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Purpose: Posttraumatic stress disorder (PTSD) often co-occurs with panic disorder (PD), with some etiological models positing a causal role of panic reactivity in PTSD onset; however, data addressing the temporal ordering of these conditions are lacking. The aim of this study was to examine the bi-directional associations between PD and PTSD in a nationally representative, epidemiologic sample of trauma-exposed adults., Methods: Participants were community-dwelling adults (62.6% women; M age  = 48.9, SD 16.3) with lifetime DSM-IV PTSD criterion A trauma exposure drawn from the 2001/2 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) and re-interviewed in 2004/5 (N = 12,467). Cox discrete-time proportional hazards models with time-varying covariates were used to investigate the bi-directional associations between lifetime PD and PTSD, accounting for demographic characteristics, trauma load, and lifetime history of major depression, generalized anxiety disorder, and social anxiety disorder., Results: PD was significantly associated with subsequent onset of PTSD (HR 1.210, 95%CI = 1.207-1.214, p < .001), and PTSD was significantly associated with onset of PD (HR 1.601, 95% CI 1.597-1.604, p < .001). The association between PTSD and subsequent PD was stronger in magnitude than that between PD and subsequent PTSD (Z = - 275.21, p < .01). Men evidenced stronger associations between PD and PTSD compared to women., Conclusions: Results were consistent with a bidirectional pathway of risk, whereby PD significantly increased risk for the development of PTSD, and PTSD significantly increased risk for PD. Given the association between PTSD and subsequent PD, particularly among men, clinicians may consider supplementing PTSD treatment with panic-specific interventions, such as interoceptive exposure, to prevent or treat this disabling comorbidity.

Self-reported anxiety, and potentially physiological response, to maintained inhalation of carbon dioxide (CO 2 ) enriched air shows promise as a putative marker of panic reactivity and vulnerability. Temporal stability of response systems during low-dose, steady-state CO 2 breathing challenge is lacking. Outcomes on multiple levels were measured two times, one week apart, in 93 individuals. Stability was highest during the CO 2 breathing phase compared to pre-CO 2 and recovery phases, with anxiety ratings, respiratory rate, skin conductance level, and heart rate demonstrating good to excellent temporal stability (ICCs≥0.71). Cognitive symptoms tied to panic were somewhat less stable (ICC=0.58) than physical symptoms (ICC=0.74) during CO 2 breathing. Escape/avoidance behaviors and DSM-5 panic attacks were not stable. Large effect sizes between task phases also were observed. Overall, results suggest good-excellent levels of temporal stability for multiple outcomes during respiratory stimulation via 7.5% CO 2 ., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Background and Objectives: Carbon dioxide (CO2) hypersensitivity is hypothesized to be a robust endophenotypic marker of panic spectrum vulnerability. The goal of the current study was to explore the latent class trajectories of three primary response systems theoretically associated with CO2 hypersensitivity: subjective anxiety, panic symptoms, and respiratory rate (fR)., Methods: Participants (n = 376; 56% female) underwent a maintained 7.5% CO2 breathing task that included three phases: baseline, CO2 air breathing, and recovery. Growth mixture modeling was used to compare response classes (1…n) to identify the best-fit model for each marker. Panic correlates also were examined to determine class differences in panic vulnerability., Results: For subjective anxiety ratings, a three-class model was selected, with individuals in one class reporting an acute increase in anxiety during 7.5% CO2 breathing and a return to pre-CO2 levels during recovery. A second, smaller latent class was distinguished by elevated anxiety across all three phases. The third class reported low anxiety reported during room air, a mild increase in anxiety during 7.5% CO2 breathing, and a return to baseline during recovery. Latent class trajectories for fR yielded one class whereas panic symptom response yielded two classes., Limitations: This study examined CO2 hypersensitivity in one of the largest samples to date, but did not ascertain a general population sample thereby limiting generalizability. Moreover, a true resting baseline measure of fR was not measured., Conclusions: Two classes potentially representing different risk pathways were observed. Implications of results will be discussed in the context of panic risk research., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

The association between trauma exposure and panic attacks has received increased attention over the past decade, with mounting evidence suggesting an overlapping etiologic pathway. This study examined the incidence of new onset panic attacks in 775 Vietnamese individuals in the 2-3 months following Typhoon Xangsane. Pre-typhoon (Wave 1) and post-typhoon (Wave 2) assessments were conducted, allowing for consideration of factors occurring prior to the typhoon in addition to typhoon-relevant responding. Of the 775 participants, 11.6% (n=90) met criteria for lifetime panic attack pre-typhoon and 2.8% (n=22) met post-typhoon panic attack criteria. Individuals with pre-typhoon panic were significantly older and reported less education compared to the no-panic group. Individuals in both panic groups were more likely to screen positive on a Wave1 psychiatric screening measure, endorse greater typhoon exposure and prior traumatic event exposure and were significantly more likely to meet DSM-IV criteria for posttraumatic stress disorder (PTSD) and major depression (MDD) post-typhoon compared with persons reporting no history of panic attacks. Pre and post-typhoon panic exhibited similar patterns across variables and both panic conditions were associated with the development of PTSD and MDD, suggesting that persons experiencing panic attacks may represent a vulnerable population in need of early intervention services., (© 2013 Elsevier Ireland Ltd. All rights reserved.)

Few naturalistic, longitudinal studies of panic disorder with and without agoraphobia (PD/PDA) exist, limiting our knowledge of the temporal rates of incidence, relapse, and chronicity, or the factors that predict category transition. Data from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) wave 1 (n=43,093) and wave 2 (n=34,653) were utilized to determine transitional rates, and predictors of category transitions, over a 3-year period. Analyses revealed very high 3-year remission rates for PD and PDA (75% and 67%, respectively), although relapse also was relatively frequent (PD=12%; PDA=21%). Logistic regression revealed previous history of panic attacks, generalized anxiety disorder/major depression (GAD/MDD), nicotine dependence, female sex, younger age, and major financial crises to be reliable predictors of incidence and relapse. The direction and magnitude of association of many predictor variables were similar for PD and PDA, with notable exceptions for social anxiety and romantic relationship factors. Clinicians should be aware of the relapsing-remitting nature of PD and PDA and, thus, take caution to not reduce or eliminate effective treatments prematurely. Similarly, the current study suggests clinicians pay particular attention to concurrent factors relevant to relapse in PD/PDA that may also be clinically addressed (e.g., co-morbid MDD/GAD and nicotine dependence)., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Background: Childhood separation anxiety disorder (SAD) is hypothesized to share etiologic roots with panic disorder. The aim of this study was to estimate the genetic and environmental sources of covariance between childhood SAD and adult onset panic attacks (AOPA), with the primary goal to determine whether these two phenotypes share a common genetic diathesis., Methods: Participants included parents and their monozygotic or dizygotic twins (n = 1,437 twin pairs) participating in the Virginia Twin Study of Adolescent Behavioral Development and those twins who later completed the Young Adult Follow-Up (YAFU). The Child and Adolescent Psychiatric Assessment was completed at three waves during childhood/adolescence followed by the Structured Clinical Interview for DSM-III-R at the YAFU. Two separate, bivariate Cholesky models were fit to childhood diagnoses of SAD and overanxious disorder (OAD), respectively, and their relation with AOPA; a trivariate Cholesky model also examined the collective influence of childhood SAD and OAD on AOPA., Results: In the best-fitting bivariate model, the covariation between SAD and AOPA was accounted for by genetic and unique environmental factors only, with the genetic factor associated with childhood SAD explaining significant variance in AOPA. Environmental risk factors were not significantly shared between SAD and AOPA. By contrast, the genetic factor associated with childhood OAD did not contribute significantly to AOPA. Results of the trivariate Cholesky reaffirmed outcomes of bivariate models., Conclusions: These data indicate that childhood SAD and AOPA share a common genetic diathesis that is not observed for childhood OAD, strongly supporting the hypothesis of a specific genetic etiologic link between the two phenotypes., (© 2012 Wiley Periodicals, Inc.)

Background: The phenotypic variance observed in panic disorder (PD) appears to be best captured by a respiratory and non-respiratory panic subtype. We compared respiratory and non-respiratory panic subtypes across a series of external validators (temporal stability, psychiatric co-morbidity, treatment response) to determine whether subtypes are best conceptualized as differing: (1) only on their symptom profiles with no other differences between them; (2) on a quantitative (i.e. severity) dimension only; or (3) qualitatively from one another., Method: Data from a large epidemiological survey (National Epidemiologic Survey on Alcohol and Related Conditions) and a clinical trial (Cross-National Collaborative Panic Study) were used. All analytic comparisons were examined within a latent class framework., Results: High temporal stability of panic subtypes was observed, particularly among females. Respiratory panic was associated with greater odds of lifetime major depression and a range of anxiety disorders as well as increased treatment utilization, but no demographic differences. Treatment outcome data did not suggest that the two PD subtypes were associated with differential response to either imipramine or alprazolam., Conclusions: These data suggest that respiratory and non-respiratory panic represent valid subtypes along the PD continuum, with the respiratory variant representing a more severe form of the disorder.

Background: Panic disorder (PD) is a heterogeneous syndrome that can present with a variety of symptom profiles that potentially reflect distinct etiologic pathways. The present study represents the most comprehensive examination of phenotypic variance in PD with and without agoraphobia for the purpose of identifying clinically relevant and etiologically meaningful subtypes., Method: Latent class (LC) and factor mixture analysis were used to examine panic symptom data ascertained from three national epidemiologic surveys [Epidemiological Catchment Area (ECA), National Comorbidity Study (NCS), National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), Wave 1], a twin study [Virginia Adult Twin Study of Psychiatric and Substance Use Disorders (VATSPSUD)] and a clinical trial (Cross-National Collaborative Panic Study [CNCPS])., Results: Factor mixture models (versus LC) generally provided better fit to panic symptom data and suggested two panic classes for the ECA, VATSPSUD and CNCPS, with one class typified by prominent respiratory symptoms. The NCS yielded two classes, but suggested both qualitative and quantitative differences. The more contemporary NESARC sample supported a two and three class model, with the three class model suggesting two variants of respiratory panic. The NESARC's three class model continued to provide the best fit when the model was restricted to a more severe form of PD/panic disorder with agoraphobia., Conclusions: Results from epidemiologic and clinical samples suggest two panic subtypes, with one subtype characterized by a respiratory component and a second class typified by general somatic symptoms. Results are discussed in light of their relevance to the etiopathogenesis of PD.

Background: Similar patterns of vulnerability to carbon dioxide (CO(2)) inhalation have been reported in adults with panic disorder (PD) and children with separation anxiety disorder (SAD), suggesting a link between the adult and child conditions. This study examines the influence of familial risk for PD on CO(2) responses in children with SAD. We hypothesized that offspring with SAD of parents with PD would have distinct CO(2) responses., Methods: Two hundred twelve 9- to 20-year-old offspring of parents with or without PD were exposed to maintained 5% CO(2) inhalation in the participants' homes. Anxiety symptoms, panic attacks, and respiratory physiology (respiratory frequency and tidal volume) were monitored during baseline and 15-min maintained CO(2) breathing., Results: As hypothesized, significant offspring SAD x parent PD interactions were obtained for anxiety symptoms, respiratory frequency, tidal volume, and a panting index during CO(2) inhalation. Offspring with both SAD and parental PD exhibited more anxiety symptoms at termination of 5% CO(2) breathing than the other offspring groups and had the most extreme values on measures of respiratory physiology., Conclusions: Youth with both SAD and parental PD have respiratory responses to CO(2) similar to adult PD. They might be a subtype of SAD at particularly high risk for adult PD.

Objective: A previous laboratory-based study found elevated cortisol levels in anxious children susceptible to CO(2)-induced panic, but the effects of parent diagnosis were not considered. The current home-based study tested the hypothesis that parental panic disorder and offspring response to CO(2) are associated with elevated cortisol levels in juvenile offspring., Method: A total of 131 offspring (ages 9-19) of parents with panic disorder, major depression, and no mental disorder underwent CO(2) inhalation. Parent and child diagnoses were assessed. Salivary cortisol was assayed before and after CO(2) inhalation., Results: Neither parents with panic disorder, parents with major depression, or offspring anxiety predicted offspring cortisol levels. Independent of parent and child diagnoses, anxiety response to CO(2) predicted elevated cortisol levels in offspring., Conclusions: As in adults, anxiety response to CO(2) in juveniles is associated with elevated cortisol levels, but elevated cortisol levels are not related to parent or child diagnoses.

Background: Carbon dioxide (CO(2)) sensitivity is postulated to be a familial risk marker of panic disorder (PD). Exaggerated responses to CO(2) inhalation have been reported in adults with PD and their unaffected adult relatives, as well as in clinic-referred children with anxiety disorders., Objective: To test in a family-based design whether CO(2) hypersensitivity is a familial risk marker for PD and associated with current anxiety disorders in children and adolescents., Setting and Participants: One hundred forty-two offspring (aged 9-19 years) of parents with PD, major depressive disorder, or no disorder. Forty-five (32%) had a current anxiety disorder, excluding specific phobia., Design and Main Outcome Measures: Parents and offspring received diagnostic assessments. Offspring underwent 5% CO(2) inhalation at home. Panic symptoms and panic attacks were rated with the Acute Panic Inventory at baseline, while anticipating CO(2) delivery ("threat"), and during CO(2) inhalation. Respiratory rate and volume were measured with spirometry., Results: No group differences were found in Acute Panic Inventory ratings at baseline or in respiratory measures during threat. Risk for PD was not associated with CO(2) sensitivity (panic symptoms and respiratory physiologic response). During CO(2) inhalation, offspring with anxiety disorders, relative to offspring without anxiety disorders, experienced significantly more panic symptoms and panic attacks, as well as elevated respiratory rates. During threat, panic symptoms were significantly and independently associated with both parental PD and offspring anxiety disorders., Conclusions: No support was obtained for CO(2) hypersensitivity as a familial risk marker for PD in children and adolescents. Links between childhood anxiety disorders and CO(2) sensitivity were replicated. Familial risk for PD in children and adolescents may be associated with vulnerability to anticipatory anxiety.

Twenty-eight individuals with panic disorder were provided with a copy of Mastery of Your Anxiety and Panic II and received either four sessions of group cognitive-behavior therapy (Group) or one meeting with a therapist plus three telephone contacts (Telephone). Between group repeated measures analyses revealed significant improvement over the course of treatment and maintenance of gains over the follow-up period with few treatment by trials interactions. A higher percentage of participants in the Telephone condition achieved high end-state functioning status at posttreatment compared to those who participated in group CBT (72% vs. 24%), but this difference disappeared at 6 months posttreatment (45% vs. 55%). Participants with characteristics of either borderline, dependent, or depressive personality disorders, as assessed by the MCMI-III, were unlikely to achieve high end-state functioning status at posttreatment. Trends in the data suggest that participants who met criteria for panic disorder with agoraphobia, and those with comorbid generalized anxiety disorder, were also less likely to achieve clinically significant outcome. These findings add to the growing literature indicating that self-directed treatment with brief therapist contact is a viable option for many people with panic disorder. Furthermore, the study provides preliminary data suggesting that certain comorbid conditions negatively impact self-directed treatment outcome.