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Journal articles on the topic 'Anxiety, panic disorder, anxiety sensitivity, CO2 challenge'

Author: Grafiati

Published: 10 March 2023

Last updated: 11 March 2023

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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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Argyropoulos, S. "Sensitivity of the Generalised Anxiety Disorder Inventory (GADI) to Detect Changes in Two Experimental Models of Human Anxiety." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70749-7.

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We developed and validated a new questionnaire for the assessment of the symptom profile and severity of generalised anxiety, the Generalised Anxiety Disorder Inventory (GADI). The 18-item scale (Argyropoulos et al, 2007, J Psychopharmacology, 21: 145-152) showed good reliability, convergent and divergent validity. The scale comprises three factors, relating to cognitive, somatic and sleep symptoms. It distinguishes accurately GAD patients from non-patient controls. The cognitive factor also distinguishes GAD from other anxiety disorders and depression. The sensitivity of the GADI to detect changes in symptom levels was tested in two experimental models of anxiety induction; the inhalation of 7.5% CO2 over a period of 20 minutes, which models generalised anxiety, and a single vital capacity inhalation of 35% CO2, which models panic anxiety (Bailey et al, 2005, Depression & Anxiety, 21: 18-25; Bailey et al, 2007, J Psychopharmacology, 21: 42-49). We found that the GADI was able to detect the differential drug effect of a benzodiazepine (alprazolam) and placebo in the anxiety induced by these tests in healthy volunteers.

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Schmidt, Norman B., and Jeffrey H. Cook. "Effects of anxiety sensitivity on anxiety and pain during a cold pressor challenge in patients with panic disorder." Behaviour Research and Therapy 37, no. 4 (April 1999): 313–23. http://dx.doi.org/10.1016/s0005-7967(98)00139-9.

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NARDI, ANTONIO EGIDIO, ALEXANDRE M. VALENÇA, WALTER ZIN, and ISABELLA NASCIMENTO. "Carbon dioxide induced panic attacks and short term clonazepam treatment: preliminary study." Arquivos de Neuro-Psiquiatria 57, no. 2B (June 1999): 361–65. http://dx.doi.org/10.1590/s0004-282x1999000300003.

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AIMS: 1. To verify the sensibility of panic patients to a mixture of 35% CO2 and 65% O2. 2. To determine if a ten days treatment with clonazepam attenuates the panic attacks induced by the inhalation of 35% carbon dioxide in panic disorder. METHOD: We randomly selected six panic disorder subjects, using the Structured Clinical Interview for DSM-IV. All subjects went double-blindly through an inhalation of 35% CO2 and compressed gas (atmospheric air) on two occasions. First, at baseline, when they were drug free. Second, after a 10 days clonazepam treatment. RESULTS: Neither at baseline nor after treatment any patient had a panic attack during compressed gas inhalation. At the first test five patients (83.3%) had a severe panic attack with high levels of subjective anxiety during carbon dioxide inhalation. After 9.6 (± 3.4) days of clonazepam treatment, only two (33.3%) patients experienced a mild panic attack. CONCLUSION: This pilot study suggests the efficacy of the short term clonazepam therapy in attenuating panic attacks and supports the usefulness of the 35% carbon dioxide challenge test as an analogue method for study the efficacy of anti-panic drugs. Further placebo-controlled studies to pharmacological treatment are warranted.

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Battaglia, Marco, Anna Ogliari, Francesca D’Amato, and Richard Kinkead. "Early-life risk factors for panic and separation anxiety disorder: Insights and outstanding questions arising from human and animal studies of CO2 sensitivity." Neuroscience & Biobehavioral Reviews 46 (October 2014): 455–64. http://dx.doi.org/10.1016/j.neubiorev.2014.04.005.

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Battaglia, Marco, Paola Pesenti-Gritti, Sarah E. Medland, Anna Ogliari, Kristian Tambs, and Chiara A. M. Spatola. "A Genetically Informed Study of the Association Between Childhood Separation Anxiety, Sensitivity to CO2, Panic Disorder, and the Effect of Childhood Parental Loss." Archives of General Psychiatry 66, no. 1 (January 1, 2009): 64. http://dx.doi.org/10.1001/archgenpsychiatry.2008.513.

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Kyriakoulis, Peter, Michael Kyrios, Antonio Egidio Nardi, Rafael C. Freire, and Mark Schier. "The Implications of the Diving Response in Reducing Panic Symptoms." Frontiers in Psychiatry 12 (November 29, 2021). http://dx.doi.org/10.3389/fpsyt.2021.784884.

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Increased CO2 sensitivity is common in panic disorder (PD) patients. Free divers who are known for their exceptional breathing control have lower CO2 sensitivity due to training effects. This study aimed to investigate the immediate effects of cold facial immersion (CFI), breath holding and CO2 challenges on panic symptoms. Healthy participants and patients with PD were subjected to four experimental conditions in a randomly assigned order. The four conditions were (a) breath-holding (BH), (b) CFI for 30 s, (c) CO2 challenge, and (d) CO2 challenge followed by CFI. Participants completed a battery of psychological measures, and physiological data (heart rate and respiration rate) were collected following each experimental condition. Participants with PD were unable to hold their breath for as long as normal controls; however, this finding was not significant, potentially due to a small sample size. Significant reductions in both physiological and cognitive symptoms of panic were noted in the clinical group following the CFI task. As hypothesized, the CFI task exerted demonstrable anxiolytic effects in the clinical group in this study by reducing heart rate significantly and lessening self-reported symptoms of anxiety and panic. This outcome demonstrates the promise of the CFI task for clinical applications.

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Schopman, Simone M. E., Renske C. Bosman, Anna D. T. Muntingh, Anton J. L. M. van Balkom, and Neeltje M. Batelaan. "Effects of tryptophan depletion on anxiety, a systematic review." Translational Psychiatry 11, no. 1 (February 11, 2021). http://dx.doi.org/10.1038/s41398-021-01219-8.

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AbstractVulnerability markers for onset of anxiety disorders are scarce. In depression, patients at risk tend to respond with a negative mood to ‘acute tryptophan depletion’ (ATD), while healthy volunteers and current patients do not. The serotonergic system thus provides indications for vulnerability for depression. It is unknown whether ATD reveals vulnerability in anxiety too. This study systematically reviews the effects of ATD on anxiety and assesses whether challenging anxiety modifies the response. PubMed, Embase and PsychInfo were systematically searched up to April 2019 for studies in which (1) healthy volunteers or patients with a (remitted) anxiety disorder underwent ATD and (2) levels of anxiety were reported. In total, 21 studies were included. Studies conducted in healthy volunteers (n = 13), and patients with a remitted (n = 6) or current (panic, social or generalised) anxiety disorder (n = 4). Studies were mostly of poor quality and heterogeneous regarding population, challenge test used and outcome measures. ATD did not consistently affect anxiety in any of the groups. Moreover, a challenge test after ATD (n = 17 studies) did not consistently provoke anxiety in healthy volunteers or remitted patients. A 35% CO2 challenge did consistently increase anxiety in patients with a current panic disorder (PD). To conclude, this systematic review found no clear indications that ATD provokes anxiety in those at risk for anxiety disorders. Hence, unlike in depression, ATD does not indicate vulnerability to develop an anxiety disorder. Because included studies were heterogeneous and mostly of poor quality, there is an urgent need for high quality research in homogeneous samples.

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