging during four scanning blocks: baseline, sad mood, mood recovery and following return to baseline. Comparing mood recovery to baseline, both whole brain analyses and template-based region-of-interest analyses revealed greater amygdala activity for the S vs the L-group. There were no significant amygdala differences found during the induced sad mood. These results demonstrate the effect of the S allele on amygdala activity during intentional mood regulation and suggest that amygdala hyperactivity during recovery from a sad mood may be one mechanism by which the S allele confers depression risk.

Activation of the TrkB Neurotrophin Receptor Is Induced by Antidepressant Drugs and Is Required for Antidepressant-Induced Behavioral Effects

Recent studies have indicated that exogenously administered neurotrophins produce antidepressant-like behavioral effects. We have here investigated the role of endogenous brain-derived neurotrophic factor (BDNF) and its receptor trkB in the mechanism of action of antidepressant drugs. We found that trkB.T1-overexpressing transgenic mice, which show reduced trkB activation in brain, as well as heterozygous BDNF null (BDNF(+/)-) mice, were resistant to the effects of antidepressants in the forced swim test, indicating that normal trkB signaling is required for the behavioral effects typically produced by antidepressants. In contrast, neurotrophin-3(+/)- mice showed a normal behavioral response to antidepressants. Furthermore, acute as well as chronic antidepressant treatment induced autophosphorylation and activation of trkB in cerebral cortex, particularly in the prefrontal and anterior cingulate cortex and hippocampus. Tyrosines in the trkB autophosphorylation site were phosphorylated in response to antidepressants, but phosphorylation of the shc binding site was not observed. Nevertheless, phosphorylation of cAMP response element-binding protein was increased by antidepressants in the prefrontal cortex concomitantly with trkB phosphorylation and this response was reduced in trkB.T1-overexpressing mice. Our data suggest that antidepressants acutely increase trkB signaling in a BDNF-dependent manner in cerebral cortex and that this signaling is required for the behavioral effects typical of antidepressant drugs. Neurotrophin signaling increased by antidepressants may induce formation and stabilization of synaptic connectivity, which gradually leads to the clinical antidepressive effects and mood recovery.

Attentional Bias and Mood Persistence as Prospective Predictors of Dysphoria

This study examined whether either a negative attentional bias or mood persistence would interact with intervening life stress to predict future increases in dysphoria among college students (N = 77). Dysphoria was assessed in the lab, and then attentional bias was measured with a dot-probe task before and after a negative mood induction. Mood recovery following the induction was also assessed. Seven weeks later, dysphoria and intervening life stress were measured. Prior shifts in attention toward negative information following a negative mood induction interacted with intervening life stress to predict increases in dysphoria 7 weeks later. Slower mood recovery following the mood induction also combined with intervening life stress to predict increased dysphoria at follow-up. These vulnerabilities each explained unique variance in follow-up dysphoria. Results suggest that both attentional bias and mood persistence may have significant roles in depression susceptibility.

Anti-bipolar therapy: mechanism of action of lithium.

This review introduces the concepts that multiple actions of lithium are critical for its therapeutic effect, and that these complex effects stabilize neuronal activities, support neural plasticity, and provide neuroprotection. Three interacting systems appear most critical. (i) Modulation of neurotransmitters by lithium likely readjusts balances between excitatory and inhibitory activities, and decreased glutamatergic activity may contribute to neuroprotection. (ii) Lithium modulates signals impacting on the cytoskeleton, a dynamic system contributing to neural plasticity, at multiple levels, including glycogen synthase kinase-3beta, cyclic AMP-dependent kinase, and protein kinase C, which may be critical for the neural plasticity involved in mood recovery and stabilization. (iii) Lithium adjusts signaling activities regulating second messengers, transcription factors, and gene expression. The outcome of these effects appears likely to result in limiting the magnitudes of fluctuations in activities, contributing to a stabilizing influence induced by lithium, and neuroprotective effects may be derived from its modulation of gene expression.

Need for a Revision of the Normal Limits of Resting Heart Rate

The current definition of sinus tachycardia is a heart rate >100 beats per minute (bpm).1 This limit was set arbitrarily when heart rate was not yet regarded as a risk factor for cardiovascular disease, probably with the main purpose of distinguishing between a disease state (fever, thyrotoxicosis, anemia, congestive heart failure, etc) and a normal condition. In recent years, interest has been aroused by the awareness that fast heart rate is a potent precursor of hypertension, atherosclerosis, and their sequelae.2 3 4 5 6 7 8 9 10 In addition, many leading epidemiological studies have shown that tachycardia is associated with an increased risk of death from cardiovascular and noncardiovascular causes. This relationship has been found in general populations,3 4 5 6 7 in elderly individuals,9 and in hypertensive cohorts.10 In all of these studies, the heart rate value above that in which a significant increase in risk was observed was below the 100 bpm threshold (Table 1⇓). Only in the study by Levy et al3 was tachycardia defined as a heart rate >99 bpm, but in that study the cutoff between normal and high heart rate was chosen arbitrarily, and the highest heart rate value measured during the examination was taken to define the subject’s heart rate. In all the other studies, the threshold level between normal and fast heart rate was between 79 and 90 bpm. View this table: Table 1. Heart Rate Values Above Which a Significant Increase in Risk Was Found: Data From 9 Epidemiological Studies The normalcy limits of a clinical variable can be established according to different criteria. For many parameters, such as most biochemical indexes, the 95% confidence interval is calculated to identify the upper normal limit of the variable. This statistical approach does not appear suitable for those clinical variables …

A comparative epidemiological study of the effects of regular exercise on health level.

To reveal the relationship between regular exercise and physical fitness, life style, mental health, and other cardiovascular risk factors among the Japanese. cross-sectional study. Three thousands, one hundred and thirty-two individuals (1,795 men and 1,336 women) over 40 years old who were examinees at one of seven centers for health promotion. A questionnaire survey on the life style, a physical fitness tests and clinical laboratory tests were performed. Continuing regular exercise was associated with high levels of physical strength and their odds ratio (OR) was 2.09 (95% confidence interval(CI) 1.74-2.50). Many individuals in this group had good mental health: the OR for their sensation of fatigue (swift recovery) was 1.40(95% CI; 1.17-1.68) and that for mood recovery (fast) was 1.44(95% CI; 1.20-1.72). Thinness and obesity were scarce in this group. High physical fitness level, good mental health, standard body weight are more common in regular exercise group.

A comparative epidemiological study on the effects of physical fitness on health level.

Clinical tests, a questionnaire on life style and mental health, and physical fitness tests were conducted on 3,132 individuals (1,796 men and 1,336 women) to find the relationships between physical fitness level and life style, mental health, or cardiovascular risk factors among Japanese. Individuals with an advanced physical fitness level also exhibited optimum mental health: the odds ratio (OR) and 95% confidence interval (CI) for their sensation of fatigue (fast recovery) was 1.16 (95% CI = 1.00 to 1.35) and that for mood recovery (fast) was 1.29 (95% CI = 1.12 to 1.49). Among those with an advanced physical fitness level, the following were rare (OR): daily smoking [0.78]; obesity (over 120%) [0.73 (95% CI = 0.62 to 0.87)]; thick subcutaneous fat (over 20 mm on the back) [0.77 (95% CI = 0.66 to 0.90)]; high blood sugar level [0.64 (95% CI = 0.50 to 0.82)]; and hypertension [0.67 (95% CI = 0.49 to 0.91)]. These are risks for circulatory diseases. These data show that risk factors associated with cardiovascular disease are more common in those with a low physical fitness level.