A Case Report of Problem Solving Therapy for Reducing Suicide Risk in Older Adults with Anxiety Disorders.

Objectives: Suicide is a global public health problem among older adults. Problem-solving therapy (PST) has demonstrated promise in reducing late-life suicide risk, chiefly in secondary analyses of studies on late-life depression. PST mitigates negative beliefs about one's problem-solving abilities and maladaptive problem-solving styles, which suicidal older adults report. The effects of PST on suicide risk in older adults with primary anxiety disorder diagnoses have not been examined. Anxiety is a risk factor for suicide, but it is less studied in research on suicide compared to depression. This paper describes two cases of older individuals with anxiety disorders and suicidal ideation who completed six sessions of PST. Methods: Assessments of suicide risk, anxiety, depressive symptoms, and problem-solving ability were administered. Results: Both cases exhibited a clinically significant reduction in suicide risk, along with reductions in anxiety, worry, and depressive symptoms by posttreatment. Conclusions & Clinical Implications: Findings highlight the potential for PST as a psychotherapeutic intervention for reducing suicide risk in older adults with anxiety disorders.

Older adults report more sadness and less jealousy than young adults in response to worry induction.

OBJECTIVES: The present study examined age differences in descriptions of the experience of worry and worry content. METHOD: Twenty-eight older and 25 younger adults participated in an experimental manipulation of worry (i.e. 5-minute worry induction). Participants identified their three main worries and completed an emotion checklist before and after the induction. RESULTS: After the induction, younger adults endorsed feeling fearful, impatient, and irritated, whereas older adults endorsed feeling tense or worrying. Older adults were more likely than younger adults to report feeling sad (χ2(53) = 7.52, p = .01), whereas younger adults were marginally more likely to report feeling jealous (χ2(53) = 4.34, p = .05). With regards to worry content, older adults worried more about community/world affairs (χ2 = 6.59, p = .01), whereas younger adults worried more about school (χ2 = 17.61, p < .001). Only age differences in worry about school remained significant after applying the Holm-Bonferroni correction. CONCLUSION: Following a worry induction, older and younger adults endorsed a wide variety of negative affect beyond the typical emotions associated with worry. Greater sadness experienced by older compared with younger adults highlights the importance of considering negative affect states, particularly depression, when working with older adult worriers.

Association of Anxiety Symptom Clusters with Sleep Quality and Daytime Sleepiness.

Objectives: To better understand links between anxiety and sleep disturbances in older adults, we examined the association of different phenotypic presentations of anxiety (i.e., affective, cognitive, and somatic clusters) with global sleep quality and daytime sleepiness. Methods: 109 community-dwelling adults aged 66-92 years old (57% female) completed assessments of global sleep quality (Pittsburgh Sleep Quality Index), daytime sleepiness (Epworth Sleepiness Scale), affective anxiety symptoms (Geriatric Anxiety Scale (GAS) affective subscale), cognitive anxiety symptoms (GAS cognitive subscale), and somatic anxiety symptoms (GAS somatic subscale). Results: In hierarchical regression models adjusted for depressive symptoms and health status, greater affective and somatic anxiety were associated with poorer global sleep quality (affective B = 0.30, p = .01; somatic B = 0.41, p = .01). Somatic and cognitive anxiety were associated with greater daytime sleepiness (somatic B = 0.74, p < .001; cognitive B = 0.30, p = .03), but these associations were attenuated by covariates added to the models. Discussion: These findings indicate that anxiety symptom clusters are differentially associated with specific sleep-related disturbances, underscoring the complex relationship of late-life anxiety to sleep. Results suggest that personalized treatments, such as targeted sleep interventions, may improve specific anxiety-symptom domains, or vice versa.

Unlocking Neurocognitive Substrates of Late-Life Affective Symptoms Using the Research Domain Criteria: Worry Is an Essential Dimension.

While investigations have sought to identify the distinct and shared contributions of anxiety and depression to neurocognitive processes in late life, less is known regarding the further contribution of worry, a unique and critical dimension of affective dysregulation. Capturing the full range of symptoms, as inspired by the NIH Research Domain Criteria (RDoC), may provide finer-grained information on inter-relationships among worry, anxiety and depression on neurocognitive processing in later life. The objective of this study was to determine if the dimensional trait of worry intensifies known negative associations of dimensional measures of anxiety and depressive symptoms with neurocognitive processes, specifically cognitive control and memory processes. Using a cross-sectional and observational design, this study was conducted within a translational research center located with a Veterans medical center in Northern California. One hundred and nineteen community-residing older adults ages 65-91 years participated, and were characterized with psychiatric and neurocognitive dimensional measures. Affective symptom severity was assessed with the Penn State Worry Questionnaire, the Beck Anxiety Inventory (BAI), and the Beck Depression Inventory-II. Primary neurocognitive outcomes were inhibitory control assessed using a Stroop paradigm and delayed verbal memory assessed with the Rey Auditory Verbal Learning Test. Secondary outcomes included other less frequently examined cognitive control mechanisms (working memory, information processing, and verbal fluency) and memory processes (visual delayed memory). Contrary to prediction, the dimensional trait of worry attenuated negative associations between anxiety and depressive symptoms and inhibitory control on the one hand, and between depressive symptoms and delayed verbal memory processes on the other. In the secondary models, symptom dimensions were not associated with other cognitive control or visual delayed memory processes. Our fine-grained approach, in line with the NIMH RDoC model, suggests the neurocognitive processes associated with dimensional measures of late-life affective symptoms are dissociable. Specifically, dimensional measures of worry operate independently from other anxiety and depression symptoms to reveal differential patterns of neurocognitive processes associated with affective dysregulation.

Inflammation-induced anhedonia: endotoxin reduces ventral striatum responses to reward.

BACKGROUND: Although inflammatory activity is known to play a role in depression, no work has examined whether experimentally induced systemic inflammation alters neural activity that is associated with anhedonia, a key diagnostic symptom of depression. To investigate this, we examined the effect of an experimental inflammatory challenge on the neural correlates of anhedonia-namely, reduced ventral striatum (VS) activity to reward cues. We also examined whether this altered neural activity related to inflammatory-induced increases in depressed mood. METHODS: Participants (n = 39) were randomly assigned to receive either placebo or low-dose endotoxin, which increases proinflammatory cytokine levels in a safe manner. Cytokine levels were repeatedly assessed through hourly blood draws; self-reported and observer-rated depressed mood were assessed regularly as well. Two hours after drug administration, neural activity was recorded as participants completed a task in which they anticipated monetary rewards. RESULTS: Results demonstrated that subjects exposed to endotoxin, compared with placebo, showed greater increases in self-reported and observer-rated depressed mood over time, as well as significant reductions in VS activity to monetary reward cues. Moreover, the relationship between exposure to inflammatory challenge and increases in observer-rated depressed mood was mediated by between-group differences in VS activity to anticipated reward. CONCLUSIONS: The data reported here show, for the first time, that inflammation alters reward-related neural responding in humans and that these reward-related neural responses mediate the effects of inflammation on depressed mood. As such, these findings have implications for understanding risk of depression in persons with underlying inflammation.

The future and promise of cognitive behavioral therapy: a commentary.

The Academy for Psychological Clinical Science and the independent accrediting entity it created, the Psychological Clinical Science Accreditation system, have recently launched a movement aimed at reforming all of clinical psychology. If this movement is successful, it will result in a greater emphasis on empirical science in the practice of clinical psychology. As cognitive behavioral therapy (CBT) is the approach that currently has the greatest number of controlled scientific studies supporting it, this should be an impetus for CBT to grow. The very same scientific evidence that supports the efficacy of CBT, however, also shows that CBT is far from fully efficacious. Several recent trends that hold great promise to enhance the effectiveness of CBT are discussed, such as greater integration of CBT with biological approaches, cognitive science, systemic approaches, motivational interviewing, and strengths-based approaches.

Inflammation and social experience: an inflammatory challenge induces feelings of social disconnection in addition to depressed mood.

Although research has established links between feelings of social isolation and inflammation, the direction of these effects is unclear. Based on the role that proinflammatory cytokines play in initiating "sickness behavior," which includes symptoms such as social withdrawal, it is possible that inflammatory processes heighten feelings of 'social disconnection.' Here, we examined whether exposure to an inflammatory challenge increased self-reported feelings of social disconnection. In addition, because both inflammatory processes and feelings of social disconnection contribute to depressive symptoms, we also explored whether increases in feelings of social disconnection played a role in the link between inflammation and depressed mood. Participants were randomly assigned to either receive endotoxin, an inflammatory challenge, or placebo. Proinflammatory cytokines (IL-6, TNF-alpha) were collected at baseline and then hourly for 6h. Participants completed self-reports of sickness symptoms ("fatigue"), social disconnection ("I feel disconnected from others"), and depressed mood ("unhappy") hourly. Results revealed that endotoxin led to significant increases (from baseline) in IL-6 and TNF-alpha levels as well as feelings of social disconnection and depressed mood. Moreover, controlling for increases in social disconnection eliminated the relationship between exposure to inflammatory challenge and depressed mood. This study demonstrates that inflammation can have social psychological consequences, which may play a role in cytokine-related depressive symptoms.

An fMRI study of cytokine-induced depressed mood and social pain: the role of sex differences.

Although research has demonstrated a relationship between proinflammatory cytokine activity and depressive symptoms, the neurocognitive processes underlying this relationship have remained largely unexplored. Here, we examined the effect of proinflammatory cytokine activation on the neural correlates of socially painful experience and associated depressed mood. Participants received either low-dose endotoxin or placebo through intravenous injection. Levels of the proinflammatory cytokine, IL-6, were repeatedly assessed through hourly blood draws; self-reported depressed mood was assessed hourly as well. Two hours post-injection, participants completed a neuroimaging session in which they were socially excluded during an online ball-tossing game. Replicating previous research, individuals exposed to endotoxin, compared to placebo, showed increases in IL-6 levels and depressed mood. Although there were no meaningful differences between the endotoxin and control groups in neural responses to social exclusion, there were sex differences in the relationships between IL-6 increases and neural responses to exclusion among subjects exposed to endotoxin. Among females, but not males, exposed to endotoxin, increases in IL-6 were associated with increases in social pain-related neural activity (dorsal anterior cingulate cortex, anterior insula) that mediated the relationship between IL-6 increases and depressed mood increases. Implications of these sex differences in the neural correlates of cytokine-associated depressed mood and social pain are discussed.