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Objective: To investigate whether capnometry-assisted antihyperventilation respiratory training, successful in treating panic, and sleep hygiene instructions would reduce posttraumatic stress disorder (PTSD) hyperarousal symptoms in U.S. military veterans., Method: We conducted a parallel, nonblinded clinical trial and randomized 80 veterans with PTSD hyperarousal into treatment or wait list. Primary treatment outcomes from baseline to 1st follow-up were analyzed using mixed modeling. Baseline physiological measures were compared between the PTSD hyperarousal group and a no-PTSD group ( n = 68)., Results: Baseline respiration rate but not partial-pressure of end-tidal carbon dioxide (PCO₂) was higher in the PTSD hyperarousal group than in the no-PTSD group during 3 min of quiet sitting, indicating no difference in baseline hyperventilation. There was no significant effect of the intervention on PTSD hyperarousal symptoms or hyperventilation compared to wait list, but treatment did lower respiratory rate., Conclusion: This intervention did not reduce PTSD hyperarousal symptoms, perhaps due to differences between underlying mechanisms of PTSD hyperarousal and panic disorder or to differences between veteran and civilian populations. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Psychophysiological theories postulate respiratory dysregulation as a mechanism contributing to panic disorder (PD). Additionally, symptomatic and respiratory recovery from voluntary hyperventilation (HVT-recovery) have been shown to lag in PD and it is unclear if HVT-recovery normalizes with treatment. Thirty-seven panic disorder patients were randomized to hypoventilation therapy (TX, n = 20) or waitlist control (WL, n = 17) (Meuret et al., 2008). In a secondary analysis, their HVT-recovery was analyzed at pre- and post-TX/WL, compared to 29 healthy controls (HC). HVT included three phases: 5-min baseline, 3-min hyperventilation, and 8-min recovery. HVT-elicited symptom severity and anxiety were rated following each phase, and end-tidal PCO 2 and respiratory rate (RR) were recorded throughout. Treatment, compared to WL, was highly effective in reducing PD pathology (d=2.21, Meuret et al., 2008). At pre-TX/WL, PD demonstrated delayed HVT-recovery PCO 2 and higher RR. Treated patients demonstrated normalization of HVT-recovery for PCO 2 and RR; however, improvements of HVT-recovery for symptom severity and anxiety did not differ between TX and WL. Results replicate pretreatment HVT respiratory recovery abnormalities in PD and further demonstrate normalization, comparable to HC, following successful treatment. The results provide support for respiratory dysregulation as a feature of PD and demonstrate the utility of HVT respiratory recovery as treatment outcome measure for respiration-based PD therapy., (Copyright © 2020. Published by Elsevier Ltd.)

Objective/background: Wrist-worn sleep actigraphs are limited for evaluating sleep, especially in sleepers who lie awake in bed without moving for extended periods. Sleep logs depend on the accuracy of perceiving and remembering times of being awake. Here we evaluated pressing an event-marker button while lying awake under two conditions: self-initiated pressing every 5 to 10 minutes or pressing when signaled every 5 minutes by a vibration pulse from a wristband. We evaluated the two conditions for acceptability and their concordance with actigraphically scored sleep., Participants and Methods: Twenty-nine adults wore actigraphs on six nights. On nights 1 and 4, they pressed the marker to a vibration signal, and on nights 2 and 5, they self-initiated presses without any signal. On nights 3 and 6, they were told not to press the marker. Every morning they filled out a sleep log about how they had slept., Results: The vibration band was unacceptable to 42% of the participants, who judged it too disturbing to their sleep. Self-initiated pressing was acceptable to all, although it reduced log reported sleep depth compared to a no pressing condition. Estimations of sleep onset latency were considerably longer by button pressing than by actigraphy. Agreement of epoch-by-epoch sleep scoring by actigraphy and by button pressing was poor (kappa = 0.23) for self-initiated pressing and moderate (kappa = 0.46) for pressing in response to a vibration., Conclusions: Self-initiated button pressing to indicate being awake while lying in bed is acceptable to many, interferes little with sleep, and adds substantially to the information given by actigraphy., Competing Interests: The authors have declared that no competing interests exist.

Both intense physical activity and potent psychosocial stressors increase blood lactate. Raising lactate levels by infusing the chemical can have an anxiogenic effect. Here, we compare the relationship between changes in lactate and anxiety levels resulting from two standardized stressors. We investigated the effects of the Multiple Wingate All-Out Performance Test (WG), a strong physical stressor, and the Trier Social Stress Test (TSST), a well-documented psychosocial stressor, in 32 healthy young men using a crossover design. Before and after each stressor, venous blood was analyzed for lactate levels and the State-Trait-Anxiety Inventory (STAI) was given. Both stressors raised both lactate and anxiety significantly above their baseline levels. While the rise in lactate was much higher for the WG than for the TSST, the rises in anxiety were nearly equal. Individual fitness did not influence the results for lactate or anxiety. No significant relation between lactate and anxiety changes were found. Thus, our results as well as the literature suggest that lactate is an important variable for understanding the impact of sport participation.

Sleep disturbance is commonly reported by participants with post-traumatic stress disorder, but objective evidence of poor sleep is often absent. Here we compared self-report and actigraphic evaluations of sleep between veterans with post-traumatic stress disorder and controls. Participants reported their sleep retrospectively for the month before the recording night and on the recording night. On the recording night, they wore an Actiwatch-64 and were instructed to press the marker button upon getting into bed, each time they awoke, and at their final awakening. The post-traumatic stress disorder group reported much worse sleep than controls on the Pittsburgh Sleep Quality Index for the previous month and somewhat poorer sleep on the recording night. However, on the recording night, neither diary nor actigraphic measures of number of awakenings, total time in bed, nor time lying awake after sleep onset differed between participants with and without post-traumatic stress disorder. Diary-reported number of awakenings was fewer than actigraphically captured awakenings. These results suggest a memory bias towards remembering worse sleep on the nights before the recording night., (© 2017 European Sleep Research Society.)

Background: Previous research has shown that hypoventilation therapy reduces panic symptoms in part by increasing basal partial pressure of carbon dioxide (PCO 2 ) levels. We tested an additional pathway by which hypoventilation therapy could exert its therapeutic effects: through repeated interoceptive exposure to sensations of dyspnea., Methods: A total of 35 patients with panic disorder were trained to perform exercises to raise their end-tidal PCO 2 levels using a portable capnometry device. Anxiety, dyspnea, end-tidal PCO 2 , and respiratory rate were assessed during each exercise across 4 weeks of training. Mixed-model analysis examined whether within-exercise levels of dyspnea were predictive of reduction of panicogenic cognitions., Results: As expected, within-exercise anxiety and respiratory rate decreased over time. Unexpectedly, PCO 2 dropped significantly from the beginning to the end of exercise, with these drops becoming progressively smaller across weeks. Dyspnea increased and remained consistently above basal levels across weeks. As hypothesized, greater dyspnea was related to significantly lower panicogenic cognitions over time even after controlling for anxiety and PCO 2 . Additional exploratory analyses showed that within-exercise increases in dyspnea were related to within-exercise increases in anxiety but were not related to within-exercise increases in PCO 2 ., Conclusions: In support of the interoceptive exposure model, we found that greater dyspnea during hypoventilation exercises resulted in lower panicogenic cognitions even after the effect of PCO 2 was taken into account. The findings offer an additional important target in panic treatment., (Copyright © 2018 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

The authors investigated the effects of the quality of the therapeutic alliance, expectancy of improvement, and credibility of treatment on the outcome of two breathing therapies for anxiety and panic. Data were collected during a randomized clinical trial evaluating the efficacy of two theoretically opposing, end-tidal pCO2 feedback-assisted breathing therapies for patients experiencing anxiety attacks. In this study, five weekly individual breathing therapy sessions were administered for the patients who were experiencing anxiety attacks as symptoms of various anxiety disorders. The outcome of this trial indicated that regardless of the opposing breathing instructions (raise or lower pCO2) used in the two breathing therapies, patients in both treatment groups improved equally after treatment. Nonspecific factors rather than the different directions of pCO2 changes could have played a role in the improvement. Regression analyses showed that for both therapies patient-rated therapeutic alliance was predictive of improvement at the 1-month follow-up, and that patient-rated confidence that the therapy would produce improvement, an aspect of its credibility, accounted for almost half of the variance in improvement at the 6-month follow-up. Thus, two factors usually considered nonspecific were identified to be potent predictors of treatment outcome.

Physiological hyperarousal is manifested acutely by increased heart rate, decreased respiratory sinus arrhythmia, and increased skin conductance level and variability. Yet it is uncertain to what extent such activation occurs with the symptomatic hyperarousal of posttraumatic stress disorder (PTSD). We compared 56 male veterans with current PTSD to 54 males who never had PTSD. Subjects wore ambulatory devices that recorded electrocardiograms, finger skin conductance, and wrist movement while in their normal environments. Wrist movement was monitored to estimate sleep and waking periods. Heart rate, but not the other variables, was elevated in subjects with PTSD equally during waking and during actigraphic sleep (effect sizes, Cohen's d, ranged from 0.63 to 0.89). The length of the sleep periods and estimated sleep fragmentation did not differ between groups. Group heart rate differences could not be explained by differences in body activity, PTSD hyperarousal symptom scores, depression, physical fitness, or antidepressant use., (Published 2014. This article is a US Government work and is in the public domain in the USA.)

On July 22, 2011, Anders Breivik, a Norwegian citizen, detonated a fertilizer bomb near government buildings in Oslo, killing eight people, and then proceeded to a nearby island where the Labor Party was holding a youth camp. There, he killed 69 people before being arrested. Just before these events, he posted a "compendium" on the Web explaining his actions and encouraging others to do likewise. Much of the ensuing media coverage and trial focused on whether he was sane and whether he had a psychiatric diagnosis. One team of court-appointed psychiatrists found him to be psychotic with a diagnosis of paranoid schizophrenia and legally insane. A second team found him neither psychotic nor schizophrenic and, thus, legally sane. Their contrary opinions were not reconciled by observing his behavior in court. We discuss why experienced psychiatrists reached such fundamentally opposing diagnostic conclusions about a "home-grown" terrorist holding extreme political views.

Psychometric studies indicate that anxiety sensitivity (AS) is a risk factor for anxiety disorders such as panic disorder (PD). To better understand the psychophysiological basis of AS and its relation to clinical anxiety, we examined whether high-AS individuals show similarly elevated reactivity to inhalations of carbon dioxide (CO2) as previously reported for PD and social phobia in this task. Healthy individuals with high and low AS were exposed to eight standardized inhalations of 20% CO2-enriched air, preceded and followed by inhalations of room air. Anxiety and dyspnea, in addition to autonomic and respiratory responses were measured every 15 s. Throughout the task, high AS participants showed a respiratory pattern of faster, shallower breathing and reduced inhalation of CO2 indicative of anticipatory or contextual anxiety. In addition, they showed elevated dyspnea responses to the second set of air inhalations accompanied by elevated heart rate, which could be due to sensitization or conditioning. Respiratory abnormalities seem to be common to high AS individuals and PD patients when considering previous findings with this task. Similarly, sensitization or conditioning of anxious and dyspneic symptoms might be common to high AS and clinical anxiety. Respiratory conditionability deserves greater attention in anxiety disorder research., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Background: Commonly used trait measures might not accurately capture the relationship between worry and sleep difficulties in real life., Methods: In a 24-h ambulatory monitoring study, high and low trait worriers maintained a log of worry and sleep characteristics while actigraphy, heart rates (HR), skin conductance (SC), and ambient temperature were recorded., Results: Worrying in bed on the night of the recording was associated with longer self-reported and actigraphic nocturnal awakenings, lower actigraphic sleep efficiency, higher HR, lower HR variability, elevated SC level, and more non-specific SC fluctuations compared to not worrying in bed. High trait worriers had higher HR during waking and sleep, and reported shorter total sleep time and poorer sleep quality., Conclusions: While trait worry is mainly associated with subjective sleep difficulties, worrying in bed impairs sleep according to both subjective and objective sleep parameters, including heightened sympathetic and reduced parasympathetic activation., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Background: Individuals with asthma have been shown to respond to unpleasant stimuli with bronchoconstriction, but little is known about the time course of responding during sustained emotional stimulation and whether it varies with patients' experience., Objective: To examine the time course of oscillatory resistance (R(os)) during emotionally evocative films in 15 asthma patients and 14 healthy controls., Methods: Participants viewed unpleasant, surgery, and neutral films, each ranging 3-5min in duration. R(os) and the respiratory pattern (respiration rate, tidal volume, minute ventilation) were monitored continuously. Following each film, participants rated their affective response and symptoms. The time course of R(os) during films was explored using multilevel modeling., Results: Compared to neutral film sequences, unpleasant films (including those with surgery scenes) elicited a uniform pattern of initial increases in R(os) with peaks within the first 1-2min, followed by a gradual decline. Increases were more pronounced in asthma and during surgery films. Including additional respiratory parameters as time-varying covariates did not affect the temporal course of R(os) change. The rate of decline in R(os) (after the initial increase) was less in participants who experienced greater arousal and in patients who reported more shortness of breath. Patients more susceptible to psychological triggers in daily life showed slower rates of decline in R(os)., Conclusion: The temporal course of bronchoconstriction to unpleasant stimulation is highly uniform in asthma, with strong constriction in early stages of stimulation. More sustained constriction in emotion-induced asthma could be a risk factor for developing asthma exacerbation in daily life., (Copyright © 2012 Elsevier B.V. All rights reserved.)

This committee was appointed by the SPR Board to provide recommendations for publishing data on electrodermal activity (EDA). They are intended to be a stand-alone source for newcomers and experienced users. A short outline of principles for electrodermal measurement is given, and recommendations from an earlier report (Fowles et al., ) are incorporated. Three fundamental techniques of EDA recording are described: (1) endosomatic recording without the application of an external current, (2) exosomatic recording with direct current (the most widely applied methodology), and (3) exosomatic recording with alternating current-to date infrequently used but a promising future methodology. In addition to EDA recording in laboratories, ambulatory recording has become an emerging technique. Specific problems that come with this recording of EDA in the field are discussed, as are those emerging from recording EDA within a magnetic field (e.g., fMRI). Recommendations for the details that should be mentioned in publications of EDA methods and results are provided., (Copyright © 2012 Society for Psychophysiological Research.)

Background: Teaching anxious clients to stop hyperventilating is a popular therapeutic intervention for panic. However, evidence for the theory behind this approach is tenuous, and this theory is contradicted by an opposing theory of panic, the false-suffocation alarm theory, which can be interpreted to imply that the opposite would be helpful., Objective: To test these opposing approaches by investigating whether either, both, or neither of the 2 breathing therapies is effective in treating patients with panic disorder., Method: We randomly assigned 74 consecutive patients with DSM-IV-diagnosed panic disorder (mean age at onset = 33.0 years) to 1 of 3 groups in the setting of an academic research clinic. One group was trained to raise its end-tidal P(CO₂) (partial pressure of carbon dioxide, mm Hg) to counteract hyperventilation by using feedback from a hand-held capnometer, a second group was trained to lower its end-tidal P(CO₂) in the same way, and a third group received 1 of these treatments after a delay (wait-list). We assessed patients physiologically and psychologically before treatment began and at 1 and 6 months after treatment. The study was conducted from September 2005 through November 2009., Results: Using the Panic Disorder Severity Scale as a primary outcome measure, we found that both breathing training methods effectively reduced the severity of panic disorder 1 month after treatment and that treatment effects were maintained at 6-month follow-up (effect sizes at 1-month follow-up were 1.34 for the raise-CO(2) group and 1.53 for the lower-CO(2) group; P < .01). Physiologic measurements of respiration at follow-up showed that patients had learned to alter their P(CO₂) levels and respiration rates as they had been taught in therapy., Conclusions: Clinical improvement must have depended on elements common to both breathing therapies rather than on the effect of the therapies themselves on CO(2) levels. These elements may have been changed beliefs and expectancies, exposure to ominous bodily sensations, and attention to regular and slow breathing., Trial Registration: ClinicalTrials.gov identifier: NCT00183521., (© Copyright 2012 Physicians Postgraduate Press, Inc.)

Background: Separation anxiety disorder (SAD) is one of the most common anxiety disorders in childhood and is predictive of adult anxiety disorders, especially panic disorder. However, the disorder has seldom been studied and the attempt to distinguish SAD from other anxiety disorders with regard to psychophysiology has not been made. We expected exaggerated anxiety as well as sympathetic and respiratory reactivity in SAD during separation from the mother., Method: Participants were 49 children with a principal diagnosis of SAD, 21 clinical controls (CC) with a principal diagnosis of anxiety disorder other than SAD, and 39 healthy controls (HC) not meeting criteria for any current diagnosis. Analyses of covariance controlling for age were used to assess sympathetic and parasympathetic activation (preejection period and respiratory sinus arrhythmia) as well as cardiovascular (heart rate, mean arterial pressure, total peripheral resistance), respiratory (total breath time, minute ventilation, tidal volume, end-tidal CO(2) , respiratory variability), electrodermal, and self-report (anxiety, cognitions, symptoms) variables during baseline, 4-min separation from, and reunion with the mother., Results: Children with a diagnosis of SAD were characterized by elevated self-reported anxiety responses to separation and increased sympathetic reactivity compared with CC and HC groups. The SAD group also displayed greater vagal withdrawal and higher reactivity in multiple cardiovascular, respiratory, and electrodermal measures compared with the HC group, while corresponding responses were less in the CC group and not significantly different from the other groups., Conclusions: Separation from the mother elicits greater autonomic, respiratory, and experiential responses in children with SAD. Our findings based on brief experimental separation demonstrate differential subjective and physiological manifestations of specific anxiety diagnoses, thus supporting the validity of the diagnostic category of SAD., (© 2011 The Authors. Journal of Child Psychology and Psychiatry © 2011 Association for Child and Adolescent Mental Health.)

Background: Spontaneous or unexpected panic attacks, per definition, occur "out of the blue," in the absence of cues or triggers. Accordingly, physiological arousal or instability should occur at the onset of, or during, the attack, but not preceding it. To test this hypothesis, we examined if points of significant autonomic changes preceded the onset of spontaneous panic attacks., Methods: Forty-three panic disorder patients underwent repeated 24-hour ambulatory monitoring. Thirteen natural panic attacks were recorded during 1960 hours of monitoring. Minute-by-minute epochs beginning 60 minutes before and continuing to 10 minutes after the onset of individual attacks were examined for respiration, heart rate, and skin conductance level. Measures were controlled for physical activity and vocalization and compared with time matched control periods within the same person., Results: Significant patterns of instability across a number of autonomic and respiratory variables were detected as early as 47 minutes before panic onset. The final minutes before onset were dominated by respiratory changes, with significant decreases in tidal volume followed by abrupt carbon dioxide partial pressure increases. Panic attack onset was characterized by heart rate and tidal volume increases and a drop in carbon dioxide partial pressure. Symptom report was consistent with these changes. Skin conductance levels were generally elevated in the hour before, and during, the attacks. Changes in the matched control periods were largely absent., Conclusions: Significant autonomic irregularities preceded the onset of attacks that were reported as abrupt and unexpected. The findings invite reconsideration of the current diagnostic distinction between uncued and cued panic attacks., (Copyright © 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

The hypothesis of physiological emotion specificity has been tested using pattern classification analysis (PCA). To address limitations of prior research using PCA, we studied effects of feature selection (sequential forward selection, sequential backward selection), classifier type (linear and quadratic discriminant analysis, neural networks, k-nearest neighbors method), and cross-validation method (subject- and stimulus-(in)dependence). Analyses were run on a data set of 34 participants watching two sets of three 10-min film clips (fearful, sad, neutral) while autonomic, respiratory, and facial muscle activity were assessed. Results demonstrate that the three states can be classified with high accuracy by most classifiers, with the sparsest model having only five features, even for the most difficult task of identifying the emotion of an unknown subject in an unknown situation (77.5%). Implications for choosing PCA parameters are discussed., (Copyright © 2011 Society for Psychophysiological Research.)

Anxiety disorders are associated with respiratory abnormalities. Breathing training (BT) aimed at reversing these abnormalities may also alter the anxiogenic effects of biological challenges. Forty-five Panic Disorder (PD) patients, 39 Episodic Anxiety patients, and 20 non-anxious controls underwent voluntary hypoventilation and hyperventilation tests twice while psychophysiological measures were recorded. Patients were randomized to one of two BT therapies (Lowering vs. Raising pCO(2)) or to a waitlist. Before treatment panic patients had higher respiration rates and more tidal volume instability and sighing at rest than did non-anxious controls. After the Lowering therapy, patients had lower pCO(2) during testing. However, neither reactivity nor recovery to either test differed between patients and controls, or were affected by treatment. Although the two treatments had their intended opposite effects on baseline pCO(2), other physiological measures were not affected. We conclude that baseline respiratory abnormalities are somewhat specific to PD, but that previously reported greater reactivity and slower recovery to respiratory challenges may be absent.

Little is known how much skin conductance (SC) recordings from the fingers are affected by factors such as electrode site deterioration, ambient temperature (TMP), or physical activity (ACT), or by age, sex, race, or body mass index. We recorded SC, TMP, and ACT in 48 healthy control subjects for a 24-hour period, and calculated SC level (SCL), its standard deviation, the coefficient of SC variation, and frequency and amplitude of non-specific SC fluctuations. One method of assessing electrode site deterioration showed an average decline of 20%, while a second method found no significant change. All SC measures were higher during waking than sleep. Other factors influenced different measures in different ways. Thus, 24-hour SC recording outside the laboratory is feasible, but some measures need to be corrected for the influence of confounding variables., (Copyright © 2011 Elsevier B.V. All rights reserved.)

It has been suggested that high arousal negative affective states, but not low arousal negative affective states, potentiate the startle response. Because sadness has generally been studied as a low arousal emotion, it remains unclear whether high arousal sadness would produce startle potentiation to a similar degree as high arousal fear. To address this issue, 32 participants viewed two sets of 10-min film clips selected to induce two affective states of high subjective arousal (fear, sadness) and a neutral state of low subjective arousal, while the eyeblink startle response associated with brief noise bursts was assessed using orbicularis oculi EMG. Larger blink magnitude was found for fearful than for sad or neutral clips. Implications for conceptualizing sadness are discussed., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Earlier research found autonomic and airway reactivity in asthma patients when they were exposed to blood-injection-injury (BII) stimuli. We studied oscillatory resistance (R(os)) in asthma and BII phobia during emotional and disease-relevant films and examined whether muscle tension counteracts emotion-induced airway constriction. Fifteen asthma patients, 12 BII phobia patients, and 14 healthy controls viewed one set of negative, positive, neutral, BII-related, and asthma-related films with leg muscle tension and a second set without. R(os), ventilation, cardiovascular activity, and skin conductance were measured continuously. R(os) was higher during emotional compared to neutral films, particularly during BII material, and responses increased from healthy over asthmatic to BII phobia participants. Leg muscle tension did not abolish R(os) increases. Thus, the airways are particularly responsive to BII-relevant stimuli, which could become risk factors for asthma patients., (Copyright © 2010 Society for Psychophysiological Research.)

Skin conductance, physical activity, ambient temperature and mood were recorded for 24 h in 22 panic disorder (PD) patients and 29 healthy controls. During the day, subjects performed standardized relaxation tests (ARTs). We hypothesized that tonically elevated anticipatory anxiety in PD during waking and sleeping would appear as elevated skin conductance level (SCL) and greater skin conductance (SC) variability. Mean SCL was higher during both usual waking activities and sleeping in PD, but not during the ARTs. Group SC variability differences did not reach significance, perhaps because of variance unrelated to anxiety. Analyses indicated that in the PD group, antidepressant medication reduced mean SCL whereas state anxiety had the opposite effect during the day. Depressive symptoms reported during the day were related to elevated mean SCL on the night of the recording. The rate and extent of SCL deactivation over the night was equal in the two groups. However, PD patients had more frequent interruptions of deactivation that could have arisen from conditioned arousal in response to threat cues during sleep., (Published by Elsevier Ltd.)

Twenty-five panic disorder (PD) patients, 19 social phobics (SP), and 20 healthy controls (HC) sat quietly for 15 min, rating their anxiety and dyspnea every 30s while respiratory, cardiovascular, and electrodermal responses were recorded. No panic attacks were reported. For self-reported anxiety and dyspnea, within-subject variability over time was higher in PD than in SP or HC. In PD within-subject correlations across 30-s epochs were significant for (a) self-reported anxiety versus dyspnea, end-tidal pCO2, minute volume, duty cycle, skin conductance level, and interbeat interval, and for (b) dyspnea versus end-tidal pCO2, minute volume, tidal volume, and inspiratory flow rate. Several positive or negative correlations were greater in PD than in other groups. Thus in PD, experienced anxiety and dyspnea are temporally unstable but are correlated with each other and with fluctuations in respiratory and autonomic variables, even in the absence of panic attacks., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Inhalation of carbon dioxide (CO₂) enriched air triggers anxiety in panic disorder (PD) patients, which is often interpreted as a sign of biological vulnerability. However, most studies have not measured respiration in these tasks. We compared patients with PD (n=20) and social phobia (SP, n=19) to healthy controls (n=18) during eight inhalations of 20% CO₂, preceded and followed by two inhalations of room air, while continuously measuring subjective anxiety and dyspnea as well as autonomic and respiratory variables. PD patients showed increased reactivity and delayed recovery during CO₂ inhalations for most measures. Unlike both other groups, the PD group's tidal volume responses did not habituate across CO₂ inhalations. However, PD patients did not differ from SP patients on most other measures, supporting a continuum model of CO₂ sensitivity across anxiety disorders. Both patient groups showed continued reactivity during the last air inhalations, which is unlikely to be due to a biological sensitivity., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Statistical methods for detecting changes in longitudinal time series of psychophysiological data are limited. ANOVA and mixed models are not designed to detect the existence, timing, or duration of unknown changes in such data. Change point (CP) analysis was developed to detect distinct changes in time series data. Preliminary reports using CP analysis for fMRI data are promising. Here, we illustrate the application of CP analysis for detecting discrete changes in ambulatory, peripheral physiological data leading up to naturally occurring panic attacks (PAs). The CP method was successful in detecting cardio-respiratory changes that preceded the onset of reported PAs. Furthermore, the changes were unique to the pre-PA period, and were not detected in matched non-PA control periods. The efficacy of our CP method was further validated by detecting patterns of change that were consistent with prominent respiratory theories of panic positing a relation between aberrant respiration and panic etiology., (Copyright © 2010 Elsevier B.V. All rights reserved.)

By comparing efficacious psychological therapies of different kinds, inferences about common effective treatment mechanisms can be made. We selected six therapies for review on the basis of the diversity of their theoretical rationales and evidence for superior efficacy: psychoanalytic psychotherapy, hypercapnic breathing training, hypocapnic breathing training, reprocessing with and without eye-movement desensitization, muscle relaxation, and cognitive behavior therapy. The likely common element of all these therapies is that they reduce the immediate expectancy of a panic attack, disrupting the vicious circle of fearing fear. Modifying expectation is usually regarded as a placebo mechanism in psychotherapy, but may be a specific treatment mechanism for panic. The fact that this is seldom the rationale communicated to the patient creates a moral dilemma: Is it ethical for therapists to mislead patients to help them? Pragmatic justification of a successful practice is a way out of this dilemma. Therapies should be evaluated that deal with expectations directly by promoting positive thinking or by fostering non-expectancy.

To determine if improvement in mood would ameliorate autonomic dysregulation, HPA dysfunction, typical risk factors and C-reactive protein in depressed patients with elevated cardiovascular disease risk (CVD), 48 depressed participants with elevated cardiovascular risk factors were randomized to a cognitive behavioral intervention (CBT) or a waiting list control (WLC) condition. Twenty non-depressed age and risk-matched controls were also recruited. Traditional risk factors (e.g., lipids, blood pressure) and C-reactive protein were assessed pre- and post-treatment six months later. Subjects also underwent a psychophysiological stress test while cardiovascular physiology was measured. Salivary cortisol was measured during the day and during the psychological stress test. At post-treatment, the CBT subjects were significantly less depressed than WLC subjects. There was no significant difference in change scores on any of the traditional risk factors or C-reactive protein, cortisol measures, or cardiovascular physiology, except for triglyceride levels and heart rate, which were significantly lower in treatment compared to control subjects. The normal controls exhibited no change in the variables measured during the same time. A significant improvement in mood may have little impact on most traditional or atypical risk factors, cortisol or cardiophysiology.

The purpose of the study was to examine whether changes in pCO(2) mediate changes in fear of bodily sensation (as indexed by anxiety sensitivity) in a bio-behavioral treatment for panic disorder that targets changes in end-tidal pCO(2). Thirty-five panic patients underwent 4 weeks of capnometry-assisted breathing training targeting respiratory dysregulation. Longitudinal mediation analyses of the changes in fear of bodily symptoms over time demonstrated that pCO(2), but not respiration rate, was a partial mediator of the changes in anxiety sensitivity. Results were supported by cross lag panel analyses, which indicated that earlier pCO(2) levels predicted later levels of anxiety sensitivity, but not vice versa. PCO(2) changes also led to changes in respiration rate, questioning the importance of respiration rate in breathing training. The results provide little support for changes in fear of bodily sensations leading to changes in respiration, but rather suggest that breathing training targeting pCO(2) reduced fear of bodily sensations in panic disorder.

In a recent pilot study with asthma patients we demonstrated beneficial outcomes of a breathing training using capnometry biofeedback and paced breathing assistance to increase pCO(2) levels and reduce hyperventilation. Here we explored the time course changes in pCO(2), respiration rate, symptoms and lung function across treatment weeks, in order to determine how long training needs to continue. We analyzed in eight asthma patients whether gains in pCO(2) and reductions in respiration rate achieved in home exercises with paced breathing tapes followed a linear trend across the 4-week treatment period. We also explored the extent to which gains at home were manifest in weekly training sessions in the clinic, in terms of improvement in symptoms and spirometric lung function. The increases in pCO(2) and respiration rate were linear across treatment weeks for home exercises. Similar increases were seen for in-session measurements, together with gradual decreases in symptoms from week to week. Basal lung function remained stable throughout treatment. With our current protocol of paced breathing and capnometry-assisted biofeedback at least 4 weeks are needed to achieve a normalization of pCO(2) levels and reduction in symptoms in asthma patients.

Recent studies have shown that end-tidal PCO(2) is lower during anxiety and stress, and that changing PCO(2) by altering breathing is therapeutic in panic disorder. However, end-tidal estimation of arterial PCO(2) has drawbacks that might be avoided by the transcutaneous measurement method. Here we compare transcutaneous and end-tidal PCO(2) under different breathing conditions in order to evaluate these methods in terms of their comparability and usability. Healthy volunteers performed two hypoventilation (slow vs. paused breathing) and two hyperventilation tests (25 mm Hg at 18 vs. 30 breaths per minute). Three measurements of PCO(2) (two end-tidal and one transcutaneous device), tidal volume, and respiration rate were recorded. Before and after each test, subjects filled out a symptom questionnaire. The results show that PCO(2) estimated by the two methods was comparable except that for transcutaneous measurement registration of changes in PCO(2) was delayed and absolute levels were much higher. Both methods documented that paused breathing was effective for raising PCO(2), a presumed antidote for anxious hyperventilation. We conclude that since the two methods give comparable results choosing between them for specific applications is principally a matter of whether the time lag of the transcutaneous method is acceptable.

Background: Recently we found that patients with blood-injection-injury (BII) phobia tend to hyperventilate when exposed to feared stimuli. Hyperventilation results from increases in minute ventilation above levels required by metabolic demand and can result from increases in either frequency or depth of breathing, or a combination of both., Method: In order to determine which of these factors contributed most to hyperventilation in BII phobia we analyzed breathing patterns of BII phobia patients (N=12) and non-anxious controls (N=14), recorded with respiratory inductance plethysmography. Participants viewed ten film clips of either an emotionally positive, negative, or neutral quality, as well as surgery and asthma-relevant clips. During five film clips (one from each category) they also tensed their leg muscles., Results: Minute ventilation was markedly increased in blood phobia patients compared to other groups during surgery films. Also, tidal volume and irregularity of tidal volume showed strong increases, while respiration rate was not affected. Leg muscle tension increased ventilation in general but far below the extent brought about by hyperventilation in BII phobia. Patients who were breathing deeper during exposure reported stronger symptoms of dizziness, light-headedness and faintness. In general, patients showed a higher rate of spontaneous sighs throughout all film presentations, but not at baseline., Conclusion: Thus, hyperventilation in blood phobia is produced by excessively deep and irregular breathing and may contribute to fainting responses. Behavioral interventions for BII phobia could benefit from attention to this aspect of dysfunctional breathing., ((c) 2008 Wiley-Liss, Inc.)

Depression is a risk factor for cardiovascular disease (CVD) perhaps mediated by hypothalamic-pituitary-adrenal (HPA) axis or vagal dysregulation. We investigated circadian mood variation and HPA-axis and autonomic function in older (55 years) depressed and nondepressed volunteers at risk for CVD by assessing diurnal positive and negative affect (PA, NA), cortisol, and cardiopulmonary variables in 46 moderately depressed and 19 nondepressed volunteers with elevated CVD risk. Participants sat quietly for 5-min periods (10:00, 12:00, 14:00, 17:00, 19:00, and 21:00), and then completed an electronic diary assessing PA and NA. Traditional and respiration-controlled heart rate variability (HRV) variables were computed for these periods as an index of vagal activity. Salivary cortisols were collected at waking, waking+30min, 12:00, 17:00, and 21:00h. Cortisol peaked in the early morning after waking, and gradually declined over the day, but did not differ between groups. PA was lower and NA was higher in the depressed group throughout the day. HRV did not differ between groups. Negative emotions were inversely related to respiratory sinus arrhythmia in nondepressed participants. We conclude that moderately depressed patients do not show abnormal HPA-axis function. Diurnal PA and NA distinguish depressed from nondepressed individuals at risk for CVD, while measures of vagal regulation, even when controlled for physical activity and respiratory confounds, do not. Diurnal mood variations of older individuals at risk for CVD differ from those reported for other groups and daily fluctuations in NA are not related to cardiac autonomic control in depressed individuals.

Background: Given growing evidence that respiratory dysregulation is a central feature of panic disorder (PD) interventions for panic that specifically target respiratory functions could prove clinically useful and scientifically informative. We tested the effectiveness of a new, brief, capnometry-assisted breathing therapy (BRT) on clinical and respiratory measures in PD., Methods: Thirty-seven participants with PD with or without agoraphobia were randomly assigned to BRT or to a delayed-treatment control group. Clinical status, respiration rate, and end-tidal pCO(2) were assessed at baseline, post-treatment, 2-month and 12-month follow-up. Respiratory measures were also assessed during homework exercises using a portable capnometer as a feedback device., Results: Significant improvements (in PD severity, agoraphobic avoidance, anxiety sensitivity, disability, and respiratory measures) were seen in treated, but not untreated patients, with moderate to large effect sizes. Improvements were maintained at follow-up. Treatment compliance was high for session attendance and homework exercises; dropouts were few., Conclusions: The data provide preliminary evidence that raising end-tidal pCO(2) by means of capnometry feedback is therapeutically beneficial for panic patients. Replication and extension will be needed to verify this new treatment's efficacy and determine its mechanisms.

Panic disorder (PD) patients usually react with more self-reported distress to voluntary hyperventilation (HV) than do comparison groups. Less consistently PD patients manifest physiological differences such as more irregular breathing and slower normalization of lowered end-tidal pCO(2) after HV. To test whether physiological differences before, during, or after HV would be more evident after more intense HV, we designed a study in which 16 PD patients and 16 non-anxious controls hyperventilated for 3 min to 25 mmHg, and another 19 PD patients and another 17 controls to 20 mmHg. Patients reacted to HV to 20 mmHg but not to 25 mmHg with more self-reported symptoms than controls. However, at neither HV intensity were previous findings of irregular breathing and slow normalization of pCO(2) replicated. In general, differences between patients and controls in response to HV were in the cognitive-language rather than in the physiological realm.

Muscle relaxation therapy assumes that generalized anxiety disorder (GAD) patients lack the ability to relax but can learn this in therapy. We tested this by randomizing 49 GAD patients to 12 weeks of Applied Relaxation (AR) or waiting. Before, during, and after treatment participants underwent relaxation tests. Before treatment, GAD patients were more worried than healthy controls (n=21) and had higher heart rates and lower end-tidal pCO2, but not higher muscle tension (A. Conrad, L. Isaac, & W.T. Roth, 2008). AR resulted in greater symptomatic improvement than waiting. However, 28% of the AR group dropped out of treatment and some patients relapsed at the 6-week follow-up. There was little evidence that AR participants learned to relax in therapy or that a reduction in anxiety was associated with a decrease in activation. We conclude that the clinical effects of AR in improving GAD symptoms are moderate at most and cannot be attributed to reducing muscle tension or autonomic activation.

Generalized anxiety disorder (GAD) patients have been reported to have more muscle tension than controls, which has provided a rationale for treating them with muscle relaxation therapies (MRT). We tested this rationale by comparing 49 GAD patients with 21 controls. Participants underwent 5-min relaxation tests, during which they either just sat quietly (QS) or sat quietly and tried to relax (R). GAD patients reported themselves to be more worried during the assessment than the controls, had higher heart rates and lower end-tidal pCO2, but not higher muscle tension as measured by multiple EMGs. QS and R did not differ on most psychological and physiological measures, indicating that intention to relax did not affect speed of relaxation. In the GAD group, self-reported anxiety was not associated with electromyographic or autonomic measures. We conclude that GAD is not necessarily characterized by chronic muscle tension, and that this rationale for MRT should be reconsidered.

The definition of generalized anxiety disorder (GAD) has been narrowed in successive editions of DSM by emphasizing intrusive worry and deemphasizing somatic symptoms of hyperarousal. We tried to determine the clinical characteristics of more broadly defined chronically anxious patients, and whether they would show physiological signs of sympathetic activation. A group whose chief complaint was frequent, unpleasant tension over at least the last six weeks for which they desired treatment, was compared with a group who described themselves as calm. Participants were assessed with structured interviews and questionnaires. Finger skin conductance, motor activity, and ambient temperature were measured for 24h. Results show that during waking and in bed at night, runs of continuous minute-by-minute skin conductance level (SCL) declines were skewed towards being shorter in the tense group than in the calm group. In addition, during waking, distributions of minute SCLs were skewed towards higher levels in the tense group, although overall mean SCL did not differ. Thus, the tense group showed a failure to periodically reduce sympathetic tone, presumably a corollary of failure to relax. We conclude that broader GAD criteria include a substantial number of chronically anxious and hyperaroused patients who do not fall within standard criteria. Such patients deserve attention by clinicians and researchers.

Responses to fear- and sadness-inducing films were assessed using a broad range of cardiovascular (heart rate, T-wave amplitude, low- and high-frequency heart rate variability, stroke volume, preejection period, left-ventricular ejection time, Heather index, blood pressure, pulse amplitude and transit time, and finger temperature), electrodermal (level, response rate, and response amplitude), and respiratory (rate, tidal volume and its variability, inspiratory flow rate, duty cycle, and end-tidal pCO(2)) measures. Subjective emotional experience and facial behavior (Corrugator Supercilii and Zygomaticus Major EMG) served as control measures. Results indicated robust differential physiological response patterns for fear, sadness, and neutral (mean classification accuracy 85%). Findings are discussed in terms of the fight-flight and conservation-withdrawal responses and possible limitations of a valence-arousal categorization of emotion in affective space.