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Examination of Differential Anxiety Sensitivities in Panic Disorder: A Test of Anxiety Sensitivity Subdomains Predicting Fearful Responding to a 35% CO2 Challenge
Abstract
Cognitive conceptualizations of panic disorder suggest that panic is produced and maintained by threatening beliefs associated with autonomic arousal. The present study tested the discriminant validity of the anxiety sensitivity model of panic by assessing the differential predictions of particular anxiety sensitivity domains. A factor analysis of the Body Sensations Questionnaire indicated four nested anxiety sensitivity factors assessing fears of cardiopulmonary, dissociation, numbness, and gastrointestinal sensations. The symptoms assessed by each factor possess varying levels of correspondence to the sensations typically produced during a 35% CO_2 inhalation (i.e., Cardiopulmonary Fears/High Correspondence, Dissociation Fears/Moderate Correspondence, Numbness Fears/Moderate Correspondence, Gastrointestinal Fears/Low Correspondence). It was hypothesized that anxiety sensitivity to the high-correspondence sensations, compared to anxiety sensitivity to moderate- and low-correspondence sensations, would predict greater fearful responding to a 35% CO_2 challenge. Fifty-six participants meeting DSM-IV criteria for panic disorder completed a single vital capacity 35% CO_2 challenge. Consistent with prediction, Cardiopulmonary Fears was the only index that predicted provocation-induced anxiety and symptoms. These findings suggest that specific anxiety sensitivities can provide a more powerful explanatory model for predicting emotional responding in panic disorder.
... The vast majority of laboratory challenge work has focused on CO 2 inhalation or hyperventilation exercises that produce symptoms relevant to ASCC (i.e., derealization) but simultaneously produce many prominent physical sensations (e.g., tachycardia, trouble breathing, chest pain/tightness). Previous work has shown specificity in the perception of internal bodily sensations (Schmidt, 1999). Individuals with high anxiety sensitivity show greater vigilance to sensations corresponding with specific symptom domains (e.g., physical, cognitive, social). ...
... Individuals with high anxiety sensitivity show greater vigilance to sensations corresponding with specific symptom domains (e.g., physical, cognitive, social). Prior studies indicate high levels of specificity for specific domains and are predictive of increased symptom endorsement for the corresponding sensations (Schmidt, 1999;Schmidt et al., 2002). Given the increasing recognition of ASCC as a correlate of psychopathology, it follows that greater evaluation of ASCC specific laboratory challenges, without the confounding effects of related physical sensations, is warranted. ...
... However, this study also did not report specifically on ASCC or fear reactivity. It is also noteworthy that hyperventilation is associated with significant activation of AS physical concerns (Schmidt, 1999). Only one non-hyperventilation task (i.e., standing in a dark room with a strobe light for 3 min) produced significantly greater derealization than dot/mirror staring and no non-hyperventilation tasks produced significantly greater derealization than dot staring. ...
Background:
Anxiety sensitivity cognitive concerns (ASCC), refer to fears of mental catastrophe or losing control over mental processes. Recent findings show that ASCC are related to suicide risk, mood disorders and trauma-related disorders. Using controlled experimental psychopathology paradigms could be one heretofore unutilized method of increasing understanding of ASCC. Our goal was to test fear reactivity to four head-mounted display perceptual illusion challenges designed to bring on feelings of cognitive dyscontrol (i.e., derealization, depersonalization) in a group of high and low anxiety sensitivity cognitive concerns participants.
Methods:
Participants (N=49) with Anxiety Sensitivity Index-3 cognitive scores at least 1.5 SD above or below the mean completed four cognitive dyscontrol challenges utilizing head-mounted display technology.
Results:
Results showed all four challenges successfully elicited high cognitive anxiety symptoms. Consistent with other laboratory challenge studies; high versus low ASCC participants reported comparable cognitive symptoms but reported significantly greater fear.
Limitations:
This was an initial proof of concept study designed to examine fear reactivity to cognitive dyscontrol challenges. Therefore, no control exercises were evaluated.
Conclusions:
The finding that fear reactivity to the laboratory challenges can potentially serve as a viable behavioral correlate of ASCC provides a potentially useful exposure exercise for clients experiencing high levels of ASCC. Given the association between ASCC and severe psychopathology, with further investigation and refinement, such exposure exercises could be integrated into cognitive-behavioral treatments.
... Within this context, there is emerging evidence that the greater the degree of specificity between preexisting fear about bodily 3 sensations and symptoms induced during challenge, the better anxiety-related responding can be predicted (Eifert, Zvolensky, Sorrell, Hopko, & Lejuez, 1999;Rachman & Taylor, 1993). For instance, Schmidt (1999) recently found that cardiopulmonary fears were the only dimension that predicted anxiety and bodily sensations produced by 35% CO 2 inhalation (see also Aikens, Zvolensky, & Eifert, 2000;McNally & Eke, 1996;Zvolensky, Goodie, McNeil, Sperry, & Sorrell, in press). These convergent findings suggest that particular psychological variables are involved in the pathogenesis of anxious and fearful responding, and in fact may be a mechanism or vulnerability dimension involved in the development of anxiety disorders, particularly PD. ...
... Our first goal was to further evaluate whether multiple AS dimensions (i.e., fears of respiratory symptoms, publicly observable anxiety reactions, cardiovascular symptoms, and cognitive dyscontrol) predicted anxiety and fear in response to CO 2 challenge, relative to other theoretically relevant variables (e.g., trait anxiety). Consistent with existing research Rachman & Taylor, 1993;Schmidt, 1999), we expected that concerns about the negative consequences of respiratory symptoms, cardiac symptoms, and cognitive dyscontrol, all of which can be produced by CO 2 inhalation, would be more predictive of provocation-induced anxiety than other concerns not related to those 8 symptoms (i.e., fear of publicly observable symptoms of anxiety) and trait anxiety. The second aim of this study was to provide an initial test as to whether the use of avoidant coping strategies, as measured by the COPE Inventory (Carver, Scheier, & Weintraub, 1989) independently predicted particular aspects of anxious and fearful responding to interoceptive provocation. ...
... ASI-R. Based on previous research (e.g., Eifert et al., 1999;Rachman & Taylor, 1993;Schmidt, 1999), we expected that challenge-relevant concerns about the negative consequences of respiratory symptoms, cardiac symptoms, and cognitive dyscontrol, would be more predictive of provocation-induced anxiety than other concerns less related to challenge-induced sensations (i.e., fear of publicly observable symptoms of anxiety) and trait anxiety. Consistent with this hypothesis, the Fear of Cardiac Symptoms subscale uniquely predicted an increased number and intensity of challenge-induced cognitive symptoms of panic, including catastrophic cognitions. ...
... Each item assesses concern about the possible negative consequences of anxiety symptoms. The ASI has demonstrated adequate internal consistency (22) and test-retest reliability (23). Moreover, the ASI appears to tap fear of anxiety symptoms as opposed to state or trait anxiety (24). ...
... Patients with panic disorder generally exhibit high levels of anxiety' sensitivity' (21). Despite this general tendency toward high anxiety sensitivity, patients vary in terms of the relative level and type of fears (22). For some, high anxiety sensitivity scores may be clue to cardiacspecific fears (e.g., "it scares me when my heart beats rapidly) (23). ...
... It is important to recognize that anxiety sensitivity is not isomorphic with a panic disorder diagnosis. High levels of anxiety sensitivity are commonly seen in panic disorder but there are individual differences in the manner in which anxiety sensitivity manifests itself in these patients (22). In general, it appears that anxiety sensitivity affects fitness estimates but not actual fitness levels. ...
To date, primary research in the area of panic disorder and similar anxiety, pathology has been laboratory-based. A wealth of primary research in panic disorder in particular has been gleaned from laboratory research using biological challenge paradigms by which panic is experimentally provoked. The present work reviews the knowledge based gleaned from the biological challenge paradigm and the competing (and often agreeing) models of panic and anxiety, narrowing to a focus on Reiss' (1991) expectancy theory. Within expectancy theory, emphasis is placed upon the role of anxiety sensitivity. Expectancy theory proposes that anxiety sensitivity may serve as a premorbid risk factor for the development of anxiety pathology (Reiss, 1991). Next, this work presents a series of five reports investigating the role of anxiety sensitivity and psychological vulnerability in a number of areas. In addition, the concept of psychological vulnerability factors in general is explored, and other possible risk factors for anxiety, pathology, depression, disability, and impairment are examined. The first three reports presented here stem from a large sample of data collected at the U.S. Air Force Academy (USAFA) during Basic Cadet Training (BCT) in the summer of 1995. The remaining two studies examine the theoretical position of anxiety sensitivity in terms of pathology, specificity, and other more distal effects of elevated anxiety? sensitivity such as decreased cardiovascular fitness.
... There is emerging evidence that the greater the degree of specificity between pre-existing fear about bodily sensations and symptoms experienced, the better self-reported anxiety-related responding can be predicted (Eifert, Zvolensky, Sorrell, Hopko, & Lejuez, 1999; Rachman & Taylor, 1993). For instance, Schmidt (1999) recently found that cardiopulmonary fears, a subcomponent of anxiety sensitivity physical concerns, was the only dimension that predicted reported anxiety and bodily sensations during 35% CO 2 inhalation in panic disorder patients. These findings are consistent with the idea that different dimensions of anxiety sensitivity may be uniquely related to theoretically similar aspects of negative emotional responding (Eifert, Zvolensky, & Lejuez, 2000). ...
... For instance, contemporary models of panic and related disorders emphasise that individuals expect somatic events to be threatening and that there is an exaggerated vigilance on internal sensations (Bouton, Mineka, & Barlow, 2001). Similar to behavioural inhibition theory, such conceptualisations posit that heightened anxious and fearful responding occurs in response to bodily sensations perceived as dangerous, contributing to increased attention on somatic events (Ehlers & Breuer, 1992; McNally, 1998; Schmidt, Lerew, & Trakowski, 1997; Schmidt & Trakowski, 1999). It is plausible, then, a cognitive-based BIS might represent one process variable that may produce elevated anxious responding to bodily sensations. ...
... We utilised a multimethod assessment protocol to provide a comprehensive evaluation of emotional responding. Consistent with existing research (Schmidt, 1999), we expected that concerns about the negative consequences of psychological and physical sensations commonly produced by the CO 2 (i.e., anxiety sensitivity psychological and physical concerns, respectively) would be more predictive of provocation-induce d anxiety than other concerns not related to those symptoms (i.e., anxiety sensitivity social concerns) and trait anxiety. It also was hypothesised that BIS would be significantly predictive of emotional displeasure, arousal, and dyscontrol as highlighted in various contemporary perspectives of behavioural inhibition (Gray & McNaughton, 1996). ...
The present study explored psychological predictors of response to a series of three 25 second inhalations of 20% carbon dioxide-enriched air in 60 nonclinical participants. Multiple regression analyses indicated that only anxiety sensitivity physical concerns predicted self-reported fear, whereas both physical anxiety sensitivity concerns and behavioural inhibition sensitivity independently predicted affective ratings of emotional arousal. In contrast, the psychological concerns anxiety sensitivity dimension predicted ratings of emotional displeasure (valence), and both psychological anxiety sensitivity concerns and behavioural inhibition sensitivity independently predicted emotional dyscontrol. No variables significantly predicted heart rate. These data are in accord with current models of emotional reactivity that highlight the role of cognitive variables in the production of anxious and fearful responding to somatic perturbation, and help further clarify the particular predictors of anxiety-related responding to biological challenge.
... In fact, anxiety sensitivity, across numerous studies, is concurrently and prospectively associated with more severe anxiety symptoms and panic psychopathology; effects not attributable to trait anxiety or negative affectivity (Feldner, Zvolensky, Schmidt, & Smith, 2008; Hayward, Killen, Kraemer, & Taylor, 2000; Li & Zinbarg, 2007; Maller & Reiss, 1992; McLeish, Zvolensky, & Bucossi, 2007; Schmidt, Lerew, & Jackson, 1997, 1999; Schmidt, Zvolensky, & Maner, 2006). Additionally, laboratory studies have consistently confirmed that anxiety sensitivity measured prior to a biological challenge paradigm is a significant predictor of post-challenge anxiety symptoms and panic attacks (Eke & McNally, 1996; Leen-Feldner, Feldner, Bernstein, McCormick, & Zvolensky, 2005; Rabian, Embry, & McIntyre, 1999; Schmidt, 1999; Zvolensky, Feldner, Eifert, & Stewart, 2001); effects, again, evident above and beyond negative affectivity and trait anxiety. Although empirical work on anxiety sensitivity has indicated that it represents a central cognitive factor in fear acquisition to interoceptive stimuli, there has been considerably less effort to integrate conceptually related work on tolerance (cf, sensitivity) of aversive stimuli, which is of theoretical relevance to models of panic psychopathology (Bernstein, Zvolensky, Vujanovic, & Moos, in press; Zvolensky & Otto, 2007). ...
... Although empirical work on anxiety sensitivity has indicated that it represents a central cognitive factor in fear acquisition to interoceptive stimuli, there has been considerably less effort to integrate conceptually related work on tolerance (cf, sensitivity) of aversive stimuli, which is of theoretical relevance to models of panic psychopathology (Bernstein, Zvolensky, Vujanovic, & Moos, in press; Zvolensky & Otto, 2007). Such limitation is unfortunate, as anxiety sensitivity is related to distress tolerance constructs (e.g., Bernstein et al., in press), and as discussed below, distress tolerance factors may be related to panic psychopathology (Marshall, Zvolensky, Vujanovic, et al., 2008; Schmidt & Trakowski, 1999). Indeed, like anxiety sensitivity, distress tolerance variables may theoretically motivate avoidance and paradoxically amplify anxiety states. ...
... Discomfort intolerance has been initially explored in relation to anxious and fearful responding to laboratory stressors. For example, using a carbon dioxide-enriched air (CO 2 ) paradigm among clinical (n = 45) and non-clinical (n = 45) samples, Schmidt and Trakowski (1999) found discomfort intolerance was significantly predictive of a greater fear response only among the nonclinical group. The lack of an effect in the clinical group may have been due to a truncated range of discomfort intolerance among that group (Schmidt & Trakowski, 1999). ...
The current study investigated anxiety sensitivity, distress tolerance (Simons & Gaher, 2005), and discomfort intolerance (Schmidt, Richey, Cromer, & Buckner, 2007) in relation to panic-relevant responding (i.e., panic attack symptoms and panic-relevant cognitions) to a 10% carbon dioxide enriched air challenge. Participants were 216 adults (52.6% female; M(age)=22.4, SD=9.0). A series of hierarchical multiple regressions was conducted with covariates of negative affectivity and past year panic attack history in step one of the model, and anxiety sensitivity, discomfort intolerance, and distress tolerance entered simultaneously into step two. Results indicated that anxiety sensitivity, but not distress tolerance or discomfort intolerance, was significantly incrementally predictive of physical panic attack symptoms and cognitive panic attack symptoms. Additionally, anxiety sensitivity was significantly predictive of variance in panic attack status during the challenge. These findings emphasize the important, unique role of anxiety sensitivity in predicting risk for panic psychopathology, even when considered in the context of other theoretically relevant emotion vulnerability variables.
... Across studies, it appears the three first-order factors measure fears of adverse physical outcomes (Physical Concerns), cognitive concerns (Psychological Concerns), and fears of the public display of anxiety symptoms (Social Concerns) (Stewart, Taylor, & Baker, 1997;Zinbarg, Brown, & Barlow, 1997;Zvolensky, McNeil, Porter, & Stewart, in press). Furthermore, these first-order anxiety sensitivity factors appear to differentially predict anxious and fearful responding across populations with different types of interoceptive concerns (Schmidt, 1999), and therefore may represent different psychological mechanisms for certain types of psychopathology (Cox, 1996). For example, researchers have found that the Physical Concerns dimension of the ASI best predicts fear and panic responding in both laboratory and naturalistic contexts relative to other ASI first-order factors (Aikens, Zvolensky, & Eifert, in press;Schmidt, 1999;Zvolensky, Goodie, McNeil, Sperry, & Sorrell, in press). ...
... Furthermore, these first-order anxiety sensitivity factors appear to differentially predict anxious and fearful responding across populations with different types of interoceptive concerns (Schmidt, 1999), and therefore may represent different psychological mechanisms for certain types of psychopathology (Cox, 1996). For example, researchers have found that the Physical Concerns dimension of the ASI best predicts fear and panic responding in both laboratory and naturalistic contexts relative to other ASI first-order factors (Aikens, Zvolensky, & Eifert, in press;Schmidt, 1999;Zvolensky, Goodie, McNeil, Sperry, & Sorrell, in press). These findings, in conjunction with related research, sug-gest that predictions of anxious and fearful responding improve with higher levels of correspondence between the particular anxiety sensitivity domain and events that closely match that fear. ...
This article reviews the concept of heart-focused anxiety that may occur in response to cardiac-related stimuli and sensations. Our aim was to examine the relation between chest pain, panic, and heart-focused anxiety in persons with and without heart disease. We identify a preoccupation with the heart and its functioning based on the belief that it will lead to negative consequences (e.g., death, pain) as an important psychological variable in the production of anxious and fearful responding. We then discuss heart-focused anxiety in relation to other clinically relevant variables in anxiety-related problems such as hypochondriacal concerns, including physical symptoms, disease fear, disease conviction, and safety-seeking behavior. Finally, we briefly discuss the clinical importance of heart-focused anxiety in the assessment and treatment of certain anxiety and cardiac-related problems.
... One explanation of the panic-like symptoms after inhalation of 35% CO 2 observed in panic disorder patients and their relatives is the tendency to misinterpret and catastrophize novel bodily sensations, like an "interoceptive phobia" regarding the physical well-being (Griez and Schruers, 2003). Anxiety sensitivity, and especially cardiopulmonary fears, may predict 35% CO 2induced panic in patients with panic disorder (Schmidt, 1999). Perna et al. (2003) showed that in patients with panic disorder anxiety sensitivity predicted the somatic, but not the cognitive, symptomatology induced by 35% CO 2 . ...
... Panic disorder patients with prominent respiratory symptoms are more sensitive to CO 2 than "non-respiratory" panic disorder patients (Biber and Alkin, 1999;Freire et al., 2008). In this sense, CO 2 reactivity may depend upon the triggering of sensations of dyspnea and suffocation, in both patients and healthy volunteers (Schmidt, 1999). Griez et al. (2007) suggested that the very Psychiatry Research 179 (2010) 194-197 mechanism causing false suffocation alarms in panic patients might correspond to a normal system in healthy individuals that gets activated with high doses of CO 2 . ...
The aim of this study was to examine the effects of history of suffocation, state-trait anxiety, and anxiety sensitivity on response to a 35% carbon dioxide (CO₂) challenge in panic disorder patients, their healthy first-degree relatives and healthy comparisons. Thirty-two patients with panic disorder, 32 first-degree relatives, and 34 healthy volunteers underwent the 35% CO₂ challenge. We assessed baseline anxiety with the Anxiety Sensitivity Index (ASI) and State-Trait Anxiety Inventory (STAI1), and panic symptoms with the Panic Symptom List (PSL III-R). A history of suffocation was associated with greater risk of CO₂ reactivity in the combined sample. Patients had more anxiety sensitivity and state and trait anxiety than relatives and healthy comparisons; the difference between relatives and healthy comparisons was not significant. In female patients, trait anxiety predicted CO₂-induced panic. Having a CO₂-sensitive panic disorder patient as a first-degree relative did not predict CO₂-induced panic in a healthy relative. History of suffocation may be an important predictor of CO₂-induced panic. Trait anxiety may have a gender-specific relation to CO₂ reactivity.
... A number of independent lines of research demonstrate that this cognitive vulnerability factor increases the risk for anxiety symptoms and disorders, perhaps most particularly panic attacks and panic disorder (Ginsburg & Drake, 2002;Kearney, Albano, Eisen, Allan, & Barlow, 1997;Lau, Calamari, & Waraczynski, 1996;Rabian, Peterson, Richters, & Jensen, 1993;Taylor, Koch, & McNally, 1992;Vasey, Daleiden, Williams, & Brown, 1995). For example, prospective studies indicate that AS predicts the future occurrence of panic attacks and anxiety symptoms among adults and youth (Hayward, Killen, Kraemer, & Taylor, 2000;Schmidt, Lerew, & Jackson, 1997, 1999Schmidt, Zvolensky, & Maner, 2006;Weems, Hayward, Killen, & Taylor, 2002). Other work indicates that AS predicts fear responses to bodily sensations (Rabian, Embry, & MacIntyre, 1999;Unnewehr, Schneider, Margraf, Jenkins, & Florin, 1996;Zinbarg, Brown, Barlow, & Rapee, 2001). ...
... The purpose of the present investigation was to provide an initial test of the possible explanatory utility of AS in relation to anxiety and somatization symptoms as well as depressive symptoms among an adult population with HIV/AIDS. Given evidence that AS subfactors are differentially related to specific anxiety and other negative emotional symptoms (Schmidt, 1999;Schmidt, Lerew, & Joiner, 1998;Zvolensky, Feldner, Eifert, & Stewart, 2001;Zvolensky, Goodie, McNeil, Sperry, & Sorrell, 2000), it was hypothesized that the AS-physical concerns subscale would best predict somatization symptoms, whereas the AS-mental concerns subscale would best predict anxiety and depressive symptoms. In all tests, it was expected that the AS relations would be evident above and beyond the variance accounted for by negative affectivity (neuroticism) and gender. ...
This investigation explored facets of anxiety sensitivity (AS-social, physical and mental concerns) in regard to somatization, anxiety and depression symptoms among people with HIV/AIDS. Significant relations were found for AS-physical concerns and somatization symptoms (beta = .52, p = .007) and AS-mental concerns and anxiety symptoms (beta = .29, p < .05), controlling for negative affectivity, gender and shared variance with other AS subscales. Together, AS subscales were significantly related to depression symptoms (DeltaR(2) = .11; p = .006), but no one subscale was independently related. Findings are discussed in terms of examining AS in better understanding the HIV/AIDS-anxiety relation.
... Elevated AS also predicts stress reactions to novel laboratory stresses including biological challenges (e.g. Asmundson et al., 1994;McNally and Eke, 1996;Schmidt, 1999) as well as trauma films (Boffa et al., 2016;Olatunji and Fan, 2015) and exposure to actual trauma such as a campus shooting (Boffa et al., 2016). Further, AS is associated with a range of maladaptive coping behaviors including compulsive behaviors such as hoarding and excessive washing (e.g. ...
Background
Anxiety sensitivity (AS) is a well-studied transdiagnostic risk construct that is believed to amplify responses to many forms of stress. The COVID-19 pandemic is a broad stressor with significant physical and social threats. In the current study, we were interested in ascertaining the degree to which AS would relate to distress and disability in the context of COVID-19. We hypothesized that AS would be associated with increased distress and disability. Moreover, we hypothesized that AS would be uniquely predictive while controlling for other relevant risk factors such as age, race, and perceived local COVID infection rates.
Method
Participants (N = 249) were U.S. adults assessed using online data resourcing and followed one month later.
Results
At the first time point, during the beginning phases of the COVID-19 pandemic, AS was significantly related to COVID distress and disability with a moderate effect size. AS was longitudinally associated with higher COVID worry and depression.
Limitations
Our findings are limited by the use of a relatively small online sample. Additionally, assessment of pre-pandemic and post-pandemic symptoms and functioning would be beneficial for future research.
Conclusions
Taken together, the current study provided evidence consistent with AS as a causal risk factor for the development of distress and depression during the COVID-19 pandemic.
... Whether the activation of these neurons trigger or not nausea remains to be determined. Of 428 note, however, a role for CO2 in mediating nausea remains to be reconciled with the 429 observation that exposure to a 35% CO2 inhalation challenge to test for anxiety is rarely 430 associated with nausea (46). ...
Introduction:
Nausea caused by exhaustive sprinting is associated with high lactate ([La-]) and hydrogen ion concentrations ([H+]) and fall in blood pCO2, thus raising the issue of whether there is a causal link between nausea and these variables. For this reason, this study aimed to determine whether interspersing repeated sprints (RS) with periods of active, compared with passive, recovery results in lower levels of both nausea and changes in [La-], [H+], and pCO2.
Methods:
Twelve male participants completed two separate sessions comprising four 30-s sprints separated by 20 min of either active (AR; cycling at 40% V˙O2peak) or passive recovery (PR). At 6 and 18 min of each recovery period, nausea was assessed via a visual analog scale (VAS), and blood samples were collected to measure [La-], [H+], and pCO2.
Results:
RS significantly increased VAS score in both AR (P < 0.001) and PR (P < 0.01). After the first sprint, VAS was higher than preexercise in only AR (P < 0.01). AR was associated with lower VAS, [La-], [H+], and higher pCO2 (all P = 0.001) compared with PR after sprints 2-4. Linear mixed modeling indicated that each of the variables significantly predicts VAS scores (P < 0.0001). Repeated-measures correlation (rrm2) indicated that [La-] had the closest association with VAS (rrm2 = 0.22, P < 0.0001).
Conclusion:
The lower levels of both nausea and changes in [La-], [H+], and pCO2 in response to AR suggest that nausea associated with RS may be causally related with these variables. However, the absence of a close relationship between these variables after the first sprint and the findings that [La-], [H+], and pCO2 only account for 13%-22% of the variation in VAS indicate that other mechanisms may also mediate nausea.
... Another possibility relates to the observation that there are chemosensitive neurons within the NTS that respond to changes in pCO 2 via activation of CO 2 -sensing proteins (Dean, Bayliss, Erickson, Lawing, & Millhorn, 1990;Putnam, Filosa, & Ritucci, 2004). It is important to note, however, that our interpretation that CO 2 is a mediator of nausea is challenged by the observation that nausea is only "rarely" reported during exposure to a 35% CO 2 inhalation challenge test for anxiety (Schmidt, 1999). ...
This study aims to determine if there is a relationship between nausea level and lactic acidosis during recovery from sprinting. Thirteen recreationally active males completed a 60-s bout of maximal intensity cycling. Prior to and for 45 mins following exercise, blood pH, pCO2 and lactate levels were measured together with nausea. In response to sprinting, nausea, lactate and H+ concentrations increased and remained elevated for at least 10 min (P<0.001) whereas pCO2 increased only transiently (P < 0.001) before falling below pre-exercise levels (P<0.001), with all these variables returning toward pre-exercise levels during recovery. Both measures of nausea adopted for analyses (nausea profile, NP; visual analogue scale, VAS), demonstrated significant repeated measures correlation (rmcorr) post-exercise between nausea and plasma lactate (VAS and NPrrm>0.595, P<0.0001) and H+ concentrations (VAS and NPrrm >0.689, P <0.0001), but an inconsistent relationship with pCO2 (VAS rrm=0.250, P=0.040; NP rrm=0.144, P=0.248) and bicarbonate levels (VAS rrm=-0.252, P=0.095; NP rrm=-0.397, P=0.008). Linear mixed modelling was used to predict the trajectory of nausea over time, with both lactate and H+ concentrations found to be key predictors of nausea (P <0.0001). In conclusion, this study reveals a strong positive relationship between nausea and both H+ and lactate concentrations during recovery from sprinting, a finding consistent with H+ and lactate being potential mediators of nausea post-sprinting. However, as the timing of the recovery of both H+ and lactate was delayed, compared to that of nausea, further research is required to confirm these findings and investigate other potential mechanisms.
... These findings are consistent with previous work highlighting the importance of anxiety sensitivity in individuals with respiratory conditions (e.g., asthma; Avallone et al., 2012;Caccappolo-van Vliet et al., 2002;Carr et al., 1994) and extends previous findings in both the PTSD and respiratory As hypothesized, anxiety sensitivity added unique variance to LRS above and beyond PTSD symptom severity and this relationship was specific to the somatic concerns. This finding is consistent with the literature implicating somatic concerns in the prediction of interoceptive anxiety symptoms such as those experienced during respiratory distress (Eifert et al., 1999;Schmidt, 1999). Further analyses also suggested that anxiety sensitivity contributed significantly to explaining the relationship between PTSD and LRS. ...
Respiratory problems and posttraumatic stress disorder (PTSD) are the signature health consequences associated with the September 11, 2001 (9/11), World Trade Center disaster and frequently co-occur. The reasons for this comorbidity, however, remain unknown. Anxiety sensitivity is a transdiagnostic trait that is associated with both PTSD and respiratory symptoms. The present study explored whether anxiety sensitivity could explain the experience of respiratory symptoms in trauma-exposed smokers with PTSD symptoms. Participants (N = 135; Mage = 49.18 years, SD = 10.01) were 9/11-exposed daily smokers. Cross-sectional self-report measures were used to assess PTSD symptoms, anxiety sensitivity, and respiratory symptoms. After controlling for covariates and PTSD symptoms, anxiety sensitivity accounted for significant additional variance in respiratory symptoms (ΔR(2) = .04 to .08). This effect was specific to the somatic concerns dimension (β = .29, p = .020); somatic concerns contributed significantly to accounting for the overlap between PTSD and respiratory symptoms, b = 0.03, 95% CI [0.01, 0.07]. These findings suggest that the somatic dimension of anxiety sensitivity is important in understanding respiratory symptoms in individuals with PTSD symptoms. These findings also suggest that it may be critical to address anxiety sensitivity when treating patients with comorbid respiratory problems and PTSD.
... Furthermore, if somatic complaints are truly multidimensional, relationships between global measures of somatic concerns and measures of specific anxiety symptoms may be misleading. For example, the relation between overall somatic concerns and response to CO 2 challenge may be less pronounced than the relation between the somatic concerns specific to the cardiovascular and respiratory systems and fearful responses to CO 2 (e.g., Schmidt, 1999). ...
Somatic complaints are often key features of anxiety pathology. Although most measures of anxiety symptoms capture somatic complaints to some degree, the Self-Rating Anxiety Scale (SAS) was developed primarily as a measure of somatic symptoms associated with anxiety responding. We evaluated the psychometric properties and factor structure of the SAS in two large undergraduate samples who completed the SAS and measures of anxiety and depression. Exploratory factor analysis revealed four lower-order SAS factors in both samples: (1) anxiety and panic; (2) vestibular sensations; (3) somatic control; and, (4) gastrointestinal/muscular sensations. The SAS demonstrated good reliability in both samples, and the correlations between the SAS factors and other anxiety variables provide supportive evidence for convergent validity, though evidence for discriminant validity was limited. The strengths and limitations of the SAS are offered as well as the implications of our findings for the nature and assessment of somatic complaints in anxiety disorders. (c) 2005 Elsevier Inc. All rights reserved.
... Numerous studies have examined the relationship between AS and anxiety disorders, with a majority of these investigations focusing the association between AS and panic (Schmidt et al. 1997. It has been shown that higher levels of AS are associated with increased panic responding as measured by CO 2 challenge studies (Korte and Schmidt 2012;Schmidt 1999;Schmidt and Mallott 2006) and exaggerated responding in hyperventilation studies (Brown et al. 2003). Further, AS has been shown to prospectively predict the development of panic (Schmidt et al. 1997. ...
Anxiety sensitivity (AS), the fear of anxiety and its potential consequences, places individuals at an increased risk for the development of anxiety disorders. While elevated AS is correctable, often through very brief interventions, individuals high in AS may be unaware of the risks associated with this risk factor and, therefore, may be unaware or unmotivated to address this potential risk. The purpose of the present investigation was to examine the use of motivation enhancement therapy (MET) to enhance motivation to utilize a preventive intervention in a non-intervention seeking population with elevated levels of AS. We examined this issue in a randomized controlled pilot study. Participants (N = 23) were randomized to one of two groups: (1) a MET group (n = 12) group or (2) a control group focused on healthy behaviors (n = 11). Those in the MET group received MET focused on enhancing motivation to reduce AS, whereas those in the control group received psychoeducation about health and general well being. At the end of the study, all of the participants were given the option to receive a computerized intervention previously found to be effective at reducing AS. Results revealed that the MET group had significant changes in motivation to change anxiety and motivation to attend the AS preventative intervention. Moreover, 50 % of individuals in the MET group completed the preventative intervention in comparison to 0 % in the control group. Implications of the findings are discussed.
... Research indicates that the factor structure of the ASI is comprised of three lower-order factors (i.e., Physical, Psychological, and Social Concerns), which all load on a single higher-order factor (Global Anxiety Sensitivity; Stein, Jang, & Livesley, 1999). The total and subscale ASI scores are distinct from trait anxiety and are commonly used as indices of anxiety sensitivity (Schmidt, 1999). ...
... Since the initial validation of the ASI, dozens of studies have established the reliability and validity of the scale in a diverse range of clinical and nonclinical samples. High ASI scores have been associated with a diagnosis of panic disorder as opposed to other anxiety disorders (e.g., Taylor, Koch, & McNally, 1992), anxious responding to panic challenge tasks (e.g., Rapee & Medoro, 1994), and prospective development of panic attacks (e.g., Schmidt, Lerew, & Jackson, 1997, 1999). Consistent with the theory that elevated AS drives the vicious circle of panic, even among individuals without panic disorder (Reiss & McNally, 1985; Reiss, 1987 ...
The goal of the present study was to examine the factor structure of the Anxiety Sensitivity Index (ASI; S. Reiss, R. A. Peterson, D M. Gursky, & R. J. McNally, 1986) and the replicability, reliability, and validity of its dimensions in a nonclinical sample. One-thousand-and-seventy-one undergraduate volunteers completed the ASI and a modified version of the Panic Attack Questionnaire (PAQ; G. R. Norton, J. Dorward, & B. J. Cox, 1986). A principal components analysis, using oblique rotation and parallel analysis, yielded three ASI dimensions that were highly consistent with those reported in previously published studies. Individuals classified as nonclinical panickers scored higher than nonpanickers on the Physical Concerns and Cognitive Concerns subscales of the ASI. Although spontaneous panic attacks were not significantly related to scores on any ASI scale, the occurrence of panic attacks in the past month was related to higher scores on the Cognitive Concerns subscale. The results are discussed in terms of cognitive theories of panic, and limitations of the present study and directions for future research are addressed.
... The last several decades of research on panic disorder have revealed a number of factors relevant to the prediction of panic, both over the long-term (i.e., prospectively) and the short-term (i.e., within a laboratory setting). Numerous prospective studies have shown that anxiety sensitivity (Reiss and McNally 1985), which reflects a fear of anxiety-related symptoms, predicts elevated rates of future onset of panic and related anxiety disorders, even when controlling for general trait anxiety (e.g., Hayward et al. 2000;Schmidt 1999;Schmidt et al. 2006). Anxiety sensitivity is theoretically linked to the underlying belief that anxiety symptoms have catastrophic consequences '[e.g., a quickened heart rate (HR) is interpreted as a sign of a heart attack]. ...
Theoretical models of panic disorder posit a unique role for external anxiety-related control attributions (i.e., lack of perceived control over the onset and maintenance of one’s anxiety symptoms) in predicting panic reactivity, even beyond well-established cognitive risk factors such as anxiety sensitivity. The present study examined whether anxiety-related control attributions would uniquely predict a range of anxious responses across multiple phases and sessions of a biological stressor. Undergraduate students (N = 317) completed measures of anxiety-related control attributions and anxiety sensitivity prior to undergoing a 7.5 % carbon dioxide (CO2) challenge. A subset of these participants (N = 102) returned 1 week later for a second administration. Self-reported subjective distress, physical panic symptoms, and panic-related threat cognitions were measured at baseline and again during several phases of the challenge procedure. Physiological measures of heart rate, skin conductance, and respiration rate were also recorded throughout the challenge. Consistent with theoretical models, higher external control attributions uniquely predicted greater reactivity on all self-report indices across challenge phases and sessions; findings were more mixed for the physiological indices, with higher external control attributions predicting higher heart rate but lower skin conductance, and no prediction for respiration rate. Implications for theory and treatment of panic pathology are discussed.
... Schmidt also observed the importance of cardio respiratory symptoms (over symptoms like numbness or nausea) in response to 35% CO 2 . 24 Welkowitz et al. 25 concluded that CO 2 -induced panic is a biological effect, independent of cognitive stimuli such as illusion of control over the test or reassurance of safety. ...
This systematic review assesses the current state of clinical and preclinical research on panic disorder (PD) in which the carbon dioxide (CO2) challenge was used as a trigger for panic attacks (PAs). A total of 95 articles published from 1984 to 2012 were selected for inclusion. Some hypotheses for PD evolved greatly due to the reproducibility of PAs in a controlled environment using the safe and noninvasive CO2 test. The 35% CO2 protocol was the method chosen by the majority of studies. Results of the test report specific sensitivity to hypercapnia in PD patients of the respiratory PD subtype. The CO2 challenge helped assess the antipanic effects of medication and non-pharmaceutical approaches such as physical exercise and cognitive behavioral therapy. The test was also used in studies about the genetic component of PD, in which twins and relatives of PD patients were analyzed.
... Those with higher levels of AS show increased panic related responding as measured by exaggerated responding to biological challenge agents such as high concentrations of CO 2 (Schmidt 1999; Schmidt and Mallott 2006; Zinbarg et al. 2001). Moreover, it has been shown that being high in AS serves as a predisposition for the development of panic attacks (Schmidt et al. 1997, 1999, 2006). ...
Elevated levels of anxiety sensitivity (AS), the fear of anxiety and its consequences, places individuals at an increased risk for the development of anxiety disorders, especially panic disorder. Research has shown that treating AS may reduce the future development of anxiety psychopathology. However, individuals high in AS may be unaware of the risks associated with this risk factor and, therefore, may tend to be unaware or unmotivated to change AS. The purpose of the current study was to investigate the effect of providing high-risk feedback in those at-risk for developing anxiety psychopathology. Participants consisted of 55 non-treatment seeking individuals with clinically significant levels of AS. Participants completed a battery of baseline questionnaires, received high-risk feedback about their level of anxiety sensitivity, and completed post-study questionnaires. Results revealed significant increases in motivation. Specifically, there were significant increases in the importance and confidence to change anxiety after receiving the high-risk feedback. Implications of the findings and future directions are discussed.
... Prior work on the nature of AS established the potential for individuals with elevated AS to experience impairment under a number of circumstances. For example, those with high levels of AS show increased panic related responding as measured by exaggerated responding in hyperventilation studies (Brown et al., 2003) and CO 2 challenge studies (Schmidt, 1999;Schmidt and Mallott, 2006;Zinbarg et al., 2001). Further, elevated AS is also associated with increased risk for the development of panic attacks and serves as a predisposition for the development of panic disorder . ...
Mounting evidence suggests that specific psychological risk factors increase the likelihood for the development of anxiety psychopathology. Anxiety sensitivity (AS), the fear of the consequences of anxiety, is one such risk factor. However, very little is known about the consequences of having elevated AS prior to the development of diagnosable psychopathology. We hypothesized that elevated AS may create impairment among premorbid individuals. The aims of the present study were twofold. The first aim was to examine whether having elevated AS would be predictive of impairment in a nonclinical sample. The second aim was to examine whether subclinical anxiety symptoms would partially mediate the association between AS and impairment in daily life.
These aims were examined in two studies utilizing samples of individuals with elevated levels of AS. Study 1 (N=387) and Study 2 (N=79) were comprised of participants with elevated AS. Participants completed a battery of questionnaires and a diagnostic interview to assess for risk status. Only participants without an anxiety disorder were eligible to participate in the study to ensure that they were in the premorbid stage.
In Study 1, there was a direct effect of AS on impairment. Additionally, there was evidence for anxiety symptoms acting as a partial mediator in the relation between AS and impairment. Study 2 revealed the same pattern of results, with AS having a significant direct effect on impairment that was partially mediated by anxiety symptoms.
The samples utilized in the present sample were primarily Caucasian females, thereby potentially limiting the generalizability of these findings.
This study provides evidence that a premorbid risk factor is associated with impairment before the actual development of an anxiety disorder. Implications of the present investigation and future directions are discussed.
... A substantial number of studies have examined the relationship between AS and anxiety disorders (Bernstein et al. 2005; Deacon and Abramowitz 2006; Rector et al. 2007; Zinbarg et al. 1997) with much of this work focusing on the relationship between AS and panic disorder (McNally 2002; Taylor et al. 1992). Those with higher levels of AS show increased panic related responding as measured by exaggerated responding to biological challenge agents such as high concentrations of CO 2 (Schmidt 1999; Schmidt and Mallott 2006; Zinbarg et al. 2001). Moreover, it has been shown that being high in AS serves as a predisposition for the development of panic attacks (Schmidt et al. 1997Schmidt et al. , 1999). ...
Anxiety sensitivity (AS), the fear of the consequences of anxiety, is known to be a risk factor in the
development and maintenance of anxiety psychopathology. In recent years, AS has been shown to be responsive to a variety of interventions aimed at reducing this malleable risk factor. Motivational interviewing (MI) and motivation enhancement treatment (MET) have been shown to be effective in enhancing the treatment of anxiety disorders. Thus, it was hypothesized that motivational interventions may also be effective in those with elevated AS. The aim of the present study was to examine whether the use of MI/
MET would be effective in reducing AS. Participants (N = 80) with elevated AS were randomized into an MET
or health-focused psychoeducation control group. Results revealed that the MET condition showed a significant reduction in AS in comparison to the control group. These findings are comparable to reductions in AS observed in other AS interventions. Further, changes in motivation mediated the association between experimental group and post-intervention AS. This study is the first to demonstrate the efficacy of MI/MET strategies in the reduction of AS. Implications of the findings and directions for future research are discussed
... Third, specific AS dimensions predict unique aspects of anxious and fearful responding to bodily sensations across diverse populations Zvolensky, Goodie, McNeil, Sperry, & Sorrell, 2001). Fourth, research examining ASI in relation to response to panicogenic challenge procedures have shown that AS is strongly related with a tendency to report greater panic, fear, and distress in response to such challenges, but not to experience greater autonomic arousal (Forsyth, Eifert, & Canna, 2000;Forsyth, Palav, & Duff, 1998;McNally & Eke, 1996;Schmidt, 1999;Zvolensky, Eifert, & Lejuez, 2001). ...
The present study evaluated 2 interrelated hypotheses concerning the relation between specific anxiety sensitivity dimensions and how one responds to bodily sensations in a population with no known history of psychopathology (N = 214). Specifically, the Physical Concerns subscale of the Anxiety Sensitivity Index (ASI; S. Reiss, R. A. Peterson, M. Gursky, & R. J. McNally, 1986) was found to be uniquely and statistically predictive of bodily vigilance, whereas the Mental Incapacitation ASI subscale was predictive of emotional avoidance. These effects were above and beyond the variance accounted for by demographic variables, treatment history for common interoceptive medical conditions, subclinical panic attack history, and trait anxiety. We discuss these findings in relation to differential predictive validity conceptualizations of anxiety sensitivity, with implications for understanding models of health functioning and panic disorder.
... Finally, learning to observe without judgment may counteract the tendency among PTSD patients to negatively interpret internal and external experiences. For example, anxiety sensitivity, which is fear of anxiety and anxiety-related sensations, is a risk factor for the development of panic disorder (Schmidt, 1999) and has been shown to be elevated in individuals with PTSD (Lang, Kennedy, & Stein, 2002). There is a significant negative correlation between anxiety sensitivity and mindfulness, and high anxiety sensitivity is associated with heightened anxious arousal in the context of low mindfulness (Vujanovic, Zvolensky, Bernstein, Feldner, & McLeish, 2007) but less negative effect when paired with high mindfulness (Arch & Craske, 2010). ...
In spite of the existence of good empirically supported treatments for posttraumatic stress disorder (PTSD), consumers and providers continue to ask for more options for managing this common and often chronic condition. Meditation-based approaches are being widely implemented, but there is minimal research rigorously assessing their effectiveness. This article reviews meditation as an intervention for PTSD, considering three major types of meditative practices: mindfulness, mantra, and compassion meditation. The mechanisms by which these approaches may effectively reduce PTSD symptoms and improve quality of life are presented. Empirical evidence of the efficacy of meditation for PTSD is very limited but holds some promise. Additional evaluation of meditation-based treatment appears to be warranted.
... [7][8][9] The ASI provides an overall index of AS, as well as three conceptually distinct subscales measuring Physical Concerns (e.g., it scares me when my heart beats rapidly), Mental Incapacitation Concerns (e.g., when I am nervous, I worry that I might be mentally ill), and Social Concerns (e.g., it is important to me not to appear nervous). [10] Total ASI scores predict the severity of experimentally induced panic, [11,12] the duration of panic disorder, [13] and the likelihood of receiving an anxiety disorder diagnosis. [14] Some evidence suggests that the three subscale factors may be associated with specific clinical conditions. ...
Anxiety Sensitivity (AS), the tendency to fear the thoughts, symptoms, and social consequences associated with the experience of anxiety, is associated with increased risk for developing anxiety disorders. Some evidence suggests that higher scores on the Anxiety Sensitivity Index (ASI), a measure of the AS construct, are associated with activation of the anterior insular cortex during overt emotion perception. Although the ASI provides subscale scores measuring Physical, Mental Incapacitation, and Social Concerns of AS, no study has examined the relationship between these factors and regional brain activation during affect processing. We hypothesized that insular responses to fear-related stimuli would be primarily related to the Physical Concerns subscale of the ASI, particularly for a sample of subjects with specific phobias.
Adult healthy controls (HC; n = 22) and individuals with specific phobia, small animal subtype (SAP; n = 17), completed the ASI and underwent functional magnetic resonance imaging while engaged in a backward-masked affect perception task that presents emotional facial stimuli below the threshold of conscious perception.
Groups did not differ in ASI, state or trait anxiety scores, or insula activation. Total ASI scores were positively correlated with activation in the right middle/anterior insula for the combined sample and for the HC and SAP groups separately. Multiple regression analysis revealed that the relationship between AS and insular activation was primarily accounted for by Physical Concerns only.
Findings support the hypothesized role of the right anterior insula in the visceral/interoceptive aspects of AS, even in response to masked affective stimuli.
Background and objectives:
Anxiety sensitivity (AS) social concerns, the fear of observable anxiety symptoms is posited as a risk factor for social anxiety by increasing fear reactivity in social situations when observable anxiety symptoms are present. Experimental evaluation of AS social concerns is limited. The current study utilized several manipulations designed to be relevant to AS social concerns or fear of negative evaluation (FNE), a distinct social anxiety risk factor. The effects of these manipulations on fear reactivity to a speech were examined.
Methods:
Participants (N = 124 students; M age = 19.44, SD = 2.45; 64.5% female) were randomized to one of four conditions in a 2 (100 mg niacin vs 100 mg sugar pill) X 2 (instructional set) design. For the instructional set manipulation, participants were told their speech performance would be evaluated by a judge based on their performance (i.e., FNE-relevant) or their observable anxiety symptoms (i.e., AS social concerns-relevant).
Results:
There was a main effect for vitamin condition with participants in the niacin condition reporting higher panic symptoms post-speech relative to those in the placebo condition. There was no main effect for speech instructions. As hypothesized, these effects were qualified by an interaction indicating that AS social concerns significantly predicted panic symptoms for those receiving niacin.
Limitations:
Limitations include the reliance on self-reports of outcome variables and the use of an undergraduate student sample.
Conclusions:
These findings highlight a distinct role of AS social concerns in fear responding to socially evaluative situations in the context of physically observable arousal.
Background:
Anxiety sensitivity cognitive concerns (ASCC), or fear of cognitive dyscontrol sensations, confers risk for anxiety and mood psychopathology. Recent work demonstrated that novel perceptual challenges generated by a head mounted display can elicit fear among those with elevated ASCC. This suggests that interoceptive exposure to perceptual challenges may offer a means to mitigate ASCC. This study was designed to evaluate whether repeated exposure to novel perceptual challenges can reduce ASCC, and if these effects are stronger among those experiencing greater negative emotionality as a proxy for individuals likely to present for treatment.
Methods:
Participants with elevated ASCC (N = 57) were randomized to one of three experimental conditions utilizing a head-mounted display. In the rotations condition (n = 20), participants viewed themselves spinning in a circle. In the opposite directions condition (n = 20), participants turned their head while the camera moved in the opposite direction creating dissonance in their visual field. In the control condition (n = 17), participants completed a series of simple arithmetic problems.
Results:
Participants in the rotation condition, relative to control, reported significant reductions in ASCC from pre- to post-exposure and these effects were strongest for those with elevated negative affect. The main effect of the opposite directions exposure on post-treatment ASCC was non-significant, but follow-up analyses revealed that reductions in ASCC were observed among those with elevated negative affectivity.
Discussion:
Perceptual illusion challenges appear to have utility for reducing ASCC through repeated exposure. There was evidence for the perceptual illusion exercises, particularly the rotations condition, specifically reducing ASCC, making this challenge the first we are aware of that specifically targets ASCC-related concerns.
Limitations:
As a proof-of-concept study, the present sample was not recruited for clinically-significant psychopathology, and only a brief follow-up was utilized. Future research should utilize a longer follow-up and test if these exposures mitigate ASCC-relevant psychopathology among clinical samples.
Suicide remains a public health concern with suicide rates showing a consistent increase over the last 20 years. Recent studies have found a relationship between anxiety sensitivity (i.e., the fear of anxiety related symptoms)and suicidality. Specifically, a relationship has been found between anxiety sensitivity cognitive concerns (ASCC)and suicidality. The knowledge around this relationship, however, has relied mostly on self-report measures. This study seeks to expand on the current literature by exploring the association between ASCC and suicidality, through the use of head-mounted display perceptual illusion challenges (e.g., using tactile sensations and mannequins to create illusions that the participant has switched bodies). A head-mounted display was used to elicit symptoms (e.g., depersonalization, derealization)related to ASCC in a sample of undergraduate students (N = 54). Suicidality and depression were measured by the Inventory of Depression and Anxiety Symptoms-2 (IDAS-II), anxiety sensitivity cognitive concerns by the Anxiety Sensitivity Index-3 (ASI-3), and distress by the Subjective Units of Distress Scale (SUDS). Findings indicated that suicidality was associated with self-reported ASCC as well as the fear generated from the challenges. Furthermore, our results found that challenge-induced fear predicted suicidality scores above and beyond the traditional self-report measures of ASCC. The small sample size and low suicide risk of the current sample limits generalizations to more severe populations.
Cannabis is among the most widely used psychoactive substances in the United States, and rates of cannabis use and cannabis-related problems are increasing. Anxiety sensitivity, or the fear of aversive interoceptive sensations, may be relevant to better understanding cannabis use problems and other significant cannabis use processes (e.g., beliefs about quitting). Previous research has primarily focused on the global anxiety sensitivity construct; however, anxiety sensitivity lower-order facets (Cognitive Concerns, Physical Concerns, and Social Concerns) tend to be differentially related to substance use processes in non-cannabis specific studies. The current study therefore explored anxiety sensitivity lower-order facets in relation to cannabis use problems, perceived barriers for cannabis cessation, and abstinence phobia (fear of not using cannabis) among a community sample of 203 cannabis-using adults. Results indicated that anxiety sensitivity Cognitive Concerns were significantly associated with each of the dependent measures and these effects were not explained by shared variance with the other lower-order factors or a range of other covariates (e.g., tobacco use). The present findings suggest future work may benefit from focusing on the role of anxiety sensitivity Cognitive Concerns in the maintenance of cannabis use.
Within a hierarchical framework for depressive and anxiety disorders, negative affect (NA) is posited to be indirectly related to social anxiety and depression through cognitive vulnerabilities, including intolerance of uncertainty (IU) and anxiety sensitivity (AS). However, few prior studies have considered whether the lower-order dimensions of IU (i.e., prospective and inhibitory IU) and AS (i.e., physical, cognitive, and social concerns) better explain the indirect relation between NA and social anxiety and depression. The indirect relations between NA and social anxiety and depression through these cognitive vulnerabilities were examined using structural equation modeling in a clinical sample (N = 298). NA and social anxiety symptoms were indirectly related through AS social concerns and inhibitory IU, although a direct effect of NA was also found. Only AS social concerns explained the relation between NA and a social anxiety disorder diagnosis. AS cognitive concerns was the only cognitive vulnerability factor to indirectly explain the relation between NA and depressive symptoms, although a direct effect of NA was also found. These findings suggest that the lower-order dimensions of AS and IU demonstrate more specific and less transdiagnostic associations with social anxiety and depression.
Difficulty tolerating emotional distress is a core feature in theoretical accounts of borderline personality disorder (BPD). However, few studies have attempted to parse emotional sensitivity in BPD in terms of specific qualities of negative affect. The present study compares the incremental validity of anxiety sensitivity (AS) and disgust sensitivity (DS) in predicting concurrent symptoms of BPD. Prior to receiving treatment, patients at a partial hospital (n = 134) completed measures of AS and DS in addition to a larger survey battery and clinical interview. This study found that AS, but not DS, was correlated with BPD symptoms, and AS continued to predict concurrent BPD symptoms when controlling for demographic variables, symptoms of anxiety and depression, and experiential avoidance. However, the relationship between AS and BPD symptoms was partially mediated by experiential avoidance, consistent with prior research using a categorical approach to BPD symptoms. The AS domain of cognitive concerns was most robustly related to BPD symptoms. These findings highlight the importance of distinguishing between specific negative affects when conceptualizing emotional sensitivity in BPD and may suggest new avenues for treatment through targeting specific sensitivities.
Prior research has found that health anxiety is related to poor patient outcomes in primary care settings. Health anxiety is characterized by at least two presentations: with either severe or no/mild somatic symptoms. Preliminary data indicate that anxiety sensitivity may be important for understanding the presentation of health anxiety with severe somatic symptoms. We further examined whether the combination of health anxiety and somatic symptoms was related to anxiety sensitivity. Participants were adults presenting for treatment at a community health center (N=538). As predicted, the interactive effect between health anxiety and somatic symptoms was associated with anxiety sensitivity cognitive concerns. Health anxiety shared a stronger association with anxiety sensitivity cognitive concerns when coupled with severe, relative to mild, somatic symptoms. Contrary to predictions, the interactive effect was not associated with the other dimensions of anxiety sensitivity. We discuss the potential relevancy of anxiety sensitivity cognitive concerns to the combined presentation of health anxiety and severe somatic symptoms, as well as how this dimension of anxiety sensitivity could be treated in primary care settings.
The cognitive model of panic (Clark, 1988) suggests that panic attacks result from the catastrophic misinterpretation of bodily sensations rather than the sensations themselves. Anxiety sensitivity (AS) is fear of anxious bodily sensations (Reiss, 1991) and has implications in panic
development, maintenance, and severity. Although previous work has demonstrated that AS amplifies symptoms in response to provocations, few have analyzed the role of AS in the relationship between panic symptoms and panic disorder severity. The purpose of this investigation was to determine
if AS, a cognitive risk for panic, has an indirect effect on the association between self-reported panic symptoms and panic severity, both self-reported and clinician-assessed, among 67 treatment-seeking individuals with a primary diagnosis of panic disorder with or without agoraphobia. Data
were analyzed using the bootstrapped conditional process indirect effects model. Results indicated that the overall total mediational effect on Panic Disorder Severity Scale (PDSS) was significant with evidence of partial mediation. The direct effect of Beck Anxiety Inventory (BAI) on PDSS
remained significant although there was also a significant indirect effect of BAI via AS. Results showed a similar relationship when Clinician Severity Rating was the outcome. Moderation analyses were not significant. Therefore, AS was a significant partial mediator of the relationship between
symptom intensity and panic severity, whether clinician-rated or self-reported. This investigation provides support for the importance of AS in panic, highlighting its importance but suggesting that it is not sufficient to explain panic disorder.
Anxiety sensitivity (AS) and emotion regulation (ER) difficulty have been identified as risk factors for anxiety symptoms. Few studies have examined the unique relations between these risk factors and anxiety and even less have examined whether AS and ER difficulty interact in their relations with anxiety. The current study used latent variable modeling to examine the unique and interactive effects of AS and ER difficulty on worry, panic, and social anxiety symptoms in a sample of 526 individuals (M age = 34.87 years, SD = 12.41). It was hypothesized that AS and ER difficulty would be uniquely associated with all anxiety symptoms and that significant, negative interactions would emerge. The hypotheses of the current study were supported, except ER difficulty was only associated with panic at low levels of AS. These findings indicate that the effects of one risk factor was diminished at high levels of the other risk factor.
Whereas it has been speculated that the psychopathology risk factors anxiety sensitivity (AS) and distress tolerance (DT) are highly overlapping, no studies have examined whether a core affect sensitivity construct explains this relation. It was hypothesized that, in a sample of 808 treatment-seeking individuals (Mage=35.11, SD=14.94), the best-fitting confirmatory factor analysis model of AS and DT would comprise a common underlying affect sensitivity factor orthogonal to DT and lower-order AS factors (physical, cognitive, and social concerns). It was also hypothesized that specific relations between the factors and fear, distress, and alcohol/substance use disorders would emerge. The best-fitting model comprised a common affect sensitivity factor orthogonal to DT and lower-order AS factors. Whereas the affect sensitivity and DT factors were associated with fear, distress, and alcohol/substance use disorders, AS cognitive concerns was only related to distress disorders and AS social concerns was only related to fear disorders.
Copyright © 2015. Published by Elsevier Ltd.
Current diagnostic criteria suggest that some individuals experience health anxiety and severe somatic symptoms, whereas others experience health anxiety and either no or mild somatic symptoms. However, to date, our understanding of potential differences among individuals with health
anxiety and varying severity of somatic symptoms remains limited. Adopting a dimensional approach, we completed this study to help fill this gap in the literature by examining whether the interactive effect between health anxiety and somatic symptoms was related to health-related beliefs among
men (n = 211) and women (n = 220). Among both men and women, health anxiety was related to certain health-related beliefs, particularly anxiety sensitivity, only when coupled with severe somatic symptoms. Conceptual and therapeutic implications of these results are discussed.
This study examined the relationship between public speaking anxiety and physiological stress indicators at four different milestones or stages in the delivery of a public speech. Specifically, public speakers' gastrointestinal body sensations were compared at different times and across different levels of psychological trait anxiety. Results indicated significant differences in both the magnitude and the patterns of somatic responses between high- and low-trait-anxiety groupings. First, as the groups of speakers moved from anticipation to confrontation, their somatic responses changed in opposite directions. Subsequently, high-anxiety speakers reported a significant increase in stress symptoms immediately after the speech had ended, indicating anxious remorse or fear of negative evaluation. These findings provided important new information about speech anxiety patterns, particularly as they differ in high- and low-anxiety speakers.
The present investigation evaluated affective style in terms of anxiety sensitivity, emotional reactivity, and distress tolerance in heavy smokers. Specifically, heavy smokers (≥20 cigarettes per day) were partitioned into those who were able to quit for at least 7 days (n=10) and those who were able to quit for less than 7 days (n=12). All participants completed measures of anxiety sensitivity and maximum breath-holding duration and then were exposed to a 20% carbon dioxide-enriched air challenge. Results indicated that heavy smokers who had not been able to remain abstinent from smoking for at least 1 week during a quit attempt demonstrated significantly greater cognitive-affective reactivity to the challenge relative to their counterparts but did not differ at a physiological level of analysis. Contrary to our hypotheses, neither anxiety sensitivity scores nor maximum breath-holding duration significantly differed between the groups. These findings are discussed in relation to better understanding affective style among heavy smokers.
Consensus is beginning to emerge in the literature on the dimensionality of the Anxiety Sensitivity Index [ASI; Behav. Res. Ther. 24 (1986) 1] in the form of a hierarchical model consisting of three group factors and one general factor. One important limitation in the literature on AS is that no studies have tested the invariance of the structure of the ASI over time or across conditions differing in terms of the degree of stressors impacting the participants. We conducted a test of invariance across conditions differing in the degree of stressors impacting participants by administering the ASI on three occasions to a sample of 881 first year undergraduate students from the United States Air Force Academy undergoing Basic Cadet Training. Both exploratory and confirmatory factor analyses produced results that supported the invariance of the consensual hierarchical model of the structure of the ASI. These findings suggest that changes in any of the four scores that can be derived from the ASI (the total score and three ASI subscale scores) associated with changes in levels of stress can be attributed to changes in the degree, rather than changes in meaning, of the corresponding AS factor.
We have provided a laboratory evaluation of emotional reactivity to physiological (hyperventilation), cognitive (mental arithmetic), and social (speech) challenge procedures, and investigated how preexperimental levels of perceived stress, anxiety sensitivity, and negative-evaluation sensitivity predicted anxious and fearful responding. Participants were 37 nonclinical individuals. Dependent measures included a multimethod assessment involving self-reported anxiety, frequency and intensity of bodily sensations, and heart rate and blood pressure responses to the challenges. Our results indicated that preexperimental levels of perceived stress were more predictive than other theoretically relevant variables of self-reported anxiety-related reactivity to cognitive and social challenges, whereas anxiety sensitivity was a better predictor of the emotional response to hyperventilation. Collectively, these findings are consistent with theoretical accounts of anxiety pathology, and suggest that perceived stress is an important process variable to consider in understanding the determinants of anxiety-related responding.
Anxiety sensitivity (AS), a belief that symptoms of anxiety (e.g., autonomic arousal) can be harmful (Reiss & McNally, 1985), predisposes individuals to the development of panic disorder (PD). A pathoplasty relationship between two variables is defined when a dispositional variable is associated with the expression or course of a clinical condition. The theoretical and empirical literature on the pathoplastic relationship between AS and PD has only addressed limited aspects of the expression and course of PD in relation to the total AS score. In addition, there has been no evaluation of the pathoplastic relationship between lower-order empirically-established AS dimensions and the full range of PD expression and course This study examined the pathoplasty relationship of total AS and its lower-order sub-factors with variables representing a full range of the expression and course of panic disorder. One hundred and thirty one adults with formally-diagnosed PD volunteered for participation in a PD assessment and treatment research protocol. Information on the expression and course of PD (Panic frequency, intensity, anticipation, avoidance, and core fears) was derived from clinician-rated and self-report measures collected at pre- and post-treatment phases of the study. The three major findings include: (1) AS is related to the major features of PD expression and course, (2) changes in AS correspond to changes in these features, and (3) AS lower- order factors possess specific relationships with features of PD expression and course. These findings suggest that AS is related to the maintenance and treatment of PD. In addition, the specific relationships among AS lower-order factors and PD expression and course features help clarify the means by which AS contributes to the maintenance and treatment of PD, which may lead to improved assessment and treatment models.
The purpose of this study was to determine if higher and lower anxiety sensitive speakers would exhibit differential levels of four types of body sensations (gastrointestinal, cardiopulmonary, disorientation, and numbness) while anticipating giving a public speech. The participants were eighty‐seven undergraduate students who gave five‐minute informative speeches. The Anxiety Sensitivity Index was used to measure anxiety sensitivity, and the Body Sensations Questionnaire was used to measure body sensations during the anticipatory period. The results showed a significant difference in body sensations between higher and lower anxiety sensitivity speakers for gastrointestinal, cardiopulmonary and numbness sensations. There were no significant differences found for disorientation between higher and lower anxiety sensitive speakers.
This study examined the relationships among a public speaker's body sensations, state of mind, and anticipatory public speaking state anxiety. A negative relationship was found to exist between speaker state of mind and anticipatory public speaking anxiety, and a positive relationship was found between speaker body sensations and anticipatory public speaking anxiety. Moreover, speaker state of mind and body sensations combined to predict anticipatory public speaking anxiety.
While reports of anxiety about public speaking are common, the specific ways in which individual speakers are impacted varies considerably. Researchers of public speaking state anxiety have found support for the operation of Gray’s (1995a32.
Gray , J. A. 1995a . The contents of consciousness: A neuropsychological conjecture . Behavioral and Brain Sciences , 18 : 659 – 722 . [CrossRef], [Web of Science ®]View all references) comparator theory of emotion. The present study extends this perspective by examining the association of higher mental processes (worry) and body sensations. In the present study, conscious rumination and uncomfortable physical sensations were found to coincide during the anticipation milestone, i.e., approximately 1 minute before presenting a public speech. This finding supports the operation of Gray’s comparator theory. Recommendations for future research that focus on recursive patterns of body sensations and worry are advanced.
The purpose of this chapter is to provide a comprehensive review of what is known about the etiology and pathology of anxiety disorders across the lifespan, highlighting in particular developmental differences in the expression of individual anxiety disorders. Anxiety is implicated heavily across the full range of psychopathology. Anxiety is a future-oriented emotion characterized by marked negative affect, bodily symptoms of tension, and chronic apprehension. Fear, on the other hand, is an immediate alarm reaction to present danger characterized by strong escapist action tendencies. Anxiety, fear, and panic are the building blocks of anxiety disorders, arranging themselves in different ways as they focus on varying internal and external stimuli that have become imbued with threat or danger to form the commonly recognized variants of anxiety disorder. Included within this chapter will be separation anxiety disorder, obsessive-compulsive disorder, specific phobias, social phobia, panic disorder (with and without agoraphobia), and generalized anxiety disorder. Covered for each disorder will be clinical presentation, prevalence, demographics, comorbidity, cultural influences, developmental changes, and etiology.
An imaginal challenge was designed to determine the degree to which cognitive manipulations, in isolation from specific biological challenge agents, might be sufficient for the production of panic in patients with panic disorder. Patients with panic disorder (n = 20) and nonclinical controls (n = 18) were exposed to four audiotaped vignettes (physical threat, social threat, loss of control threat, control). In relation to a composite measure of panic, the experimental vignettes produced panic in 30% of the patient sample compared to 0% of the control sample. There was also evidence for increased subjective reactivity to personally relevant panicogenic stimuli.
Increasing evidence suggests that anxiety sensitivity (AS) may be a premorbid risk factor for the development of anxiety pathology. Perceived control and predictability have also been implicated as factors relevant to the genesis of anxiety. The principal aim of this study was to extend this work to examine independent and interactive effects of perceived control, predictability, and AS in the pathogenesis of panic. A large nonclinical sample of young adults (N = 1296) was prospectively followed over a 5- week highly stressful period of time (i.e., military basic training). Perceived control and predictability did not independently predict panic. However, there was evidence suggesting that AS interacted with perceived control such that high perceived control regarding basic training was protective against panic for individuals with high AS. Similarly, high perceived predictability during basic training reduced anxiety symptoms for individuals with high AS.
Anxiety sensitivity (AS) is a trait-like characteristic capturing fears of the experience of anxiety and the potential psychological, somatic, or social consequences associated with anxiety. Recently, research has provided evidence for the latent structure of AS suggesting two discrete types, i.e. a taxonic class and a complement class. Investigations have identified combinations from the 16-items of the Anxiety Sensitivity Index (ASI) that are able to predict the taxon class of AS, referred to as the ASI taxon scales.
The current study investigated the ability of a new ASI taxon scale, comprised of the seven overlapping items of the previously identified ASI taxon scales, to predict CO(2) challenge responses. This was examined in a sample of 387 nonclinical participants presenting for an AS treatment program. Participants completed a battery of questionnaires and a 20% CO(2) challenge as part of the program.
Analyses indicated that the ASI taxon scale uniquely predicted CO(2) challenge response, whereas the complement scale did not have a significant association.
The present study provides the first evidence of the AS taxon having the ability to predict an exaggerated fear response to a novel stressor known to be associated with anxiety psychopathology. Implications of these findings are discussed.
The present study evaluated anxiety sensitivity, along with depression and pain severity, as predictors of pain-related fear and anxiety in a heterogeneous chronic pain population (n=68). The results indicated that the global anxiety sensitivity factor, as indexed by the Anxiety Sensitivity Index (ASI: Reiss, Peterson, Gursky & McNally, 1986: Reiss, S., Peterson, R. A., Gursky, M. & McNally, R. J. (1986). Anxiety, sensitivity, anxiety frequency, and the prediction of fearfulness. Behaviour Research and Therapy, 24, 1–8) total score, was a better predictor of fear of and anxiety about pain relative to the other relevant variables. Additionally, the physical concerns subscale of the ASI was a better predictor of pain-related fear dimensions characterized by high degrees of physiological symptoms and behavioral activation on both the Fear of Pain Questionnaire-III (FPQ-III; McNeil & Rainwater, 1998: McNeil, D. W. & Rainwater, A. J. (1998). Development of the Fear of Pain Questionnaire-III. Journal of Behavioral Medicine.) and Pain Anxiety Symptoms Scale (PASS; McCracken, Zayfert & Gross, 1992: McCracken, L. M., Zayfert, C. & Gross, R. T. (1992). The Pain Anxiety Symptoms Scale: Development and validation of a scale to measure fear of pain. Pain, 50, 67–73). In a related way, the ASI psychological concerns subscale was a better predictor of pain-related anxiety dimensions characterized by cognitive symptoms of anxiety. Overall, these findings reiterate the importance of anxiety sensitivity in understanding pain-related fear and anxiety, and suggest anxious and fearful responding can be predicted more accurately with higher levels of correspondence between a particular anxiety sensitivity domain and events that closely match that fear.
Patients with panic disorder show attentional hypervigilance to internal bodily sensations (i.e., body vigilance), but the role of body vigilance in the genesis of anxiety has not been evaluated. The present study utilized an experimental paradigm to examine the relationship between attentional focus and fearful responding to biological challenge. Patients with panic disorder (n = 45) and matched nonclinical controls (n = 45) were randomly assigned to one of three experimental conditions in which their attentional focus was directed toward internal bodily sensations (Internal Focus) or external cues (External Focus), or was allowed to alter freely (No Focus Control) in the context of a 35% CO2 challenge. Subjective and physiological measures were taken at baseline and during the biological challenge procedure. Consistent with prediction, patients showed greater attention to internal arousal cues prior to the challenge, but patient status did not interact with condition to predict response to the challenge. On the other hand, level of anxiety sensitivity was found to interact with attentional focus in the expected direction. These findings add support for cognitive models of panic disorder.
Thesis (M.A.)--Northern Illinois University, 1999. Dept. of Psychology. Includes bibliographical references (leaves [112]-123).
Expectancy theory posits that anxiety sensitivity may serve as a premorbid risk factor for the development of anxiety pathology (S. Reiss, 1991). The principal aim of the present study was to determine whether anxiety sensitivity acts as a specific vulnerability factor in the pathogenesis of anxiety pathology. A large, nonclinical sample of young adults (N = 1,401) was prospectively followed over a 5-week highly stressful period of time (i.e., military basic training). Anxiety sensitivity was found to predict the development of spontaneous panic attacks after controlling for a history of panic attacks and trait anxiety. Approximately 20% of those scoring in the upper decile on the Anxiety Sensitivity Index (R. A. Peterson & S. Reiss, 1987) experienced a panic attack during the 5-week follow-up period compared with only 6% for the remainder of the sample. Anxiety sensitivity also predicted anxiety symptomatology, functional impairment created by anxiety, and disability. These data provide strong evidence for anxiety sensitivity as a risk factor in the development of panic attacks and other anxiety symptoms.
In the field of anxiety research much attention has recently been focussed on panic attacks. Freedman and Glass (1984) devoted their recent review of progress in psychiatry in the Journal of the American Medical Association almost exclusively to this topic. As we discuss in detail in the chapter by Margraf, Ehlers, and Roth in this book, the major impetus for this development has come from the claim that panic is a biologically unique form of anxiety (Klein 1981; Sheehan 1982). This assumption, however, remains controversial (Marks 1983; Foa et al. 1984; Hand 1984).
D. F. Klein (see record 1993-37796-001 ) proposed that patients with panic disorder ( PD) have a hypersensitive suffocation monitor that predisposes them to experience panic attacks under certain conditions. The suffocation alarm theory predicts differential emotional responding to biological challenges that affect arterial partial pressure of carbon dioxide ( PCO₂ ). These PD patients should exhibit (a) lower fear and less likelihood of panic in response to biological challenges that lower PCO₂ levels (e.g., hyperventilation), and (b) increased fear and greater likelihood of panic in response to biological challenges that raise PCO₂ levels (e.g., inhalation of 35% CO₂ gas). The following indicators of the suffocation monitor were assessed: (a) severity of dyspnea symptoms, (b) frequency of dyspnea symptoms, (c) heightened respiration rate, and (d) lowered PCO₂ levels. Ratings of physiological and subjective responding, as well as panic, were obtained during both a hyperventilation and a 35% CO₂ challenge. None of the classification methods predicted differential emotional responding to hyperventilation versus 35% CO₂ challenge. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Provides simple but accurate methods for comparing correlation coefficients between a dependent variable and a set of independent variables. The methods are simple extensions of O. J. Dunn and V. A. Clark's (1969) work using the Fisher
z transformation and include a test and confidence interval for comparing 2 correlated correlations, a test for heterogeneity, and a test and confidence interval for a contrast among
k (>2) correlated correlations. Also briefly discussed is why the traditional Hotelling's
t test for comparing correlations is generally not appropriate in practice. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
D. F. Klein (see record
1993-37796-001) proposed that patients with panic disorder ( PD) have a hypersensitive suffocation monitor that predisposes them to experience panic attacks under certain conditions. The suffocation alarm theory predicts differential emotional responding to biological challenges that affect arterial partial pressure of carbon dioxide ( PCO₂ ). These PD patients should exhibit (a) lower fear and less likelihood of panic in response to biological challenges that lower PCO₂ levels (e.g., hyperventilation), and (b) increased fear and greater likelihood of panic in response to biological challenges that raise PCO₂ levels (e.g., inhalation of 35% CO₂ gas). The following indicators of the suffocation monitor were assessed: (a) severity of dyspnea symptoms, (b) frequency of dyspnea symptoms, (c) heightened respiration rate, and (d) lowered PCO₂ levels. Ratings of physiological and subjective responding, as well as panic, were obtained during both a hyperventilation and a 35% CO₂ challenge. None of the classification methods predicted differential emotional responding to hyperventilation versus 35% CO₂ challenge. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The Anxiety Sensitivity Index (ASI) is one of the most widely used measures of the construct of anxiety sensitivity. Until the recent introduction of a hierarchical model of the ASI by S. O. Lilienfeld, S. M. Turner, and R. G. Jacob (1993), the factor structure of the ASI was the subject of debate, with some researchers advocating a unidimensional structure and others proposing multidimensional structures. In the present study, involving 432 outpatients seeking treatment at an anxiety disorders clinic and 32 participants with no mental disorder, the authors tested a hierarchical factor model. The results supported a hierarchical factor structure consisting of 3 lower order factors and 1 higher order factor. It is estimated that the higher order, general factor accounts for 60% of the variance in ASI total scores. The implications of these findings for the conceptualization and assessment of anxiety sensitivity are discussed. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Anxiety sensitivity (fear of anxiety) is thought to play an important role in the development and maintenance of anxiety disorders. One of the most widely used measures of anxiety sensitivity is the Anxiety Sensitivity Index (ASI). The originators of this scale regarded it as a measure of a unidimensional construct (S. Reiss et al, 1986). Recent investigations have challenged this claim, and several 4-factor solutions have been proposed. If the dimension(s) of this scale are to guide theory and research, then it is necessary to determine the most stable factor structure. ASI responses were obtained from 142 spider-phobic college students and 327 psychiatric patients presenting with anxiety or stress-related (psychophysiological) disorders. The results of a series of confirmatory analyses indicated that the ASI is best regarded as unifactorial. The implications for the conceptualization of anxiety sensitivity are considered, and directions for further investigation are set out. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The present study examined the efficacy of an 8-wk, cognitive-behavioral group treatment for panic disorder. Patients meeting DSM-III-R criteria for panic disorder with or without agoraphobia were randomly assigned to treatment (N = 34) or delayed treatment control (N = 33). The treatment consisted of: (a) education and corrective information; (b) cognitive therapy; (c) training in diaphragmatic breathing; and (d) interoceptive exposure. At posttreatment, 85% of treated Ss were panic free, compared to 30% of controls. Treated Ss also showed clinically significant improvement on indices of anxiety, agoraphobia, depression and fear of fear. Recovery, as estimated conservatively by the attainment of normal levels of functioning on each of the major clinical dimensions of the disorder (i.e. panic, anxiety and avoidance), was achieved in 64% of the treated Ss and 9% of the controls. At the 6 month follow-up, 63% of the treated patients met criteria for recovery. These findings mirror those from recently-completed trials of individually-administered cognitive-behavioral treatment, and suggest that CBT is a viable alternative to pharmacotherapy in the treatment of panic disorder.
Anxiety disorder patients (n = 198; under criteria of the Diagnostic and Statistical Manual of Mental Disorders; rev. 3rd ed.; American Psychiatric Association, 1987) and nonanxious control subjects (n = 25) underwent challenges of 90 s of voluntary hyperventilation and 15 min of 5.5% carbon dioxide in air. Panic disorder subjects showed a greater subjective response to both challenges than did subjects with other anxiety disorders, who in turn responded more than did control subjects. Furthermore, subjects with panic disorder as an additional diagnosis tended to report more subjective response than did anxiety disorder subjects without panic disorder. The best prechallenge predictor of response to each procedure was a measure of fear of physical symptoms. The findings support previous results that have pointed to a greater fear or anxiety-inducing effect of these challenge procedures in panic disorder patients, as compared with other subjects.
The current study tested the notion that a sense of control can mitigate anxiety and panic attacks caused by the inhalation of 5.5% carbon dioxide (CO2)-enriched air. Twenty patients with panic disorder inhaled a mixture of 5.5% CO2-enriched air for 15 minutes. All patients were instructed that illumination of a light directly in front of them would signal that they could decrease the amount of CO2 that they were receiving, if desired, by turning a dial attached to their chair. For ten patients, the light was illuminated during the entire administration of CO2. For the remaining ten patients, the light was never illuminated. In fact, all patients experienced the full CO2 mixture, and the dial was ineffective. When compared with patients who believed they had control, patients who believed they could not control the CO2 administration (1) reported a greater number of DSM-III-revised panic attack symptoms, (2) rated the symptoms as more intense, (3) reported greater subjective anxiety, (4) reported a greater number of catastrophic cognitions, (5) reported a greater resemblance of the overall inhalation experience to a naturally occurring panic attack, and (6) were significantly more likely to report panic attacks. These data illustrate the contribution of psychologic factors to laboratory induction of panic attacks through inhalation of 5.5% CO2-enriched air.
This study examined the effect of having a safe person present on artificially induced anxiety following a biological challenge among panic-disordered patients. Anxiety symptoms were induced using a 5.5% CO2-inhalation procedure. Panic patients underwent the inhalation procedure either in the presence or absence of their safe person. Nonanxious controls underwent the procedure without a safe person. Panic patients exposed to CO2 without their safe person present reported greater distress, a greater number of catastrophic cognitions, and a greater level of physiological arousal than did panic patients exposed with their safe person. The latter group did not differ from controls on most measures at postexposure. The attenuation of self-reported anxiety and catastrophic cognitions is consistent with the safety-signal theory and the cognitive model of panic, respectively. The results, however, are inconsistent with a biological model of panic.
The Anxiety Sensitivity Index (ASI) is one of the most widely used measures of the construct of anxiety sensitivity. Until the recent introduction of a hierarchical model of the ASI by S. O. Lilienfeld, S. M. Turner, and R. G. Jacob (1993), the factor structure of the ASI was the subject of debate, with some researchers advocating a unidimensional structure and others proposing multidimensional structures. In the present study, involving 432 outpatients seeking treatment at an anxiety disorders clinic and 32 participants with no mental disorder, the authors tested a hierarchical factor model. The results supported a hierarchical factor structure consisting of 3 lower order factors and 1 higher order factor. It is estimated that the higher order, general factor accounts for 60% of the variance in ASI total scores. The implications of these findings for the conceptualization and assessment of anxiety sensitivity are discussed. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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.
We tested the hypothesis that the Anxiety Sensitivity Index (ASI) measures a unitary personality variable. College students (N = 840) were administered the ASI along with a questionnaire assessing panic and anxiety symptomatology. The ASI demonstrated adequate internal reliability (α = .82) and showed modest discrimination on two of three anxiety disorder indices (i.e., anxiety medication usage and panic history). Results of a principal components analysis with varimax rotation revealed a four-factor solution which explained 53.5% of the total variance. Our findings seriously challenge previous claims that the ASI measures a single factor. Rather, our data suggest that the ASI measures several loosely-related cognitive appraisal domains concerned with the anticipated negative consequences of anxiety. The four factors that emerged from our analysis were (a) concern about physical sensations, (b) concern about mental/cognitive incapacitation, (c) concern about loss of control, and (d) concern about heart/lung failure. It is concluded that the ASI is a convenient and reliable instrument for assessing perceived physical consequences of anxiety but that the instrument is lacking in its coverage of anxiety consequences related to social concerns. Implications of the findings for 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)
Reports an error in "The role of anxiety sensitivity in the pathogenesis of panic: Prospective evaluation of spontaneous panic attacks during acute stress" by Norman B. Schmidt, Darin R. Lerew and Robert J. Jackson (Journal of Abnormal Psychology, 1997[Aug], Vol 106[3], 355-364). The article contained an error in the scoring of the Anxiety Sensitivity Index (ASI). A data conversion error led to transformation of ASI scores that dramatically truncated this measure (scores of 0-2 recoded to 0, 3 receded to 1, and 4 recoded to 2). The corrected values (items scored 0-4), revised statistics, and amended conclusions are presented in the corrected text. (The following abstract of the original article appeared in record 1997-05214-001.) Expectancy theory posits that anxiety sensitivity may serve as a premorbid risk factor for the development of anxiety pathology (S. Reiss, 1991). The principal aim of the present study was to determine whether anxiety sensitivity acts as a specific vulnerability factor in the pathogenesis of anxiety pathology. A large, nonclinical sample of young adults (N = 1, 401) was prospectively followed over a 5-week highly stressful period of time (i.e., military basic training). Anxiety sensitivity was found to predict the development of spontaneous panic attacks after controlling for a history of panic attacks and trait anxiety. Approximately 20% of those scoring in the upper decile on the Anxiety Sensitivity Index (R. A. Peterson & S. Reiss, 1987) experienced a panic attack during the 5-week follow-up period compared with only 6% for the remainder of the sample. Anxiety sensitivity also predicted anxiety symptomatology, functional impairment created by anxiety, and disability. These data provide strong evidence for anxiety sensitivity as a risk factor in the development of panic attacks and other anxiety symptoms. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
(Publisher-supplied data) The classic text is Psychometric Theory. Like the previous edition, this text is designed as a comprehensive text in measurement for researchers and for use in graduate courses in psychology, education and areas of business such as management and marketing. It is intended to consider the broad measurement problems that arise in these areas and is written for a reader who needs only a basic background in statistics to comprehend the material. It also combines classical procedures that explain variance with modern inferential procedures.
12 21–42 yr olds with panic disorder or agoraphobia with panic attacks, who received a standard infusion of sodium lactate (10 ml/mg), were Ss in an investigation to determine whether naloxone HCl would precipitate or exacerbate Ss' panic attacks. Four Ss received doses of naloxone (2.5, 5, 10, and 20 mg) alone, while 1 S received naloxone (2.5 mg, iv) followed by a standard lactate infusion, and 7 Ss received 2.5 mg, iv, naloxone followed by another standard infusion of lactate followed again by 20 mg, iv, naloxone. Results indicate that Ss given naloxone alone reported that naloxone produced none of the symptoms reminiscent of a panic attack. In the remaining 8 Ss administered naloxone with lactate, there were 4 panic attacks with lactate alone and 4 panic attacks during the lactate phase of naloxone-lactate trial. There were no consistent differences in intensity, time of onset, duration, or nature of symptoms between lactate and naloxone-lactate panic attacks. Findings suggest that the endogenous opiate system is not chronically active in suppressing panic attacks and does not support the involvement of endogenous opiates in the pathogenesis or control of panic attacks. (10 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
cognitive model of panic attacks is described . . . based on the clinical observation that panic-prone patients are particularly sensitive to the experience of any physical sensation or mental state that they cannot dismiss as normal
major hypotheses of the model: the catastrophic misinterpretation hypothesis and the cognitive dysfunction hypothesis
catastrophic content of ideation / loss of reappraisal capability
treatment / induction of "minipanic attacks" / graded exposure
preliminary study of 25 patients with panic disorder indicates that these methods have a robust effect on the frequency of panic attacks / total elimination of panic attacks (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Lilienfeld, Turner, and Jacob recently presented a critical review of conceptual and methodological issues pertaining to anxiety sensitivity. Their review raised several important issues, and advanced two novel hypotheses. The latter were (1) the interaction between anxiety sensitivity and trait anxiety is an important determinant of fear responding, and (2) trait anxiety and fundamental fears are hierarchically structured. Despite the many strengths of their critique, Lilienfeld et al. made several questionable claims, which are challenged in the present article. Contrary to Lilienfeld et al., the present article concludes (1) there is a sound theoretical rationale for expecting anxiety sensitivity to increase fear-proneness, (2) the Anxiety Sensitivity Index (ASI) is not confounded with the assessment of panic symptoms, and (3) the ASI is unifactorial. The present article also presents an empirical evaluation of Lilienfeld et al.'s hypotheses. Results failed to support the interaction hypotheses, although support was found for the hierarchical model. The latter represents an important advancement that deserves further investigation.
Guttman's classic lower bound for the number of common factors is extended to the completely general case where communalities may lie in the closed interval from zero to one.
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.
Lactate infusions were conducted in 12 male panic patients and 8 male normal controls with arterial catheters in place to reassess previously reported acid-base changes based on venous blood samples. The analysis of arterial pH, carbon dioxide pressure, and bicarbonate concentration confirmed most venous findings. At baseline, before the infusion, venous blood shows evidence of mixed chronic and acute respiratory alkalosis in patients while arterial blood gasses are most consistent with developing acute respiratory alkalosis. During the infusion both bloods are consistent with mixed metabolic and respiratory alkalosis with the patients hyperventilating more than normal controls and panicking patients hyperventilating more than nonpanicking patients. Arterial blood seems more sensitive than venous blood in detecting baseline differences between panicking and nonpanicking patients. A baseline arterial carbon dioxide pressure of 40 mmHg or higher and an arterial pH below 7.40 may predict no subsequent panic to lactate infusion.
The present study investigated the singular and joint effects of fear of somatic sensations and perceived safety of hypocapnia-induced bodily cues on nonclinical subjects' subjective and psychophysiological response to a hyperventilation challenge. Fear of fear was assessed with the Body Sensations Questionnaire (BSQ; High versus Low), and subjects were randomly assigned to one of two informational conditions (Safety Information versus No Safety Information). When anticipating hyperventilation, High BSQ-Safety Information subjects reported higher subjective anxiety compared to Low BSQ-Safety Information subjects. Similarly, High BSQ-Safety Information subjects reported significantly more symptoms during the anticipatory phase compared to subjects in each of the other three conditions. During hyperventilation, fear of somatic cues and safety information exerted independent effects on subjective responding. High BSQ subjects reported higher levels of subjective fear and physical symptoms compared to Low BSQ subjects; subjects who received safety information reported lower levels of anxiety and physical symptoms compared to those who did not receive safety information. High BSQ subjects' heightened subjective fear response persisted through the hyperventilation recovery period. There were no group differences on the psychophysiological variables across any of the experimental phases. These findings provide further support both that fear of fear contributes to heightened emotional responding to biological challenges and that emotional responding is also affected by conditions that alter the perceived threat of the challenge-induced cues.
Anxiety sensitivity (AS) is the fear of anxiety-related sensations arising from beliefs that these sensations have harmful physical, psychological, or social consequences. AS is measured using the Anxiety Sensitivity Index (ASI), a 16-item self-report questionnaire. Little is known about the origins of AS, although social learning experiences (including sex-role socialization experiences) may be important. The present study examined whether there were gender differences in: (a) the lower- or higher-order factor structure of the ASI; and/or (b) pattern of ASI factor scores. The ASI was completed by 818 university students (290 males; 528 females). Separate principal components analyses on the ASI items of the total sample, males, and females revealed nearly identical lower-order three-factor structures for all groups, with factors pertaining to fears about the anticipated (a) physical, (b) psychological, and (c) social consequences of anxiety. Separate principal components analyses on the lower-order factor scores of the three samples revealed similar unidimensional higher-order solutions for all groups. Gender × AS dimension analyses on ASI lower-order factor scores showed that: females scored higher than males only on the physical concerns factor; females scored higher on the physical concerns factor relative to their scores on the social and psychological concerns factors; and males scored higher on the social and psychological concerns factors relative to their scores on the physical concerns factor. Finally, females scored higher than males on the higher-order factor representing the global AS construct. The present study provides further support for the empirical distinction of the three lower-order dimensions of AS, and additional evidence for the theoretical hierarchical structure of the ASI. Results also suggest that males and females differ on these various AS dimensions in ways consistent with sex role socialization practices.
The effects of anxiety sensitivity and perceived control on emotional responding to a caffeine challenge were assessed in 72 subjects without a history of panic disorder. Subjects high and low in anxiety sensitivity (AS) were randomly assigned to either a perceived control (PC) or a no perceived control (NPC) instructional set. Compared to subjects low in AS, subjects high in AS displayed heightened emotional responding to the caffeine challenge. As predicted, high-AS subjects in the NPC condition displayed significantly greater emotional responding compared to high-AS subjects in the PC condition. In contrast, low AS subjects' emotional response to caffeine was not affected by the perceived control manipulation. Consistent with recent psychological formulations of panic, the present findings suggest that a fear of arousal (i.e., anxiety sensitivity) exerts a significant effect on emotional responding. Moreover, for those who display high anxiety sensitivity, greater emotional responding occurs when perceived control over arousal is low.
We report the results of a long-term clinical outcome study testing variations of behavioral treatments for panic disorder without agoraphobic avoidance. Exposure to somatic cues combined with cognitive therapy was compared to relaxation therapy designed specifically for panic disorder. In a third treatment condition, these techniques were combined. All three treatments were superior on a variety of measures to a wait-list control group. In the two treatment conditions containing exposure to somatic cues and cognitive therapy, 85% or more of clients were panic free at posttreatment. These were the only groups significantly better than wait-list control on this measure. Relaxation, on the other hand, tended to effect greater reductions in generalized anxiety associated with panic attacks but was associated with high drop-out rates. These results suggest that we have a successful behavioral treatment for panic disorder, but leave questions on effective components and mechanisms of action unanswered.
The purposes of this article are to summarize the author's expectancy model of fear, review the recent studies evaluating this model, and suggest directions for future research. Reiss' expectancy model holds that there are three fundamental fears (called sensitivities): the fear of injury, the fear of anxiety, and the fear of negative evaluation. Thus far, research on this model has focused on the fear of anxiety (anxiety sensitivity). The major research findings are as follows: simple phobias sometimes are motivated by expectations of panic attacks; the Anxiety Sensitivity Index (ASI) is a valid and unique measure of individual differences in the fear of anxiety sensations; the ASI is superior to measures of trait anxiety in the assessment of panic disorder; anxiety sensitivity is associated with agoraphobia, simple phobia, panic disorder, and substance abuse; and anxiety sensitivity is strongly associated with fearfulness. There is some preliminary support for the hypothesis that anxiety sensitivity is a risk factor for panic disorder. It is suggested that future researchers evaluate the hypotheses that anxiety and fear are distinct phenomena; that panic attacks are intense states of fear (not intense states of anxiety); and that anxiety sensitivity is a risk factor for both fearfulness and panic disorder.
The construct of anxiety sensitivity (AS) has occupied an increasingly important place in theorizing and research on anxiety and anxiety disorders. Although a number of recent studies have provided support for the construct validity of the principal operationalization of AS, the Anxiety Sensitivity Index (ASI), the relation of the AS construct and the ASI to trait anxiety continues to be a source of controversy. Key issues in the AS-trait anxiety debate include the assimilative nature of traits and the concept of incremental validity. Recent research on AS lends some support to the claim that trait anxiety cannot fully account for AS findings. Important areas for future AS research include (1) demonstrating that AS is a risk factor for panic disorder and related conditions, lather than simply a consequence of these conditions, (2) developing and utilizing multiple operationalizations of constructs, (3) minimizing the impact of potentially inapplicable items, (4) testing for interactions between AS and other variables, and (5) testing hierarchical factor models that allow trait anxiety and AS to coexist as higher- and lower-order factors, respectively. Researchers in this area will need to develop alternative measures of the AS construct, recognize the distinction between different levels of trait specificity, clarify a number of theoretical issues relevant to the AS construct, and continue to subject predictions to stringent theoretical risks.
Reliability, factor structure, and factor independence from other anxiety measures for the Anxiety Sensitivity Index (ASI) was assessed. One hundred and twenty-two anxious college students were administered the ASI, Cognitive-Somatic Anxiety Questionnaire, and the Reactions to Relaxation and Arousal Questionnaire. The results suggest that the ASI is a reliable measure which is factorially independent of other anxiety measures. Further, the ASI was supported as a measure of the variable anxiety sensitivity which has been suggested as an important personality variable in fear behavior.
The factor structure of the Anxiety Sensitivity Index was assessed in 166 agoraphobic clients who had applied to a behavioral treatment programme and 120 age and sex-matched normal controls. In both samples a four factor solution emerged as the most useful, and it explained more than 60% of the total variance. The item loading in the agoraphobic sample revealed a coherent theme with factors reflecting fear of heart and breathing symptoms, fear of loss of mental control, fear of gastrointestinal difficulties, and concern about other people detecting anxiety. The item loading in the normal sample made less psychological sense. The results are discussed both in the light of the trait model of anxiety sensitivity and with respect to the clinical implications of anxiety sensitivity.
We investigated cardiac perception in panic disorder with both self-report and objective measures. In Study 1, 120 patients with panic disorder, 86 infrequent panickers, and 38 patients with other anxiety disorders reported greater cardiac and gastrointestinal awareness than 62 normal control subjects. Subjects with panic attacks reported greater cardiac awareness, but not gastrointestinal awareness, than those with other anxiety disorders. Studies 2 and 3 included a test of heart rate perception in which subjects silently counted their heart-beats without taking their pulse. In Study 2, 65 panic disorder patients showed better performance than 50 infrequent panickers, 27 patients with simple phobias, and 46 normal control subjects. No group differences were found in ability to estimate time intervals. In Study 3, 13 patients with panic disorder and 15 with generalized anxiety disorder showed better heart rate perception than 16 depressed patients.
We studied the action of cholecystokinin tetrapeptide (CCK-4) in patients with panic disorder and normal controls. Subjects received, in random order, one injection of CCK-4 and one injection of placebo (saline) on two separate days in a double-blind crossover design. Two doses of CCK-4, 50 and 25 micrograms, were administered to two different samples of subjects. The panic rate with 50 micrograms of CCK-4 was 100% (12/12) for patients and 47% (7/15) for controls. The panic rate with 25 micrograms of CCK-4 was 91% (10/11) for patients and 17% (2/12) for controls. Nine percent of patients compared with 0% of controls panicked with placebo. These findings concur with previous reports of a panicogenic effect of CCK-4 and suggest that patients with panic disorder are more sensitive to the panicogenic effect of the peptide than are normal controls.
We evaluated the functional sensitivity of the gamma-aminobutyric acid-benzodiazepine supramolecular complex in 9 patients with panic disorder and 10 psychiatrically healthy control subjects by comparing the effects of four logarithmically increasing doses of intravenous diazepam on saccadic eye movement velocity, memory, and self-rated sedation. Patients with panic disorder were less sensitive than controls to diazepam using eye velocity as the dependent measure. Sedation and memory effects did not distinguish the two groups. These findings suggest that panic disorder is associated with functional subsensitivity of the gamma-aminobutyric acid-benzodiazepine supramolecular complex in brain-stem areas controlling saccadic eye movements.
A cognitive explanation of the association between acute hyperventilation and panic attacks has been proposed: the extent to which sensations produced by hyperventilation are interpreted in a negative and catastrophic way is said to be a major determinant of panic. Non-clinical subjects were provided with a negative or a positive interpretation of the sensations produced by equivalent amounts of voluntary hyperventilation. As predicted, there was a significant difference between positive and negative interpretation conditions on ratings of positive and negative affect. Subjects in the positive interpretation condition experienced hyperventilation as pleasant, and subjects in the negative interpretation condition experienced hyperventilation as unpleasant, even though both groups experienced similar bodily sensations and did not differ in their prior expectations of the affective consequences of hyperventilation. When the subjects were given a positive interpretation, the number of their sensations correlated with positive affect; when a negative interpretation was given, the number of bodily sensations correlated with negative affect. The results provide support for a cognitive model of panic and are inconsistent with the view that panic is simply a symptom of hyperventilation syndrome.
The effects of double breath inhalation of a 35% CO2 mixture in oxygen and placebo air inhalation were compared in 14 women seeking treatment for marked premenstrual dysphoric changes who did not have panic disorder and 12 control women. The first exposure to CO2 inhalation induced a panic attack reaction (severe subjective anxiety with autonomic symptoms) in 9 of 14 women with premenstrual dysphoria but none of the controls. Neither patients nor controls panicked in response to the air inhalation. Control subjects experienced mild anxiety and/or somatic symptoms after CO2 inhalation, but these did not resemble panic attacks and were clearly different from the response of the patient group.
The possibility that a disorder of brain alpha 2-adrenoceptor sensitivity might contribute to the etiology of panic disorder was examined using a challenge paradigm with the alpha 2-adrenoceptor agonist clonidine. The cardiovascular, psychological, and endocrine actions of 1.5-microgram/kg clonidine hydrochloride given intravenously were assessed in 16 patients and compared with age- and sex-matched controls. Patients with panic disorder showed an increased fall in blood pressure and decreased sedative and endocrine responses as compared with controls. These results suggest that there may be subsensitivity of some, and supersensitivity of other, brain alpha 2-adrenoceptors in panic disorder. In view of the increased cardiovascular responses seen in the present study and other reports of increased responses to the alpha 2-adrenoceptor antagonist yohimbine, there may exist an increased lability (decreased damping) of cardiovascular control mechanisms in panic disorder. Such a dysfunction could contribute to the symptoms of panic attacks, such as dizziness, palpitations, and faintness.
Fenfluramine, and indirect serotonergic agonist, was administered to nine women with panic disorder, nine women with major depressive disorder, and nine women controls. Panic disorder patients revealed significantly greater anxiogenic responses to fenfluramine administration at all 5 hourly measurement points than either depressed patients or control subjects. Prolactin and cortisol responses to fenfluramine were also significantly greater in panic disorder patients than in either depressed patients or control subjects. Placebo administration did not elicit robust or significantly different anxiety or hormonal responses in panic disorder patients or control subjects. These data offer evidence that serotonergic hyperresponsivity must be considered as an important factor in the mechanism of events provoking overt panic attacks.
The present study examined several dimensions of panic cognitions to test whether panic appraisals predict phobicity among panic sufferers. Thirty-five patients meeting DSM-III-R criteria for panic disorder with minimal or no phobic avoidance were compared to 40 patients meeting DSM-III-R criteria for panic disorder with agoraphobia (severe). The two groups looked strikingly similar on measures of panic symptoms, panic frequency and panic severity. As expected, patients diagnosed as having panic disorder with agoraphobia reported significantly more depression and phobic avoidance than patients with PD. Striking differences emerged on each of the following panic appraisal dimensions: (a) anticipated panic, (b) perceived consequences of panic, and (c) perceived self-efficacy in coping with panic. In each case, patients with panic disorder and agoraphobia reported significantly more dysfunctional panic appraisals than patients with panic disorder and no avoidance. Of those panic appraisal dimensions studied, anticipated panic emerged as the most potent correlate of agoraphobic avoidance. These findings support the hypothesis that cognitive appraisal factors may play an important role in the genesis or maintenance of phobic avoidance among panic patients.
The immediate effects of a single inhalation of a 35% CO2 mixture in oxygen were examined in 12 patients with panic disorders and 11 normal control subjects. Compared to a placebo air inhalation, the CO2 inhalation provoked short-lived autonomic panic symptoms in both patients and normals; it also elicited high subjective anxiety in patients with panic disorders. The latter rated the overall CO2-induced state as very similar to a real-life panic attack.
Biological models have had major consequences for the therapy and theory of panic disorder and agoraphobia. Authors such as Klein and Sheehan propose a qualitative biological distinction between panic attacks and other types of anxiety. Central arguments for their models include drug specificity, panic induction, family data, spontaneity of panic attacks and separation anxiety. A look at the evidence, however, shows surprisingly little empirical support for these arguments. In spite of the great heuristic value of Klein's and Sheehan's models, alternative approaches focusing on an interaction of physiological and psychological factors seem more capable of integrating the relevant findings.
To determine whether endogenous opiates are involved in panic anxiety, the authors challenged 12 patients with panic attacks with intravenous naloxone hydrochloride alone or combined with sodium lactate. Naloxone did not produce panic attacks or alter responses to lactate.
The effects of inhaling a mixture of 35 per cent carbon dioxide and 65 per cent oxygen on the occurrence of panic symptoms defined by the DSM III, was investigated. Compared to a placebo (air), carbon dioxide produced more panic symptoms. If carbon dioxide inhalation was preceded by intake of a beta-blocker (60 mg propranolol), less symptoms occurred than if preceded by a placebo. The results are compared with earlier reports on the effects of lactate infusion. It is argued that panic disorders can be conceptualized as a fear of internal (panic) sensations and that inhalation of a mixture of carbon dioxide and oxygen may constitute an effective exposure treatment.
Describes the development of the Agoraphobic Cognitions Questionnaire and the Body Sensations Questionnaire, companion measures for assessing aspects of fear of fear (panic attacks) in agoraphobics. The instruments were administered to 175 agoraphobics (mean age 37.64 yrs) and 43 controls (mean age 36.13 yrs) who were similar in sex and marital status to experimental Ss. Results show that the instruments were reliable and fared well on tests of discriminant and construct validity. It is concluded that these questionnaires are useful, inexpensive, and easily scored measures for clinical and research applications and fill a need for valid assessment of this dimension of agoraphobia. (22 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
UNTIL recently panic disorder was viewed almost exclusively in psychological terms. It was believed that the patient was overreacting to a life stress or an "unconscious" conflict.1 A growing body of evidence now suggests that we revise this view in favor of a medical-illness model.2 , 3 This model suggests that in contrast to stress-related situational anxiety, panic disorder is associated with a biochemical abnormality in the nervous system, to which there is a genetic vulnerability.3 4 4a This new view has important implications for treatment and research. Natural History Panic disorder usually starts with paroxysmal attacks of anxiety that strike suddenly, without warning, . . .
Cholecystokinin (CCK) has well-documented anxiogenic effects in animals and normal people, and panicogenic effects in patients with panic disorder, but little is known about its neuroendocrine profile. We examined neuroendocrine responses to intravenous infusions of pentagastrin, a selective CCK-B receptor agonist, in 10 patients with panic disorder and 10 normal control subjects. Pentagastrin potently activated the hypothalamic-pituitary-adrenal (HPA) axis, but did not release growth hormone or any of several vasoactive peptides (neurokinin A, substance P, vasoactive intestinal peptide). The HPA axis response was unrelated to increases in symptoms. Panic patients did not differ from controls in neuroendocrine responses to the CCK agonist. Differential sensitivity to novelty stress accounted for the only patient-control differences in neuroendocrine profiles. The data suggest that CCK may help modulate normal HPA axis activity, but its anxiogenic effects are unrelated to its stimulatory effects on the HPA axis. Pentagastrin provides a safe and readily available probe for further study of CCK receptor systems in humans.
Results on cardiac awareness in panic disorder are inconsistent. The present study attempted to clarify whether differences in instructions or the inclusion of patients taking antidepressant medication could account for these inconsistencies. 112 patients with panic disorder with agoraphobia were compared to 40 normal controls on the heartbeat perception task developed by Schandry (1981) [Schandry, R., Psychophysiology, 18, 483-488] using a standard instruction ("count all heartbeats you feel in your body") and a strict instruction ("count only those heartbeats about which you are sure"). Superior heartbeat perception for patients was only found with the standard instruction. Similarly, only with the standard instruction, patients taking medication affecting the cardiovascular system performed worse than patients without medication, as expected based on the relationship between stroke volume and heartbeat perception. The pattern of group differences indicates that agoraphobic patients have a better feeling for how fast their heart is beating than controls although these differences may be due to a tendency to interpret weak sensations as heartbeats. Furthermore, we tested in a subgroup of 40 patients whether cardiac awareness changes with exposure treatment. No changes in heartbeat perception were observed.
The primary aim of this study was to determine if pretreatment with a single dose of alprazolam reduces anxiety and panic provoked by the inhalation of 35% carbon dioxide (CO2) in patients with panic disorder. Ten panic disorder patients participated in a CO2 challenge test after pretreatment with a single dose of alprazolam (1 mg p.o.) or placebo in a randomized, double-blind, within-subjects design. Seventy percent of the subjects had a panic attack with placebo, compared to only 10% with alprazolam. Alprazolam reduced the number and severity of panic symptoms and baseline anxiety significantly more than placebo. This study demonstrates the efficacy of the acute administration of alprazolam to block panic attacks and supports the usefulness of the CO2 challenge as an analogue method to study panic disorder.