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Добірка наукової літератури з теми "Anxiety, panic disorder, anxiety sensitivity, CO2 challenge"

Автор: Grafiati

Опубліковано: 10 березня 2023

Оновлено: 11 березня 2023

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Статті в журналах з теми "Anxiety, panic disorder, anxiety sensitivity, CO2 challenge"

Schutters, Sara IJ, Wolfgang Viechtbauer, Inge J. Knuts, Eric JL Griez, and Koen RJ Schruers. "35% CO2 sensitivity in social anxiety disorder." Journal of Psychopharmacology 26, no. 4 (January 6, 2012): 479–86. http://dx.doi.org/10.1177/0269881111430750.

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The 35% carbon dioxide (CO2) challenge is a well-established model of panic. This study aimed to investigate 35% CO2 sensitivity in patients with social anxiety disorder (SAD) compared with patients with panic disorder (PD) and normal controls. First, a 35% CO2 challenge was conducted including 16 patients with generalized SAD, 16 with PD and 16 normal subjects. Outcome was assessed by a Visual Analogue Scale for Fear (VAS-F) and the Panic Symptom List (PSL). Second, meta-analyses of fear and panic scores were performed, including data from the present experiment and from previous 35% CO2 challenge studies in patients with SAD. The present 35% CO2 challenge found equal increases in VAS-F and PSL in patients with SAD compared with normal controls, whereas the CO2 response in patients with PD was significantly stronger than in controls. The meta-analyses confirmed the experimental data from this study, and in addition showed an intermediate panic rate in SAD patients, in between that of normal controls and patients with PD. In conclusion, neither our experiment nor the meta-analyses found evidence for a similarly exaggerated 35% CO2 sensitivity in SAD and PD, suggesting that the pathogenesis of SAD is different from PD, although patients with SAD may be slightly more sensitive than non-anxious controls.

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Sardinha, Aline, Rafael Christophe da Rocha Freire, Walter Araújo Zin, and Antonio Egidio Nardi. "Respiratory manifestations of panic disorder: causes, consequences and therapeutic implications." Jornal Brasileiro de Pneumologia 35, no. 7 (July 2009): 698–708. http://dx.doi.org/10.1590/s1806-37132009000700012.

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Multiple respiratory abnormalities can be found in anxiety disorders, especially in panic disorder (PD). Individuals with PD experience unexpected panic attacks, characterized by anxiety and fear, resulting in a number of autonomic and respiratory symptoms. Respiratory stimulation is a common event during panic attacks. The respiratory abnormality most often reported in PD patients is increased CO2 sensitivity, which has given rise to the hypothesis of fundamental abnormalities in the physiological mechanisms that control breathing in PD. There is evidence that PD patients with dominant respiratory symptoms are more sensitive to respiratory tests than are those who do not manifest such symptoms, and that the former group constitutes a distinct subtype. Patients with PD tend to hyperventilate and to panic in response to respiratory stimulants such as CO2, triggering the activation of a hypersensitive fear network. Although respiratory physiology seems to remain normal in these subjects, recent evidence supports the idea that they present subclinical abnormalities in respiration and in other functions related to body homeostasis. The fear network, composed of the hippocampus, the medial prefrontal cortex, the amygdala and its brain stem projections, might be oversensitive in PD patients. This theory might explain why medication and cognitive-behavioral therapy are both clearly effective. Our aim was to review the relationship between respiration and PD, addressing the respiratory subtype of PD and the hyperventilation syndrome, with a focus on respiratory challenge tests, as well as on the current mechanistic concepts and the pharmacological implications of this relationship.

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Garcia de Miguel, Berta, David J. Nutt, Sean D. Hood, and Simon JC Davies. "Elucidation of neurobiology of anxiety disorders in children through pharmacological challenge tests and cortisol measurements: a systematic review." Journal of Psychopharmacology 26, no. 4 (July 19, 2010): 431–42. http://dx.doi.org/10.1177/0269881110372818.

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Anxiety disorders are common both in adults and children. While there have been major advances in understanding the neurobiology of anxiety disorders in adults, progress has been more limited in the elucidation of the mechanisms underlying these disorders in childhood. There is a need to delineate childhood biological models, since anxiety represents a significant clinical problem in children and is a risk factor for the subsequent development of anxiety and depression in adulthood. We conducted a review of the literature regarding pharmacological challenge tests and direct hypothalamic–pituitary–adrenal axis measurement in children with anxiety disorders, with emphasis on panic disorder and social anxiety disorder. Studies identified were contrasted with those in adult panic disorder and social anxiety disorder. Despite this broad approach few studies emerged in children, with only 22 studies meeting inclusion criteria. When contrasted with adult neurobiological models of panic disorder and social anxiety disorder, children studied showed some abnormalities which mirrored those reported in adults, such as altered baseline respiration, altered responses to CO2 challenge tests and blunted growth hormone response to yohimbine. However, results differed from adults with panic disorder and social anxiety in some aspects of noradrenergic and serotonergic function. For endpoints studied in panic disorder children, unlike adults, displayed a lack of baseline end-tidal CO2 abnormalities and a different hypothalamic–pituitary–adrenal pattern response under low-dose CO2. The biology of these anxiety disorders in children may only partially mirror that of adult anxiety disorders. However, caution is required as the evidence is limited, and many studies combined patients with panic disorder and social anxiety disorder with other disorders or non-specific anxiety. Further research is required to fully understand the biology and progression of childhood anxiety disorders.

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Overbeek, Thea, Koen Schruers, Ine Docters van Leeuwen, Tineke Klaassen, and Eric Griez. "Experimental Affective Symptoms in Panic Disorder Patients." Canadian Journal of Psychiatry 50, no. 3 (March 2005): 175–78. http://dx.doi.org/10.1177/070674370505000307.

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Objective: To date, carbon dioxide (CO2) challenge tests in panic disorder (PD) patients have focused on anxiety as the sole outcome measure. This study assesses a broader range of symptoms in patients with PD. Method: We administered a gas mixture of 35% CO2 and 65% oxygen (O2) to 25 patients with PD. Nine patients met the criteria for a comorbid major depressive disorder (MDD), and 16 did not. We assessed not only subjects' symptoms of anxiety but also their symptoms of depression and aggression. Results: Baseline ratings did not differ across the 2 subgroups. Postchallenge ratings were higher for PD and MDD patients on all the assessed affective symptoms, except for specific panic symptoms. Conclusion: These findings suggest that, in addition to anxiety, CO2 challenge induces depressive and aggressive symptoms, specifically in PD patients with comorbid depression.

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Miller, H. E. J., J. F. W. Deakin, and I. M. Anderson. "Effect of acute tryptophan depletion on CO2-induced anxiety in patients with panic disorder and normal volunteers." British Journal of Psychiatry 176, no. 2 (February 2000): 182–88. http://dx.doi.org/10.1192/bjp.176.2.182.

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BackgroundUncertainties remain about the role of serotonin in the aetiology and treatment of panic disorder.AimsTo investigate the effect of reducing brain serotonin function on anxiety at rest, and following 5% CO2 provocation in normal controls and patients with panic disorder.MethodTwenty drug-free patients with DSM–III–R panic disorder and 19 controls received a tryptophan-free amino acid drink on one occasion and a control drink on the other in a double-blind, balanced protocol. 5% CO2 was given as a panic challenge after 270 minutes.ResultsPlasma tryptophan fell by more than 80% both patients and controls after the tryptophan-free drink. Tryptophan depletion did not alter resting anxiety. In patients alone, tryptophan depletion caused a greater anxiogenic response and an increased rate of panic attacks (9 v. 2, P<0.05) after 5% CO2 challenge. No normal volunteers panicked.ConclusionsSerotonin may directly modulate panic anxiety in patients with panic disorder. This may underlie the efficacy of serotonergic antidepressants in treating panic disorder.

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Muhtz, C., J. Daneshi, M. Braun, and M. Kellner. "The effects of CO2 inhalation in patients with chronic post-traumatic stress disorder (PTSD)." European Psychiatry 26, S2 (March 2011): 168. http://dx.doi.org/10.1016/s0924-9338(11)71879-x.

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IntroductionPanic disorder and post-traumatic stress disorder (PTSD), which is currently classified as an anxiety disorder in DSM-IV, share some clinical characteristics. Emerging evidence suggests that CO2-induced fear reactivity is associated with anxiety disorders, especially panic disorder. However, there are only very few data available about the sensitivity of patients with PTSD to carbon dioxide.AimTo examine the psychometric effects of CO2 on panic anxiety and PTSD symptoms in subjects with PTSD.MethodsIn 10 patients with PTSD, 10 sex- and age-matched healthy subjects and additional 8 patients with panic disorder we assessed anxiety, panic, dissociative and PTSD symptoms before and after a single vital capacity inhalation of 35% CO2.ResultsInhalation of a single deep breath of 35% of carbon dioxide resulted in significant panicogenic and anxiogenic effects in PTSD patients versus healthy controls, which were similar to the well known responses of patients with panic disorder. Furthermore, significant pro-dissociative effects and significant provocation of post-traumatic flashbacks and PTSD symptoms were observed in PTSD patients.ConclusionsThese data provide novel evidence that panic disorder and PTSD share a common hypersensitivity to CO2 and thus might belong to the same spectrum of vulnerability.

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Cosci, Fiammetta, Koen Schruers, Carlo Faravelli, and Eric Griez. "The influence of alcohol oral intake on the effects of 35% CO2 challenge. A study in healthy volunteers." Acta Neuropsychiatrica 16, no. 2 (April 2004): 107–9. http://dx.doi.org/10.1111/j.0924-2708.2004.0077.x.

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Objective:Alcohol use disorders and panic disorder co-occur at a rate that exceeds chance significantly. The underlying mechanism of alcoholism associated with anxiety has rarely been examined using experimental methodologies. The present study in healthy volunteers tested whether alcohol consumption reduces anxiety associated with a panic-challenge procedure (35% CO2 challenge).Methods:The study design was placebo-controlled, double-blind, randomized. Eight healthy volunteers were enrolled; all subjects had an alcohol and a placebo oral intake according to a crossover design. After each consumption the subjects underwent the 35% CO2 challenge and a series of anxiety symptom assessments.Results:After the alcohol intake, the subjects presented a significant reduction in the anxiety state associated with the challenge procedure. The Panic Symptom List score is significantly lower after alcohol intake (P = 0.032), as compared with the placebo, and the Visual Analogue Anxiety Scale shows a trend to be lower after alcohol intake (P = 0.111).Conclusions:Moderate doses of alcohol acutely decrease the response to a 35% CO2 challenge in healthy volunteers. These results lend support to the pharmacological anxiolytic effect of alcohol and suggest that this property may reinforce the drinking behaviour among those with high levels of anxiety.

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Perna, Giampaolo, Pietra Romano, Daniela Caldirola, Michele Cucchi, and Laura Bellodi. "Anxiety sensitivity and 35% CO2 reactivity in patients with panic disorder." Journal of Psychosomatic Research 54, no. 6 (June 2003): 573–77. http://dx.doi.org/10.1016/s0022-3999(02)00468-3.

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Verburg, Kees, Henk Pols, Thea Overbeek, and Eric Griez. "Vulnerability to the 35% CO2 panic provocation challenge in anxiety disorder patients." European Psychiatry 11 (January 1996): 379s. http://dx.doi.org/10.1016/0924-9338(96)89224-8.

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Abrams, Kenneth, Laura Schlosser, Kate Leger, Katelyn Donisch, Andrew Widmer, and Anna Minkina. "Panic-Relevant Cognitive Processes Among Smokers." Journal of Cognitive Psychotherapy 25, no. 1 (2011): 71–81. http://dx.doi.org/10.1891/0889-8391.25.1.71.

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To further understand the frequent co-occurrence of smoking and panic disorder (PD), we examined panic-relevant cognitive processes among heavy smokers, half of whom were in 12-hour withdrawal, and nonsmokers. All participants (N = 85) underwent a 5-minute carbon dioxide rebreathing challenge. Prior to the challenge, participants completed questionnaires on reasons for smoking, anxiety sensitivity, and suffocation fear. Results are consistent with a model in which smokers with predisposing risk factors (high anxiety sensitivity and high suffocation fear) misappraise bodily sensations and experience panicky symptoms. No evidence was found that being in acute withdrawal heightened this risk. Overall, findings highlight (a) cognitive vulnerabilities that may place smokers at elevated risk for developing PD and hence (b) potential targets for intervention.

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Дисертації з теми "Anxiety, panic disorder, anxiety sensitivity, CO2 challenge"

BERTOLI, GIULY. "The effect of anxiety sensitivity and expectancy manipulation on panic-like response to the 35% CO2 challenge." Doctoral thesis, 2017. http://hdl.handle.net/2158/1089785.

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The Anxiety Sensitivity (AS) theory, developed by Reiss and McNally, refers to the fear of anxiety related bodily sensation, due to the belief that they are psychologically, physiologically, and socially harmful. In this field several researches established the relationship between AS and panic: subjects with High AS (HAS), compared to Low AS (LAS), had greater panic-like responses when the carbon-dioxide (CO2) challenge was administered. Telch and colleagues suggested that the standardized instructions for the CO2 challenge might influence the anxiety response to the test in healthy subjects. Surprisingly, they found that HAS subjects (versus LAS), randomized to Expected Relaxation instructions (ER) (versus standard Expected Arousal instructions - EA) had higher panic response to the 35% CO2 challenge compared to room air inhalation. Thus, the aim of the present research was to replicate Telch and colleagues’ study in order to overcome some methodological limitations and verify if AS, and the manipulation of expectations, might affect the psychological and physiological responses to the 35% CO2 challenge. Sixty-eight healthy subjects, matched for sex, age, and opposite level of AS (HAS versus LAS), as measure by the Anxiety Sensitivity Index - 3 (ASI-3), were randomized to one of two instructional set (ER versus EA). Immediately before and after the 35% CO2 challenge and room air inhalation, they filled the Visual Analogue Scale of Anxiety (VAAS), of Fear (VAS-F), of Discomfort (VAS-D), and the Panic Symptom List (PSL). Physiological parameters (i.e., systolic and diastolic blood pressure, heart rate) were also measured. Hierarchical multiple regression showed greater psychological responses at VAAS, VAS-F, VAS-D, and PSL, and higher systolic blood pressure under CO2 compared to room air. The psychological and physiological response to the test was not affected by the level of AS (HAS versus LAS) or the instructional set (Expected Arousal versus Expected Relaxation). The present study confirmed the psychological effect of CO2 challenge on emotional responses of healthy subjects and strengthens the goodness of the standardized instructions used to administer it.

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Частини книг з теми "Anxiety, panic disorder, anxiety sensitivity, CO2 challenge"

Battaglia, Marco, and Waqas Ullah Khan. "Reappraising Preclinical Models of Separation Anxiety Disorder, Panic Disorder, and CO2 Sensitivity: Implications for Methodology and Translation into New Treatments." In Biomarkers in Psychiatry, 195–217. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/7854_2018_42.

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