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PubMed1988

Lactate- and isoproterenol-induced panic attacks in panic disorder patients and controls.

In a double-blind study using sodium lactate and isoproterenol infusions to provoke panic attacks, 73 of 86 panic disorder patients and 10 of 45 controls panicked with lactate, and 58 of 86 patients and 4 of 45 controls panicked with isoproterenol. We measured baseline and peak anxiety ratings in 10 controls with lactate-induced panic attacks, 31 controls who did not panic during lactate infusions, and 63 panic disorder patients who did panic during lactate infusions. The controls who panicked with lactate had robust increases in their anxiety ratings very similar to the increases experienced by patients who panicked with lactate.

Adolescent↗
PubMed2004

Does coping predict CO2-induced panic in patients with panic disorder?

Patients with panic disorder (PD) show maladaptive coping but the role of coping in the pathogenesis of panic is unclear. This study examined general coping and panic-specific coping as predictors of fear responding to CO2 inhalation. Subjective and physiological responses including panic attacks were assessed in 45 patients with PD and 45 matched nonclinical controls. Measures of coping were the primary predictors used in the analyses. Consistent with other reports, patients with PD reported increased emotion-focused coping and there was an association between emotion-focused coping and subjective reactivity. However, only panic-specific coping predicted panic attacks in response to the CO2 challenge.

Adaptation, Psychological↗
PubMed2005

Smoking and panic attacks, panic disorder, and agoraphobia: a review of the empirical literature.

The empirical literature regarding panic-spectrum problems (i.e., panic attacks, panic disorder, and agoraphobia) and cigarette smoking is reviewed. In the first section of the paper, empirical studies that document the prevalence of smoking and panic-related problems are presented and discussed. In the second section of the paper, studies pertaining to the role cigarette smoking may play in the onset and maintenance of panic-related problems are critically reviewed. In the third section of the paper, studies related to the association between panic vulnerability factors and the nature of smoking behavior are presented. In the fourth section of the paper, specific areas not otherwise covered in the review are presented to stimulate further development in these areas (e.g., specialized treatment development).

Agoraphobia↗
PubMedDate not supplied

Recurrent sleep panic, insomnia, and suicidal behavior in patients with panic disorder.

The purpose of this study was to examine the association between recurrent sleep, panic, and suicidal behavior in panic disorder. We compared the recurrent sleep panickers (N = 33) with other panickers (N = 34). The Schedule for Affective Disorders and Schizophrenia (SADS) suicide subscale was used to rate the severity of active suicidality. We found that recurrent sleep panickers also had a higher percentage of insomnia and comorbid major depression than the others. A multivariate analysis demonstrated an association between recurrent sleep panic and suicidal tendencies in patients with panic disorder. Although recurrent sleep panic alone is not an independent risk factor for suicidal behavior, it may modify the severity of illness in patients with panic disorder.

Adult↗
PubMed1998

Cardiovascular death from panic disorder and panic-like anxiety: a critical review of the literature.

Several symptoms of panic disorder mimic those of cardiovascular diseases and patients with this disorder frequently consult physicians with the fear of dying from a heart attack. The salient question is: Can the patient with panic disorder die from the cardiovascular consequences of his/her panic attacks? We critically review the six studies that have examined the association between panic disorder (or panic-like anxiety) and cardiovascular mortality or complications associated with the cardiovascular system. We then briefly review the evidence by which mechanisms panic may be linked to cardiovascular mortality and conclude with proposed guidelines for patient management.

Cardiovascular Diseases↗
PubMed1990

Risk factors for the onset of panic disorder and other panic attacks in a prospective, population-based study.

A total of 383 cases of incident panic attack were identified among 12,823 participants in the Epidemiologic Catchment Area Program over various 12-month periods in 1980-1983. These cases not phobia-stimulated were compared with 766 controls. Risk factors were examined for the onset of panic attacks, with attacks categorized as panic disorder, severe and unexplained panic attacks, or other panic attacks. Risk factors were also examined for the onset of attacks in which cardiovascular symptoms were experienced and those in which psychologic symptoms were experienced. Females were at greater risk than males for each category of attacks (relative odds ranged from 1.36 to 2.25). Persons aged 65 years or older were at lower risk than younger persons (relative odds, compared with 30- to 44-year-olds, ranged from 0.26 to 0.71). A history of cardiac symptoms, shortness of breath, depression or a major grief episode, drug abuse or dependence, alcohol abuse or dependence, and seizures were each strongly associated with panic attacks. A history of cardiac symptoms was more strongly associated with attacks in which cardiovascular symptoms were experienced than with attacks in which psychologic symptoms were experienced (relative odds, 8.36 vs. 2.23). A history of seizures was more strongly associated with attacks with psychologic symptoms than with attacks with cardiovascular symptoms (relative odds, 5.21 vs. 1.58).

Adolescent↗
PubMed1997

Differences in symptom structure between panic attack and limited symptom panic attack: a study using cluster analysis.

We had investigated the clinical characteristics of panic disorder (PD) in a Japanese outpatient population comprised of more than 250 patients diagnosed as having PD during a 13-year study period and observed that some PD patients had both panic attacks (PA) and limited symptom panic attacks (LPA). In the criteria for PD based on the Diagnostic and Statistics Manual of Mental Disorders, third edition-revised (DSM-III-R), episodes involving four or more symptoms are classified as PA, while those involving fewer than four symptoms are described as LPA. Therefore, LPA is identified as part of an episode of PA, since the difference between the two episodes is only in the number of symptoms. However, some recent research suggests that there is a distinct subgroup of individuals who suffer LPA. Using cluster analysis, we investigated the differences between PA and LPA groups in terms of the structures of several panic symptoms, which included anticipatory anxiety, agoraphobia and 13 clinical symptoms based on the DSM-III-R at the time of panic attacks, in 247 patients with PD. Cluster analysis revealed clusters of three and four panic symptoms in the PA group and LPA group, respectively, and there were also differences in symptom structure between the two groups. These results suggest that there may be a subgroup of individuals who show LPA among PD patients.

Adult↗
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↗
PubMed1987

Neurobiological mechanisms of panic anxiety: biochemical and behavioral correlates of yohimbine-induced panic attacks.

The effects of yohimbine, an alpha 2-adrenergic receptor antagonist, on anxiety, blood pressure, heart rate, and plasma levels of the norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) and cortisol were determined in 20 healthy subjects and 68 patients who had agoraphobia with panic attacks or panic disorder. Yohimbine produced panic attacks meeting DSM-III criteria in 37 patients and one healthy subject. The patients reporting yohimbine-induced panic attacks had significantly larger increases in plasma MHPG, cortisol, systolic blood pressure, and heart rate than the healthy subjects. These findings support the hypothesis relating high noradrenergic neuronal activity to the pathophysiology of panic attacks in a subgroup of panic disorder patients.

Adult↗
PubMed1996

Family history of panic disorder and hypersensitivity to CO2 in patients with panic disorder.

OBJECTIVE: The authors investigated the relationships between hypersensitivity to CO2 and familial-genetic risk for panic disorder in patients with panic disorder. METHOD: Morbidity risks for panic disorder were calculated for families of 203 patients with panic disorder, each of whom was challenged with 35% CO2. RESULTS: Patients who reacted with a positive response to the 35% CO2 challenge showed a genetic risk for panic disorder (morbidity risk = 14.4%) that was significantly higher than that for patients who did not react (morbidity risk = 3.9%). CONCLUSIONS: These findings support the idea that hypersensitivity to CO2 might be associated with a subtype of panic disorder specifically related to a greater familial loading.

Adult↗
PubMed2000

Panic: course, complications and treatment of panic disorder.

Panic disorder is a chronic condition typically associated with significant distress and disability. In addition to the acute distress associated with the panic attack itself, the disorder often leads to distressing anticipatory anxiety and phobic avoidance. Affected individuals experience significant impairment in social and vocational functioning, high utilization of medical resources, constriction of function, premature mortality and diminution in overall quality of life. Panic disorder is frequently comorbid with other conditions, particularly depression, as well as alcohol and other substance abuse, and other anxiety disorders including social phobia, generalized anxiety disorder, obsessive-compulsive disorder and post-traumatic stress disorder. A number of pharmacological agents and cognitive-behavioural treatments have been shown to be effective in the treatment of panic disorder, with the selective serotonin reuptake inhibitors (SSRIs) becoming first-line pharmacotherapy for this condition. Among these, the SSRI sertraline appears effective not only in improving symptoms of panic, but also in reducing anticipatory anxiety and improving multiple aspects of quality of life. For patients who remain partly or fully symptomatic despite adequate first-line treatment, a variety of strategies are emerging for the management of refractory conditions. We provide an overview of the prevalence, presentation and associated complications of panic disorder, review the therapeutic options and discuss the management of refractory patients.

Humans↗
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↗
PubMed2004

Clinical features of panic patients sensitive to hyperventilation or breath-holding methods for inducing panic attacks.

Our aim was to compare the clinical features of panic disorder (PD) patients sensitive to hyperventilation or breath-holding methods of inducing panic attacks. Eighty-five PD patients were submitted to both a hyperventilation challenge test and a breath-holding test. They were asked to hyperventilate (30 breaths/min) for 4 min and a week later to hold their breath for as long as possible, four times with a 2-min interval. Anxiety scales were applied before and after the tests. We selected the patients who responded with a panic attack to just one of the tests, i.e., those who had a panic attack after hyperventilating (HPA, N = 24, 16 females, 8 males, mean age +/- SD = 38.5 +/- 12.7 years) and those who had a panic attack after breath holding (BHPA, N = 20, 11 females, 9 males, mean age +/- SD = 42.1 +/- 10.6 years). Both groups had similar (chi(2) = 1.28, d.f. = 1, P = 0.672) respiratory symptoms (fear of dying, chest/pain discomfort, shortness of breath, paresthesias, and feelings of choking) during a panic attack. The criteria of Briggs et al. [British Journal of Psychiatry, 1993; 163: 201-209] for respiratory PD subtype were fulfilled by 18 (75.0%) HPA patients and by 14 (70.0%) BHPA patients. The HPA group had a later onset of the disease compared to BHPA patients (37.9 +/- 11.0 vs 21.3 +/- 12.9 years old, Mann-Whitney, P < 0.001), and had a higher family prevalence of PD (70.8 vs 25.0%, chi(2) = 19.65, d.f. = 1, P = 0.041). Our data suggest that these two groups--HPA and BHPA patients--may be specific subtypes of PD.

Adolescent↗
PubMed1990

[Psychosocial and biological correlates of panic attacks and panic syndrome].

The definition of a separate nosological entity "panic disorder" in the Diagnostic and Statistical Manual of Mental Disorders, 3rd revision (DSM III) of the American Psychiatric Association triggered a flood of empirical research into this disorder. In this article the literature is surveyed to find out to what extent panic attacks and panic disorder bear specific relationships to measurable variables from the psychosocial and biological spheres. The investigated psychosocial variables are: experiences of separation in childhood; separation anxieties in childhood; sociodemographic correlates as they are known from epidemiological studies; personality factors; life events as possible triggering events of periods with panic attacks; and, finally, socalled "cognitive correlates". The results obtained in this field are just as inhomogeneous as they continue to be in the sphere of biological variables. Of these, the following factors are discussed: genetic factors; neurological and psycho-physiological correlates; the problem of mitral valve prolapse; endocrinal correlates and neurotransmitters. Present findings do not supply conclusive evidence either for or against separation of panic attacks from free-floating anxiety. The relationship between panic attacks and depressive disorders is equally unclear if judged on the basis of the results from empirical research which are far from uniform.

Anxiety Disorders↗
PubMed1988

Thyroid hormones in panic disorder, panic disorder with agoraphobia, and generalized anxiety disorder.

Fifty-two patients with generalized anxiety disorder who had symptoms persisting for at least 6 months, 41 patients suffering from either panic disorder (32 patients) or panic disorder with agoraphobia (9 patients), and 14 control subjects were screened for thyroid disease. Total serum thyroxine (TT4), serum-free thyroxine index (FT4I), and triiodothyronine resin uptake (T3RU), were examined for the entire sample, using a one-way analysis of variance (ANOVA). No significant differences were found in TT4 (p = .24), FT4I (p = .24), and T3RU (p = .19). Thyroid-stimulating hormone (TSH) was examined in a subsample of 10 patients with generalized anxiety disorder, 11 with panic disorder or panic disorder with agoraphobia, and 10 controls. One-way ANOVA again showed no significant differences, although there was a trend (p = .07). This is the first report that compares generalized anxiety disorder patients, panic disorder patients, and patients with panic disorder and agoraphobia with controls on measures of thyroid function. It is also the first to report normal values in the thyroid indices of generalized anxiety disorder patients.

Adult↗
PubMed1987

Therapeutic response to phenelzine in patients with panic disorder and agoraphobia with panic attacks.

The therapeutic response to phenelzine sulfate was evaluated during 6 months' treatment of 35 outpatients meeting DSM-III criteria for panic disorder or agoraphobia with panic attacks. The possible influence of nonspecific predictors of drug efficacy and some biochemical parameters were investigated. Therapeutic response was assessed on standardized rating scales. Agoraphobic patients showed a significantly higher frequency of panic attacks when compared to the subjects with uncomplicated panic disorder. Phenelzine treatment blocked panic attacks in 100% of the patients with panic disorder and in 94.7% of the agoraphobics. Anticipatory anxiety and avoidant behavior improved markedly, although not statistically significantly, in 73.6% of the agoraphobics.

Adolescent↗
PubMed2000

Effects of tryptophan depletion on carbon dioxide provoked panic in panic disorder patients.

Results of an earlier study in healthy volunteers suggest that the serotonergic system is involved in anxiety-related mechanisms. We studied the influence of tryptophan depletion on the response to a 35% carbon dioxide challenge. Twenty-four panic disorder patients received a mixture of amino acids, either with or without tryptophan, under double-blind conditions. There was a significant increase in anxiety as well as in neurovegetative symptoms in the depletion group, compared to the placebo condition. Furthermore, when we compare the results of the placebo group with earlier panic provocation studies, it also seems that a balanced amino acid mixture might have a protective effect against a panic provocation. We conclude that the panic-enhancing effect of tryptophan depletion as well as the potential protective effect of tryptophan administration in panic disorder patients can be explained by the Deakin-Graeff theory of anxiety.

Adult↗
PubMed2001

Hyperventilation challenge test in panic disorder and depression with panic attacks.

Our aim was to determine whether panic disorder (PD) patients, major depressive patients without panic attacks (MD) and major depressive patients with panic attacks (MDP) respond similarly to hyperventilation challenge tests. We randomly selected 35 PD patients, 33 MDP patients, 27 MD patients and 30 normal volunteers with no family history of anxiety or mood disorder. The patients had not been treated with psychotropic drugs for at least 1 week. They were induced to hyperventilate (30 breaths/min) for 4 min, and anxiety was assessed before and after the test. A total of 16 (45.7%) PD patients, 12 (36.4%) MDP patients, four (11.1%) MD patients, and two (6.7%) normal volunteers had a panic attack after hyperventilating. The PD and MDP patients were significantly more responsive to hyperventilation than the MD patients and the normal volunteers. The MD patients had a significantly lower heart-rate response to the test than all the other groups. There is growing evidence that PD patients are more sensitive to the vasoconstrictive effects on basilar arterial blood flow caused by hyperventilation-induced hypocapnia than are comparison subjects. Our data suggest that there is an association between panic attacks and hyperreactivity to an acute hyperventilation challenge test.

Adult↗