Anxiety Dysfunction Research Articles

The Efficacy of Downward Counterfactual Thinking for Regulating Emotional Memories in Anxious Individuals.

Aversive autobiographical memories sometimes prompt maladaptive emotional responses and contribute to affective dysfunction in anxiety and depression. One way to regulate the impact of such memories is to create a downward counterfactual thought–a mental simulation of how the event could have been worse–to put what occurred in a more positive light. Despite its intuitive appeal, counterfactual thinking has not been systematically studied for its regulatory efficacy. In the current study, we compared the regulatory impact of downward counterfactual thinking, temporal distancing, and memory rehearsal in 54 adult participants representing a spectrum of trait anxiety. Participants recalled regretful experiences and rated them on valence, arousal, regret, and episodic detail. Two to six days later, they created a downward counterfactual of the remembered event, thought of how they might feel about it 10 years from now, or simply rehearsed it. A day later, participants re-rated the phenomenological characteristics of the events. Across all participants, downward counterfactual thinking, temporal distancing, and memory rehearsal were equally effective at reducing negative affect associated with a memory. However, in individuals with higher trait anxiety, downward counterfactual thinking was more effective than rehearsal for reducing regret, and it was as effective as distancing in reducing arousal. We discuss these results in light of the functional theory of counterfactual thinking and suggest that they motivate further investigation into downward counterfactual thinking as a means to intentionally regulate emotional memories in affective disorders.

Emotion and Emotion Preferences in Daily Life: The Role of Anxiety.

People vary in their emotion preferences (i.e., desired emotional states). No study, however, has examined the nature of emotion preferences in anxiety. The current study utilized a 14-day ecological momentary assessment (EMA) paradigm to investigate the daily dynamics of emotion preferences and state emotion as they relate to individual differences in trait anxiety and anxiety symptom severity. Individuals with higher levels of trait anxiety and with more severe anxiety symptoms report greater preferences for state anxiety compared to their low anxiety counterparts. Relations between anxiety preferences and subsequent anxiety vary as a function of trait anxiety and symptom severity, and different associations are observed between the two measures of anxiety. The current findings suggest that aberrant emotion preferences may contribute to emotion dysfunction in anxiety, and highlight emotion preferences as a novel treatment target for interventions that aim to improve emotion functioning among people with elevated levels of anxiety.

The impact of cognitive load on processing efficiency and performance effectiveness in anxiety: evidence from event-related potentials and pupillary responses.

Anxiety has been associated with poor attentional control, as reflected in lowered performance on experimental measures of executive attention and inhibitory control. Recent conceptualisations of anxiety propose that individuals who report elevated anxiety symptoms worry about performance and will exert greater cognitive effort to complete tasks well, particularly when cognitive demands are high. Across two experiments, we examined the effect of anxiety on task performance and across two load conditions using (1) measures of inhibitory control (behavioural reaction times and eye-movement responses) and (2) task effort with pupillary and electrocortical markers of effort (CNV) and inhibitory control (N2). Experiment 1 used an oculomotor-delayed-response task that manipulated load by increasing delay duration to create a high load, relative to a low load, condition. Experiment 2 used a Go/No-Go task and load was manipulated by decreasing the No-Go probabilities (i.e., 20% No-Go in the high load condition and 50% No-Go in the low load condition). Experiment 1 showed individuals with high (vs. low) anxiety made more antisaccade errors across load conditions, and made more effort during the high load condition, as evidenced by greater frontal CNV and increased pupillary responses. In Experiment 2, individuals with high anxiety showed increased effort (irrespective of cognitive load), as characterised by larger pupillary responses. In addition, N2 amplitudes were sensitive to load only in individuals with low anxiety. Evidence of reduced performance effectiveness and efficiency across electrophysiological, pupillary, and oculomotor systems in anxiety provides some support for neurocognitive models of frontocortical attentional dysfunction in anxiety.

Ecological Assessment of Executive Dysfunction in Anxiety

Introduction: The specialized literature states that anxiety can interfere with cognition, particularly in complex cognitive processes such as those related to executive functioning. Neuropsychological studies in anxiety disorders have confirmed the presence of deficits in executive functions, with significant changes in its components. The main aim of this study was to compare the executive performance of a sample with anxiety disorder to a control group, using an instrument that differs from the others by high ecological validity, revealing a higher predictive evidence on daily tasks. Methods: This study included 60 participants aged between 18 and 53 years that were allocated to an experimental group (n=30; mean = 31.93; standard deviation [SD] =10.99) and a control group (n=30; mean = 29.63; SD=9.07). Anxiety symptoms and the executive functioning were assessed using the Beck Anxiety Inventory (BAI) and the Behavioural Assessment of the Dysexecutive Syndrome (BADS), respectively. Results: Participants with anxiety disorders presented a significant impairment on executive functioning in general. However, we found a significant impact in tasks that involve control inhibition, design of action strategies according to the functionality and probability of success, the ability to predict or estimate and the ability to plan the action. In addition, the EG required significantly more time to execute all the tests (mean = 440.33, SD = 97.17), compared to the CG (mean = 320.90; SD = 51.27). Conclusions: Individuals with anxiety disorders have a significant impairment in their executive functioning in general, which is reflected in activities of daily living. Keywords : Anxiety disorders; executive functions; BADS; cognitive and affective evaluation

Distinct Associations Between Low Positive Affect, Panic, and Neural Responses to Reward and Threat During Late Stages of Affective Picture Processing

BackgroundAbnormal patterns of attention to threat and reward have been proposed as potential mechanisms of dysfunction in anxiety and mood disorders. However, research on this topic has been inconsistent, perhaps because of both clinical heterogeneity in the samples assessed and measurement of attentional biases that is temporally imprecise. MethodsThe present study measured transdiagnostic symptoms of anxiety and depression in 205 young adults and recorded affect-modulated event-related potentials in response to task-irrelevant pictures in a speeded response task. ResultsLow positive affect was uniquely associated with reduced modulation of later event-related potentials (i.e., the P300 and the late positive potential) by rewarding images, suggesting deficits in sustained attention to reward. Low positive affect was also associated with a blunted threat-elicited late positive potential. Symptoms of panic were associated with an increased N1 to rewarding images, as well as an increased late positive potential to all picture types. ConclusionsThese data suggest that dysfunction in neural markers of sustained attention to threat and reward relate in specific ways to transdiagnostic symptom dimensions of anxiety and depression. Moreover, event-related potentials are likely to be useful in investigations of the time course of attentional abnormalities associated with these symptom dimensions.

Depression and reduced neural response to emotional images: Distinction from anxiety, and importance of symptom dimensions and age of onset.

Abnormal patterns of attention to threat and reward have been proposed as potential mechanisms of dysfunction in anxiety and unipolar depressive disorders. However, few studies have simultaneously examined whether these patterns of attention are shared among disorders or distinguish between them. In the present study, we recorded the Late Positive Potential (LPP), an event-related potential and putative index of motivated attention, from 145 patients with anxiety and unipolar depressive disorders and 32 controls, as they viewed blocks of rewarding and threatening images, respectively. We found that a current diagnosis of depression was associated with a reduced LPP to rewarding visual stimuli. This appeared to be specific to a subgroup of individuals with early onset depression; this subgroup was also characterized by a reduced LPP to threatening images. Anxiety diagnosis and age of onset of anxiety, whether comorbid with depression or not, was unrelated to the magnitude of the LPP. Finally, a transdiagnostic symptom dimension measuring current severity of suicidal ideation was related to a reduced LPP to both rewarding and threatening images. These data suggest that dysfunction in neural markers of attention to threat and reward can effectively distinguish features of depression from anxiety, particularly early onset depression, and may track suicidal ideation across disorders.

A psychophysiological investigation of threat and reward sensitivity in individuals with panic disorder and/or major depressive disorder.

Heightened sensitivity to threat and reduced sensitivity to reward are potential mechanisms of dysfunction in anxiety and depressive disorders, respectively. However, few studies have simultaneously examined whether these mechanisms are unique or common to these disorders. In this study, sensitivity to predictable and unpredictable threat (measured by startle response during threat anticipation) and sensitivity to reward (measured by frontal electroencephalographic [EEG] asymmetry during reward anticipation) were assessed in 4 groups (N = 191): those with (1) panic disorder (PD) without a lifetime history of depression, (2) major depression (MDD) without a lifetime history of an anxiety disorder, (3) comorbid PD and MDD, and (4) controls. General distress/negative temperament (NT) was also assessed via self-report. Results indicated that PD (with or without comorbid MDD) was uniquely associated with heightened startle to predictable and unpredictable threat, and MDD (with or without comorbid PD) was uniquely associated with reduced frontal EEG asymmetry. Both psychophysiological measures of threat and reward sensitivity were stable on retest approximately 9 days later in a subsample of participants. Whereas the comorbid group did not respond differently on the tasks relative to the PD-only and MDD-only groups, they did report greater NT than these 2 groups (which did not differ from each other). Results suggest that heightened sensitivity to threat and reduced sensitivity to reward may be specific components of PD and MDD, respectively. In addition, relative to noncomorbid depression and PD, comorbid MDD and PD may be characterized by heightened NT, but not abnormal levels of these "specific" components.

Neurocognitive Dysfunction in Anxiety and Depression

Neurocognitive Dysfunction in Anxiety and Depression

GABAergic and Endocannabinoid Dysfunction in Anxiety - Future Therapeutic Targets?

With a lifetime prevalence of up to 25% anxiety disorders are among the most frequently occurring psychiatric disorders. The etiology of anxiety is considered to be multifactorial with an interaction of neurobiological, psychological and environmental factors. With regard to neurobiological factors, several neurochemical systems and neuroanatomical circuits have been discussed to be involved. In particular, anxiety might be a result of insufficient inhibitory control, pointing towards a major role of the gamma-amino-butyric acid (GABA) system in these disorders. Preclinical and clinical studies discuss a decreased GABAergic inhibition in anxiety and patients with anxiety disorders. In view of these findings it is intriguing that benzodiazepines, which currently represent the most potent and powerful anxiolytic agents, act through an enhancement of GABAergic inhibition targeting the GABAA receptor. Thus, it has been suggested that the GABAergic system might represent a promising future target for new pharmacologic strategies for the treatment of anxiety. Closely linked to the GABAergic system is the endocannabinoid system, which might also play an important role in this group of disorders. The endocannabinoid system has particularly been involved in extinction learning, suggesting a key role of this system in the process of fear extinction. In this paper, both the GABAergic and the endocannabinoid system will be reviewed with regard to their role in anxiety and anxiety disorders in humans with particular attention to findings from genetic and neuroimaging studies. Moreover, both systems will be discussed as potential therapeutic targets.

A cognitive dysfunction in anxiety and its amelioration by effective treatment with SSRIs

There is extensive research suggesting an abnormal selective attention to threat in anxiety disorders. We assessed the processing of emotional cognitions of physical anxiety, psycho-social fears, depression and positive affect in a cohort of 15 patients with active anxiety disorder (mostly panic) in comparison with a group of 15 depressed patients and 15 recovered panic patients after treatment with antidepressants (all selective serotonin re-uptake inhibitors) and an age- and sex-matched normal control group. Anxious patients showed delayed processing of emotional words (both negative and positive) compared with depressed patients. The successfully treated group showed no such interference and their responses were indistinguishable from controls. It would therefore appear that anxious patients (panic and generalized anxiety disorder) are affected primarily (but not exclusively) by themes of self-harm and psycho-social fears, and that this cognitive dysfunction in pathological anxiety is a state rather than trait feature of the condition, which is responsive to pharmacological intervention.