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PubMed1995

Panic attacks and panic disorder: the great neurologic imposters.

Patients who experience panic attacks, panic disorder, or agoraphobia have significant impairment associated with their disorders. The cost to society in health care costs as well as the human suffering and mortality is high and may be even higher than necessary because of misdiagnosis and inadequate treatment of these patients. Although we do not have many answers in the areas of pathophysiology or neurochemistry of panic disorder, we do have effective treatments for panic disorder and agoraphobia. If these are conceptualized as distinct disorders with specific symptoms, making a diagnosis of panic disorder or agoraphobia is relatively easy. Making the correct diagnosis may save the patient many months or years of suffering and many inappropriate tests or treatments.

Agoraphobia↗
PubMed1994

Relationship of panic, anticipatory anxiety, agoraphobia and global improvement in panic disorder with agoraphobia treated with alprazolam and exposure.

In a controlled trial of alprazolam and exposure in 154 patients with panic disorder with agoraphobia, relations between panic, anticipatory anxiety, and phobic avoidance were examined. The three symptoms were independent of one another at baseline and improved largely independently during treatment; only early improvement in avoidance predicted global improvement after treatment. Global improvement was more related to reduction of avoidance than a decrease in panics. Panic was not a valuable outcome measure in panic disorder with agoraphobia.

Adult↗
PubMed1996

[From inducers of panic attack to neurobiology of panic disorder].

Various provocative agents, including sodium lactate, carbon dioxide (CO2), caffeine, yohimbine and cholecystokinin (CCK), have been utilized as panicogenics in studies on healthy volunteers as well as in panic disorder patients. Most provocative agents are lacking in specificity, limiting their use in identifying neurotransmitter systems involved in panic attacks. CCK appears to offer several advantages over other challenge strategies since it is a putative neurotransmitter in the CNS, with its own neuronal pathways and receptors, and reliably provokes panic attacks in a dose-dependent manner. It is important to clarify the relationships between CCK and other neurotransmitter systems in order to further understand the neurobiology of panic disorder. The possible roles of some of these neurotransmitters in panic disorder are discussed in this review.

Arousal↗
PubMed1989

Electroencephalographic sleep in panic disorder. A focus on sleep-related panic attacks.

Sleep electroencephalograms were studied in 13 patients with panic disorder, six of whom experienced panic from sleep, and seven controls. Sleep was disturbed in the patients, as manifested by increased sleep latency, decreased sleep time, and decreased sleep efficiency. Rapid eye movement (REM) latencies were not reduced in the patient group. All six of the panic awakenings were preceded by non-REM sleep, which could be further characterized as a transition from stage II toward delta sleep. The overall degree of sleep disturbance (ie, sleep latency, sleep efficiency) did not appear to be influenced by the occurrence of sleep panic. There was also an association of increased REM latency with nights of sleep panic.

Adult↗
PubMed2006

The epidemiology of panic attacks, panic disorder, and agoraphobia in the National Comorbidity Survey Replication.

CONTEXT: Only limited information exists about the epidemiology of DSM-IV panic attacks (PAs) and panic disorder (PD). OBJECTIVE: To present nationally representative data about the epidemiology of PAs and PD with or without agoraphobia (AG) on the basis of the US National Comorbidity Survey Replication findings. DESIGN AND SETTING: Nationally representative face-to-face household survey conducted using the fully structured World Health Organization Composite International Diagnostic Interview. PARTICIPANTS: English-speaking respondents (N=9282) 18 years or older. MAIN OUTCOME MEASURES: Respondents who met DSM-IV lifetime criteria for PAs and PD with and without AG. RESULTS: Lifetime prevalence estimates are 22.7% for isolated panic without AG (PA only), 0.8% for PA with AG without PD (PA-AG), 3.7% for PD without AG (PD only), and 1.1% for PD with AG (PD-AG). Persistence, lifetime number of attacks, and number of years with attacks increase monotonically across these 4 subgroups. All 4 subgroups are significantly comorbid with other lifetime DSM-IV disorders, with the highest odds for PD-AG and the lowest for PA only. Scores on the Panic Disorder Severity Scale are also highest for PD-AG (86.3% moderate or severe) and lowest for PA only (6.7% moderate or severe). Agoraphobia is associated with substantial severity, impairment, and comorbidity. Lifetime treatment is high (from 96.1% for PD-AG to 61.1% for PA only), but 12-month treatment meeting published treatment guidelines is low (from 54.9% for PD-AG to 18.2% for PA only). CONCLUSION: Although the major societal burden of panic is caused by PD and PA-AG, isolated PAs also have high prevalence and meaningful role impairment.

Adolescent↗
PubMed2003

Nocturnal panic: biology, psychopathology, and its contribution to the expression of panic disorder.

The latest studies on psychopathology and biology of nocturnal (or sleep) panic attacks and other findings related to sleep in panic disorder are reviewed. While some of the newer articles doubt that nocturnal panics present a more severe variation of panic disorder, older studies and some newer articles support this notion. Some studies suggest that nocturnal panic maybe also be associated with other, more severe pathology. This interesting syndrome, or variant of disorder, may have its own etiology, psychopathology, and underlying biology.

Adult↗
PubMed1994

Pentagastrin induced panic attacks: enhanced sensitivity in panic disorder patients.

The effects of pentagastrin, a synthetic analogue of the cholecystokinin tetrapeptide (CCK4), were studied in 15 patients with panic disorder and 15 healthy controls. Three different intravenous dosages of pentagastrin (0.1, 0.3 and 0.6 microgram/kg) and saline were investigated. Subjects were randomly allocated to two of the four treatment groups and tested on two separate occasions, 1 week apart, using an unbalanced double-blind incomplete block design. The mean panic rate with pentagastrin was 55% (12/22) for patients and 5% (1/22) for controls. None of the subjects panicked with saline. The frequency of panic attacks between the three pentagastrin doses in patients was not different. One control subject had a panic-like attack at the highest dose of pentagastrin. These findings concur with previous studies on the panicogenic effect of CCK4 and pentagastrin and suggest a greater sensitivity for CCK receptor agonists in patients suffering from panic disorder than in healthy controls.

Adult↗
PubMed2006

Panic attacks, panic disorder, and agoraphobia: associations with substance use, abuse, and dependence.

Anxiety and substance use disorders frequently co-occur. Despite the clinical importance of this co-occurrence, theory and research addressing the relations between anxiety-substance use disorder comorbidity remain limited. The present commentary is intended to briefly review and summarize key aspects of this literature, with a specific focus on panic-spectrum psychopathology (panic attacks, panic disorder, and agoraphobia) and its associations with tobacco, alcohol, and marijuana use, abuse, and dependence. A heuristic theoretical model for better understanding the panic-substance use relations also is offered. Extant data suggest clinically meaningful bidirectional associations are evident between panic problems and premorbid risk factors for such problems and various forms of tobacco, alcohol, and marijuana use. Key clinical implications and future directions are outlined based upon the review.

Agoraphobia↗
PubMed1989

Provocation of panic: three elements of the panic reaction in four anxiety disorders.

Subjects with agoraphobia (N = 25), panic disorder (N = 25), social phobia (N = 19) or generalized anxiety disorder (N = 10) and controls with no psychiatric history (N = 16) underwent two provocation tests, voluntary hyperventilation and inhalation of 5% CO2 in air, and three experimental control conditions. They were measured on three elements of the panic reaction: somatic symptoms, psychic anxiety and fears of impending doom, and on a standard YES/NO measure of panic attack. The provocation conditions produced increased somatic symptoms and psychic anxiety across all groups relative to the control conditions. The agoraphobic and panic disorder groups showed a significantly greater increase in fears of impending doom from control to provocation conditions than the social phobic and GAD patients. This difference was not observed on measures of somatic symptoms or psychic anxiety. The present results provide some support for the theory that panic attacks result from the catastrophic misinterpretation of anxious symptoms, in this case produced by the two provocation tests.

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↗
PubMed1994

Exposure reduced agoraphobia but not panic, and cognitive therapy reduced panic but not agoraphobia.

Earlier studies showed that cognitive therapy has anti-panic effects and exposure has anti-agoraphobic effects while other studies suggest that agoraphobia is a secondary complication of panic disorder. It was therefore hypothesized that cognitive therapy not only reduces panic but also agoraphobia and that it potentiates the effects of exposure in vivo. Two groups of 12 severe agoraphobics were treated with 4 sessions of cognitive therapy followed by 8 sessions of cognitive therapy combined with in vivo exposure. The other 12 received 4 sessions of 'associative therapy', a presumably inert treatment that controls for therapist attention, followed by 8 sessions of in vivo exposure that was framed in common behavioral terms. The initial cognitive therapy produced a significant reduction in panic frequency, while associative therapy did not affect panic. Neither cognitive therapy alone, nor associate therapy alone significantly reduced depression, state or trait anxiety, self-rated agoraphobia or behavioral avoidance. After adding exposure however, these parameters were clearly and significantly reduced. Cognitive therapy did not potentiate exposure effects. The results are discussed.

Adult↗
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↗
PubMed2006

Panic and avoidance in panic disorder with agoraphobia: clinical relevance of change in different aspects of the disorder.

Different aspects of change were examined in 62 patients who fulfilled the DSM-IV criteria for a primary diagnosis of panic disorder with agoraphobia of moderate to severe magnitude, and who were treated with 16 sessions of behavioral therapy. The treatment resulted in substantial effects on panic attacks and agoraphobic avoidance. Panic-free status only differentiated the patients regarding mood at pre- and post-treatment. Changes in panic and avoidance were related to each other, but change in avoidance was more related to change in negative affect. Change in quality of life (QOL) was also more associated with change in avoidance at post-treatment. At follow-up change in QOL was more related to change in panic than change in avoidance.

Agoraphobia↗
PubMedDate not supplied

A test of the cognitive model of panic: primed lexical decision in panic disorder.

The aim of the present study was to investigate whether individuals with panic disorder are characterised by an enhanced tendency to associate particular somatic sensations with threatening outcomes, compared with nonclinical controls. In order to test this prediction, a modified lexical decision task was employed. Panic disorder subjects and nonclinical control subjects made lexical decisions to neutral word pairs and threatening word pairs. Threatening word pairs consisted of combinations of somatic sensations and catastrophic outcomes (e.g., breathless-suffocate), which have been shown to be of salience to individuals with panic disorder. Semantic priming was found for both neutral and threatening word pairs, but was demonstrated equally by panic disorder subjects and nonclinical controls. The results did not provide support for cognitive models of panic disorder.

Cognition↗
PubMed1999

Panic disorder and memory: does panic disorder result from memory dysfunction?

It is proposed that patients with panic disorder have a defect in fear-relevant episodic memory, and their panic attacks arise from automaticity in recollecting fear-relevant emotional-autonomic cluster. The cluster as a component of fear appears to have been dissociated from cognitive structure (episodic or informative memory trace) or from "information structure". A special method was created for testing this hypothesis where 30 panic disorder patients, 12 healthy controls, and 32 patients with other psychiatric diagnoses were asked to recall and describe a fearful experience. None of the patients in the panic disorder group could recall any fearful event or episode in their past. All but one subject among healthy controls and all the subjects in the non-panic group could recall one or more fearful event or episode. Possible theoretical implications of these results are discussed in the context of some classical concepts.

Adolescent↗
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↗
PubMed1994

Remission and relapse in subjects with panic disorder and panic with agoraphobia: a prospective short-interval naturalistic follow-up.

This article reports on the course of uncomplicated panic disorder and panic with agoraphobia on 309 patients participating in the Harvard/Brown Anxiety Research Project, a prospective longitudinal study of patients with DSM-III-R-defined anxiety disorders. At 1 year, there was a .39 probability of full remission for uncomplicated panic disorder and a .17 probability of full remission for panic disorder with agoraphobia Similar differences in time to remission for these syndromes were still found when criteria for remission were made less stringent. However, even requiring less improvement for remission left a large percentage of subjects in an episode, and for those that remitted, relapse occurred quickly, indicating a chronic and recurrent course of illness. This is the first longitudinal, prospective, naturalistic study on a large cohort of subjects with anxiety disorders to have regular, structured, short-interval follow-up. Our results are consistent with the view that panic disorder has a chronic course with high rates of relapse after remission and longer episodes when agoraphobia is a part of the constellation of symptoms.

Adult↗
PubMed2002

Agoraphobia without a history of panic disorder may be part of the panic disorder syndrome.

Agoraphobia without a history of panic attacks is a disorder lacking strong support. Data from the Australian National Survey were explored in respect to panic disorder with or without agoraphobia (PDA, PD), and agoraphobia without a history of panic disorder (AG). Panic disorder, agoraphobia, and panic disorder with agoraphobia occurred in 3.5% of the adult population. People with this group of disorders were more likely to be female and more likely to seek help than people with other anxiety disorders. Significant anxiety symptoms and unease about safety when out and about occur in all three disorders. People with the double disorder PDA report more comorbid disorders, are more disabled, and have higher neuroticism scores than people with PD or AG. People with AG are older and consult less than people with PD or PDA. Agoraphobia has been devalued as a cause of human suffering. This idea is wrong. Agoraphobia is as common, comorbid, and disabling as PD, but less disabling than the double disorder of PDA.

Adolescent↗