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Respiratory Muscle Tension as Symptom Generator in Individuals With High Anxiety Sensitivity
Abstract
Objective:
Anxiety and panic are associated with the experience of a range of bodily symptoms, in particular unpleasant breathing sensations (dyspnea). Respiratory theories of panic disorder have focused on disturbances in blood gas regulation, but respiratory muscle tension as a source of dyspnea has not been considered. We therefore examined the potential of intercostal muscle tension to elicit dyspnea in individuals with high anxiety sensitivity, a risk factor for developing panic disorder.
Methods:
Individuals high and low in anxiety sensitivity (total N=62) completed four tasks: electromyogram biofeedback for tensing intercostal muscle, electromyogram biofeedback for tensing leg muscles, paced breathing at three different speeds, and a fine motor task. Global dyspnea, individual respiratory sensations, nonrespiratory sensations, and discomfort were assessed after each task, whereas respiratory pattern (respiratory inductance plethysmography) and end-tidal carbon dioxide (capnography) were measured continuously.
Results:
In individuals with high compared to low anxiety sensitivity, intercostal muscle tension elicited a particularly strong report of obstruction (M=5.1, SD=3.6 versus M=2.5, SD=3.0), air hunger (M=1.9, SD=2.1 versus M=0.4, SD=0.8), hyperventilation symptoms (M=0.6, SD=0.6 versus M=0.1, SD=0.1), and discomfort (M=5.1, SD=3.2 versus M=2.2, SD=2.1) (all p values<.05). This effect was not explained by site-unspecific muscle tension, voluntary manipulation of respiration, or sustained task-related attention. Nonrespiratory control sensations were not significantly affected by tasks (F<1), and respiratory variables did not reflect any specific responding of high-Anxiety Sensitivity Index participants to intercostal muscle tension.
Conclusions:
Respiratory muscle tension may contribute to the respiratory sensations experienced by panic-prone individuals. Theories and treatments for panic disorder should consider this potential source of symptoms.
... Given the multidimensionality of dyspnea (96), other lessstudied triggers need to be considered. For example, the contraction of respiratory muscles produces respiratory sensations independent of potential changes in PCO 2 or hyperventilation (97). These muscles are under voluntary control. ...
... Compared to asthmatics without PD, individuals with comorbid PD and asthma find dyspneic symptoms more distressing during the onset and longterm than those without PD (109). High anxiety sensitivity is associated with more intense feelings of SOB and additional panic symptoms in response to dyspnea induced through inspiratory resistive loads (110), or tensing respiratory muscles by intercostal muscle biofeedback (97). Neuroimaging studies indicate that habituation to dyspnea is influenced by an individual's level of anxiety in that individuals with low anxiety are more likely to habituate (111). ...
Panic disorder is a common psychiatric diagnosis characterized by acute, distressing somatic symptoms that mimic medically-relevant symptoms. As a result, individuals with panic disorder overutilize personal and healthcare resources in an attempt to diagnose and treat physical symptoms that are often medically benign. A biobehavioral perspective on these symptoms is needed that integrates psychological and medical knowledge to avoid costly treatments and prolonged suffering. This narrative review examines six common somatic symptoms of panic attacks (non-cardiac chest pain, palpitations, dyspnea, dizziness, abdominal distress, and paresthesia), identified in the literature as the most severe, prevalent, or critical for differential diagnosis in somatic illness, including long COVID. We review somatic illnesses that are commonly comorbid or produce panic-like symptoms, their relevant risk factors, characteristics that assist in distinguishing them from panic, and treatment approaches that are typical for these conditions. Additionally, this review discusses key factors, including cultural considerations, to assist healthcare professionals in differentiating benign from medically relevant symptoms in panic sufferers.
... This difference may be explained by the different samples tested. For example, increased intercostal muscle tension has been associated with greater self-reported symptoms of discomfort and hyperventilation for participants who scored high in anxiety sensitivity compared to low anxiety sensitivity controls (Ritz et al., 2013). Hence, it is possible that among the highly fearful sample tested in the present study the application of muscle tension increased cerebral oxygenation but also heightened perception of presyncopal symptoms. ...
... Among patients with blood phobia, the use of leg muscle tension did not produce a significant effect on P et-CO 2 relative to a no treatment control condition (Meuret et al., 2017;Ritz et al., 2005). Similarly, leg muscle tension did not produce a significant difference in P et CO 2 relative to a rest period among healthy adults with high or low in anxiety sensitivity (Ritz et al., 2013). However, these studies did not encourage abdominal muscle tension, hence it is possible that a respiratory effect would not be produced. ...
Fear of blood and needles increases risk for presyncopal symptoms. Applied muscle tension can prevent or attenuate presyncopal symptoms; however, it is not universally effective. This study examined the effects of applied muscle tension, a respiratory intervention, and a no treatment control condition, on presyncopal symptoms and cerebral oxygenation, during a simulated blood draw with individuals highly fearful of needles. Participants (n = 95) completed questionnaires, physiological monitoring, and two trials of a simulated blood draw with recovery. Presyncopal symptoms decreased across trials; however, no group differences emerged. Applied muscle tension was associated with greater cerebral oxygenation during trial two, and greater end-tidal carbon dioxide during both trials. The respiratory intervention did not differ from the no treatment control. Applied muscle tension is an intervention that can increase cerebral oxygenation and end-tidal carbon dioxide. While the respiratory intervention is promising within therapeutic settings, it was not efficacious after a brief audio training.
... Dyspnea could be caused by either high or low PCO 2 levels during the exercises because both can cause shortness of breath or suffocation symptoms. In addition, the strong voluntary control over breathing required by the exercises recruits respiratory muscles, which are known to induce dyspnea sensations independent from respiratory gas exchange (20). In line with possible mechanisms in interoceptive exposure (21), prolonged and repeated exposure to dyspnea triggered by the breathing exercises could lead to reduction of panicogenic cognitions through desensitization of the central fear network. ...
... The twin who did not report dyspnea sensations did not. Thus, respiratory muscle activation can also be a source of dyspnea independent of PCO 2 levels, and individuals with elevated anxiety sensitivity are particularly sensitive to manipulations of tension in these muscles (20). ...
Background
Previous research has shown that hypoventilation therapy reduces panic symptoms in part by increasing basal PCO2 levels. We tested an additional pathway by which hypoventilation therapy could exert its therapeutic effects: through repeated interoceptive exposure to sensations of dyspnea.
Methods
Thirty-five patients with panic disorder and agoraphobia were trained to perform exercises to raise their end-tidal PCO2 levels using a portable capnometry device. Anxiety, dyspnea, end-tidal PCO2, and respiratory rate were assessed during each exercise across four weeks of training. Mixed model analysis examined whether within-exercise levels of dyspnea were predictive of reduction of panicogenic cognitions.
Results
As expected, within-exercise anxiety and respiratory rate decreased over time. Unexpectedly, PCO2 dropped significantly from the beginning to the end of exercise, these drops becoming progressively smaller across weeks. Dyspnea increased and remained consistently above basal levels across weeks. As hypothesized, greater dyspnea was related to significantly lower panicogenic cognitions over time, even after controlling for anxiety and PCO2. Additional exploratory analyses showed that within-exercise increases in dyspnea were related to within-exercise increases in anxiety, but not related to within-exercise increases in PCO2.
Conclusions
In support of the interoceptive exposure model, we found that greater dyspnea during hypoventilation exercises resulted in lower panicogenic cognitions, even after the effect of PCO2 was taken into account. The findings offer an additional, important target in panic treatment.
... Cognitive trainings based on auditory modeling have been developed and successfully tested in different domains. For instance, in neuropsychology, positive effects of auditory training were proved in motor rehabilitation of patients with Parkinson disease and strokes (Nombela, Hughes, Owen & Grahn, 2013;Thaut & Abiru, 2010;Pelton, Johannsen, Chen & Wing, 2010); in sport psychology, performance improvements were found in hammer throw, swimming, rowing and many other sports, both in auditory and audiovisual conditions (Agostini, Righi, Galmonte & Bruno, 2004;Murgia, Forzini & Agostini, 2014;Effenberg, 2005;Schmitz, Mohammadi, Hammer, Heldmann & Samii, 2013); in music psychology, motionless listening improved motor sequence retention in novice musicians (Lahav, Katz, Chess & Saltzman, 2013); in clinical psychology and medicine, different device-guided breathing techniques facilitated patients' breathing control, inducing the synchronization of their own breathing rhythm with acoustically administered rhythms (Gavish, 2010;Ekman, Kjellström, Falk, Norman & Swedberg, 2011, Mahtani, Nunan & Heneghan, 2012Ritz, Meuret, Bhaskara & Petersen, 2013). ...
... Another important aspect regards the nature of the artificial stimuli. We decided to manipulate pitch height for simulating the dynamic of breathing, thus maintaining continuity with previous research studies in this field (Gavish, 2010;Ekman et al., 2011;Mahtani et al., 2012;Ritz et al., 2013). However, there may be other typologies of artificial stimuli that modify different sound parameters, which could have different effects on modulating the breath duration. ...
Previous research has demonstrated that auditory rhythms affect both movement and physiological functions. We hypothesized that the ecological sounds of human breathing can affect breathing more than artificial sounds of breathing, varying in tones for inspiration and expiration. To address this question, we monitored the breath duration of participants exposed to three conditions: (a) ecological sounds of breathing, (b) artificial sounds of breathing having equal temporal features as the ecological sounds, (c) no sounds (control). We found that participants' breath duration variability was reduced in the ecological sound condition, more than in the artificial sound condition. We suggest that ecological sounds captured the timing of breathing better than artificial sounds, guiding as a consequence participants' breathing. We interpreted our results according to the Theory of Event Coding, providing further support to its validity, and suggesting its possible extension in the domain of physiological functions which are both consciously and unconsciously controlled.
... The authors theorized that the participants in the study may have concluded from the sessions that their anxiety attacks were not due to an impending catastrophic event but simply related to breathing. In another study, it was found that respiratory muscle tension was an important factor (Ritz, Meuret, Bhaskara, & Petersen, 2013). Other studies examined the role of thoracic breathing as a concomitant of breathing discomfort and negative mood states. ...
This chapter describes a breathing method that has been developed over the past 50 years in Europe. It includes elements of direct respiratory retraining, as well as indirect approaches to modify respiration by way of its connections to the whole body. It is combined with a systems perspective by taking mental and physical tension states into account.
... If the authors' theory finds further support by empirical research, it will in all likelihood only explain one among a number of ways in which respiration can be involved in exaggerated manifestations of anxiety. Hypocapnia is not the only route to creating symptoms that might be experienced as distressing to vulnerable individualsdyspnea, the unpleasant sensation of not getting enough air, can be generated through a number of peripheral and central pathways, tension of respiratory muscles being another relevant one (Davenport & Vovk, 2009), which has been demonstrated to unsettle susceptible individuals beyond any change in gas exchange levels (Ritz, Meuret, Bhaskara, & Petersen, 2013). Nevertheless, it is hoped that neurobiological conceptualizations such as the one by Feinstein et al. (2022) can stimulate a new generation of studies that seek to elucidate mechanisms associated with sudden unexpected panic attacks and the generation of acute states of anxiety more broadly. ...
The Apnea-induced Anxiety model of Feinstein et al. continues a line of respiratory theories of panic, extending Klein’s false suffocation alarm theory to a broader range of fear and anxiety states. It draws on neurobiological evidence including the underappreciated role of the amygdala in eliciting periods of apnea and CO2 tolerance. Further progress can be expected from empirical testing and integration with neuromodulatory systems that support respiration, activity, fear and anxiety, in particular the orexin system.
... addressing a sensitised suffocation alarm system) [61]. Exercises may have also improved dyspnoea by reducing tension in respiratory muscles [66]. ...
Dyspnoea self-management is often suboptimal for patients with COPD. Many patients with COPD experience chronic dyspnoea as distressing and disabling, especially during physical activities. Breathing therapy is a behavioural intervention that targets reducing the distress and impact of dyspnoea on exertion in daily living.
Using a qualitative design, we conducted interviews with 14 patients after they participated in a novel mind–body breathing therapy intervention adjunct, capnography-assisted respiratory therapy (CART), combined with outpatient pulmonary rehabilitation. Comprehensive CART consisted of patient-centred biofeedback, tailored breathing exercises, a home exercise programme and motivational interviewing counselling. We assessed participants’ perceptions and reported experiences to gauge the acceptability of CART and refine CART based on feedback. Constant comparative analysis was used to identify commonalities and themes.
We identified three main themes relating to the acceptability and reported benefits of CART: (1) self-regulating breathing; (2) impact on health; and (3) patient satisfaction. Our findings were used to refine and optimise CART ( i.e. its intensity, timing and format) for COPD.
By addressing dysfunctional breathing behaviours and dysregulated interoception, CART offers a promising new paradigm for relieving dyspnoea and related anxiety in patients with COPD.
... HVS is highly prevalent in patients with psychological pathologies [3]. However, it is not clear if psychological pathologies are a cause of HVS [4,5]. ...
... HVS is highly prevalent in patients with psychological pathologies [3]. However, it is not clear if psychological pathologies are a cause of HVS [4,5]. ...
Introduction
Measurement of ventilatory efficiency, defined as minute ventilation per unit carbon dioxide production (VE/VCO2), by cardiopulmonary exercise testing (CPET) has been proposed as a screen for hyperventilation syndrome (HVS). However, increased VE/VCO2 may be associated with other disorders which need to be distinguished from HVS. A more specific marker of HVS by CPET would be clinically useful. We hypothesized ventilatory control during exercise is abnormal in patients with HVS.
Methods
Patients who underwent CPET from years 2015 through 2017 were retrospectively identified and formed the study group. HVS was defined as dyspnea with respiratory alkalosis (pH >7.45) at peak exercise with absence of acute or chronic respiratory, heart or psychiatric disease. Healthy patients were selected as controls. For comparison the Student t-test or Mann-Whitney U test were used. Data are summarized as mean ± SD or median (IQR); p<0.05 was considered significant.
Results
Twenty-nine patients with HVS were identified and 29 control subjects were selected. At rest, end-tidal carbon dioxide (PETCO2) was 27 mmHg (25–30) for HVS patients vs. 30 mmHg (28–32); in controls (p = 0.05). At peak exercise PETCO2 was also significantly lower (27 ± 4 mmHg vs. 35 ± 4 mmHg; p<0.01) and VE/VCO2 higher ((38 (35–43) vs. 31 (27–34); p<0.01)) in patients with HVS. In contrast to controls, there were minimal changes of PETCO2 (0.50 ± 5.26 mmHg vs. 6.2 ± 4.6 mmHg; p<0.01) and VE/VCO2 ((0.17 (-4.24–6.02) vs. -6.6 (-11.4-(-2.8)); p<0.01)) during exercise in patients with HVS. The absence of VE/VCO2 and PETCO2 change during exercise was specific for HVS (83% and 93%, respectively).
Conclusion
Absence of VE/VCO2 and PETCO2 change during exercise may identify patients with HVS.
... Hypertonicity of respiratory muscles can contribute to dyspnoea [42], and aggravate the tendency for asthma sufferers to develop hyperinflation of the lungs [43] and abnormal breathing patterns such as thoracic breathing and paradoxical breathing [44]. Increased tone and activity of inspiratory muscles at the end of expiration leads to higher than normal levels of lung inflation. ...
Various breathing training programmes may be helpful for adults with asthma. The main therapeutic aim for many of these programmes is the correction of dysfunctional breathing. Dysfunctional breathing can be viewed practically as a multidimensional entity with the three key dimensions being biochemical, biomechanical and psychophysiological. The objectives of this review are to explore how each of these dimensions might impact on asthma sufferers, to review how various breathing therapy protocols target these dimensions and to determine if there is evidence suggesting how breathing therapy protocols might be optimised.
Databases and reference lists of articles were searched for peer-reviewed English language studies that discussed asthma or dysfunctional breathing and various breathing therapies.
Biochemical, biomechanical and psychophysiological aspects of dysfunctional breathing can all potentially impact on asthma symptoms and breathing control. There is significant variation in breathing training protocols and the extent to which they evaluate and improve function in these three dimensions.
The various dimensions of dysfunctional breathing may be of greater or lesser importance in different cases and the effectiveness of breathing training protocols is likely to be improved when all three dimensions are considered. Outcomes for breathing training for dysfunctional breathing in asthma may be most successful when the three key dimensions of dysfunctional breathing are evaluated at the start of treatment and monitored during treatment. This allows breathing training protocols to be adjusted as appropriate to ensure that treatment is sufficiently comprehensive and intensive to produce measurable improvements where necessary.
... In contrast, persons who fear suffocation exhibited a reduced mouth pressure associated with a decreased volume per breath (Harver & Mahler, 1998;Shipherd, Beck, & Ohtake, 2001). This suggests that high SF persons may have decreased their workload of the respiratory muscles to avoid the unpleasant respiratory sensations associated with a higher muscle tension (Ritz, Meuret, Bhaskara, & Petersen, 2013). Interestingly, this pattern, which may be interpreted as being indicative of a behavioral avoidance strategy, did not alleviate the intensity of bodily sensations. ...
In patients with anxiety and/or respiratory diseases, body sensations, particularly from the respiratory system, may increase in intensity and aversiveness and thus lead into defensive action (e.g., escape) or panic. The processes, however, that might contribute to the culmination of symptoms and the switch into defensive action have not been well understood yet. The current study aimed at evaluating an experimental paradigm to characterize the dynamics of defensive mobilization to body sensations increasing in intensity and aversiveness. Persons reporting low and high suffocation fear (SF; N = 69) were exposed to increasingly unpleasant feelings of dyspnea induced by inspiratory resistive loads and a breathing occlusion requiring voluntary breath holding. Respiratory responses were assessed along with subjective reports of anxiety and panic symptoms. Presentation of respiratory loads with increasing physical resistance led to increasingly unpleasant feelings of dyspnea. Twenty-eight participants terminated the exposure prematurely at least once. When dyspnea was severe, high compared to low SF persons exhibited an increased respiratory rate that was accompanied by reports of more intense panic symptoms. Premature terminations of exposure were preceded by a surge in anxiety, breathing frequency, and mouth pressure, and a decrease in tidal volume. We successfully established an experimental paradigm to assess changes in defensive responding with increasing intensity of an interoceptive threat. The current data foster our understanding of behavioral expression patterns observed in patients with anxiety and/or respiratory diseases and the processes involved in the culmination of bodily sensations and anxiety into panic.
... We should note that these developments do not rule out the possibility of identifying clinically relevant biomarkers for panic disorder. For example, respiratory muscle tension has been identified as a generator of dyspnea in individuals predisposed to panic disorder (132), and levels of cortisol have been found to moderate clinical improvement during exposure therapy for individuals with panic disorder (133). ...
Disrupted interoception is a prominent feature of the diagnostic classification of several psychiatric disorders. However, progress in understanding the interoceptive basis of these disorders has been incremental, and the application of interoception in clinical treatment is currently limited to panic disorder. To examine the degree to which the scientific community has recognized interoception as a construct of interest, we identified and individually screened all articles published in the English language on interoception and associated root terms in Pubmed, Psychinfo, and ISI Web of Knowledge. This search revealed that interoception is a multifaceted process that is being increasingly studied within the fields of psychiatry, psychology, neuroscience, and biomedical science. To illustrate the multifaceted nature of interoception, we provide a focused review of one of the most commonly studied interoceptive channels, the cardiovascular system, and give a detailed comparison of the most popular methods used to study cardiac interoception. We subsequently review evidence of interoceptive dysfunction in panic disorder, depression, somatic symptom disorders, anorexia nervosa, and bulimia nervosa. For each disorder, we suggest how interoceptive predictions constructed by the brain may erroneously bias individuals to express key symptoms and behaviors, and outline questions that are suitable for the development of neuroscience-based mental health interventions. We conclude that interoception represents a viable avenue for clinical and translational research in psychiatry, with a well-established conceptual framework, a neural basis, measurable biomarkers, interdisciplinary appeal, and transdiagnostic targets for understanding and improving mental health outcomes.
Interoception research can substantially contribute to treatment modalities that improve organic disease management and mental health. Studies in asthma have demonstrated that feedback of added resistive loads can improve accuracy of detecting airway obstruction and that diaries of symptoms and spirometry self-measurement can improve estimations of lung function and asthma control. Multifaceted blood glucose perception training that combines accuracy training by self-measurement diaries with education about determinants of blood glucose can improve blood glucose control in individuals suffering from diabetes. In panic disorders, interoceptive exposure training with systematic elicitation of bodily sensations by exercises, including dyspnea by hyper- or hypoventilation, has aimed to reduce patients’ catastrophic interpretations of feared sensations. In addition, a range of relaxation and meditation techniques have been devised to enhance aspects of interoception, such as the detection of muscle tension by progressive muscle relaxation or attention to breathing via meditation techniques inspired by Buddhist practices, with the ultimate goal of improving general well-being. Although many approaches have yielded promising results, more attention to ecologically or physiologically valid selection of targets and personalization of treatment is warranted. This includes consideration of possible adverse effects of training on clinical outcomes through heightened attention to symptoms of illness.
Biomechanics and their link to anatomy are only one aspect of the complex equation that is respiration. Biochemical processes are equally important, and are already acknowledged in ancient yogic texts emphasizing breathing patterns and practices (i.e., pranayama) that optimize breath biochemistry, such as subtle breathing, tailored breath retention and suspension, four-part breathing, and others. Biochemically, respiration happens at multiple levels, including external, internal, cellular, and mitochondrial. Gas exchange at the alveolar level is known as external respiration; gas exchange at the tissue level is internal respiration. These two distinct aspects of breathing are crucial to understanding and teaching healthful breathing that supports balanced biochemistry, lasting vitality, a resilient nervous system, and a composed and stable mind. External and internal respiration can come under conscious control (external more so than internal) and are key to therapeutic breathwork that is individually tailored. This chapter elucidates both external and internal respiration, providing healthcare professionals and breathing coaches with information for optimizing breath and breathing, especially for individuals whose suffering can be ameliorated through creating and maintaining breath patterns that are biochemically wholesome and healing.
Objective:
Anxiety is highly prevalent in individuals with asthma. Asthma symptoms and medication can exacerbate anxiety, and vice versa. Unfortunately, treatments for comorbid anxiety and asthma are largely lacking. A problematic feature common to both conditions is hyperventilation. It adversely affects lung function and symptoms in asthma and anxiety. We examined whether a treatment to reduce hyperventilation, shown to improve asthma symptoms, also improves anxiety in asthma patients with high anxiety.
Method:
One-hundred-twenty English- or Spanish-speaking adult patients with asthma were randomly assigned to either capnometry-assisted respiratory training (CART) to raise PCO2 or feedback to slow respiratory rate (SLOW). Although anxiety was not an inclusion criterion, 21.7% met clinically-relevant anxiety levels on the Hospital Anxiety and Depression scale. Anxiety (HADS-A) and depression (HADS-D) scales, anxiety sensitivity (ASI), and negative affect (PANAS-N) were assessed at baseline, posttreatment,1-month follow-up, and 6-month follow-up.
Results:
In this secondary analysis, asthma patients with high baseline anxiety showed greater reductions in ASI and PANAS-N in CART than in SLOW (ps ≤ .005, Cohen's ds ≥ .58). Further, at 6-month follow-up, these patients also had lower ASI, PANAS-N, and HADS-D in CART than in SLOW (ps ≤ .012, Cohen's ds ≥ .54). Patients with low baseline anxiety did not have differential outcomes in CART than in SLOW.
Conclusions:
For asthma patients with high anxiety, our brief training designed to raise PCO2 resulted in significant and sustained reductions in anxiety sensitivity and negative affect compared to slow-breathing training. The findings lend support for PCO2 as a potential physiological target for anxiety reduction in asthma.Trial Registration:clinicaltrials.gov Identifier: NCT00975273.
Wireless Sensor Networks (WSNs) are systems with great potential for applications in the most diverse areas such as industry, security, public health, and agriculture. In general, for a WSN to achieve high performance, multiple criteria must be considered, such as coverage area, connectivity, and energy consumption. In this work an Integer Programming (IP) model to solve a Sensor Allocation Problem (SAP) is presented. The IP model considers a heterogeneous WSN and deterministic locations to positioning of sensors. The proposed model was validated using the IBM ILOG CPLEX solver. A several computational experiments were performed, and an analysis through small and medium-sized instances of the problem under study are presented and discussed. The proposed model presents good results given the problem premises, constraints and considered objectives, achieving 0.0099% optimality gap for the best scenarios where networks are fully connected and are feasible to implement. Other suboptimal evaluated scenarios with denser distribution of sensor nodes depict about 0.04% of isolated node positioning, spite maintaining overall balance between energy consumption and coverage. Therefore, the proposed model shows promise for achieving practical solutions, i.e., those with implementation feasibility in most considered heterogeneous network scenarios.
Nowadays, there is an increasing number of mental illnesses, especially anxiety, being estimated that 284 million people were living with this disorder, in 2018. This study raises awareness of this mental illness and addresses the challenge of stress/anxiety detection using a supervised machine learning system for classification. We give a focus on the respiratory system and its parameters that correlate with stress/anxiety. The developed work establishes the framework for an anxiety monitoring system using multiple physiological parameters. 5 of the most common algorithms were used for the task and the one achieving the best results was the random forest classifier with 92% accuracy and great values for precision, recall, f1-Score and cohen kappa score. Ultimately, this technology can be applied to self and autonomous stress/anxiety detection purposes or partner with specialists who deal with these problems on a day-to-day basis like psychologists or psychiatrists.
KeywordsMental health disordersBreathingMachine learningAnxiety
Objective
Respiratory abnormalities are a hallmark of anxiety symptomatology and may serve as clinically useful modifiers for alleviating anxiety symptoms. However, gold-standard anxiety treatments (e.g., cognitive-behavioral interventions) often do not directly address respiratory components despite their theoretical utility and clinical accessibility. This review examined the clinical effectiveness of respiratory interventions, interventions that directly target respiration abnormalities and processes, in treating trait anxiety symptoms.
Methods
The final analysis included 40 randomized controlled trials including at least one measure of trait anxiety, a respiratory-focused intervention group, and a non-respiratory control-group (active or inactive treatment). Overall effects of respiratory focused interventions were examined, as well as the effect of hypothesized moderators.
Results
Respiratory component interventions yielded significantly greater improvements (moderate to large effect) in anxiety symptoms than controls, with the stronger effects observed in comparison to inactive, rather than active, control conditions. Significant heterogeneity in findings suggests that variability in intervention design, population, and control comparison may obfuscate interpretation of findings.
Conclusions
Evidence supports the clinical utility of respiratory interventions as either an independent anxiety treatment, or as an adjunct to other interventions. Clinical and research implications of findings along with recommendations for ongoing investigations in this domain are discussed.
Background
Complex regional pain syndrome (CRPS) is associated with deficits in limb‐recognition. The purpose of our study was to determine whether mental load during this task affected performance, sympathetic nervous system activity or pain in CRPS‐patients.
Methods
We investigated twenty CRPS‐I patients with pain in the upper extremity and twenty age‐ and sex matched healthy controls. Each participant completed a limb‐recognition task. To experimentally manipulate mental load, the presentation time for each picture varied from 2 s (greatest mental load), 4 s, 6 s to 10 s (least mental load). Before and after each run, pain intensity was assessed. Skin conductance was recorded continuously.
Results
CRPS patients did not differ from controls in terms of limb recognition and skin conductance reactivity. However, CRPS‐patients reported an increase in pain during the task, particularly during high mental load and during the latter stages of the task. Interestingly, state anxiety and depressive symptoms were also associated with increases in pain intensity during high mental load.
Conclusions
These findings indicate that high mental load intensifies pain in CRPS. The increase of pain in association with anxiety and depression indicates a detrimental effect of negative affective states in situations of high stress and mental load in CRPS.
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Etwa 20–50 % der Patienten mit einem akuten Koronarsyndrom erleben zusätzlich zum akuten Brustschmerz Todesangst. Diese umfasst Symptome, die viele Patienten auch im weiteren Verlauf nicht mehr loslassen. Todesangst und Brustschmerzen sind deshalb wichtige Themen für die Psychotherapie von Herzpatienten. Empirische Untersuchungen zur Bedeutung der Todesangst erbrachten sehr widersprüchliche Befunde: Todesangst war einerseits deutlich mit einer stärkeren psychischen Belastung assoziiert, andererseits aber auch mit einer wesentlich besseren Prognose. Für die Aufklärung dieses Widerspruchs ist ein affektfokussierter Untersuchungs- und Behandlungsansatz hilfreich. Todesangst als Reaktion auf eine lebensbedrohliche Situation ist hochgradig adaptiv und Zeichen einer gesunden Selbstfürsorge. In anderen Fällen allerdings ist Todesangst keine adaptive emotionale Reaktion, sondern Ausdruck maladaptiver Abwehrmechanismen wie beispielsweise im Rahmen einer somatischen Belastungsstörung (nach DSM-5): Somatisierung der Angst in Form von Brustschmerzen und anhaltend unangemessene Ängste und Sorgen wegen der körperlichen Symptome. Die affektfokussierte Exploration erlaubt diese Differenzierung und ermöglicht es dem Patienten, diese Unterschiede nachzuvollziehen und adaptive Verhaltensweisen aufzubauen.
Panic disorder (PD) is unique among the anxiety disorders in that panic symptoms are primarily of a physical nature. Consequently, comorbidity with medical illness is significant. This review examines the association between PD and medical illness. We identify shared pathophysiological and psychological correlates and illustrate how physiological activation in panic sufferers underlies their symptom experience in the context of the fight-orflight response and beyond a situation-specific response pattern. We then review evidence for bodily symptom perception accuracy in PD. Prevalence of comorbidity for PD and medical illness is presented, with a focus on respiratory and cardiovascular illness, irritable bowel syndrome, and diabetes, followed by an outline for potential pathways of a bidirectional association. We conclude by illustrating commonalities in mediating mechanistic pathways and moderating risk factors across medical illnesses, and we discuss implications for diagnosis and treatment of both types of conditions. Expected final online publication date for the Annual Review of Clinical Psychology Volume 13 is May 7, 2017. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
Aim
This study aimed to develop and test the reliability and validity of a scale about fluid overload symptoms in patients with heart failure.
Background
Fluid overload symptoms are a common cause of admission of patients with heart failure. An instrument that is quick to complete and easy to use for the measurement of fluid overload symptoms would be beneficial for early intervention and avoidance of hospital admission.
Methods
Fifty-six participants were recruited from cardiology wards. Internal consistency reliability was assessed using Cronbach's alpha coefficient. Validity was assessed using Pearson's correlation coefficient and Exploratory Factor Analysis.
Results
This new instrument had a Cronbach's alpha of .81. Exploratory Factor Analysis revealed two factors (breathing symptoms and body fluid accumulation symptoms) with acceptable criterion validity.
Conclusions
The fluid overload symptoms scale exhibits reliability with construct and criterion validity. It would be more beneficial if further testing is done.
Dyspnea and fear of suffocation are burdensome to patients with respiratory disease. Inspiratory resistive loads offer an experimental respiratory stimulus to quantify the discriminative domain of respiratory perception. Resistive (R) load magnitude estimation (ME) and subjective ratings were measured over sustained multiple breaths in healthy subjects. There was no significant group difference between the ME for Breath 1 and 20 for small R loads, but a significant gender difference for large R loads. Subjective responses of fear, fear of suffocation, displeasure, chest pressure, faintness, dizziness, fear of losing control, trembling, and tingling were significantly greater for females. These results demonstrate that ME of large resistive sustained loads elicits nonsignificant increases in ME in females, but a significant decrease in ME for males. The maintenance of ME in females co-occurs with increased aversive processing relative to males.
In the article by S. Schachter and J. Singer, which appeared in Psychological Review (1962, 69(5), 379-399) the following corrections should be made: The superscript "a" should precede the word "All" in the footnote to Table 2. The superscript "a" should appear next to the column heading "Initiates" in Table 3. The following Tables 6-9 should be substituted for those which appeared in print. (The following abstract of this article originally appeared in record 196306064-001.) It is suggested that emotional states may be considered a function of a state of physiological arousal and of a cognition appropriate to this state of arousal. From this follows these propositions: (a) Given a state of physiological arousal for which an individual has no immediate explanation, he will label this state and describe his feelings in terms of the cognitions available to him. (b) Given a state of physiological arousal for which an individual has a completely appropriate explanation, no evaluative needs will arise and the individual is unlikely to label his feelings in terms of the alternative cognitions available. (c) Given the same cognitive circumstances, the individual will react emotionally or describe his feelings as emotions only to the extent that he experiences a state of physiological arousal. An experiment is described which, together with the results of other studies, supports these propositions. (PsycINFO Database Record (c) 2006 APA, all rights reserved).
Dyspnea is a common, distressing symptom of cardiopulmonary and neuromuscular diseases. Since the ATS published a consensus statement on dyspnea in 1999, there has been enormous growth in knowledge about the neurophysiology of dyspnea and increasing interest in dyspnea as a patient-reported outcome.
The purpose of this document is to update the 1999 ATS Consensus Statement on dyspnea.
An interdisciplinary committee of experts representing ATS assemblies on Nursing, Clinical Problems, Sleep and Respiratory Neurobiology, Pulmonary Rehabilitation, and Behavioral Science determined the overall scope of this update through group consensus. Focused literature reviews in key topic areas were conducted by committee members with relevant expertise. The final content of this statement was agreed upon by all members.
Progress has been made in clarifying mechanisms underlying several qualitatively and mechanistically distinct breathing sensations. Brain imaging studies have consistently shown dyspnea stimuli to be correlated with activation of cortico-limbic areas involved with interoception and nociception. Endogenous and exogenous opioids may modulate perception of dyspnea. Instruments for measuring dyspnea are often poorly characterized; a framework is proposed for more consistent identification of measurement domains.
Progress in treatment of dyspnea has not matched progress in elucidating underlying mechanisms. There is a critical need for interdisciplinary translational research to connect dyspnea mechanisms with clinical treatment and to validate dyspnea measures as patient-reported outcomes for clinical trials.
Despite the importance of respiration and hyperventilation in anxiety disorders, research on breathing disturbances associated with hyperventilation is rare in the field of music performance anxiety (MPA, also known as stage fright). The only comparable study in this area reported a positive correlation between negative feelings of MPA and hyperventilation complaints during performance. The goals of this study were (a) to extend these previous findings to the period before performance, (b) to test whether a positive correlation also exists between hyperventilation complaints and the experience of stage fright as a problem, (c) to investigate instrument-specific symptom reporting, and (d) to confirm gender differences in negative feelings of MPA and hyperventilation complaints reported in other studies.
We assessed 169 university students of classical music with a questionnaire comprising: the State-Trait Anxiety Inventory for negative feelings of MPA, the Nijmegen Questionnaire for hyperventilation complaints, and a single item for the experience of stage fright as a problem.
We found a significant positive correlation between hyperventilation complaints and negative feelings of MPA before performance and a significant positive correlation between hyperventilation complaints and the experience of stage fright as a problem. Wind musicians/singers reported a significantly higher frequency of respiratory symptoms than other musicians. Furthermore, women scored significantly higher on hyperventilation complaints and negative feelings of MPA.
These results further the findings of previous reports by suggesting that breathing disturbances associated with hyperventilation may play a role in MPA prior to going on stage. Experimental studies are needed to confirm whether hyperventilation complaints associated with negative feelings of MPA manifest themselves at the physiological level.
Various theories about the genesis of dyspnea have often assumed that the sensation is similar from patient to patient and is generated by a single underlying mechanism. To investigate whether breathlessness induced in normal volunteers by different stimuli represents one or more than one sensation, we studied 30 subjects in whom breathlessness was induced by each of 8 different stimuli: breath-holding, CO2 inhalation, inhalation of CO2, with ventilation voluntarily targeted below the level dictated by chemical drive, breathing with a resistive load, breathing with an elastic load, voluntary elevation of functional residual capacity, voluntary limitation of tidal volume, and exercise. For each stimulus, subjects were asked to choose description of their sensation(s) of breathlessness from a questionnaire listing 19 descriptors. The responses from this questionnaire were evaluated using cluster analysis to search for relationships among descriptors and to identify natural groupings. We found that distinct groups of descriptors emerged, i.e., subjects could distinguish different sensations of breathlessness. In addition, we found an association between certain descriptor groups and stimuli. We conclude that the term breathlessness may encompass multiple sensations, and, therefore, may not be explainable by a single physiologic mechanism.
Most current models in health psychology assume that stress adversely affects physical health. We re-examined this assumption by reviewing extensive data from the literature and from six samples of our own, in which we collected measures of personality, health and fitness, stress, and current emotional functioning. Results indicate that self-report health measures reflect a pervasive mood disposition of negative affectivity (NA); self-report stress scales also contain a substantial NA component. However, although NA is correlated with health compliant scales, it is not strongly or consistently related to actual, long-term health status, and thus will act as a general nuisance factor in health research. Because self-report measures of stress and health both contain a significant NA component, correlations between such measures likely overestimate the true association between stress and health. Results demonstrate the importance of including different types of health measures in health psychology research.
Previous research has found differences in respiratory function between panic disorder and other anxiety disorder populations. These differences have been explained as reflecting either a) a specific feature of panic disorder, b) merely a sign of increased general arousal, or c) a result of population sampling error. The current study addressed the question of such differences by using improved methodology over previous research. A preliminary evaluation of respiratory symptoms during panic attacks was undertaken as a means of identifying a respiratory-sensitive subtype of the panic patient.
Seventeen panic disorder patients (PD), 18 patients with generalized anxiety disorder (GAD), and 20 normal control (NC) subjects were administered a psychophysiological evaluation composed of baseline, stressor, and recovery phases. Panic patients were measured for the severity of respiratory symptoms during panic attacks. End-tidal CO2 (EtCO2) and respiration rate were measured throughout the psychophysiological evaluation.
PDs demonstrated significantly lower baseline EtCO2 levels than the GADs and NCs, in spite of being equivalent to GADs on baseline anxiety levels. Moreover, panic patients reporting a high level of respiratory symptoms during panic attacks seemed to account for the bulk of observed differences.
These findings lend support to a group of studies showing differences in respiratory function between panic disorder and other anxiety disorder populations. In addition, this study provides preliminary support for the presence of a distinct "hyperventilation subtype" of panic disorder. The implications of these findings for future research and treatment are discussed.
Inhalations of high concentrations of carbon dioxide (CO2) reliably produce panic attacks in patients with panic disorder. The present study evaluated whether cognitive-behavioral treatment (CBT) for panic disorder would extinguish CO2-induced panic and whether changes in panic and arousal-related cognitions were associated with the induction of panic. Patients with panic disorder (N = 54) were assigned to 1 of 3 experimental conditions: CBT with respiratory training (CBT-R), CBT without respiratory training (CBT), or delayed treatment. Participants received 5 repeated vital-capacity inhalations of 35% CO2/65% O2 prior to and following either 12 treatment sessions or a 12-week waiting period. During pretreatment assessments, 74% of patients experienced a panic attack during at least 1 inhalation. At posttreatment, only 20% of treated participants (CBT-R = 19%, CBT = 22%), compared with 64% of untreated participants, panicked. Forty-four percent of treated participants, compared with 0% of untreated participants, reported no anxiety during all posttreatment inhalations. Anxiety sensitivity as well as panic appraisals regarding the likelihood of panic and self-efficacy with coping with panic were significantly related to fearful responding to the CO2 challenge.
Dyspnea in patients could arise from both an urge to breathe and increased effort of breathing. Two qualitatively different sensations, "air hunger" and "respiratory work and effort," arising from different afferent sources are hypothesized. In the laboratory, breathing below the spontaneous level may produce an uncomfortable sensation of air hunger, and breathing above it a sensation of work or effort. Measurement of a single sensory dimension cannot distinguish these as separate sensations; we therefore measured two sensory dimensions and attempted to vary them independently. In five normal subjects we obtained simultaneous ratings of air hunger and of work and effort while independently varying PCO(2) or the level of targeted voluntary breathing. We found a difference in response to the two stimulus dimensions: air hunger ratings changed more steeply when PCO(2) was altered and ventilation was constant; work or effort ratings changed more steeply when ventilation was altered and PCO(2) was constant. We conclude that "air hunger" is qualitatively different from "work and effort" and arises from different afferent sources.
It is suggested that emotional states may be considered a function of a state of physiological arousal and of a cognition appropriate to this state of arousal. From this follows these propositions: (a) Given a state of physiological arousal for which an individual has no immediate explanation, he will label this state and describe his feelings in terms of the cognitions available to him (b) Given a state of physiological arousal for which an individual has a completely appropriate explanation, no evaluative needs will arise and the individual is unlikely to label his feelings in terms of the alternative cognitions available. (c) Given the same cognitive circumstances, the individual will react emotionally or describe his feelings as emotions only to the extent that he experiences a state of physiological arousal. An experiment is described which, together with the results of other studies, supports these propositions.
The authors examine 6 theories of panic attacks as to whether empirical approaches are capable of falsifying them and their heuristic value. The authors conclude that the catastrophic cognitions theory is least falsifiable because of the elusive nature of thoughts but that it has greatly stimulated research and therapy. The vicious circle theory is falsifiable only if the frightening internal sensations are specified. The 3-alarms theory postulates an indeterminate classification of attacks. Hyperventilation theory has been falsified. The suffocation false alarm theory lacks biological parameters that unambiguously index dyspnea or its distinction between anticipatory and panic anxiety. Some correspondences postulated between clinical phenomena and brain areas by the neuroanatomical hypothesis may be falsifiable if panic does not depend on specific thoughts. All these theories have heuristic value, and their unfalsifiable aspects are capable of modification.
This is Robert Fried's third book on the crucial role of breathing and hyperventilation in our emotional and physical health. The first, The Hyperventilation Syndrome (1987), was a scholarly monograph, and the second, The Breath Connection (1990a), was a popular version for the lay reader. This book combines the best features of both and extends Dr. Fried's seminal work to protocols for clinical psychophysiology and psy chiatry. Hoping to avoid misunderstanding, he has taken systematic care to introduce relevant electrical, physiological, and psychological concepts in operational language for the widest possible professional audience. Any clinician not thoroughly experienced in respiratory psycho physiology and biofeedback will leave these pages with profound new insight and direction into an aspect of our liveswhich we innocently take for granted as "common sense"-the role of breathing in health and illness. Einstein viewed such common sense as "that set of prejudices we acquired prior to the age of eighteen." I am impressed that Dr. Fried mirrors Einstein's uncanny genius in not accepting the obvious breathing is not "common sense" but, rather, is a pivotal psycho physiological mechanism underlying all aspects of life.
A carbon dioxide hypersensitivity theory of panic has been posited. We hypothesize more broadly that a physiologic misinterpretation by a suffocation monitor rnisfires an evolved suffocation alarm system. This produces sudden respiratory distress followed swiftly by a brief hyperventilation, panic, and the urge to flee. Carbon dioxide hypersensitivity is seen as due to the deranged suffocation alarm monitor. If other indicators of potential suffocation provoke panic, this theoretical extension is supported. We broadly pursue this theory by examining Ondine's Curse ae the physiologic and phalmacologic converse of panic disorder, splitting panic in terms of symptomatology and challenge studies, reevaluating the role of hyperventilation, and reinterpreting the contagiousness of sighing and yawning, as well ae maes hysteria. Further, the phenomena of panic during relaxation and sleep, late luteal phaee dysphoric disorder, pregnancy, childbirth, pulmonary disease, separation anxiety, and treatment are used to test and illuminate the suffocation false alann theory. Recent advances with regard to ambulatory monitoring of paI~ic disorder, catbon monoxide prevention of carbon dioxide panicogenesis, and naloxone/lactate challenge in normals will be presented.
Objective: Previous research has found differences in respiratory function between panic disorder and other anxiety disorder populations. These differences have been explained as reflecting either a) a specific feature of panic disorder, b) merely a sign of increased general arousal, or c) a result of population sampling error. The current study addressed the question of such differences by using improved methodology over previous research. A preliminary evaluation of respiratory symptoms during panic attacks was undertaken as a means of identifying a respiratory-sensitive subtype of the panic patient. Method: Seventeen panic disorder patients (PD), 18 patients with generalized anxiety disorder (GAD), and 20 normal control (NC) subjects were administered a psychophysiological evaluation composed of baseline, stressor, and recovery phases. Panic patients were measured for the severity of respiratory symptoms during panic attacks. End-tidal CO2 (EtCO2) and respiration rate were measured throughout the psychophysiological evaluation. Results: PDs demonstrated significantly lower baseline EtCO2 levels than the GADs and NCs, in spite of being equivalent to GADs on baseline anxiety levels. Moreover, panic patients reporting a high level of respiratory symptoms during panic attacks seemed to account for the bulk of observed differences. Conclusions: These findings lend support to a group of studies showing differences in respiratory function between panic disorder and other anxiety disorder populations. In addition, this study provides preliminary support for the presence of a distinct "hyperventilation subtype" of panic disorder. The implications of these findings for future research and treatment are discussed.
Inhalations of high concentrations of carbon dioxide (CO₂) reliably produce panic attacks in patients with panic disorder. The present study evaluated whether cognitive–behavioral treatment (CBT) for panic disorder would extinguish CO₂-induced panic and whether changes in panic and arousal-related cognitions were associated with the induction of panic. Patients with panic disorder (N = 54) were assigned to 1 of 3 experimental conditions: CBT with respiratory training (CBT-R), CBT without respiratory training (CBT), or delayed treatment. Participants received 5 repeated vital-capacity inhalations of 35% CO₂/65% O₂ prior to and following either 12 treatment sessions or a 12-week waiting period. During pretreatment assessments, 74% of patients experienced a panic attack during at least 1 inhalation. At posttreatments only 20% of treated participants (CBT-R = 19%, CBT = 22%), compared with 64% of untreated participants, panicked. Forty-four percent of treated participants, compared with 0% of untreated participants, reported no anxiety during all posttreatment inhalations. Anxiety sensitivity as well as panic appraisals regarding the likelihood of panic and self-efficacy with coping with panic were significantly related to fearful responding to the CO₂ challenge. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Dysregulation within both respiratory control systems and the hypothalamic-pituitary adrenal (HPA) axis has been implicated in the pathophysiological of panic disorder. However, potential linkages between respiration and the HPA axis have rarely been examined in panic patients. We have previously published neuroendocrine and psychophysiological response data from a laboratory panic model using the respiratory stimulant doxapram. We now present a new, theoretically driven re-examination of linkages between HPA axis and respiratory measures in this model. Previous analyses showed elevated corticotropin (ACTH) and persistent tidal volume irregularity in panic patients, due to a high frequency of sighs. Regression analyses now show that tidal volume irregularity and sigh frequency were strongly predicted by pre-challenge ACTH levels, but not by subjective distress or panic symptoms. We predicted this relationship on the basis of our hypothesis that both the HPA axis and respiratory control systems may be reactive to contextual cues such as novelty or anticipation of future challenge. Follow-up work is needed to directly test this hypothesis. Depression and Anxiety, 2008. Published 2007 Wiley-Liss, Inc.
Guidelines are proposed for the collection, analysis, and description of electromyographic (EMG) data. The guidelines cover technological issues in EMG recording, social aspects of EMG experimentation, and limits to inferences that can be drawn in EMG research. An atlas is proposed for facial EMG electrode placements, and standard EMG terminology is suggested.
It's logical to think that the brain's need for oxygen is what limits how long people can hold their breath. Logical, but not the whole story
Although dyspnea is a common and troubling symptom, our understanding of the neurophysiology of dyspnea is woefully incomplete. Most measurements of dyspnea treat it as a single entity. Although the multidimensional dyspnea concept has been mentioned for many decades, only recently has the concept been the subject of experimental tests. Emerging evidence has begun to favor the hypothesis that dyspnea comprises multiple dimensions or components that can be measured as different entities. Most recently, studies have begun to show that there is a separable ‘affective dimension’ (i.e. unpleasantness and emotional impact). Understanding of the multidimensional measurement of pain is far in advance of dyspnea, and has enabled progress in the neurophysiology of pain, including identification of separate neural structures subserving various elements of pain perception. We propose here a multidimensional model of dyspnea based on a state-of-the-art pain model, and review existing evidence in the light of this model.
A cognitive model of panic is described. Within this model panic attacks are said to result from the catastrophic misinterpretation of certain bodily sensations. The sensations which are misinterpreted are mainly those involved in normal anxiety responses (e.g. palpitations, breathlessness, dizziness etc.) but also include some other sensations. The catastrophic misinterpretation involves perceiving these sensations as much more dangerous than they really are (e.g. perceiving palpitations as evidence of an impending heart attack). A review of the literature indicates that the proposed model is consistent with the major features of panic. In particular, it is consistent with the nature of the cognitive disturbance in panic patients, the perceived sequence of events in an attack, the occurrence of ‘spontaneous’ attacks, the role of hyperventilation in attacks, the effects of sodium lactate and the literature on psychological and pharmacological treatments. Finally, a series of direct tests of the model are proposed.
Spontaneous or unexpected panic attacks, per definition, occur "out of the blue," in the absence of cues or triggers. Accordingly, physiological arousal or instability should occur at the onset of, or during, the attack, but not preceding it. To test this hypothesis, we examined if points of significant autonomic changes preceded the onset of spontaneous panic attacks.
Forty-three panic disorder patients underwent repeated 24-hour ambulatory monitoring. Thirteen natural panic attacks were recorded during 1960 hours of monitoring. Minute-by-minute epochs beginning 60 minutes before and continuing to 10 minutes after the onset of individual attacks were examined for respiration, heart rate, and skin conductance level. Measures were controlled for physical activity and vocalization and compared with time matched control periods within the same person.
Significant patterns of instability across a number of autonomic and respiratory variables were detected as early as 47 minutes before panic onset. The final minutes before onset were dominated by respiratory changes, with significant decreases in tidal volume followed by abrupt carbon dioxide partial pressure increases. Panic attack onset was characterized by heart rate and tidal volume increases and a drop in carbon dioxide partial pressure. Symptom report was consistent with these changes. Skin conductance levels were generally elevated in the hour before, and during, the attacks. Changes in the matched control periods were largely absent.
Significant autonomic irregularities preceded the onset of attacks that were reported as abrupt and unexpected. The findings invite reconsideration of the current diagnostic distinction between uncued and cued panic attacks.
To examine bidirectional influences of onset of psychiatric disorders and nicotine dependence among adolescent smokers.
A prospective longitudinal cohort of adolescents and mothers drawn from a large city school system. Adolescents were interviewed five times and mothers three times over 2 years.
Chicago, Illinois.
Subsample of adolescent smokers (n = 814).
Selected DSM-IV psychiatric disorders, nicotine dependence and selected risk factors were ascertained.
Among lifetime smokers, 53.7% experienced at least one nicotine dependence criterion; 26.1% full dependence; 14.1% experienced an anxiety disorder, 18.8% a mood disorder and 29.5% a disruptive disorder. Nicotine dependence and psychiatric disorders were comorbid: nicotine-dependent youths had higher rates of individual and multiple disorders than those not dependent. Controlling for other covariates, mood disorder and nicotine dependence did not predict each other; anxiety disorder predicted nicotine dependence. Bidirectional influences were observed for disruptive disorder and nicotine dependence. Predictors of onset of full nicotine dependence included earlier onset age of tobacco use, high initial pleasant sensitivity to tobacco, alcohol and illicit drug use, abuse and dependence and parental nicotine dependence. Predictors of psychiatric disorder onset included gender, race/ethnicity, other psychiatric disorders, illicit drug abuse or dependence and parental depression and delinquency.
Initial pleasant experiences of smoking are predictive of later development of nicotine dependence. There may be reciprocal influences between disruptive disorder and development of nicotine dependence in adolescence, and intergenerational transmission of parental nicotine dependence and psychopathology.
The mechanisms and pathways of the sensation of dyspnea are incompletely understood, but recent studies have provided some clarification. Studies of patients with cord transection or polio, induced spinal anesthesia, or induced respiratory muscle paralysis indicate that activation of the respiratory muscles is not essential for the perception of dyspnea. Similarly, reflex chemostimulation by CO₂ causes dyspnea, even in the presence of respiratory muscle paralysis or cord transection, indicating that reflex chemoreceptor stimulation per se is dyspnogenic. Sensory afferents in the vagus nerves have been considered to be closely associated with dyspnea, but the data were conflicting. However, recent studies have provided evidence of pulmonary vagal C-fiber involvement in the genesis of dyspnea, and recent animal data provide a basis to reconcile differences in responses to various C-fiber stimuli, based on the ganglionic origin of the C fibers. Brain imaging studies have provided information on central pathways subserving dyspnea: Dyspnea is associated with activation of the limbic system, especially the insular area. These findings permit a clearer understanding of the mechanisms of dyspnea: Afferent information from reflex stimulation of the peripheral sensors (chemoreceptors and/or vagal C fibers) is processed centrally in the limbic system and sensorimotor cortex and results in increased neural output to the respiratory muscles. A perturbation in the ventilatory response due to weakness, paralysis, or increased mechanical load generates afferent information from vagal receptors in the lungs (and possibly mechanoreceptors in the respiratory muscles) to the sensorimotor cortex and results in the sensation of dyspnea.
Our objective is to summarize the new findings concerning the respiratory subtype (RS) of panic disorder (PD) since its first description.
Two searches were made in the Institute for Scientific Information Web of Science: with the keywords "panic disorder" and "respiratory symptoms," and all articles that cited Briggs and colleagues' 1993 article "Subtyping of Panic Disorder by Symptom Profile" (Br J Psychiatry 1993;163:201-9). Altogether, 133 articles were reviewed.
We describe and discuss RS epidemiology, genetics, psychopathology, demographic features, clinical features, correlations with the respiratory system, traumatic suffocation history, provocative tests, and nocturnal panic. Compared to patients with the nonrespiratory subtype (non-RS), the RS patients had higher familial history of PD, lower comorbidity with depression, longer duration of illness, lower neuroticism scores, and higher scores in severity scales, such as the Panic and Agoraphobia Scale, Panic-Agoraphobia Spectrum scale and the Clinical Global Impression scale. Tests to induce panic attacks, such as those with CO(2), hyperventilation, and caffeine, produce panic attacks in a higher proportion of RS patients than non-RS patients. Differences in the subtypes' improvement with the pharmacologic treatment were found. There are also some controversial findings regarding the RS, including the age of onset of PD, and alcohol and tobacco use in RS patients.
Some characteristics, such as the increased sensitivity to CO(2) and the higher familial history of PD, clearly distinguish the RS from the non-RS. Nevertheless, there are also controversial findings. More studies are needed to determine the validity of the RS subtype.
Blood-injection-injury (BII) phobia patients sometimes faint during exposure to relevant stimuli. However, mechanisms and timing of physiological adjustments in BII phobia remain poorly understood. In a larger sample of 60 patients and 20 controls, we sought to replicate findings of a prior study demonstrating the role of hyperventilation in the phobic response. We also investigated the timing of respiratory adjustment across an extended exposure recovery period. In addition, because intense disgust is commonly reported by patients, responses to surgery films were compared to a pure disgust film. End-tidal PCO(2) dropped significantly while volume and flow increased during the surgery film in patients compared to controls and to other emotional films except disgust. Patients recovered quickly following the disgust film but not the surgery film. PCO(2), volume, and flow parameters showed robust associations with anxiety, disgust, and physical symptoms. Findings suggest that respiratory adjustments during and after phobic exposure may provide a critical missing link in the understanding of the psychophysiology of this singular disorder, including why fainting often occurs after the stimulus is removed.
Dyspnea is defined as an uncomfortable awareness of the need to breathe. Verbal report of dyspnea can be a valuable source of diagnostic information. However, little is known about the cognitive representation of respiratory sensations and about their affective evaluation in individuals not suffering from respiratory disease. Such knowledge would be important in evaluating the comparability of respiratory sensation report between healthy controls and patient groups.
Five hundred and eighty-two healthy individuals rated 20 descriptors of respiratory sensation with regard to frequency, valence, and situational incidence. Ratings were analysed on the level of subgroups of items found with cluster analysis and Multidimensional Scaling (MDS).
Not all respiratory sensations commonly subsumed under dyspnea are perceived to be uncomfortable by healthy individuals. Two higher-order clusters were found, interpreted as (1) compensation of dyspnea and (2) breathing deficiencies. Breathing deficiencies were unknown by approximately 50% of participants and rated to be less frequent and more uncomfortable than compensation of dyspnea. Furthermore, three dimensions of respiratory sensations were found using MDS interpreted as (1) fit between need for air and actual breathing, (2) effort, and (3) attempt of voluntary control.
The extent to which respiratory sensation ratings can be compared between patients and healthy individuals is limited. Latent dimensions of dyspnea might be less affected by differences in interpretation and evaluation of language descriptors of dyspnea and could help to assess comparability of sensation report between groups with different experiential background regarding breathlessness.
Using surface electrodes we have measured the shift in the power spectrum of intercostal and diaphragmatic EMG as an indicator of inspiratory muscle fatigue. The ECG was gated and the unfiltered EMG was passed through two band-pass filters with ranges of 20-46.7 Hz (L) and 150-350 Hz (H) respectively. The signals were subsequently rectified, integrated and the integrals expressed as a ratio of high to low frequency power (H/L). This ratio declines when the muscle is performing fatiguing work. We have observed a fall in intercostal H/L during exercise in patients with chronic airflow limitation and with ankylosing spondylitis. Therefore, inspiratory muscle fatigue may be an important factor limiting exercise in patients with respiratory disease. If so, training of the respiratory muscles should improve exercise tolerance. Training can be accomplished by breathing through a resistance just sufficient to produce fatigue, placed on the inspiratory side of a Hans-Rudolph valve for 15 min twice a day. Over a 16-week training period in a group of quadriplegics maximum inspiratory mouth pressures increased 40% while the inspiratory pressure swings just sufficient to produce fatigue increased by circa 80%. Similar results are being obtained in patients with chronic airflow limitation. We conclude that inspiratory muscle training improves both strength and endurance and should lead to improved exercise tolerance in patients, in whom inspiratory muscle fatigue limits performance.
Previous research has indicated that reports of panic attacks are associated with a different set of symptoms to reports of generalized anxiety. The present two studies attempted to extend these findings to specific (situational) fears. In Study 1, 55 subjects with panic disorder were compared on their symptom profile during their panic attacks to 65 subjects with other anxiety disorders [simple phobia, social phobia and obsessive-compulsive disorder (OCD)] during response to their feared cue. The results indicated that, compared to subjects with other anxiety disorders, subjects with panic disorder were more likely to report parasthesias, dizziness, faintness, unreality, dyspnea, fear of dying and fear of going crazy/losing control. In Study 2, 90 subjects meeting diagnostic criteria for both panic disorder and another anxiety disorder (simple phobia, social phobia or OCD) were compared on the symptoms experienced during their unexpected panic attacks and their situationally-triggered fears respectively. Combining the symptoms found in Study 1 to differ between the groups into a linear combination, there was a significant interaction found between the type of fear reaction (panic attack vs cued fear response) and symptom group. Taken together, these findings suggest that reports of unexpected panic attacks associated with panic disorder are characterized by a different symptom profile to reports of specific fear reactions that are part of a phobic disorder or OCD.
This report represents a pilot investigation of the role of chest muscle electromyographic (EMG) activity in developing panic episodes. Chest EMG activity was obtained as part of a larger study examining ventilatory differences between panic sufferers and normal controls. Frontalis EMG, heart rate, and minute ventilation (breathing rate and tidal volume) were also obtained during the study. The ventilatory procedure involved exposing the subjects to three periods of carbon dioxide gas inhalations (1%, 3%, 5%; balance oxygen). Subjective measures of frightening cognitions and body sensations were obtained across the inhalation phases as well. The panic disorder subjects were divided, on the basis of subjective anxiety ratings obtained throughout the study, into high anxious (HA) and low anxious (LA) panic disorder groups. The HA panic disorder patients exhibited significantly higher chest EMG activity than the LA panic disorder patients and controls across all phases of the experiment. In addition, the chest EMG predicted, better than the other physiologic measures, the number of frightening cognitions and sensations reported by the subjects during the baseline and 5% CO2 inhalation phases. Overall, the results were supportive of the further study of chest wall EMG activity in the pathogenesis of panic attacks.
The purpose of this study was to determine the predictor variables for breathlessness and to investigate the criteria of reliability and responsiveness for measuring breathlessness during progressive, incremental exercise on the cycle ergometer. We studied a heterogeneous group of patients with stable asthma (mean +/- SEM age, 46 +/- 4 yr) for four visits at weekly intervals. Predictor variables were determined at the first visit. Nine independent physiologic variables were obtained at each minute during exercise; the Borg rating of breathlessness (range 0 to 10) was used as the dependent variable. The regression model relating the physiologic parameters to the Borg rating of breathlessness was highly significant (model F = 43.4; p = 0.0001). Backward elimination selected the strongest predictors of the Borg rating: peak inspiratory flow (VI); tidal volume (VT)/FVC; frequency of respiration (f); and peak inspiratory mouth pressures (Pm). These four variables explained 63% of the variance in the rating of dyspnea. Each of the four variables exhibited a linear relationship with the Borg rating. Test-retest reliability was assessed by comparing results at the first and second visits. Individual slopes (except for VT/FVC) and intercepts for the four predictor variables versus Borg ratings were highly reliable. The slope for work intensity (watts) and Borg ratings, but not the intercept, was highly reliable. Responsiveness was evaluated by randomly administering inhaled methacholine or inhaled metaproterenol, alternately, at the third and fourth visits to induce acute changes in lung function before exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
This paper explains how a hyperventilation theory of panic disorder accounts for panic attacks during relaxation and relaxation-induced anxiety. The explanation is based on the observation that chronic hyperventilators maintain a steady state of low pCO2 (arterial carbon dioxide tension) and are, therefore, sensitive to relatively small increases in ventilation when metabolism is low and to relatively sudden reductions in metabolism when ventilation is relatively constant. Thus, if minute volume of air breathed remains constant while the metabolic production of CO2 decreases, as in the case of one who sits down or lies down to relax, respiratory hypocapnea may increase in intensity until it produces the familiar sensations which mark the panic attack. Data from relevant studies of panic attacks during relaxation support the hyperventilation interpretation.
Guidelines are proposed for the collection, analysis, and description of electromyographic (EMG) data. The guidelines cover technological issues in EMG recording, social aspects of EMG experimentation, and limits to inferences that can be drawn in EMG research. An atlas is proposed for facial EMG electrode placements, and standard EMG terminology is suggested.
A distinction is proposed between anxiety (frequency of symptom occurrence) and anxiety sensitivity (beliefs that anxiety experiences have negative implications). In Study 1, a newly-constructed Anxiety Sensitivity Index (ASI) was shown to have sound psychometric properties for each of two samples of college students. The important finding was that people who tend to endorse one negative implication for anxiety also tend to endorse other negative implications. In Study 2, the ASI was found to be especially associated with agoraphobia and generally associated with anxiety disorders. In Study 3, the ASI explained variance on the Fear Survey Schedule—II that was not explained by either the Taylor Manifest Anxiety Scale or a reliable Anxiety Frequency Checklist. In predicting the development of fears, and possibly other anxiety disorders, it may be more important to know what the person thinks will happen as a result of becoming anxious than how often the person actually experiences anxiety. Implications are discussed for competing views of the ‘fear of fear’.
Characteristics of the subjective symptomatology of asthma were explored within a group of 100 asthma inpatients. Patients rated the relative frequency with which 77 symptom adjectives were associated with asthma attacks. Key cluster analysis of the full set of 77 adjectives identified 5 symptom clusters: Two Mood clusters, Panic Fear and Irritability, describe affective states concomitant with asthma, while two Somatic clusters, Hyperventilation Hypocapnia and Bronchoconstriction, describe reports of more specific bodily symptoms. The fifth symptom cluster, Fatigue, describes the reduced energy level accompanying acute asthma. For the Mood symptom clusters, an increase in Panic Fear and Irritability was reported to occur frequently by 42% and 34% of the patients respectively. For the Somatic symptom clusters, 9% and 91% of the patients reported the frequent occurrence of Hyperventilation Hypocapnia and Bronchoconstriction symptoms. 78% reported the frequent occurrence of Fatigue. Reports of Bronchoconstriction were almost independent of the Mood clusters, Panic Fear (r = 0.20) and Irritability (r = 0.18), although associated with increased reports of Fatigue (r = 0.43). In contrast, Hyperventilation Hypocapnia was more highly related to both reports of Panic Fear (r = 0.38) and Irritability (r = 0.39) during acute asthma episodes. This study suggests that complex patterning of subjective symptomatology is common in asthma. Symptom patterns described across each of the 5 symptom clusters may help to define coping styles related to the role of emotions in asthma and the course of illness.
The effects of bilateral alternating out-of-phase vibrations were studied in 10 normal healthy subjects and five asthmatic patients. The second or third intercostal spaces were vibrated during expiration, and the seventh to ninth intercostal spaces were vibrated during inspiration. Most subjects sensed breathlessness during such vibrations, and 100 Hz was most effective. The degree of breathlessness correlated positively with increased respiratory rate. Respiratory rate increased from 14.1 +/- 3.78 (mean +/- SD) to 22.3 +/- 7.14 breaths/min (P less than 0.05) during relatively severe breathlessness and to 20.39 +/- 5.66 breaths/min (P less than 0.05) during less uncomfortable sensation. Slight or negligible breathlessness induced no significant increase in rate (15.33 +/- 4.19 breaths/min). All asthma patients described the sensations during vibration as similar to those during asthma attacks, and their respiratory rates increased 20.7 +/- 11.03% during 100 Hz vibration (P less than 0.01). It is suggested that the uncomfortable sensation of breathlessness may be induced by muscle spindles in the intercostal muscles being activated out of phase with the respiratory cycle. The central mechanism that receives the intercostal afferents may have a certain gate that operates in relation to the sensation of breathlessness.
The purpose of this article is to offer a comprehensive, data-based explanation of the relationship between hyperventilation and panic disorder linking CO2 hypersensitivity, cognitive/behavioral factors, and the respiratory effects of antipanic pharmacologic and psychological treatments.
The authors conducted a computerized search of MEDLINE for relevant articles.
Some panic patients have a chronic, subtle respiratory disturbance. Acute hyperventilation is neither necessary nor sufficient for panic to occur. Respiratory abnormalities in panic patients may adaptively aim at coping with a hypersensitive CO2 chemoreceptor system. Pharmacologic panicogens also stimulate the respiratory system, causing hyperventilation. Triggering this hypersensitive respiratory control mechanism may incite panic. Antipanic medications may reset the receptor threshold. Misattribution and catastrophic interpretation of somatic symptoms or the sense of loss of control may contribute to panic symptoms. Behavioral interventions such as desensitization or breathing retraining may block the full-blown attack. Cognitive strategies through cognitive control of respiration may supplement and accentuate these interventions.
Panic disorder may be due to an inherently unstable autonomic nervous system, coupled with cognitive distress.
A carbon dioxide hypersensitivity theory of panic has been posited. We hypothesize more broadly that a physiologic misinterpretation by a suffocation monitor misfires an evolved suffocation alarm system. This produces sudden respiratory distress followed swiftly by a brief hyperventilation, panic, and the urge to flee. Carbon dioxide hypersensitivity is seen as due to the deranged suffocation alarm monitor. If other indicators of potential suffocation provoke panic this theoretical extension is supported. We broadly pursue this theory by examining Ondine's curse as the physiologic and pharmacologic converse of panic disorder, splitting panic in terms of symptomatology and challenge studies, reevaluating the role of hyperventilation, and reinterpreting the contagiousness of sighing and yawning, as well as mass hysteria. Further, the phenomena of panic during relaxation and sleep, late luteal phase dysphoric disorder, pregnancy, childbirth, pulmonary disease, separation anxiety, and treatment are used to test and illuminate the suffocation false alarm theory.
Hyperventilation has been posed as an important symptom-producing mechanism in panic attacks. Some arguments and experimental findings, such as the possibility of inducing panic symptoms by voluntary hyperventilation in panic disorder patients, seem to favor this suggestion. This study was undertaken to clarify the role of hyperventilation in panic disorder. Long-term ambulatory measurement of transcutaneous arterial CO2 pressure (PCO2) offers an opportunity to test directly the co-occurrence of panic and hyperventilation under natural conditions.
Transcutaneous PCO2 was measured during three to four sessions of approximately 7 hours each in 28 panic disorder patients. Patients were instructed to expose themselves to fear-provoking situations and to press a button as soon as they experienced panic. One-half of the patients experienced one or more panic attacks during these sessions.
A decrease in PCO2 was observed during only one of the 24 registered panic attacks that lasted at least 3 minutes. Even during this particular attack, the degree of hyperventilation was not impressive.
These findings indicate that the hypothesis that hyperventilation is an important symptom-producing mechanism in panic may be dismissed.
The effect of sympathetic activation on the spindle afferent response to vibratory stimuli eliciting the tonic vibration reflex in jaw closing muscles was studied in precollicularly decerebrate rabbits. Stimulation of the cervical sympathetic trunk, at frequencies within the physiologic range, consistently induced a decrease in spindle response to muscle vibration, which was often preceded by a transient enhancement. Spindle discharge was usually correlated with the EMG activity in the masseter muscle and the tension reflexly developed by jaw muscles. The changes in spindle response to vibration were superimposed on variations of the basal discharge which exhibited different patterns in the studied units, increases in the firing rate being more frequently observed. These effects were mimicked by close arterial injection of the selective alpha 1-adrenoceptor agonist phenylephrine. Data presented here suggest that sympathetically-induced modifications of the tonic vibration reflex are due to changes exerted on muscle spindle afferent information.
Pulmonary hyperinflation is usually defined as an abnormal increase in functional residual capacity, i.e. lung volume at the end of tidal expiration. As such, it is virtually universal in patients with symptomatic diffuse airway obstruction. Hyperinflation inferred from a standard chest radiograph implies an increase in total lung capacity. The relaxation volume of the respiratory system (Vr) increases in patients with chronic airway disease as a result of changes in the elastic properties of the lungs and chest wall. In addition, a variable degree of dynamic hyperinflation may be present. This results from the onset of inspiration before lung volume has fallen to Vr. Dynamic hyperinflation is frequently present at rest in patients with moderate-to-severe airway obstruction, and it increases further on exercise, thereby increasing the mechanical load on the inspiratory muscles and at the same time reducing their mechanical advantage. Important clinical consequences and associations of hyperinflation include: distortions of chest wall motion; impaired inspiratory muscle function; increased oxygen cost of breathing; greater likelihood of hypercapnia; impaired exercise performance; and greater severity of breathlessness. The symptomatic improvement after treatment with a bronchodilator may be due, in part, to lessening of hyperinflation.
The purpose of the present study was to investigate the diagnostic specificity of bodily symptoms and respiratory behavior at rest and after a hyperventilation provocation test (HVPT) in patients that were either grouped according to the DSM classification or diagnosed as suffering from hyperventilation syndrome. Nine hundred three anxiety and somatoform patients, showing symptoms supposedly caused by psychogenic hyperventilation, and 170 healthy subjects, were studied. Breathing pattern and end-tidal CO2 concentration were recorded during breathing at rest and following a HVPT. Subjective symptoms in daily life and after HVPT were measured. A principal-components analysis was performed on both the symptoms and breathing variables and their specificity levels were compared in the two classifications of patients. Some symptoms in daily life were grouped together with the same symptoms after the HVPT, other symptoms were not. This suggests that the HVPT elicited partly specific symptoms, and partly reproduced the symptoms experienced in daily life. Similar findings were observed with respect to the breathing variables. Patients with panic differed from other patients with anxiety disorders by an increased level of symptoms and a FETCO2 decline at rest. The HVPT may be informative for diagnosis because it provokes some of the typical somatic and psychological symptoms, and it identifies the breathing instability that is characteristic of both patients with HVS and with anxiety. The same symptoms and breathing variables characterized the patients, whatever their classification. Overall, the specificity of breathing variables is rather low.
We tested the hypothesis that descriptors of breathlessness represent distinct and separable cognitive constructs, and predicted that the use of descriptors of breathlessness by healthy individuals is the same as their use by patients with cardiopulmonary disease.
Cluster analyses obtained in healthy individuals were compared with those obtained previously in patients who complained of breathing discomfort. In addition, we used multidimensional scaling (MDS) techniques to analyze relationships among descriptors in healthy individuals.
Public university.
The participants were 100 healthy individuals (48 men and 52 women) ranging in age between 18 and 65 years (mean, 27.9+/-11.7 years). Measurements and results: Participants judged the dissimilarity among pairs of 15 descriptors of breathlessness that were used previously to examine the experience of dyspnea in patients who complained of breathing discomfort. Cluster analysis solutions obtained in the healthy individuals were virtually identical to those obtained previously in patients. Three dimensions (attributes) of breathing discomfort were uncovered with MDS: "Depth and frequency of breathing," "Perceived need, or urge, to breathe," and "Difficulty breathing and phase of respiration." The results did not depend on age, sex, levels of education, or the presence of uncomfortable awareness of breathing with activities.
The relations among descriptors of breathlessness obtained in healthy individuals support the contention that the association of different clusters with different disease states reflects distinct and separable cognitive constructs that are not simply dependent on the presence of an underlying pathophysiology or on a specific disease condition. Our results in healthy individuals also suggest that distinct qualities of breathlessness relate to different physiologic mechanisms underlying respiratory discomfort.
Dyspnea is a cardinal symptom of asthma and may arise from several pathophysiological mechanisms, including pulmonary hyperinflation, stimulation of vagal receptors, and, rarely, chemoreceptor stimulation. The language that patients use to describe their breathlessness may provide important clues about the physiology underlying symptoms in a particular patient. Several physiological derangements may contribute to dyspnea in a given individual. The variability in the severity of breathlessness for any given degree of airflow obstruction may relate to differences in the relative importance of these physiological changes and/or to a range of perceptual abilities in asthmatic patients. One hypothesis that is under current investigation is that defective perception of asthma symptoms may lead to undertreatment and the potential for greater morbidity and mortality from asthma.
Anxiety sensitivity refers to fears of anxiety-related sensations. Most often measured by the Anxiety Sensitivity Index (ASI), anxiety sensitivity is a dispositional variable especially elevated in people with panic disorder. Regardless of diagnosis, ASI scores often predict panic symptoms in response to biological challenges (e.g., carbon dioxide inhalation) that provoke feared bodily sensations. Prospective longitudinal studies indicate that scores on the ASI predict subsequent spontaneous attacks, indicating that elevated anxiety sensitivity is a risk factor for panic and perhaps panic disorder. Cognitive behavioral treatment reduces anxiety sensitivity in panic patients, perhaps protecting against relapse. Imipramine likewise decreases anxiety sensitivity.
Patients with panic disorder often report a history of respiratory pathology. Furthermore, panic disorder patients are vulnerable to CO2 challenges. The increased CO2 vulnerability displayed by panic disorder patients may be related to lifetime respiratory pathology. We examined whether panic disorder patients with a history of respiratory disorders are more vulnerable to a 35% CO2 challenge than those without such a history. Ninety-six patients with panic disorder were interviewed about their lifetime respiratory status (asthma, bronchitis and various other respiratory conditions) and underwent the challenge. Immediately before and after the CO2 inhalation, the patients filled out the Visual Analogue Scale for Anxiety (VAS-A) and the Panic Symptom List (PSL). We found no differences between the two panic disorder groups on anxiety (VAS-A), panic symptoms (PSL) or panic attacks after the CO2 challenge. Our results suggest that having a PD is an important factor in CO2 vulnerability independent of a history of respiratory disorders.
Dyspnea is a key symptom in panic attacks. This study investigated different types of dyspnea induced by the 35% CO2 challenge test given to patients with panic disorder (PD). The types of dyspnea provide room for possible conjectures on neurophysiological pathways involved in the experience of breathing discomfort in PD and in the panic-respiration connection. Factor analysis applied to the Dyspnea Questionnaire identified three main factors: breathing effort, sense of suffocation, and rapid breath. Factor scores for breathing effort and sense of suffocation significantly discriminated between patients who did and those who did not report CO2-induced panic attacks. Factor scores for breathing effort significantly discriminated between patients whose reaction resembled their unexpected panic attacks and those whose reaction did not. A dissociation between an increased central respiratory command and a decreased mechanical efficiency of the respiratory response in patients with PD may underlie the breathing effort factor during the CO2 challenge. The sense of suffocation factor was found to be linked to chemosensitivity. Although involved in CO2 reactivity, it may not be a central factor in unexpected panic attacks.