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PubMed1996

Carbon dioxide induced panic attack in panic disorder in Japan.

1. The authors investigated the psychological and biochemical factors associated with challenge by 5% CO2-95% O2 inhalation for 20 min. While fifteen healthy people were used as control, thirteen cases who were diagnosed by DSM-III-R as suffering from panic disorder were used as subjects. CO2 inhalation induced panic in 38% of the panic disorder patients, but did not cause panic in any of the control cases (0%). 2. Acute panic inventory (API), heart rate and breathing rate of the panic group increased significantly after CO2 inhalation compared with the values in the control and non-panic groups. 3. Heart rates and systolic blood pressure were significantly higher those in the panic disorder and non-panic groups than in the control group prior to CO2 inhalation. The cortisol values in the panic and non-panic groups also were significantly higher than those in the control group before and after CO2 inhalation. 4. These results suggest elevated activity of the sympathetic nervous system during panic. The significantly higher heart rate, systolic blood pressure and cortisol values of the panic disorder subjects relative to the control before CO2 inhalation may have been due to circumstantial factors. The present findings of convincing evidence for behavioral, physiological, and biochemical hypersensitivity to CO2 in patients with panic disorders are consistent with a model of interoceptive conditioning in these patients.

Acute Disease↗
PubMed1994

Panic and panic disorder in the United States.

OBJECTIVE: The goal of this study was to determine the prevalence of DSM-III-R panic disorder and to describe its correlates. METHOD: The study was part of the National Comorbidity Survey, the first psychiatric epidemiologic survey of the entire U.S. population and the first to use DSM-III-R criteria for diagnosis. The 8,098 survey respondents, aged 15-54 years, were given the Composite International Diagnostic Interview. For this report, the data on panic were analyzed, and from them the prevalence of panic disorder and related experiences in the U.S. population was estimated. RESULTS: About 15% of the survey respondents reported the occurrence of a panic attack over their lifetimes, and 3% reported a panic attack in the preceding month. About 1% met the DSM-III-R criteria for panic disorder in the month preceding the interview. Panic attacks and panic disorder had a bimodal age distribution and were associated with female sex and lower educational achievement. Fifty percent of the survey respondents with panic disorder reported no symptoms of agoraphobia. The pattern of prevalence of correlated sociodemographic factors was similar for persons with panic attacks, panic disorder, and panic disorder with agoraphobia. CONCLUSIONS: There appears to be no obvious threshold for the diagnosis of panic disorder. Panic disorder and agoraphobia, although highly comorbid, also occur separately.

Adolescent↗
PubMed2001

Specificity of panic response to CO(2) inhalation in panic disorder: a comparison with major depression and premenstrual dysphoric disorder.

OBJECTIVE: The behavioral response to CO(2) inhalation has been used to differentiate panic disorder patients from normal subjects and other clinical populations. This study extended examination of the diagnostic specificity of CO(2)-induced anxiety by testing panic disorder patients and clinical populations with reported low and high sensitivity to CO(2) inhalation (patients with major depression and patients with premenstrual dysphoric disorder, respectively). METHOD: The behavioral responses to inhalation of 5% and 7% CO(2), administered by means of a respiratory canopy, were studied in 50 patients with panic disorder, 21 with major depression, and 10 with premenstrual dysphoric disorder and in 34 normal comparison subjects. Occurrence of panic attacks was judged with DSM-IV criteria by a blind rater. Subjects were rated on three behavioral scales at baseline and after each CO(2) inhalation. RESULTS: Panic disorder patients had a higher rate of CO(2)-induced panic attacks than depressed patients and normal subjects, whose panic rates were not distinguishable. The panic rate for patients with premenstrual dysphoric disorder was similar to that for panic disorder patients and higher than that for normal subjects. Subjects with CO(2)-induced panic attacks had similarly high ratings on the behavioral scales, regardless of diagnosis, including the small number of panicking normal subjects. Seven percent CO(2) was a more robust panicogen than 5%, and response to 7% CO(2 )better distinguished panic disorder patients from normal subjects than response to 5% CO(2). CONCLUSIONS: Patients with panic disorder and patients with premenstrual dysphoric disorder are highly susceptible to CO(2)-induced panic attacks, and depressed patients appear to be insensitive to CO(2) inhalation. The symptoms of CO(2)-induced panic attacks have a similar intensity regardless of the subject's diagnosis.

Administration, Inhalation↗
PubMed2002

Panic termination and the post-panic period.

A comprehensive theory of panic must explain not only the cause(s) of episodes of panic but also why and when panic episodes terminate. Accordingly, we conducted a set of three studies on participants with panic disorder in order to investigate these aspects of panic episodes. In Study 1, we asked participants to monitor their panics prospectively, paying particular attention to the episodes' conclusions and the time period which followed. Results from Study 1 were consistent with earlier retrospective studies, showing that people engage in safety and other behaviors in an attempt to end their panics. We also collected information from the participants on beliefs about panic termination and the post-panic period. Study 2 was designed to determine if a post-panic refractory period occurs. Participants were asked to complete a hyperventilation exercise, and then to repeat the exercise a second time. Results from this study provide scant evidence of a post-panic refractory period. Study 3 was a more ecologically valid version of Study 2, in which participants were asked to re-trigger panics that occurred in their natural surroundings. Again, there was little support for a post-panic refractory period. Results are discussed in terms of cognitive-behavioral and biological theories of panic disorder.

Adult↗
PubMed1990

The Zurich Study. IX. Panic disorder and sporadic panic: symptoms, diagnosis, prevalence, and overlap with depression.

The purpose of the present epidemiological study is to investigate and describe panic disorder and sporadic panic attacks among a cohort of young adults, aged 28 years, from the Canton of Zurich in Switzerland. Both DSM-III panic disorder and sporadic panic are characterized by frequent symptoms of somatic anxiety and tension, as well as by frequent symptoms of depressed mood and low vitality. Sporadic panic is more prevalent than panic disorder and shows a greater excess of females over males. The association with depressions (major depression and recurrent brief depression) is similarly high for both types of panic syndromes, while the association with other anxiety disorders is negligible. Several indicators suggest a marked similarity between sporadic panic and DSM-III panic disorder. More impressive differences were observed between subjects with panic disorder alone and subjects with comorbidity of panic and depression. For the latter group, the SCL-90R scores indicated higher severity. Comparison of the scores of life events, conflicts, self-esteem, and the number of chronic problems in childhood suggests a more specific nosological pattern for subjects with panic and depression as compared with those with panic alone.

Adult↗
PubMedDate not supplied

Panic plaques: panic disorder & coronary artery disease in patients with chest pain.

BACKGROUND: The purpose of this systematic review was to identify characteristics of the chest pain associated with the presence of panic disorder, to determine the strength of the association between panic disorder and coronary artery disease (CAD), and to determine the association between panic disorder and known cardiovascular risk factors. METHODS: Potential studies were identified via computerized search using MEDLINE and PSYCINFO databases, and review of bibliographies. MeSH headings used included "panic disorder" with "chest pain," "panic disorder" with "coronary disease or cardiovascular disorders or heart disorders," and "panic disorder" with "cholesterol or essential hypertension or tobacco smoking." Studies had to base their diagnosis of panic disorder on criteria from the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, and objective criteria of CAD and risk factors had to be used. Only case-control and cohort studies were included. RESULTS: The relative risk of panic disorder in patients with nonanginal chest pain is 2.03 [confidence interval (CI), 1.41 to 2.92]. Concerning the relationship between panic disorder and CAD, studies conducted in emergency departments found a relative risk of 1.25 (CI, 0.87 to 1.80). However, there is an inverse relationship between the prevalence of CAD in the study and the prevalence of panic disorder among the patients with CAD (r = -.469, P =.086). Panic disorder has also been linked to cardiac risk factors. CONCLUSIONS: Panic disorder and CAD are correlated in noncardiology settings, and recurrent panic attacks may actually cause CAD. Recognition of either condition should lead the family physician to consider the other, resulting in increased vigilance and possible screening.

Chest Pain↗
PubMed1998

Can panic be induced in deep sleep? Examining the necessity of cognitive processing for panic.

This study examines the relative contribution of biological and psychological processes to the induction of panic attacks by a biochemical challenge agent. Panicogenic doses of caffeine were administered to 8 panic disorder (PD) patients and 11 healthy volunteers during stage 3-4 sleep, when cognitive processing is minimal and the threshold to external stimuli is high. Panic attacks were induced directly from sleep in 3 subjects and subclinical panics in an additional 3. Subjects who experienced full panic attacks spent periods of time ranging from 4 to 52 minutes in stage 2 sleep before awakening in a panic, while those who awakened in subclinical panic awakened almost directly from stage 4 sleep. PD patients experienced significantly more panic symptoms than healthy volunteers. Although limited by a small sample size, this study suggests a combined biological-psychological model of panic induction in which panic disorder patients are more biologically predisposed than healthy controls to panic symptoms but may require cognitive processing for the elaboration of a full panic attack.

Adolescent↗
PubMed1994

Consistencies between recalled panic and lactate-induced panic.

This study investigated the frequency and severity of symptoms during naturally occurring panic attacks recollected as "usual" and during sodium lactate-induced attacks. Seventy-six male and 126 female patients with panic disorder or agoraphobics with panic attack (DSM-III criteria) underwent lactate infusion studies and were serially administered the Acute Panic Inventory (API). Fifty-nine percent of the subjects were rated by an attending psychiatrist to have experienced lactate-induced panic attacks. Patients were also asked to API symptom rate their "usual" panic attacks. For panic recollected as usual, the most frequently reported symptoms (> or = 75%) at the moderate to severe levels included: afraid in general, difficulty concentrating, difficulty performing a job, desire to flee, afraid of losing control, palpitations, feeling hot or cold or both, dyspnea, dizzy-lightheaded. During lactate infusion, 25 of 29 API symptoms increased significantly from prelactate to point of panic; however, particularly robust effect sizes were exhibited for the desire to flee, dyspnea, tingling, twitching/trembling and difficulty doing a job. Comparison of panic recollected as usual and lactate-induced panic showed that more than half of the symptoms did not differ after Bonferroni correction; however, the most notable were fear in general, dyspnea, chest pain/discomfort, difficulty swallowing, feeling weak, desire to flee, and feeling hot/cold or both. These data point to a very distinctive role during both recollected and lactate-induced panic attacks for fearfulness the desire to flee (by definition), and for dyspnea, difficulty performing a job and fear of losing control. During lactate-induced panic, dyspnea exhibited the most robust effect size of all physical symptoms.

Adolescent↗
PubMed2005

Electrocortical evidence for an early abnormal processing of panic-related words in panic disorder patients.

Panic patients are hypothesized to have particularly elaborated cortical networks for panic-related stimuli, and this characteristic should be associated with an abnormal automatic processing of these stimuli. Panic-related and neutral words were presented to 25 panic patients and 25 matched healthy controls either at individually determined perception thresholds (threshold condition) or for 1000 ms (above threshold condition). Word recognition for words presented at perception threshold (threshold words), and event-related brain potentials (ERPs) triggered by threshold and above threshold words were analyzed. In the threshold condition, both panic patients and control participants correctly recognized more panic-related than neutral words. An additional analysis restricted to participants who used an intuitive strategy for word identification revealed an enhanced frequency of correctly identified panic-related words in panic patients. In the ERPs, only panic patients exhibited enhanced positive potentials during early time windows (200-400 ms after stimulus presentation) triggered by panic-related compared to neutral threshold words. In late (400-600 ms) and very late (600-1000 ms) time windows, both groups showed a greater ERP positivity for panic-related than for neutral words. These data suggest that panic patients are characterized by an early automatic and elaborated processing of disorder-relevant stimuli.

Adult↗
PubMed2002

Priming panic interpretations in children of patients with panic disorder.

Cognitive and psycho-physiological models of panic disorder stress the role of interpretation bias in the maintenance of the disorder. Several studies have reported results consistent with this hypothesis, but it is still unclear whether this bias precedes panic disorder or is a consequence of it. In the present study, we compared the interpretations of ambiguous scenarios of children of individuals with panic disorder, children of individuals with animal phobia, and children of healthy controls. Children were presented with three types of scenarios each including one of the following descriptions: panic-relevant physical sensations, animal-relevant stimuli, and panic-irrelevant physical sensations (i.e., cold symptoms). To test, if children's interpretation bias is affected by priming, we compared their responses to the scenarios before and after watching a panic, a spider phobic, and a cold model. The results revealed that (a) children of panic disordered parents but not of parents with animal phobia and of healthy controls showed a significant increase in anxious interpretations after priming; and (b) this significant increase emerged only after priming through presentation of a panic-relevant model and not after priming through presentation of a phobia-relevant or cold-relevant model. Because the children of panic disordered parents did not have panics themselves, their increase in panic interpretations can be viewed as a vulnerability factor. Longitudinal studies should clarify the role of interpretation style in the etiology of panic disorder.

Adult↗
PubMed2005

Childhood abuse and familial violence and the risk of panic attacks and panic disorder in young adulthood.

BACKGROUND: The objectives of the study were to examine linkages between exposure to childhood abuse and interparental violence and the subsequent development of panic attacks and panic disorder using data gathered on a birth cohort of 1265 New Zealand young people studied to the age of 21 years. METHOD: Data on: (a) exposure to child abuse and interparental violence; (b) the development of panic attacks and panic disorder; and (c) other childhood and related factors were gathered over the course of a 21-year longitudinal study. RESULTS: After adjustment for childhood and related factors, exposure to childhood physical abuse was associated with a significantly increased risk of later panic attack (OR 2.3, 95% CI 1.1-4.9) and panic disorder (OR 3.0, 95% CI 1.1-7.9); childhood sexual abuse was associated with a significantly increased risk of panic attack (OR 4.1, 95% CI 2.3-7.2) and a marginally significant increase risk of panic disorder (OR 2.2; 95% CI 0.98-5.0). Exposure to interparental violence was unrelated to later panic attack or disorder after adjustment. CONCLUSIONS: Exposure to childhood sexual and physical abuse was associated with increased risks of later panic attack/disorder even after adjustment for prospectively assessed confounding factors. However, exposure to interparental violence during childhood was not related to increased risk of later panic attack/disorder after adjustment. These data suggest the need for clinicians to be aware that patients with histories of childhood physical and sexual abuse may be at increased risk for panic during young adulthood.

Adolescent↗
PubMed1993

Valproate treatment of panic disorder and lactate-induced panic attacks.

Several lines of evidence suggest that the anticonvulsant drug valproate may have antipanic properties: (1) It enhances gamma-aminobutyric acid activity in the brain; (2) it has anxiolytic effects in animal models of anxiety; and (3) it has been reported to be effective in panic disorder in several preliminary studies; however, valproate has not been studied in the prevention of lactate-induced panic attacks. Sixteen patients with panic disorder underwent a lactate infusion followed by a 28-day treatment period with valproate and subsequent rechallenge with lactate. Response was measured by change in panic attack frequency and Hamilton Anxiety Scale (HAS) scores and by the ability of valproate to block lactate-induced panic on rechallenge. Of the 14 patients completing the 28-day trial, 10 (71%) experienced a greater than 50% reduction in the weekly frequency of panic attacks. Six (43%) had complete remission. HAS scores dropped significantly from a baseline mean of 30.8 +/- 9.4 (SD) to 12.6 +/- 7 after 4 weeks of treatment. Valproate blocked reinduction of panic symptoms on lactate rechallenge in 10 (83%) of 12 patients who had initially experienced panic symptoms on initial infusion. The significant reduction in spontaneous panic attacks and the blockade of lactate-induced panic symptoms by valproate support earlier studies suggesting that the drug may be an effective treatment for panic disorder.

Adult↗
PubMed1996

The DSM-IV panic disorder field trial: panic attack frequency and functional disability.

The goal of the DSM-IV panic disorder field trial was to provide an empirical basis for choosing between alternate proposals (DSM-III-R and proposed DSM-IV) for the diagnostic threshold for panic disorder, in particular the number and frequency of panic attacks required for diagnosis. The two criteria sets were compared with respect to their ability to identify individuals whose panic attacks were associated with distress, impairment, or help-seeking. Subjects were a convenience sample screened in three geographically diverse primary care clinics for presence (past 6 months) or absence (lifetime) of panic attacks. Each underwent a clinician-administered semistructured interview which included assessment of panic frequency, panic-related impairment, psychiatric diagnosis, health services utilization, and medical illness. Self-perceived health-related quality of life was assessed using the Medical Outcome Study SF-36 Health Survey Questionnaire. Although both proposals diagnosed the same proportion of panic-impaired individuals, they were not completely overlapping. Twenty percent of subjects diagnosed by each criteria set were excluded by the other. Subjects who had been excluded by the DSM-III-R but included by the DSM-IV proposal were those with fewer than 4 attacks in 4 weeks who also denied worry about the "next" attack. Broadening the worry criterion to include concerns about the health implications of attacks enabled diagnosis of this group. Subjects who met DSM-III-R, but not the proposed DSM-IV criteria, had 4 attacks in 4 weeks but denied any panic related worry. Modification of the DSM-IV proposal to include a month of worry or "a significant change in behavior related to the attacks" allowed inclusion of this group in the diagnostic category. These data suggest that the finalized DSM-IV panic disorder criteria will diagnose a greater proportion of individuals whose panic attacks are associated with impairment without inflating the diagnostic category or significantly reducing specificity.

Adult↗
PubMed2004

The effects of tianeptine or paroxetine on 35% CO2 provoked panic in panic disorder.

Antidepressants that inhibit the reuptake of serotonin (5-HT) are particularly effective in the treatment of panic disorder. Evidence suggests that increased 5-HT availability is important for the anti-panic effect of serotonergic drugs and in maintaining the response to selective serotonin reuptake inhibitors (SSRIs). Tianeptine is an antidepressant with 5-HT reuptake enhancing properties (i.e. the opposite pharmacological profile to that of SSRIs). Therefore, no effect would be expected in panic disorder. The aim of the present study was to compare the effect of tianeptine with that of paroxetine, a selective 5-HT reuptake inhibitor with demonstrated efficacy in panic disorder, on the vulnerability to a laboratory panic challenge in panic disorder patients. Twenty panic disorder patients were treated with either tianeptine or paroxetine for a period of 6 weeks, in a randomized, double-blind, separate group design. The reaction to a 35% CO(2) panic challenge was assessed at baseline and after treatment. Improvement on several clinical scales was also monitored. Tianeptine, as well as paroxetine, showed a significant reduction in vulnerability to the 35% CO(2) panic challenge. In spite of their opposite influence on 5-HT uptake, both tianeptine and paroxetine appeared to reduce the reaction to the panic challenge. These results raise questions about the necessity of 5-HT uptake for the therapeutic efficacy of anti-panic drugs.

Adult↗
PubMed2000

Increased ACTH concentrations associated with cholecystokinin tetrapeptide-induced panic attacks in patients with panic disorder.

Preclinical findings on the role of corticotropin releasing hormone (CRH) in stress and anxiety, on the interaction of CRH and cholecystokinin (CCK) in modulating anxiety, as well as the blunted corticotropin (ACTH) response to CRH in panic disorder suggest that CRH may play a role in panic disorder. To further characterize the role of the hypothalamic-pituitary-adrenocortical (HPA) system in panic disorder, we compared patients with and without CCK tetrapeptide (CCK-4) induced panic attacks. Twenty-four patients with panic disorder were given injections of CCK-4 (25 micrograms). Panic attacks, psychopathological changes, as well as ACTH and cortisol secretion were recorded. Fifteen of the 24 patients experienced a panic attack after CCK-4. ACTH secretion was significantly higher in the patients with CCK-4-induced panic attacks than in those without such attacks. The patients without CCK-4-induced attacks had a brief but less pronounced increase in ACTH concentrations. Cortisol concentrations were not significantly increased after CCK-4 administration. The increased ACTH concentrations suggest that the activation of the HPA system in CCK-4-induced panic attacks plays a physiological role. CRH may be involved in experimentally-occurring and perhaps in naturally-occurring panic attacks as well.

Adrenocorticotropic Hormone↗
PubMed1998

Sympathetic activity in patients with panic disorder at rest, under laboratory mental stress, and during panic attacks.

BACKGROUND: The sympathetic nervous system has long been believed to be involved in the pathogenesis of panic disorder, but studies to date, most using peripheral venous catecholamine measurements, have yielded conflicting and equivocal results. We tested sympathetic nervous function in patients with panic disorder by using more sensitive methods. METHODS: Sympathetic nervous and adrenal medullary function was measured by using direct nerve recording (clinical microneurography) and whole-body and cardiac catecholamine kinetics in 13 patients with panic disorder as defined by the DSM-IV, and 14 healthy control subjects. Measurements were made at rest, during laboratory stress (forced mental arithmetic), and, for 4 patients, during panic attacks occurring spontaneously in the laboratory setting. RESULTS: Muscle sympathetic activity, arterial plasma concentration of norepinephrine, and the total and cardiac norepinephrine spillover rates to plasma were similar in patients and control subjects at rest, as was whole-body epinephrine secretion. Epinephrine spillover from the heart was elevated in patients with panic disorder (P=.01). Responses to laboratory mental stress were almost identical in patient and control groups. During panic attacks, there were marked increases in epinephrine secretion and large increases in the sympathetic activity in muscle in 2 patients but smaller changes in the total norepinephrine spillover to plasma. CONCLUSIONS: Whole-body and regional sympathetic nervous activity are not elevated at rest in patients with panic disorder. Epinephrine is released from the heart at rest in patients with panic disorder, possibly due to loading of cardiac neuronal stores by uptake from plasma during surges of epinephrine secretion in panic attacks. Contrary to popular belief, the sympathetic nervous system is not globally activated during panic attacks.

Adrenal Medulla↗
PubMed2004

Sensitivity to carbon dioxide in subjects with a single lifetime panic attack: possible clinical "bedside" predictive test for panic disorder after a first attack.

There is currently no way of knowing whether a patient who has recently had a single panic attack has incipient panic disorder. Sensitivity to carbon dioxide (CO2) is lower in healthy volunteers than in panic disorder patients. If this is also true of people who experience a single lifetime panic attack, it could be used as a prognostic test. Subjects with a single lifetime panic attack and subjects with panic disorder received an inhalation of 35% CO2. Subjects completed the panic symptoms scale (PSS), and also stated whether they considered that they had experienced an attack. None of 14 subjects with a single lifetime panic attack, compared to 7 of 17 subjects with panic disorder (P=.009), had an attack. The PSS also distinguished between the groups. The 35% CO2 challenge warrants further investigation as a predictive test after a first panic attack.

Administration, Inhalation↗
PubMed2002

Acute L-5-hydroxytryptophan administration inhibits carbon dioxide-induced panic in panic disorder patients.

Previous research showed that lowering the availability of serotonin to the brain by tryptophan depletion increases the vulnerability of panic disorder patients for an experimental 35% CO(2) panic challenge. The results also suggested that increased availability of serotonin inhibits the response to such a challenge. In the present study, this latter possibility is examined. The reaction of 24 panic disorder patients and 24 healthy volunteers to a 35% CO(2) panic challenge was assessed following administration of 200-mg L-5-hydroxytryptophan (the immediate precursor of serotonin) or placebo. L-5-Hydroxytryptophan significantly reduced the reaction to the panic challenge in panic disorder patients, regarding subjective anxiety, panic symptom score and number of panic attacks, as opposed to placebo. No such effect was observed in the healthy volunteers. L-5-Hydroxytryptophan acts to inhibit panic, which supports a modulatory role of serotonin in panic disorder.

5-Hydroxytryptophan↗