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PubMedDate not supplied

Characteristics of panic attack subtypes: assessment of spontaneous panic, situational panic, sleep panic, and limited symptom attacks.

We report the analyses of daily journal descriptions of 790 self-defined panic attacks from 59 patients meeting DSM-III criteria for panic disorder or agoraphobia with panic attacks. The DSM-III-R specified symptoms occurred with frequencies ranging from choking (17% of attacks) to palpitations (63% of attacks). The mean weekly panic attack severity correlated significantly with the number of symptoms per attack, but not their weekly frequency. Within a given person, situational and spontaneous panic attacks did not significantly differ over a number of characteristics, including severity, duration, frequency per week, diurnal distribution, and the number of symptoms per attack. Limited symptom attacks were less severe, but were otherwise similar to panic attacks. Also, panic attacks during sleep were less frequent than panic attacks in the awake state, but did not significantly differ on other descriptive characteristics. These data support the validity of the symptoms specified for panic attacks by DSM-III-R. They also suggest that within an individual, panic attacks of various subtypes may be descriptively similar, despite the differing contexts in which they arise. In addition, these data question the diagnostic significance of the limited symptom attack-panic attack distinction.

Adult↗

PubMed1991

Chronology of panic and avoidance, age of onset in panic disorder, and prediction of treatment response. A report from the Cross-National Collaborative Panic Study.

The relevance of the chronology between panic disorder and avoidance behavior and of an early, medium or late onset of panic disorder was tested. Groups from the sample of the cross-national collaborative panic study (CNCPS) were compared for differences in basic characteristics and for the ability to predict treatment response. Patients who developed avoidance behavior before the full syndrome of panic disorder had less often a full agoraphobia but were not different in their response to treatment. Patients with an early onset of panic disorder suffered more often from agoraphobia. The treatment response was similar in the groups with early, medium or late onset of panic disorder. Neither the chronology between panic disorder and avoidance behavior nor the age of onset of panic disorder predicted outcome in short-term treatment with alprazolam or imipramine.

Adult↗

PubMed1992

Panic disorder in the families of patients with normal coronary arteries and non-fear panic disorder.

Patients with non-fear panic disorder (NFPD) meet DSM-III-R criteria for panic disorder, but do not report subjective fear or anxiety. Although apparently common in medical settings, this controversial group is in need of further diagnostic validation. This study assessed family history of panic disorder in patients with chest pain and normal coronary arteries (CP/NCA) and either NFPD, panic disorder with fear, or no panic. It was hypothesized that the two panic disorder groups would have similar, elevated rates of panic disorder in their first-degree relatives, compared to patients without panic. The results support the hypothesis; about 17% of the first-degree relatives of both NFPD and panic disorder patients were diagnosable with panic disorder according to proband interviews, whereas only 4.6% of the first-degree relatives of patients without panic were so diagnosable. These results support the diagnostic validity of NFPD in CP/NCA patients, because such patients had a family history of panic disorder similar to patients with a more classical panic disorder presentation. The lack of fear symptoms and behavior in NFPD may cause panic disorder to be overlooked as a potential cause of somatic symptoms in patients with no medical explanation for their condition.

Chest Pain↗

PubMed1992

A prospective study of panic and anxiety in agoraphobia with panic disorder.

The features of panic and anxiety in the natural environment were studied by prospective self-monitoring in 39 patients with chronic agoraphobia and panic disorder. Panics overlapped greatly with anxiety episodes but were more intense. Panics occurred more often in public places than did anxiety episodes, but had otherwise similar symptom profile, time of occurrence, and antecedents. Most panics surged out of a pre-existing plateau of tonic anxiety which lasted most of the day. Spontaneous panics were less frequent than situational panics and occurred more often at home but were otherwise similar. These findings do not support the sharp distinction between panic and anxiety in DSM-III-R, not its emphasis on spontaneous panic in classifying anxiety disorders. Thoughts of dying and 'going crazy'/losing control accompanied only a minority of panic/anxiety episodes and seemed to be a product of intense panic rather than a cause.

Adult↗

PubMed1992

Noradrenergic function in panic disorder. Effects of intravenous clonidine pretreatment on lactate induced panic.

To assess the role of noradrenergic stimulation during lactate-induced panic, ten patients with panic disorder who panicked during a standard sodium-lactate infusion underwent a repeat infusion following intravenous clonidine pretreatment. Although clonidine significantly lowered prelactate systolic blood pressure, the drug did not significantly lower prelactate anxiety levels, as reflected by the Acute Panic Inventory (API). Clonidine blocked lactate-induced panic in four of ten subjects, a significant effect. Clonidine treatment also significantly attenuated lactate-panic symptoms, as reflected by time to panic and API comparison between trials. Nevertheless, over half the subjects still panicked in response to lactate despite clonidine. This preliminary study suggests that reduction of central noradrenergic activity by clonidine, at least at the dosage levels employed in the current study, only partially attenuates panic response to lactate. Noradrenergic theories of panic may not therefore fully account for lactate panicogenesis.

Adult↗

PubMed1992

Evidence for hypothalamo-growth hormone dysfunction in panic disorder: profile of growth hormone (GH) responses to clonidine, yohimbine, caffeine, glucose, GRF and TRH in panic disorder patients versus healthy volunteers.

Given the abrupt and time-limited nature of daytime-awake and nocturnal-sleep panic attacks, several chemical and neuroendocrine challenge tests have been employed to investigate the neurobiology of "spontaneous" panic attacks. Previously we demonstrated that panic disorder patients have blunted growth hormone (GH) responses to clonidine, an alpha 2-adrenergic agonist. However, the mechanism of this blunted response and the role of hypothalamic-GH dysfunction, if any, remains unclear. To further delineate the status of hypothalamic-GH function in panic disorder, we review the literature and present original data on the GH responses to a number of different chemical and neuroendocrine challenge paradigms. Although stress-mediated increases in GH are thought to be a common correlate of stress in humans, our findings indicate that panic disorder patients have significantly blunted GH responses to clonidine, yohimbine, growth-hormone releasing factor, and caffeine compared to normal control subjects. A similar trend was noted in the delayed rise in GH after glucose challenge. There was no difference in the rate of abnormal GH responses to thyrotropin-releasing hormone in panic disorder compared to normal control subjects. No drug or neuroendocrine challenge, even if associated with marked increases in anxiety, produced a significantly enhanced GH response compared to normal control subjects. These findings provide support for a hyporesponsive hypothalamic-GH system in panic disorder. These observations, combined with preliminary observations from our clinic of short stature in several cases of prepubescent children with anxiety disorders, also underscore the need for assessing early growth patterns in individuals with panic disorder. Strategies for investigating the site(s) of possible neurotransmitter or hypothalamic-GH-somatomedin dysfunction are discussed.

Caffeine↗

PubMed1992

Agoraphobic avoidance and panic frequency as predictors of laboratory induced panic reactions.

This study examined the importance of agoraphobic avoidance and frequency of panic as predictors of psychological and physiological responses of panic sufferers to a laboratory based provocation procedure. Psychophysiologic comparisons were made between 22 panic disorder patients and 15 controls, at baseline and across three periods of carbon dioxide gas inhalations (1, 3, 5%; balance oxygen). Subjective measures of anxiety, frightening cognitions and body sensations were obtained across the phases. Physiological measures of minute ventilation, breathing rate, tidal volume, end tidal CO2 and heart rate were also obtained. Between group comparisons revealed significant differences between the groups on the subjective measures with no significant differences occurring on the physiological measures. Within group analyses revealed that pre-session questionnaire measures of agoraphobia avoidance and panic frequency predicted the degree of anxiety, frightening sensations and cognitions during baseline and 5% CO2 inhalation. The results indicated that both self-reported agoraphobic avoidance and panic frequency are strong clinical predictors of psychological reactions of panic sufferers during laboratory provocation.

Adult↗

PubMed1991

Hyperventilation-induced panic attacks in panic disorder with agoraphobia.

Eight minutes of hyperventilation to an end-tidal PCO2 of less than 20 mmHg led to a panic attack in 7 of 12 patients with panic disorder with agoraphobia and only 1 of 12 normal controls. Patients experienced greater increases in panic symptoms than controls during hyperventilation. Patients who reported more distress from somatic symptoms of hyperventilation during the preceding week were more likely to panic during hyperventilation. Patients who panicked during hyperventilation exhibited a delayed recovery of normocapnia following hyperventilation. Hyperventilation by this protocol is an effective means of inducing panic attacks in the laboratory. A hyperventilation challenge may identify a subgroup of patients for whom hyperventilation symptoms are frequently associated with panic.

Adult↗

PubMed1990

Depression and panic anxiety: the effect of depressive co-morbidity on response to drug treatment of patients with panic disorder and agoraphobia.

Numerous studies have established that there is increased co-morbidity of depressive symptoms among patients with panic disorder with and without agoraphobia, but questions remain as to whether the symptom pattern and clinical course are similar to that of primary depressions. The Cross-National Collaborative Panic Study was initiated to study the effects of alprazolam, a triazolobenzodiazepine, in the treatment of panic disorder. In the first phase, which included more than 500 subjects, alprazolam was compared against placebo. In the second phase, alprazolam was compared with imipramine and placebo in a double-blind, randomized, controlled trial. Results of both the first and second phases will be reviewed as they bear on the issue of drug treatment of secondary depression accompanying panic disorder. The presence of depressive symptoms does not adversely influence anti-panic and anti-phobic response to medication. Equivalent drug-placebo differences occur on multiple measures of anxiety--including the number and intensity of panic attacks, phobias, anticipatory anxiety, and overall anxiety.

Agoraphobia↗

PubMed1992

Noradrenergic neuronal dysregulation in panic disorder: the effects of intravenous yohimbine and clonidine in panic disorder patients.

In order to evaluate possible abnormal noradrenergic neuronal functional regulation in patients with panic disorder, the behavioral, biochemical and cardiovascular effects of intravenous yohimbine (0.4 mg/kg) and clonidine (2 micrograms/kg) were determined in 15 healthy subjects and 38 patients with panic disorder. A subgroup of 24 panic disorder patients were observed to experience yohimbine-induced panic attacks and had larger yohimbine-induced increases in plasma 3-methoxy-4-hydroxyphenylglycol (MHPG) than healthy subjects and other panic disorder patients. A blunted growth hormone response to clonidine and a significant clonidine-induced decrease in plasma MHPG was also observed in this subgroup of panic disorder patients. These data replicate and extend previous investigations, which are consistent with a large body of preclinical and human data relating increased noradrenergic neuronal function to human anxiety and fear states.

Adult↗

PubMed1992

Diurnal rhythms and symptom severity in panic disorder. A preliminary study of 24-hour changes in panic attacks, generalised anxiety, and avoidance behaviour.

Diurnal changes in the frequency of panic attacks and symptoms of generalised anxiety, phobic anxiety and phobic avoidance in 34 panic-disorder patients and 40 normal controls were evaluated. The panic-disorder patients had significant diurnal changes in generalised and phobic anxiety, but not phobic avoidance. Increased severity of symptoms and prominent diurnal changes were most evident in the panic-disorder patients with a history of depression. Although panic attacks were distributed throughout the 24-hour period, patients with a current episode or history of depression tended to have more frequent panic attacks in the morning or early afternoon. These observations challenge the traditional belief that 'anxious neurotic' patients are relatively asymptomatic upon awakening in the morning and then develop more severe symptoms of anxiety later in the day.

Adult↗

PubMed1992

Panic symptoms in asthma and panic disorder: a preliminary test of the dyspnea-fear theory.

Ley's (Behaviour Research and Therapy, 27, 549-554, 1989) dyspnea-fear theory was tested on three groups of subjects: 10 with panic disorder, 24 with asthma, and 12 who were nonanxious and nonasthmatic, using measures of pulmonary function, muscle tension; and self-report measures of generalized anxiety, dyspnea, and psychopathology. Results are supportive of dyspnea-fear theory for asthmatics but not for individuals with panic disorder. Differences between groups on panic/fear measures were explained by a combination of general anxiety and dyspnea. Within-group regression analyses showed that only generalized anxiety symptoms contributed significantly to scores on the Asthma Symptom Checklist scale of panic/fear within the panic disorder group; while only dyspnea contributed to panic/fear among asthmatics. Additional results show that panic disorder subjects performed normally on pulmonary function tests but reported respiratory symptoms as severe as did asthmatics. Compared with normal subjects, both patient groups displayed lower correlations between self-rated symptoms of bronchoconstriction and objective pulmonary measures. Panic disorder subjects showed a negative relationship between pulmonary function and hyperventilation symptoms, suggesting a heightened sensitivity to, and discomfort with, sensations associated with normal pulmonary function. Asthmatics displayed a significant relationship between degree of airway obstruction and both trapezius surface EMG and ratings of hyperventilation symptoms.

Age Factors↗

PubMed1992

The National Institute of Mental Health Panic Questionnaire. An instrument for assessing clinical characteristics of panic disorder.

This paper introduces a new self-report inventory, the NIMH Panic Questionnaire (NIMH PQ), for obtaining and quantifying comprehensive information about the clinical characteristics of panic disorder in patients with previously diagnosed or suspected illness. Fifty-two patients who met DSM-III-R criteria for panic disorder completed the NIMH PQ; their responses were compared with data derived from 16 similar or identical questions on the Schedule for Affective Disorders and Schizophrenia modified for anxiety disorders. There were no significant differences between the two instruments on 15 of the 16 (93.7%) items tested. The one exception revealed a greater proportion of patients versus physicians endorsing "spontaneous" panic, and a nonsignificant trend for physicians over patients endorsing anticipatory anxiety with greater frequency. The NIMH PQ offers a potentially useful clinical and research tool in the assessment of patients with known or suspected panic disorder.

Adult↗

PubMed1992

Self-monitoring of panic attacks and retrospective estimates of panic: discordant findings.

An event sampling method was used to study the frequency of panic attacks during treatment of agoraphobics. Results revealed a much lower incidence of panic attacks in agoraphobics according to self-monitoring than was expected on account of their retrospective estimation. When more stringent criteria for panic attacks are applied, retrospective overestimation becomes even more apparent. The implication of this finding for the classification of panic disorder patients is discussed.

Agoraphobia↗

PubMed1991

The Panic-Associated Symptom Scale: measuring the severity of panic disorder.

The Panic-Associated Symptom Scale (PASS) is presented as a new measurement of the severity of the core symptoms of panic disorder. This first description addresses the rationale for its design and its scoring, score distributions, test-retest reliability, correlations within the PASS and with other scales, principal component structure, and response to drug therapy. Data are presented from a large study group of patients with panic disorder (n = 1168). Problems in measuring panic disorder are discussed.

Adult↗

PubMed1992

Center differences and cross-national invariance in help-seeking for panic disorder. A report from the cross-national collaborative panic study.

Help-seeking behaviour for treatment of panic disorder was investigated in the sample of the Cross-National Collaborative Panic Study Second Phase. A total of 1168 patients were entered into this trial in 14 countries. Although there were significant center differences in prior treatment and utilization of health services there were also similarities. Treatment had been provided mainly by general practitioners. Drug treatment consisted mostly of prescription of classical tranquilizers and had a longer duration than treatment by psychotherapy. Patients with agoraphobic avoidance, past major depression and longer duration of illness used medical and psychiatric treatment facilities more intensely. Older and more severely disabled subjects were more frequently treated by medical health care providers and were more likely to receive psychotropic drugs. The results indicate that general practitioners carry an important load in the treatment of panic disorders but may need more information about recent development in pharmacotherapy for this condition.

Adult↗

PubMed1992

The Galway Study of Panic Disorder. II: Changes in some peripheral markers of noradrenergic and serotonergic function in DSM III-R panic disorder.

Sixty six patients with panic disorders, fulfilling the DSM III criteria for panic attack, together with a group of age and sex matched controls, were studied for changes in their peripheral noradrenergic and serotonergic status before treatment and during six months treatment with either clomipramine or lofepramine. The results of this study suggest that, despite clinical improvement, the peripheral markers of both adrenergic (platelet aggregation to noradrenaline, platelet alpha 2 receptor density and lymphocyte beta receptor density) and serotonergic (platelet aggregation to serotonin, 3H-ketanserin binding to platelet 5HT2 receptors and 3H-5HT uptake into platelets) function largely remained abnormal. It is concluded that such abnormalities are trait markers of biogenic amine function in patients with panic attack. Further studies are needed to determine whether or not these parameters eventually normalize in those patients showing prolonged remission of symptoms.

Adult↗

PubMed1992

The Galway Study of Panic Disorder. I: Clomipramine and lofepramine in DSM III-R panic disorder: a placebo controlled trial.

Among 79 volunteer, unpaid, family doctor-referred psychiatric out patients with DSM III-R panic disorder, with and without agoraphobia, 66 completed a six week placebo-controlled trial of lofepramine versus clomipramine and 57 survivors were followed up for 6 months. All subjects received one hour per week concurrent behavioural counselling in the acute phase. Of 13 dropouts in the first 3 weeks, 9 (of 27) were on clomipramine, 2 (of 26) were on lofepramine and 2 (of 26) were on placebo. The high (30%) early dropout from the clomipramine group was largely due to medication intolerance. Both drugs were superior to placebo by the end of week 6 on several standard rating scales but not on panic attack frequency. No significant differences in efficacy were found between the two drugs tested to the end of 6 months. No tendency for relapse was noted in the three months following taper-off of medication from week 12 to week 24. The study provides evidence that both drugs, in the dosages used, are superior to placebo in the acute phase of panic disorder in treatment-naive subjects concurrently receiving appropriate psychotherapy.

Adult↗