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PubMed1997

Paroxetine increases heart rate variability in panic disorder.

Panic patients have decreased heart rate variability, a risk factor for sudden cardiac death, and increased rates of cardiac death and stroke. Imipramine has been found to further reduce heart rate variability in panic. This study uses power spectral analysis to compare autonomic components of heart rate variability in 16 unmedicated control subjects and 17 panic patients before and after treatment with paroxetine at 20 mg/day for 4 weeks. Patients had higher predrug reclining and standing sympathetic activity than control subjects. After drug, patients' total sympathetic activity decreased. Predrug patients failed to increase sympathetic activity on orthostasis, lacking the normal baroreflex response found in control subjects. After drug, patients normalized this sympathetic component of the baroreflex response. Before drug, patients' parasympathetic reclining and standing activity did not differ from control subjects, and patients showed the normal orthostatic parasympathetic decrease. After drug, patients' total parasympathetic activity increased, whereas the baroreflex response was preserved. Nine medicated patients had more than a 50% reduction of panic attacks. In view of paroxetine's increase of heart rate variability, potential benefits of selective serotonin reuptake inhibitors in decreasing cardiac mortality in panic disorder are discussed.

Adult↗
PubMed1993

The diagnosis and treatment of panic disorder.

Panic attacks and panic disorder often first present in the emergency room or to the family practitioner. The presentation and differential diagnosis of this disabling disorder are described in this review, together with the etiology and health effects of the syndrome. Both medication and psychological treatments are described, as are the indications, side effects, and expected outcome for each therapy alone and in combination.

Combined Modality Therapy↗
PubMedDate not supplied

Management of panic disorders.

Panic disorders are medical conditions requiring an eclectic treatment approach that often combines pharmacotherapeutics with education, cognitive-behavior therapy, and psychodynamic therapy. This article focuses on the management of medication within this framework. The medications that have been found to be effective include tricyclic antidepressants, fluoxetine, monoamine oxidase inhibitors, and higher potency benzodiazepines. Although alprazolam is the most studied medication and acts very rapidly, each type of medication has unique advantages and liabilities. The general treatment strategy with all the medications is to start with a low dose and increase it slowly until side effects develop or panic attacks cease. The treatment approach should be oriented toward a chronic illness that often requires long-term medication.

Humans↗
PubMed2003

Association of an exonic LDHA polymorphism with altered respiratory response in probands at high risk for panic disorder.

Panic disorder (PD) is a clinical syndrome characterized by recurrent discrete episodes of fear accompanied by a variety of physiological and psychological symptoms, often with prominent respiratory components. A series of clinical observations has led some investigators to hypothesize that subtle alterations in ventilatory regulation are integral to at least a subtype of PD. In order to identify genetic factors that might predispose individuals to these alterations in ventilatory response, we conducted single stranded conformation polymorphism analysis across the exons of the lactate dehydrogenase A and B genes (LDHA and LDHB) using DNA prepared from 86 subjects previously characterized by respiratory response to a CO(2) challenge with a variable genetic loading for PD. Remarkably, a single conserved LDHA exon 5 haplotype conferred increased risk for a paradoxical ventilatory response pattern to CO(2) inhalation which robustly separated well subjects at high risk for PD from low-risk control subjects. But, comparison of LDHA exon 5 genotypes in PD probands (n = 25) to that of random newborn controls (n = 182) did not demonstrate any significant differences. Given the pivotal role of LDH in the metabolism of lactate, a known inducer of panic attacks, and the dependence of LDH activity on cell pH, we suggest that LDHA polymorphisms may contribute to the variability to CO(2) respiratory challenge.

Adolescent↗
PubMed1994

Alcohol and depression in panic disorder.

Panic disorder (PD) is a common psychiatric illness, which has many complications such as major depression, increased suicide risk, agoraphobic avoidance behaviour, alcohol abuse and dependence. A number of studies have now documented increased rates of anxiety disorders among alcoholics and of alcoholism among patients presenting with anxiety disorders. In general, it appears that PD is more prevalent in alcoholics than would be expected on the basis of general population rates. Alcohol withdrawal is clearly associated with severe anxiety symptoms. It is suggested that repeated withdrawal episodes may trigger panic through a kindling process by causing subconvulsive stimuli with increasing amounts of electrical excitability or even spontaneous seizures. Serotonergic medications are effective in treating PD and depression. They also diminish interest in drinking in ethanol-dependent patients. Serotonergic agents can also affect conditioning and learning as well as behavioral control and self-administration. The treatment of panic patients with depressive and alcohol problems usually requires long-term treatment.

Alcohol Withdrawal Delirium↗
PubMed1988

Human corticotropin releasing hormone: clinical studies in patients with affective disorders, alcoholism, panic disorder and in normal controls.

1. The 41 amino acid peptide human corticotropin releasing hormone (h-CRH) and its ovine analogue o-CRH are regulators of proopiomelanocortin (POMC) derived neuropeptides and neurosteroids of the limbic-hypothalamic-pituitary-adrenocortical (LHPA) axis such as beta-endorphin, corticotropin (ACTH) and corticosteroids modulating concomitantly hormonal and behavioral systems in animal and man, e.g. adaptation to stress. 2. Challenge tests employing h-CRH stimulation with or without different kinds of pretreatment in affective disorders, alcoholism, and panic disorder demonstrate LHPA alterations that are induced by dysregulations in the limbic area. In depression, the enhanced secretory activity of pituitary corticotrophs or altered feedback regulation is compatible with endogenous CRH hypersecretion followed by enhanced production of proopiomelanocortin whose fragments activate synthesis and release of adrenal corticosteroids. These effects are accompanied by development of a functional hyperplasia of the adrenocortex and/or down-regulation of pituitary CRH-receptors and/or reduced negative feed back capacity of limbic glucocorticoid receptor containing neurones particularly in the hippocampus. Similar disturbances are found in hypercortisolemic patients withdrawn from alcohol and are less pronounced in patients with panic disorder. 3. Repetitive h-CRH administration to normal controls induces sleep-EEG and neuroendocrine effects resembling those in depression. 4. Adrenocortical hormones act back on neurotransmitter/receptor sites of brain systems relevant for neuropharmacoloy (e.g. GABA receptor activity in anxiety disorders and affective disorders). 5. The neuroendocrine approach to the LHPA axis is of value to uncover several aspects of pathology underlying various psychiatric diseases.

Adrenocorticotropic Hormone↗
PubMed1992

Psychopharmacological treatment of panic disorder.

Panic disorder is a serious, often chronic condition that warrants vigorous treatment. The benzodiazepines, particularly the high-potency compounds alprazolam and clonazepam, provide prompt relief, often with few side effects. Tricyclic antidepressants and monoamine oxidase inhibitors are also effective, although patient acceptance may be limited by a slower response and side effects that mimic some symptoms of panic attacks. The author suggests strategies for the most effective use of these agents.

Adult↗
PubMed1986

Pharmacological treatment of panic disorder.

Panic disorder has recently been recognized as a distinct sub-type of anxiety which may occur with or without phobic avoidance. Controlled prospective trials have demonstrated the efficacy of the tricyclic antidepressants and monoamine oxidase inhibitors in the treatment of this disorder. The use of benzodiazepines and beta-blockers has been more controversial. Some preliminary studies assessing other pharmacological agents are available. Methodological problems limit the conclusions which may be drawn from available data.

Anti-Anxiety Agents↗
PubMed2005

Dysfunctional beliefs in panic disorder: The Panic Belief Inventory.

The Panic Belief Inventory (PBI) was developed to assess beliefs that increase the likelihood of catastrophic reactions to physical and emotional experiences in panic disorder. In the first stage of scale development, 197 panic disorder patients completed the PBI and standard self-report inventories of psychiatric symptomatology. An exploratory factor analysis yielded a 4-factor solution from which a 35-item instrument with 4 scales was constructed. The shortened measure and its scales had good internal consistency and convergent validity and moderate discriminant validity. Subsequently, 22 panic disorder patients who received cognitive therapy completed the PBI and other self-report inventories of dysfunctional cognitions at intake, 4 weeks, 8 weeks, termination, and several follow-up intervals. Results indicated that the PBI decreased significantly across treatment, with the largest decline occurring between intake and 4 weeks into treatment. The PBI correlated more strongly with dysfunctional cognitions associated with anxiety than dysfunctional cognitions associated with depression. These results provide preliminary evidence that the PBI has adequate psychometric characteristics, is useful to assess change in dysfunctional beliefs during treatment, and has the potential to advance cognitive theories of panic.

Adult↗
PubMed2004

Heart rate variability in coronary artery disease patients with and without panic disorder.

Panic disorder (PD) and coronary artery disease (CAD) often co-occur, and CAD patients with comorbid PD suffer greater cardiovascular morbidity and mortality relative to CAD patients without PD. However, the mechanisms underlying these associations are still unknown. Reduced heart rate variability (HRV), a non-invasive measure of cardiac autonomic modulation, is an important predictor of adverse cardiac events. Interestingly, reduced HRV has been observed in patients with panic-like anxiety and PD, as well as in various CAD populations. However, the extent to which HRV is altered in patients with both PD and CAD is unknown. This study evaluated HRV in 42 CAD patients with (n=20) and without (n=22) PD. Patients underwent 48-h electrocardiographic monitoring. Power spectral analysis of HRV indicated that CAD patients with PD exhibited significantly lower LF/HF ratios, which may reflect lower sympathetic modulation, compared with non-PD patients. Additionally, total power in PD patients was made up of a significantly higher proportion of HF power and a significantly lower proportion of VLF power than in non-PD patients. No other significant differences in HRV indices were observed. Results suggest that contrary to what has been observed in the majority of PD-only and CAD-only populations; patients with both PD and CAD appear to exhibit lower sympathetic modulation during ordinary daily life conditions. Though preliminary, these findings suggest that changes in HRV may not be the mechanism underlying greater cardiovascular morbidity and mortality among CAD patients with PD.

Activities of Daily Living↗
PubMed1984

Psychophysiological factors in panic disorder.

Panic disorder patients were compared with normal subjects during intravenous infusion of sodium lactate, isoproterenol, and placebo. Panic attacks meeting the criteria of the Diagnostic and Statistical Manual, vol. 3 [American Psychiatric Association, 1980] occurred during all three conditions in patients and during the lactate and isoproterenol infusions in normals. Patients had significantly higher average levels of skin conductance, heart rate and state anxiety, and significantly lower finger temperatures compared to normal subjects. However, no measure reliably differentiated panic attacks from nonattack periods. It is concluded that the peripheral physiologic responses investigated are neither necessary nor sufficient for the occurrence of panic attacks. It is possible that reports of these attacks represent phobic responses to intense anxiety.

Anxiety Disorders↗
PubMed1986

Effects of one night's sleep deprivation on mood and behavior in panic disorder. Patients with panic disorder compared with depressed patients and normal controls.

The effects of one night's sleep deprivation on mood and behavior were evaluated in 12 patients with panic disorder, ten depressed patients, and ten controls. In contrast to the improvement in symptoms of anxiety and depression shown by the majority of depressed patients, the response of patients with panic disorder as a group did not differ from that of normal controls, although a subgroup did experience noticeable worsening in their symptoms of anxiety, with 40% experiencing panic attacks on the day following sleep deprivation. Electroencephalographic recordings with nasopharyngeal electrodes on the day following sleep deprivation were normal, further suggesting that patients with panic disorder do not have seizure activity characteristic of temporal lobe epilepsy.

Adult↗
PubMed2001

A twin study of generalized anxiety disorder symptoms, panic disorder symptoms and post-traumatic stress disorder in men.

Generalized anxiety disorder (GAD), panic disorder (PD) and post-traumatic stress disorder (PTSD) often co-occur. We investigated whether and to what degree genetic and environmental contributions overlap among symptoms of GAD, symptoms of PD and PTSD. Subjects were 3327 monozygotic and dizygotic male-male twin pair members of the Vietnam Era Twin Registry who participated in a 1992 telephone administration of the Diagnostic Interview Schedule Version 3 Revised (DIS3R). Genetic model fitting was performed to estimate the magnitude of genetic and environmental contributions to the lifetime co-occurrence of GAD symptoms, PD symptoms and PTSD. The liability for GAD symptoms was due to a 37.9% additive genetic contribution common to PD symptoms and PTSD. Liability for PD symptoms was due to a 20.7% additive genetic contribution common to GAD symptoms and PTSD, and a 20.1% additive genetic influence specific to PD symptoms. Additive genetic influences common to symptoms of GAD and PD accounted for 21.3% of the genetic variance in PTSD. Additive genetic influences specific to PTSD accounted for 13.6% of the genetic variance in PTSD. Remaining variance for all three disorders was due to unique environmental factors both common and specific to each phenotype. These results suggest that these disorders each have etiologically distinct components and also have significant genetic and unique environmental contributions in common.

Adult↗
PubMedDate not supplied

Quality of life in anxiety disorders: a comparison of obsessive-compulsive disorder, social anxiety disorder, and panic disorder.

BACKGROUND: There is growing recognition that the anxiety disorders are disabling disorders associated with substantial morbidity and impaired quality of life (QOL). Nevertheless, there have been few studies comparing QOL across these conditions. SAMPLING AND METHODS: 337 outpatients with obsessive-compulsive disorder (OCD; n = 220), panic disorder (PD; n = 53), or social anxiety disorder (SAD; n = 64) were compared using a number of assessment scales to compare objective and subjective impairment in QOL. The association of QOL with symptom severity and comorbid depression was also assessed. RESULTS: The extent of impairment due to OCD, PD or SAD appears to be similar across the QOL scales. However, various domains are differentially affected in each of the disorders; OCD patients had more impairment in family life and activities of daily living; SAD patients had more impairment in social life and leisure activities, and PD patients were less able to avoid the use of nonprescribed drugs. QOL was lower in patients with increased symptom severity as well as in those with comorbid depression. CONCLUSIONS: While the extent of impairment appears similar across a number of different anxiety disorders, characteristic symptoms of each disorder may be associated with differential impairment of various domains of function, and may require specifically tailored interventions.

Activities of Daily Living↗
PubMed1992

[Panic disorder].

Panic episodes were described as a distinct form of anxiety by Freud almost 100 years ago, and the recent publication of the Diagnostic and Statistical Manual of Mental Disorders, third edition (D.S.M.-III), has provided the basis for the separate diagnostic entity of panic disorder. In this study, we showed the historical review of research and the result of our clinical study of panic disorder in 7 patients. The following results were obtained: 1) Abnormal DSTs were observed in only two of 5 patients. 2) Five of 6 patients showed high concentration of adrenaline and noradrenaline in urine. 3) Anxiety was provoked by caffeine in two of 5 patients. 4) Depression of T-wave was shown in three of 5 patients with orthostatic E.C.G. 5) Sinus tachycardia was gained in one of 3 patients with Holter E.C.G. 6) Abnormal respiratory functions were observed in all two patients with Treadmill. 7) Only one small heart was observed on a chest radiograph. 8) Panic attacks were provoked by sodium lactate infusion in four of 7 patients.

Electrocardiography↗
PubMedDate not supplied

Correlates of DSM-III personality disorder in panic disorder and agoraphobia.

One hundred eighty-seven patients meeting DSM-III criteria for panic disorder (n = 26) or agoraphobia with panic (n = 161) were assessed with the Personality Diagnostic Questionnaire (PDQ), a self-rating scale designed to assess Axis II personality disorders and traits. Results replicated our earlier findings of a preponderance of dependent, avoidant, and histrionic features and the finding that patients exhibiting a greater number of personality traits were also significantly more symptomatic. Patients with the diagnosis of panic disorder did not differ on any personality disorder variables from patients with the diagnosis of agoraphobia with panic. Furthermore, none of the specific symptom dimensions, i.e., panic, anxiety, or agoraphobia, was selected as a unique predictor of any personality variables in the regression analyses. Rather, the most important correlates of personality disorder in these patients consisted of general factors such as dysphoric mood, social phobia, or interpersonal sensitivity, and Eysenck's neuroticism dimension. The results are discussed in light of recent findings suggesting a nonspecific link between panic disorder or agoraphobia and personality disorder.

Adult↗
PubMed2002

Recollections of parent-child relationships in patients with obsessive-compulsive disorder and panic disorder with agoraphobia.

OBJECTIVE: In previous studies, patients with different psychiatric conditions, as compared with matched controls, have reported that their parents were more protective and less caring towards them when they were children. However, studies investigating associations between parental behaviours and anxiety disorders have yielded inconsistent results. The aim of this study was to compare recalled parental behaviours in out-patients with obsessive-compulsive disorder (OCD), in out-patients with panic disorder with agoraphobia (PDA), and in non-anxious controls. METHOD: The sample included 43 out-patients with OCD, 38 with PDA, and 120 controls. Participants completed the Parental Bonding Instrument and the Egna Minnen Beträffande Uppfostran or Own Memories of Parental Rearing Experiences in Childhood. RESULTS: No differences were found between the two anxious groups. However, compared with the control group, anxious patients recalled their parents as more protective. CONCLUSION: Our findings suggest that child rearing practices such as overprotection may be a risk factor in the development of anxiety disorders.

Adult↗
PubMedDate not supplied

Life events and the 1-year prevalence of major depressive episode, generalized anxiety disorder, and panic disorder in a community sample.

A community survey was conducted in Edmonton, Alberta, Canada, in which 3,070 respondents completed the Diagnostic Interview Schedule (DIS) and the Life Events Scale (LES) of Paykel. During the year before the interview, there were 222, 234, and 38 cases of major depressive episode (MDE), generalized anxiety disorder (GAD), and panic disorder (PD), respectively, where individuals may have had more than one disorder. It was not possible to time the onset of the disorder relative to the occurrence of life events, and so correlations, no casual relationships, were examined. The LES score showed an increasing trend across disorder categories defined as follows: MDE and GAD both absent; MDE absent and GAD present; MDE present and GAD absent; and MDE and GAD both present. A similar trend was observed for most of the LES subscales studied, but only in the case of events classified as "entrance," "undesirable," and "marital" was there statistical significance. The results suggest that stressful life events are correlated with both MDE and GAD, that individuals with MDE only tend to have a greater burden of stressful events and comorbid disorders than persons with GAD only, and that the presence of both disorders is associated with an even greater level of stress and number of comorbid disorders. The similar patterns across LES subscales suggest that MDE and GAD are not related to specific types of live events, at least not those covered by the LES questionnaire.

Adaptation, Psychological↗