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At least 145 records · Page 8Linked to original sources
PubMed2005

Prediction of panic response to a respiratory stimulant by reduced orbitofrontal cerebral blood flow in panic disorder.

OBJECTIVE: Lack of appropriate top-down governance by frontal cortical regions over a hypersensitive amygdala-centered fear neurocircuitry has been hypothesized to be central in the pathophysiology of panic disorder. The aim of this study was to examine regional cerebral blood flow changes in response to anxiety/panic provocation in subjects with panic disorder and healthy comparison subjects. METHOD: Quantitative water method positron emission tomography was used to obtain brain images of five untreated subjects with panic disorder and five healthy comparison subjects before and during anxiogenic challenge with intravenous doxapram, an acute respiratory stimulant. RESULTS: Baseline perfusion of the orbitofrontal cortex predicted panic attacks: lower perfusion was associated with heightened anxiety in response to doxapram challenge. CONCLUSIONS: The orbitofrontal cortex may be important in the regulation of responding to fear and is a potential area of aberrant functioning in panic disorder.

Adult↗
PubMed1988

Preliminary report of a community survey of panic attacks and panic disorder.

This study looked at the prevalence of panic attacks and panic disorder in a British population. Three thousand people (aged 18-65) registered with a Leicester general practice were sent a postal questionnaire which screened for panic attacks. Where appropriate this was followed by a diagnostic interview. Preliminary results are reported for the first 1500 subjects sampled. Panic attacks are a common experience in the study population (7.5% of responders experienced them around the time of the interview). Panic disorder was diagnosed in about 3% of responders.

Adult↗
PubMed1989

Alprazolam, propranolol, and placebo in the treatment of panic disorder and agoraphobia with panic attacks.

Fifty-five patients completed a 5-week double-blind study comparing alprazolam, propranolol, and placebo in the treatment of panic disorder and agoraphobia with panic attacks. There was no concomitant behavioral treatment. Patient and therapist rating scales included Sheehan's Panic and Anxiety Attack Scales, the Marks-Sheehan Phobia Scale, the Hamilton Anxiety Scale, the Hamilton Depression Scale, and the Side Effects Checklist. The results generally support the efficacy of alprazolam, but not propranolol, in the treatment of panic disorder and agoraphobia with panic attacks. The significance of the results are discussed, as well as a number of the unique aspects of our procedures and patient population.

Adolescent↗
PubMed1986

Clonazepam blockade of spontaneous and CO2 inhalation-provoked panic in a patient with panic disorder.

A 30-year-old woman with panic disorder and phobic avoidance responded partially to treatment with alprazolam but recovered fully while receiving clonazepam, which blocked her panic attacks and anticipatory anxiety. Before treatment, the patient underwent a carbon dioxide inhalation test as a challenge and sustained a full-featured panic attack. After clonazepam therapy and retesting under identical conditions, no panic attack was reported. This is the first report of provoked panic blocked by clonazepam, a putative, clinically effective antipanic agent.

Adult↗
PubMed1996

[Panic attacks with cycloleptic course--differential diagnostic considerations in differentiating panic disorder from epileptic anxiety attacks].

This paper reports on a patient suffering from panic-attacks. A therapy with antidepressants and benzodiazepines was ineffective. The panic-attacks had a short duration and a cycloleptic course. Under the treatment with carbamazepine panic attacks improved. The differential diagnosis of panic disorder and epileptic panic attacks is discussed.

Anticonvulsants↗
PubMedDate not supplied

Non-fearful panic disorder: a variant of panic in medical patients?

Is it possible to have panic attacks without fear? Beitman et al. reported that 32%-41% of panic disorder (PD) patients seeking treatment for chest pain have non-fearful panic disorder (NFPD). To replicate and extend this work on NFPD, the authors compared NFPD patients (N = 48), PD patients (N = 60), and No-PD patients (N = 333) at the time of an emergency department visit and follow-up approximately 2 years later. The authors compared comorbid Axis I diagnoses, panic attack symptoms, and scores on self-report measures. A significantly greater proportion of PD patients had comorbid generalized anxiety disorder and agoraphobia than NFPD patients. NFPD patients had self-report scores that were between no-PD and PD patients or similar to no-PD patients, with the exception of the Beck Depression Inventory. At follow-up, NFPD patients, like PD patients, were still symptomatic and had either not improved or had worsened according to scores on all self-report measures. NFPD should be recognized as a variant of PD, both because of its high prevalence in medical settings and its poor prognosis.

Adult↗
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↗
PubMed1986

Carbon dioxide sensitivity in panic anxiety. Ventilatory and anxiogenic response to carbon dioxide in healthy subjects and patients with panic anxiety before and after alprazolam treatment.

One hypothesis that could account for the anxiogenic response to breathing air supplemented with carbon dioxide seen in panic anxiety patients is that panic patients might have abnormally high central medullary chemoreceptor sensitivity. Chemoreceptor sensitivity was assessed by using a rebreathing technique to measure the ventilatory response to CO2 in 14 medication-free patients with agoraphobia and panic attacks and 23 healthy subjects. Ventilatory response to CO2 was similar in patients and controls (mean +/- SEM, 1.58 +/- 0.16 vs 1.58 +/- 0.14 L/min/mm Hg), suggesting that abnormal chemoreceptor sensitivity does not explain the behavioral sensitivity of panic patients to CO2. Anxiety ratings increased markedly during rebreathing both in patients and controls; anxiety increases were significantly greater in patients than in healthy subjects matched for age, sex, and rebreathing duration. Alprazolam treatment in eight patients markedly attenuated anxiety increases during rebreathing. Differences in anxiogenic sensitivity to CO2 between patients and controls may be due to differences in the regulation of noradrenergic or other neuronal systems.

Adult↗
PubMed1997

Panic disorder versus panic disorder with major depression; defining and understanding differences in psychiatric morbidity.

The present study examined the impact of comorbid major depressive disorder (MDD) on psychiatric morbidity, panic symptomatology and frequency of other comorbid psychiatric conditions in subjects with panic disorder (PD). Four hundred thirty-seven patients with PD were evaluated at intake as part of a multicenter longitudinal study of anxiety disorders; 113 of these patients were also in an episode of MDD. Patients were diagnosed by DSM-III-R criteria utilizing structured clinical interviews. The 113 PD/MDD patients were compared with the 324 remaining PD subjects regarding panic symptoms at intake, sociodemographic, quality of life and psychiatric morbidity variables. Differences in frequency of other comorbid Axis I psychiatric disorders were assessed at intake; personality disorders were evaluated twelve months after intake. The results revealed the PD/MDD patients exhibit increased morbidity and decreased psychosocial functioning as compared to PD patients. Personality disorders were more prevalent in the PD/MDD group at six month follow-up assessment; the PD/MDD group also had an increased frequency of posttraumatic stress disorder (PTSD) and more comorbid Axis I anxiety disorders as compared to the PD group. The total number and frequency of panic symptoms was highly consistent between the two patient groups.

Adolescent↗
PubMed1999

Moclobemide and fluoxetine for panic disorder. International Panic Disorder Study Group.

An international, multicentre, double blind parallel group study compared the tolerability and efficacy of moclobemide with the selective serotonin reuptake inhibitor (SSRI) fluoxetine for panic disorder. SSRIs have been shown effective for panic. The target dose of moclobemide was 450 mg and of fluoxetine was 20 mg. There were two consecutive studies. An eight week study of acute adverse events, tolerability and efficacy was followed by a long-term extension study to 1 year. The efficacy data showed no significant difference between moclobemide and fluoxetine. Both had acute efficacy, with 63% moclobemide and 70% fluoxetine patients (ns) panic free at 8 weeks. Both agents were well tolerated to 8 weeks, but moclobemide had fewer severe adverse events (5) than fluoxetine (9). There were no severe adverse events in the extension phase with either drug, and almost all patients completing 1 year extension treatment (moclobemide 61 patients, fluoxetine 65) were much or very much improved. These data suggest moclobemide and fluoxetine are tolerated and effective for both acute panic treatment and maintenance therapy.

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↗
PubMed1994

The overprediction of fear and panic in panic disorder.

The present study examined changes in the prediction of fear and panic in a clinical sample of patients (N = 25) meeting DSM-III-R criteria for panic disorder with agoraphobia (PDA). Data were collected for approx. 2000 trials of in vivo exposure. As expected, PDA patients displayed a bias for overpredicting both the level of fear and the likelihood of panic during an exposure trial. This overprediction bias was evidenced across several domains including heights, transportation and social situations. Although patients learned to make more accurate predictions within an exposure session, the level of overprediction remained relatively stable after the third trial within a session. Changes in fear overprediction differed across fear domains. Patients showed significant reductions in overprediction during exposure to transportation and social situations, but failed to show reductions in overprediction during exposure to heights. Unexpectedly, patients did not show increased prediction accuracy across sessions. These findings concur with earlier laboratory studies indicating that anxiety patients show an overprediction bias for panic and fear which decreases with practice. However, our findings indicate that the overprediction bias does not remit even after significant practice. The persistence of the overprediction bias is discussed within an evolutionary context.

Adolescent↗
PubMed1987

Platelet [3H]imipramine binding in generalized anxiety disorder, panic disorder, and agoraphobia with panic attacks.

The density of platelet [3H]imipramine binding sites is reported to be decreased in unipolar depression and, hence, is a putative biological marker. There is considerable evidence for a phenomenological and biological relationship of panic disorder with affective disorder. We studied platelet [3H]imipramine binding site density in unmedicated subjects with generalized anxiety disorder (GAD; n = 55), panic disorder (PD) with and without agoraphobia (n = 52), and normal controls (n = 26) in order to determine whether or not patients with panic disorder differed from controls in this biological assay. We found no differences in binding site density (Bmax) or affinity (Kd) among the PD, PD with agoraphobia, GAD, and control groups. Nor did we find a relationship between Bmax or Kd and the severity of depressive symptoms or the presence of a family history of affective disorder. In view of two conflicting prior studies, the use of [3H]imipramine binding in panic disorder remains problematic.

Adult↗
PubMedDate not supplied

Derealization and panic attacks: a clinical evaluation on 150 patients with panic disorder/agoraphobia.

One hundred fifty patients with Panic Disorder (PD) with or without Phobic Avoidance were subdivided into two groups on the basis of presence/absence of derealization and/or depersonalization (D-D) during panic attacks. D-D was found in 34.7% of the sample. By comparing the two groups, the patients with D-D were found to be younger and had an earlier onset of the disorder; they had a higher prevalence of avoidance behavior and a higher severity of the agoraphobic spectrum phobias. They were also more frequently subject to concomitant disorders such as Generalized Anxiety, Obsessive-Compulsive, and depressive symptomatology. The authors have hypothesized a correlation between the presence of D-D during panic attacks and a more frequent clinical evolution toward agoraphobia. This view is supported by finding that D-D in panic attacks corresponds to severer forms of PD, both in terms of the earlier onset of PD, and because PD shows higher levels of anxiety, depression, and disability.

Adolescent↗
PubMed2006

Prediction of anti-panic properties of escitalopram in the dorsal periaqueductal grey model of panic anxiety.

Escitalopram, the active enantiomer of the selective serotonin reuptake inhibitor (SSRI) citalopram, has effects in animal models for the detection of antidepressant and anxiolytic effect and in patients with major depressive and anxiety disorders. In the present study, the effects of escitalopram in the dorsal periaqueductal grey (dPAG) stimulation model of panic anxiety were investigated and compared to a number of clinically used anti-panic agents. The SSRIs, citalopram (ED(50) 6.6mg/kg), fluoxetine (ED(50) 13.6mg/kg), paroxetine (ED(50) 2.9mg/kg) and the benzodiazepine ligand, alprazolam (ED(50) 0.3mg/kg) all reduced the flight-like escape behaviour produced by electrical stimulation of the dPAG in the rat, this is presumed to indicate a reduction in fear and/or physical sensation and is interpreted as an anti-panic effect of the drugs. Escitalopram (ED(50) 3.1mg/kg) also significantly reduced flight behaviour indicating the anti-panic potential of the compound; it is suggested that escitalopram will be twice as potent as citalopram in this context.

Adrenergic alpha-Antagonists↗
PubMed2001

Evaluating panic-specific factors in the relationship between suicide and panic disorder.

Work during the past decade has suggested an association between panic disorder and suicide (i.e., suicidal ideation and suicide attempts) that cannot simply be accounted for by co-occurring depression symptoms. To clarify the linkage between panic disorder and suicide, the association between panic-specific clinical and cognitive variables and suicide indicators were evaluated in patients with panic disorder (N=146). Analyses predicting the presence of suicidal ideation (positive, negative) after covarying the effects of a current mood disorder diagnosis and depression symptoms indicated a number of significant predictors including: (1) overall anxiety symptoms; (2) level of anticipatory anxiety; (3) avoidance of bodily sensations; (4) attentional vigilance toward bodily perturbations; and (5) phrenophobia (i.e., fear of cognitive incapacitation). Anxiety-specific variables did not account for unique variance in predicting prior history of suicide attempts.

Adult↗
PubMed2004

Mastery of Your Anxiety and Panic and brief therapist contact in the treatment of panic disorder.

Twenty-eight individuals with panic disorder were provided with a copy of Mastery of Your Anxiety and Panic II and received either four sessions of group cognitive-behavior therapy (Group) or one meeting with a therapist plus three telephone contacts (Telephone). Between group repeated measures analyses revealed significant improvement over the course of treatment and maintenance of gains over the follow-up period with few treatment by trials interactions. A higher percentage of participants in the Telephone condition achieved high end-state functioning status at posttreatment compared to those who participated in group CBT (72% vs. 24%), but this difference disappeared at 6 months posttreatment (45% vs. 55%). Participants with characteristics of either borderline, dependent, or depressive personality disorders, as assessed by the MCMI-III, were unlikely to achieve high end-state functioning status at posttreatment. Trends in the data suggest that participants who met criteria for panic disorder with agoraphobia, and those with comorbid generalized anxiety disorder, were also less likely to achieve clinically significant outcome. These findings add to the growing literature indicating that self-directed treatment with brief therapist contact is a viable option for many people with panic disorder. Furthermore, the study provides preliminary data suggesting that certain comorbid conditions negatively impact self-directed treatment outcome.

Adult↗
PubMed1997

The role of anxiety sensitivity in the pathogenesis of panic: prospective evaluation of spontaneous panic attacks during acute stress.

Expectancy theory posits that anxiety sensitivity may serve as a premorbid risk factor for the development of anxiety pathology (S. Reiss, 1991). The principal aim of the present study was to determine whether anxiety sensitivity acts as a specific vulnerability factor in the pathogenesis of anxiety pathology. A large, nonclinical sample of young adults (N = 1,401) was prospectively followed over a 5-week highly stressful period of time (i.e., military basic training). Anxiety sensitivity was found to predict the development of spontaneous panic attacks after controlling for a history of panic attacks and trait anxiety. Approximately 20% of those scoring in the upper decile on the Anxiety Sensitivity Index (R. A. Peterson & S. Reiss, 1987) experienced a panic attack during the 5-week follow-up period compared with only 6% for the remainder of the sample. Anxiety sensitivity also predicted anxiety symptomatology, functional impairment created by anxiety, and disability. These data provide strong evidence for anxiety sensitivity as a risk factor in the development of panic attacks and other anxiety symptoms.

Adolescent↗