Anxiety sensitivity and panic attacks in a nonclinical population

In the present study, we administered the Anxiety Sensitivity Index (ASI) and a modified version of the Panic Attack Questionnaire (PAQ) to 425 college students to determine whether high anxiety sensitivity ('fear of fear') occurs in the absence of a history of unpredictable ('spontaneous') panic attacks, or whether such attacks are a necessary precursor to high anxiety sensitivity. Based on their ASI scores, subjects were assigned to either the high, medium, or low anxiety sensitivity groups. High anxiety sensitivity subjects more frequently reported both a personal and family history of panic than did subjects in the other groups. Nevertheless, two-thirds of the high anxiety sensitivity subjects had never experienced an unpredictable panic attack. This suggests that the fear of anxiety can be acquired in ways other than through personal experience with panic.     

Factors influencing drinking behavior in alcoholic panickers and non-panickers

Male alcoholics who (a) experienced panic attacks prior to abusing alcohol, (b) experienced panic attacks subsequent to abusing alcohol, and (c) had not experienced panic attacks were compared on three sets of measures: the Panic Attack Questionnaire, the Restrained Drinking Scale, and the Inventory of Drinking Situations. The results showed that two groups of Ss who experienced panic attacks were more likely than non-panickers to use drugs other than alcohol, began drinking at an earlier age, had a greater proportion of parents with panic and alcohol related problems, had higher drinking restraint scores, and drank in more situations. The Ss who experienced panic attacks prior to abusing alcohol were more likely than the other groups to drink in situations similar to those related to agoraphobic fears. It was postulated that alcoholics who experience panic attacks, especially those who experienced panic attacks prior to abusing alcohol may be using alcohol to reduce anxiety or fear related to panic attacks.     

The hyperventilation provocation test in panic disorder.

Forty-eight patients with DSM-III-R Panic Disorder underwent a hyperventilation provocation Test (HVPT). Twenty-four patients rated the symptoms induced during the HVPT as similar to those occurring during panic attacks in daily life. Contrary to the classical hyperventilation model of panic, no differences were found in respiratory physiology between recognizers and non-recognizers before and during voluntary hyperventilation. Moreover, recognizers and non-recognizers reported comparable levels of panic and hyperventilation symptoms and state anxiety during panic attacks in daily life. Ten of the recognizers also had a panic attack during the HVPT, independent of any differential CO2 alterations. Compared to non-panickers, panickers obtained higher scores for agoraphobia and depression. On the basis of these results, it is concluded that recognizers or panickers do not show a tendency towards hyperventilation, but that reports of severe panic and hyperventilation symptoms are more closely related to the level of anxiety. These results are more consistent with the cognitive model of panic, which emphasizes the patient's tendency to interpret somatic symptoms catastrophically.     

Generalized anxiety and panic disorders: Response to Cox, Cohen, Direnfeld, and Swinson (1996)

Contrary to the contention of Cox, Cohen, Direnfeld and Swinson (1996, Behaviour Research and Therapy, 34, 949–954) that the Beck Anxiety Inventory (BAI; Beck & Steer, 1993, Manual for the Beck Anxiety Inventory) measures primarily symptoms associated with panic attacks rather than anxiety in general, we propose that the higher level of anxiety found in patients with panic disorders not only is not an artifact of the BAI's symptom content, but patients with panic disorders truly have more anxiety than patients with other types of anxiety disorders. Furthermore, the BAI contains symptoms present in other anxiety disorders, besides panic disorder, and specifically includes 11 symptoms of generalized anxiety disorder (GAD). The BAI and revised Hamilton Anxiety Rating Scale (HARS-R; Riskind, Beck, Brown & Steer, 1987, Journal of Nervous and Mental Disease, 175, 474–479) scores of 274 (69%) outpatients with panic disorders and 123 (31%) outpatients with GAD were found to differentiate these two diagnostic groups equally and significantly. The panic disorder outpatients had higher scores on both the BAI and the HARS-R than did the GAD patients. Thus, Cox et al.'s (1996) speculation about the BAI's yielding spuriously high levels of anxiety in patients with panic disorders revives an important issue relevant to the relation of panic disorder to GAD.     

Anxiety sensitivity and nonclinical panic attacks

The present study examined anxiety sensitivity in relation to trait anxiety and the occurrence of nonclinical panic attacks in 265 subjects. Fifty percent of high anxiety sensitivity subjects reported panic attacks (both cued and spontaneous) in the past year. In addition, almost 42% of subjects with high anxiety sensitivity but no history of panic reported a high level of trait anxiety concerning physical danger. The results suggest that anxiety sensitivity is frequently not independent of other forms of anxiety.     

Responses to false physiological feedback in individuals with panic attacks and elevated anxiety sensitivity

Participants with elevated anxiety sensitivity and a history of panic attacks were compared to a low anxiety comparison group with respect to physiological and subjective reactivity to false heart-rate feedback and reactivity to a priming procedure. Whereas accurate heart-rate feedback elicited minimal responses, participants across groups showed significant physiological and subjective responses to false feedback. High risk and low risk participants did not differ in heart-rate responses to false feedback, though panic attack frequency did predict physiological and subjective reactions to false feedback in the high risk group. Self-reported nonspecific anxiety was significantly higher in high risk female participants than in low risk female participants, while males did not different in general subjective anxiety. However, high risk participants reported more panic-specific symptoms during the false feedback task than low risk participants, regardless of the sex of the participant. Therefore, although the experimental paradigm appeared to trigger nonspecific anxiety in high risk female participants, panic attack symptoms in reaction to the task were specific to risk group, not sex, and consistent with hypotheses. Surprisingly, the priming procedure did not influence physiological or subjective responses to false feedback in either group. These results raise additional questions regarding the process and impact of interoception in individuals with panic attacks, and suggest that false perception of internal changes may contribute to risk for panic disorder when exposed to believable cues.     

Anxiety sensitivity and panic symptomatology: the mediator role of hypochondriacal concerns

The present study tests the mediating role of hypochondriasis to explain the relation between anxiety sensitivity and panic symptomatology. Fifty-seven outpatients with clinically significant levels of panic symptomatology were selected to participate in the study. Measures of anxiety sensitivity, hypochondriasis, and panic symptomatology were obtained from standardized, self-administered questionnaires: the Anxiety Sensitivity Index (ASI; Reiss, Peterson, Gursky, & McNally, 1986), the Whiteley Index of Hypochondriasis (WI; Pilowsky, 1967), and the Panic-Agoraphobic Spectrum Self-Report (PAS-SR; Cassano et al., 1997; Shear et al., 2001). Regression analyses were performed to test for the mediation models. The results show that the effect of anxiety sensitivity on panic symptomatology is not significant when controlling the hypochondriacal concerns, whereas the latter predicted panic symptoms. This result holds for the overall ASI as well as for the Physical Concerns and the Mental Incapacitation Concerns dimensions of the ASI scale. No evidence of a direct relation between the Social Concerns dimension and panic symptoms was found. The findings suggest that hypochondriacal concerns might represent the mechanism through which anxiety sensitivity is able to influence panic symptoms.     

Physiological and psychological reactivity in women with asthma: the effects of anxiety and menstrual cycle phase.

The relation between menstrual cycle timing, panic attacks, and diagnosis of asthma was explored in this study. Women with or without asthma and with or without a history of panic attacks engaged in a psychophysiological task during either the intermenstrual or premenstrual cycle phase and completed self-report measures of menstrual symptoms and attitudes, general psychological symptoms, and attitudes toward illness. No significant differences were identified for psychological or psychophysiological measures with menstrual cycle phase as a factor. However, women with both asthma and a history of panic attacks reported more general psychological distress than women in the other groups, and more state anxiety than controls. Women in the asthma, asthma and panic, and panic groups reported higher anxiety sensitivity than the control group. After listening to asthma-related scenes, women with asthma exhibited a decrease in peak expiratory air flow, and women with asthma and panic exhibited increased skin conductance response magnitude. Implications for the role of anxiety in lung function are discussed, as well as directions for future research with asthma and anxiety populations.     

The catastrophic misinterpretation model of panic disorder.

In the catastrophic misinterpretation model of panic Clark [Behav. Res. Ther. 24(1986)1461] proposes that panic attacks result from the misinterpretation of autonomic arousal stimuli as precursors to a physical or psychological emergency. The model has been widely examined, with many researchers suggesting that this specific cognitive bias is implicated in both the phenomenon of panic, and the aetiology and maintenance of panic disorder. Various research methodologies have provided only partial or inconclusive support for the model as being uniquely associated with panic, and as a cognitive process underpinning the experience of panic. This paper reviews the body of existing evidence and its implications for the model and proposes future research directions. The influence of implicit operational definitions of key terms in the catastrophic misinterpretation literature (e.g. 'catastrophe', 'threat', 'anxiety-related') are examined, and clarifications proposed. Inconsistencies and limitations in the measurement of catastrophic misinterpretation are highlighted, and subsequently developments to measurement instruments are proposed.     

Waning of panic sensations during prolonged hyperventilation

Recent theories about panic emphasize that a hyperventilatory positive feedback loop is involved in panic: catastrophic misinterpretation of bodily sensations may trigger anxiety, anxiety may stimulate hyperventilation, hyperventilation may promote the salience of feared sensations etc. Such models leave unexplained how and when panics come to an end. It was hypothesised that panic with hyperventilation may end because pronounced hyperventilation becomes, in the course of time, less powerful in generating perceivable bodily sensations. Twenty healthy subjects hyperventilated forcefully and experienced clear panic symptoms as defined by DSM IIIR. When pCO2 was kept 55% below base line for 90 min, panic symptoms waned. The mean intensity of the symptoms declined as did the number of symptoms occurring. No panic symptoms were observed in the control group (n = 20) who ventilated normally. In so far as hyperventilation is involved in the positive feedback loops that characterize panic, panic attacks may be time-limited because sensations induced by hyperventilation become less salient even if massive hyperventilation continues. As to the explanation of the reported phenomenon, it is suggested that, apart from habituation, local physiological changes due to prolonged hyperventilation may produce a decrease in interoceptive input.     

Peritraumatic and persistent panic attacks in acute stress disorder

This study examined the prevalence of peritraumatic and persistent panic symptoms following trauma. Survivors of civilian trauma (n=30) with either acute stress disorder (ASD) or no acute stress disorder (non-ASD) were administered the Panic Module of the Structured Clinical Interview for DSM-IV (SCID). Participants also completed the Impact of Event Scale, Acute Stress Disorder Scale, Beck Depression Inventory, Beck Anxiety Inventory, and the Anxiety Sensitivity Index. Panic attacks were experienced by 77% of participants during their trauma, and 47% reported recurrent panic attacks post-trauma. ASD participants demonstrated more panic symptoms during and after their trauma than non-ASD participants. Posttraumatic panic was most strongly associated with anxiety sensitivity. These findings are discussed in terms of cognitive factors that may mediate posttrauma panic and treatment implications for managing posttraumatic anxiety.There is increasing evidence that panic attacks play a role in psychopathological response to trauma. A significant proportion of people with panic disorder report a history of trauma (). Moreover, two-thirds of trauma survivors report panic attacks within the previous 2 weeks (). There is also evidence that people with posttraumatic stress disorder (PTSD) display elevated levels of anxiety sensitivity (). Recent attention has focused on acute panic reactions because of proposals that panic during trauma may condition trauma-related cues to subsequent panic (). There is evidence that panic attacks occur in 53-90% of trauma survivors during the traumatic experience (). Further, people with acute stress disorder (ASD) are more likely to report peritraumatic panic attacks than non-ASD individuals. ASD is a useful framework in which to investigate the role of panic in posttraumatic stress because ASD describes acute responses to trauma that are strongly predictive of chronic PTSD ().This study investigated the relationship between peritraumatic panic and ongoing panic attacks following trauma. Specifically, we indexed panic attacks during trauma and subsequent to trauma in trauma survivors with and without ASD. We also indexed the extent to which distorted interpretations about somatic sensations may be associated with panic attacks following trauma. We considered that the strong evidence that maladaptive appraisals of somatic sensations mediate panic () is directly relevant to posttraumatic panic. We hypothesized that ASD participants would report more peritraumatic and persistent panic than non-ASD participants, and that this panic would be associated with dysfunctional interpretations about somatic stimuli.     

Panic disorder: A product of classical conditioning

Contrary to the common view that all panic attacks have a single etiology, it is shown that a distinction must be made between initial attacks, for which there are many causes, and recurrent attacks (panic disorder) which have a common basis. Most initial panic attacks are attributable to the physiological effects of hyperventilation resulting from severe and prolonged anxiety. It has been claimed that the attacks are due to such symptoms as dyspnea, tachycardia and dizziness being misattributed to deadly illness or incipient insanity. We reject this view on several grounds, and in particular because of a pilot study that showed that such attributions follow the onset of panic. Apart from some biological cases, the common initial panic is an unconditioned response to a bizarre stimulus complex produced by excessive hyperventilation, and panic disorder is the result of contiguous stimuli, especially endogenous stimuli, being conditioned to the elicited anxiety. Treatment accords with principles of conditioning.     

Differences in panic psychopathology between smokers with and without asthma

Cigarette smoking is more common among individuals with asthma compared to those without, resulting in increased risk of morbidity and mortality. However, there has been little exploration of psychological factors that differ between smokers with and without asthma. Thus, the aim of the current study was to examine differences between smokers with and without asthma in terms of anxiety sensitivity, panic symptoms, lifetime history of panic attacks, and lifetime history of panic disorder. Participants were 115 smokers with asthma (55.3% male, M_age = 38.4 years, SD = 11.9) and 120 smokers without asthma (70.6% male, M_age = 37.0 years, SD = 12.8) who were administered a structured diagnostic interview and completed self-report measures. As hypothesized, after controlling for the effects of cigarettes per day, gender, race, and education, smokers with asthma reported higher levels of anxiety sensitivity and panic symptoms and were at an increased risk for having a lifetime history of panic attacks (OR = 3.01) and panic disorder (OR = 2.96) compared to smokers without asthma. Further, group differences in anxiety sensitivity and panic symptoms remained even after removing participants with a lifetime history of panic attacks or panic disorder. These findings suggest that smokers with asthma are a particularly ‘at-risk’ population for panic psychopathology and likely in need of specialized smoking-related prevention and intervention efforts.     

Anxiety and depression as correlates of self-reported behavioural inhibition in normal adolescents

In a previous study, Muris, Merckelbach, Wessel, and Van de Ven [Psychopathological correlates of self-reported behavioural inhibition in normal children. Behav. Res. Ther. 37 (1999) 575-584] found that children who defined themselves as high on behavioural inhibition displayed elevated levels of psychopathological symptoms compared to children who defined themselves as low or middle on behavioural inhibition. The present study further examined the relationship between self-reported behavioural inhibition and anxiety disorders and depression symptoms in a large sample of adolescents aged 12-18 years (N=968). Adolescents completed a measure of behavioural inhibition and questionnaires of anxiety and depression. Results indicated that adolescents who classified themselves as high on behavioural inhibition had higher scores of anxiety and depression than adolescents who classified themselves as low or middle on behavioural inhibition. Structural equations modelling was employed to test hypothetical models on the role of behavioural inhibition in childhood anxiety and depression. It was found that a pathway in which behavioural inhibition results in anxiety, which in turn leads to depression, provided the best fit for the data.     

Provocation of panic: three elements of the panic reaction in four anxiety disorders

Subjects with agoraphobia (N = 25), panic disorder (N = 25), social phobia (N = 19) or generalized anxiety disorder (N = 10) and controls with no psychiatric history (N = 16) underwent two provocation tests, voluntary hyperventilation and inhalation of 5% CO2 in air, and three experimental control conditions. They were measured on three elements of the panic reaction: somatic symptoms, psychic anxiety and fears of impending doom, and on a standard YES/NO measure of panic attack. The provocation conditions produced increased somatic symptoms and psychic anxiety across all groups relative to the control conditions. The agoraphobic and panic disorder groups showed a significantly greater increase in fears of impending doom from control to provocation conditions than the social phobic and GAD patients. This difference was not observed on measures of somatic symptoms or psychic anxiety. The present results provide some support for the theory that panic attacks result from the catastrophic misinterpretation of anxious symptoms, in this case produced by the two provocation tests.     

The hyperventilation syndrome in panic disorder, agoraphobia and generalized anxiety disorder

The symptom complex of panic disorder and generalized anxiety disorder suggests an etiological role for hyperventilation. The present study investigates the overlap between DSM-III-R panic disorder, panic disorder with agoraphobia and generalized anxiety disorder with hyperventilation syndrome (HVS). The anxiety disorder diagnoses were based on a structured interview, and HVS syndrome (HVS). The anxiety disorder diagnoses were based on a structured interview, and HVS determined by the so-called hyperventilation provocation test (a brief period of voluntary hyperventilation with recognition of symptoms). The overlap rates with HVS were: 48% for panic disorder, 83% for panic disorder with agoraphobia and 82% for generalized anxiety disorder. However, a pilot study on transcutaneous monitoring of carbon dioxide tension leads us to question the validity of the voluntary hyperventilation method that we used to determine HVS-status. It is unclear whether hyperventilation plays an important role in panic and general anxiety, as our overlap findings suggest. For patients who recognize the symptoms induced by voluntary hyperventilation, the hyperventilation provocation procedure provides a therapeutic means of exposure to feared bodily sensations.     

The role of anxiety sensitivity and lack of emotional approach coping in depressive symptom severity among a non-clinical sample of uncued panickers

Panic attacks and depression frequently co-occur, and the presence of this co-morbidity is often associated with worse outcomes compared with each disorder alone. Despite this, not everyone who experiences panic attacks also suffers from depression, suggesting that individual difference factors may play a role in this co-morbidity. The purpose of this study was to provide a preliminary investigation of two such individual difference factors, examining the role of anxiety sensitivity and lack of emotional approach coping in depressive symptom severity among a non-clinical sample of uncued panickers. A sample of 79 college students reporting the occurrence of uncued panic attacks within the past year completed a series of questionnaires assessing the lower-order factors of anxiety sensitivity, emotional approach coping, panic attack frequency, panic-related disability, panic symptom severity and depressive symptom severity. Participants with more severe depressive symptoms reported greater anxiety sensitivity, panic attack frequency, panic symptom severity, panic-related disability and lack of emotional approach coping. The particular anxiety sensitivity dimension of fear of cognitive dyscontrol and lack of emotional approach coping emerged as the best predictors of depressive symptom severity. Findings are discussed in terms of their implications for the improved understanding of this co-morbidity, as well as its treatment.     

Cross cultural evaluation of smokers risk for panic and anxiety pathology: a test in a Russian epidemiological sample

The present study evaluated the main and interactive effects of level of smoking (cigarettes per day) and anxiety sensitivity (fear of anxiety and anxiety related sensations) in predicting panic and anxiety variables in an epidemiologically-defined sample of smokers from Moscow (n=95). The combination of high levels of anxiety sensitivity and smoking predicted agoraphobic avoidance, but not frequency of panic attacks during the past week. These findings suggest anxiety sensitivity may moderate the relation between level of smoking and prototypical panic psychopathology variables (panic attacks and agoraphobic avoidance) even after controlling for the theoretically-relevant factors of alcohol abuse and negative affect.     

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Panic attacks and depression frequently co‐occur, and the presence of this co‐morbidity is often associated with worse outcomes compared with each disorder alone. Despite this, not everyone who experiences panic attacks also suffers from depression, suggesting that individual difference factors may play a role in this co‐morbidity. The purpose of this study was to provide a preliminary investigation of two such individual difference factors, examining the role of anxiety sensitivity and lack of emotional approach coping in depressive symptom severity among a non‐clinical sample of uncued panickers. A sample of 79 college students reporting the occurrence of uncued panic attacks within the past year completed a series of questionnaires assessing the lower‐order factors of anxiety sensitivity, emotional approach coping, panic attack frequency, panic‐related disability, panic symptom severity and depressive symptom severity. Participants with more severe depressive symptoms reported greater anxiety sensitivity, panic attack frequency, panic symptom severity, panic‐related disability and lack of emotional approach coping. The particular anxiety sensitivity dimension of fear of cognitive dyscontrol and lack of emotional approach coping emerged as the best predictors of depressive symptom severity. Findings are discussed in terms of their implications for the improved understanding of this co‐morbidity, as well as its treatment.     

Test of a Factor Mixture-Based Taxonic-Dimensional Model of Anxiety Sensitivity and Panic Attack Vulnerability among University and Clinical Samples in Mexico City

The aim of the present study was to evaluate a factor mixture-based taxonic-dimensional model of anxiety sensitivity (AS) (Bernstein et al. Behavior Therapy 41:515-521, 2010), as measured by the ASI-3 (Taylor et al. Psychological Assessment 19:176-188, 2007), in regard to panic attacks, anxiety symptoms, and behavioral impairment among a university sample (N = 150, n _females  = 107, M _age = 21.3 years, SD = 4.3) and a clinical sample (N = 150, n _females  = 102, M _age = 39.0 years, SD = 12.0) from Mexico City, Mexico. Findings demonstrated cross-national support for the conceptual and operational utility of the AS taxonic-dimensional hypothesis (Bernstein et al. Journal of Anxiety Disorders 20:1-22, 2007b). Specifically, (1) the FMM-based AS taxon class base rate was significantly greater among the clinical relative to the university sample; (2) risk for panic attacks was significantly greater among the AS taxon class relative to the AS normative class; and (3) continuous individual differences in AS physical and psychological concerns, within the AS taxon class, were associated with level of risk for panic attacks, as well as panic attack severity and anxiety symptom levels. Similar AS taxonic-dimensional effects were observed in relation to degree of behavioral impairment across domains of functioning. The study results are discussed with respect to their implications for better understanding the nature of AS-related cognitive vulnerability for panic and related anxiety psychopathology.