Annika Clamor

Effects of medical and psychological treatment of depression in patients with COPD – A review

Chronic Obstructive Pulmonary Disease (COPD) is a chronic inflammatory lung disease characterized by progressive and only partially reversible symptoms and by considerable negative consequences such as reductions in functional status and quality of life. Comorbid depression is highly prevalent in patients with COPD and related to a worse course of the disease. Despite its negative impact, depression often remains unrecognized and untreated in COPD patients. This review summarizes the current state of findings from studies examining the effects of antidepressant treatments in patients with COPD. Reviewed treatment options are antidepressant medical therapy and cognitive-behavioral therapy (CBT). Antidepressant medical trials include treatments with selective serotonin reuptake inhibitors (SSRI) or tricyclic antidepressants (TCA); CBT was applied using various components. Across both treatment types, the majority of studies included patients with a wide range of psychiatric conditions and especially comorbid symptoms of anxiety were often not controlled. Furthermore, greatly varying instruments and methods for assessing depressive symptoms, small sample sizes and rather heterogeneous results were observed. This makes the comparison of treatment options rather difficult and prevents definite conclusions. However, some important implications valuable for further research were obtained. Some limited data suggested that SSRI might show fewer side effects than TCA. A few antidepressants as well as beneficial effects in other outcomes were observed after antidepressant medical treatment. More clearly, CBT showed some potential in terms of improvements in depressive symptoms, and also in other outcome measures. Patient compliance seems more promising for CBT than for antidepressant medical treatment. Overall, the reviewed studies suggest some promising effects for both treatment types and effect sizes in studies with significant antidepressant effects were reasonable. However, future randomized controlled trials comparing antidepressant medical and cognitive-behavioral therapy will be essential to assess distinct and most favorable treatment effects. Because recent data is often limited, sound diagnostic criteria of depression and adequate sample sizes are necessary to draw firm conclusions on the effects of these antidepressant treatment options in patients with COPD and comorbid depression.

Altered autonomic arousal in psychosis: An analysis of vulnerability and specificity

Vulnerability-stress models implicate that alterations of the autonomous nervous system contribute to the development of psychosis. Previous research has found autonomic arousal alterations in psychotic disorders and at-risk individuals that are not explained by medication alone. To test whether these alterations are associated with the extent of an individuals vulnerability and whether they are specific to psychosis, we compared participants with psychosis (n=23), first-degree relatives of individuals with psychosis (n=21), and healthy participants with attenuated positive symptoms (n=23) to participants with depression (n=24) and healthy controls (n=24). At rest, skin conductance level was assessed and photoplethysmography was applied to measure time- and frequency-domain heart rate variability (HRV). Univariate and multivariate analyses of covariance with perceived stress and psychophysiological values as dependent variables showed significant between-group differences for perceived stress (p=.010), heart rate (p=.022), time-domain HRV indices (all ps≤.027), and vagal activity (p=.017). Group differences in sympathetic activity were nonsignificant (p=.069). In an additional analysis with medication as a second between-group factor, the physiological between-group differences remained significant or trend significant (all ps≤.060). With the exception of sympathetic activity, participants with psychosis exhibited more extreme arousal than the control groups. First-degree relatives and participants with attenuated symptoms showed comparable autonomic activity to healthy controls. Thus, the hypothesized association of an alteration of arousal and vulnerability to psychosis was not confirmed. However, particularly low time-domain HRV was found for psychosis, with significant differences to healthy controls (all ps≤.007) and to depression (all ps≤.004), with the latter indicating a specificity to psychosis.

Bridging psychophysiological and phenomenological characteristics of psychosis — Preliminary evidence for the relevance of emotion regulation

In psychosis, the alleged increased subjective stress-sensitivity is reflected in abnormal physiological arousal such as higher heart rate, elevated skin conductance levels, decreased vagal activity, and unusual cortisol levels. Despite ongoing research, possible mechanisms that explain the interplay between the phenomenological (i.e., subjective stress and symptoms) and psychophysiological processes are not thoroughly understood. Building on the model of neurovisceral integration by Thayer and Lane (2000) that focuses on regulative mechanisms, we postulate that emotion regulation will be associated with vagal activity, and with both subjective and physiological stress. In the present analysis, we used data from a baseline relaxation period including a 5-minute assessment of heart rate variability (HRV), salivary cortisol, and momentary subjective stress ratings from a sample of 19 participants with psychosis (mean age=40.9, SD=11.1; 36.8% female). Emotion regulation modification skills were assessed for specific emotions (i.e., stress and arousal, anxiety, anger, sadness, shame) if these were present during the previous week. Vagal HRV was significantly and moderately associated with emotion regulation. Both stress parameters (i.e., cortisol, subjective stress) were significantly associated with emotion regulation, but not with HRV. We provide preliminary support for the notion that emotion regulatory processes represent a crucial link between phenomenological and psychophysiological phenomena in psychosis. A potential model that ascribes emotion regulation a central role in the restoration of homeostasis is discussed. Future studies are needed to verify its generalizability and predictive value.

Arousal Predisposition as a Vulnerability Indicator for Psychosis: A General Population Online Stress Induction Study

Explanatory models ascribe to arousability a central role for the development of psychotic symptoms. Thus, a disposition to hyperarousal (i.e., increased arousal predisposition (AP)) may serve as an underlying vulnerability indicator for psychosis by interacting with stressors to cause symptoms. In this case, AP, stress-response, and psychotic symptoms should be linked before the development of a diagnosable psychotic disorder. We conducted a cross-sectional online study in a population sample (N = 104; M age = 27.7 years, SD = 11.2, range 18–70). Participants rated their AP and subclinical psychotic symptoms. Participants reported their stress-levels before and after two stress inductions including an arithmetic and a social stressor. The participants with an increased AP generally felt more stressed. However, AP was not associated with the specific stress-response. As expected, positive psychotic symptoms were significantly associated with AP, but this was not mediated by general stress-levels. Its association to subtle, nonclinical psychotic symptoms supports our assumption that AP could be a vulnerability indicator for psychosis. The trait is easily accessible via a short self-report and could facilitate the identification of people at risk and be a promising target for early stress-management. Further research is needed to clarify its predictive value for stress-responses.

The association of resting state heart rate variability and 24-hour blood pressure variability in spinal cord injury.

Patients with high cervical complete spinal cord injuries (tetraplegia) sustain damage to the autonomic neural pathways that influence cardiovascular functioning and produce variability in the heart rate (HR) and blood pressure (BP). In non-injured individuals, an inverse relationship exists between resting autonomic control of the heart (as evidenced by HR variability (HRV)) and BP variability (BPV). This study examined the relationship between HRV, BP and BPV in individuals with tetraplegic (n=10) and paraplegic (n=10) spinal cord injuries, and a group of healthy controls (n=14). Resting HRV at baseline and 24-hour ambulatory BP measurements were collected from electrocardiogram measures of each participant. HRV was quantified using time- and frequency-domain measures. The standard deviation of the BP measurements was used as an index of BPV. Multivariate analyses of variance were performed to examine group differences for laboratory-based and 24-h dependent variables. The MANOVAs for HRV parameters (λ(14,50)=.352, p=.010, η(2)=.407) and for BP indices and HR (λ(16,48)=.318, p=.013, η(2)=.436) were significant. Furthermore, in line with existing evidence, we found that vagally mediated HRV was inversely related to BPV in healthy controls. However, this relationship did not hold for the tetraplegia group (ρ<|.42|), and mixed results were found for the paraplegia group (e.g., ρ<|.29| for time domain HRV, ρ>|.65| for low-frequency power). These results support the conclusion that the damage to the spinal sympathetic pathways to the heart found in people with tetraplegia causes a significant disruption in baroreflex control of BP.

Paranoid Delusions as an Adaptive Response to Social Evaluative Stress

Learning mechanisms may serve as a framework for understanding the formation of paranoia. Specifically, if paranoid thoughts after social stressors produce a short-term benefit for coping (e.g., downregulating arousal), the encountered negative reinforcement could lead to their excessive application and subsequently to long-term maladaptive convictions. The Trier Social Stress Test was utilized in healthy participants to examine this putative benefit. Participants rated paranoia at baseline and after the stressor. Subjective stress levels, negative affect, heart rate, and heart rate variability were assessed in the following rest phase (N = 59). Semipartial correlations showed that participants who responded with larger increases in paranoia were characterized by a lower heart rate in the subsequent rest phase. No associations were found with heart rate variability or psychological measures. Thus, paranoid thinking in healthy individuals could be an adaptive means for reestablishing some aspects of physiological homeostasis after a social stressor but further research is needed.

Emotion regulation as a predictor of the endocrine, autonomic, affective, and symptomatic stress response and recovery

Stress is associated with the development of mental disorders such as depression and psychosis. The ability to regulate emotions is likely to influence how individuals respond to and recover from acute stress, and may thus be relevant to symptom development. To test this, we investigated whether self-reported emotion regulation predicts the endocrine, autonomic, affective, and symptomatic response to and recovery from a stressor. Social-evaluative stress was induced by the Trier Social Stress Test (TSST) in N = 67 healthy individuals (53.7% female, Mage = 29.9). Self-reported habitual emotion regulation skills were assessed at baseline. We measured salivary cortisol, heart rate, negative affect, state depression and state paranoia at three time points: pre-TSST, post-TSST, and after a 10 min recovery phase. Repeated-measures ANOVA showed all indicators to significantly increase in response to the stressor (p < .001) and decrease during the recovery phase (p < .001), except for salivary cortisol, which showed a linear increase (p < .001). The habitual use of maladaptive emotion regulation (e.g., rumination, catastrophizing) significantly predicted an increased affective and reduced cortisol response. Adaptive emotion regulation (e.g., acceptance, reappraisal) was not predictive of the stress response for any of the indicators. Neither type of emotion regulation predicted response during the stress recovery phase. Individuals who habitually resort to maladaptive emotion regulation strategies show a stronger affective and a blunted endocrine stress response, which may make them vulnerable to mental health problems. However, further research is needed to identify the full scope of skills required for effective stress-regulation before this knowledge can be used to develop effective prevention programs.

Stress levels in psychosis: Do body and mind diverge?

Discrepancies between subjective and physiological stress levels may help to explain why stress leads to psychosis. We examined self-reported and physiological stress levels (heart rate, skin conductance level, cortisol level) during two conditions (noise stressor, no stressor) in patients with psychotic disorders (n = 35), patients with depression (n = 30), and healthy controls (n = 28), expecting larger discrepancies between self-reported and physiological stress levels in patients with psychosis than in controls. Difference values were calculated from standardized stress levels. Compared to healthy controls, patients with psychosis showed larger discrepancies between self-reported stress and skin conductance levels and between self-reported stress and cortisol levels. The discrepancies were similar in both patient groups and in both conditions. Paranoid symptoms, emotion awareness and antipsychotic dose were associated with the discrepancies. Future research needs to clarify whether the discrepancies causally contribute to psychotic symptoms or reflect secondary processes.

Only by the Night: A Closer Look at Parasympathetic Nervous System Dysregulation in Chronic Pain

To the Editor: In a series of studies, we have recently shown that pain severity is inversely correlated with short-term and long-term 24-hour recordings of vagal activity, indexed by high-frequency heart rate variability (HF-HRV). Most interestingly, we found that this correlation was no longer present in individuals with chronic pain. It is noted that guidelines for the measurement of HRV suggest that analysis of 24-hour long-term HRV may not accurately reflect autonomic modulation, which may be better captured by estimates based on shorter data epochs. Specifically, analyses of nighttime recordings are of great interest to address the involvement of the vagus nerve in chronic painful conditions, as during nighttime, movement artifacts are minimized and the contribution of sympathetic influences is low. Taking a closer a look at time of day difference on HF-HRV between individuals with chronic pain and those without seems promising. We conducted a secondary analysis of our data, using smaller segments of recording time where the 24-hour interbeat interval (IBI) data were decomposed into blocks of 5.35 minutes and subjected to further analysis if the artifact rate was below 5%. The root mean square of successive differences (RMSSD) was averaged for four periods (Work, Leisure, Sleep, and Next Morning) of 6 hours each, calculated based on self-reports of bedtimes and wake-up times provided by participants. Differences between segments were analyzed using analysis of variance (ANOVA) and multivariate analysis (Wilks’ Λ) on repeated measures using a 2 (Group: chronic pain vs. no chronic pain) 9 4 (Segment: Work, Leisure, Sleep, and Next Morning) interaction with RMSSD as the dependent variable. The level of significance was determined as P ≤ 0.05. Descriptive statistics by group and period are given in Table 1. The analyses showed a significant difference on RMSSD between individuals with chronic pain and those without chronic pain during Sleep only (F(1,549) = 9.532, P = 0.002), indicating blunted increases in vagal activity during night in those with chronic pain. As illustrated in Figure 1, no differences were found during Work (F(1,603) = 0.504, P = 0.478), Leisure (F(1,586) = 1.713, P = 0.191), or the Next Morning (F(1,503) = 3.700, P = 0.055). Furthermore, a significant Group 9 Segment interaction was revealed by repeated-measures analysis (Λ = 0.977, F(3,494) = 3.914, P = 0.009), as illustrated in Figure 1. In healthy individuals, HRV shows a circadian variation, which is characterized by significant increases during the nighttime. The present analyses emphasize that circadian variation of vagal activity, indexed by RMSSD, differs in a nonclinical sample of individuals with chronic pain when compared to controls without chronic pain. Specifically, this alteration is characterized by blunted increases of vagal activity during the night, with a mean difference of 9 ms. This is in line with previous research in patients with irritable bowel syndrome by Thompson et al. who showed decreased vagal activity compared to healthy controls in rapid eye movement (REM) sleep stage but not in wake phases or non-REM sleep. Adding to the existing meta-analytical evidence and findings on the association of resting state measures of vagal activity and pain symptoms recently published in Pain Practice, we like to emphasize the importance of nighttime variation in HF-HRV. It has been shown that changes in HF-HRV at night may represent a pathway to disturbed sleep and future research should address whether blunted vagal activity during nighttime is associated with disturbed sleep reported in chronic pain patients.