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Biomedical subjects

L A Papp

Publications and source records attributed to L A Papp.

At least 37 records · Page 2Linked to original sources
PubMed1997

Multicenter collaborative panic disorder severity scale.

OBJECTIVE: To address the lack of a simple and standardized instrument to assess overall panic disorder severity, the authors developed a scale for the measurement of panic disorder severity. METHOD: Ten independent evaluators used the seven-item Panic Disorder Severity Scale to assess 186 patients with principal DSM-III-R diagnoses of panic disorder (with no or mild agoraphobia) who were participating in the Multicenter Collaborative Treatment Study of Panic Disorder. In addition, 89 of these patients were reevaluated with the same scale after short-term treatment. A subset of 24 patients underwent two independent assessments to establish interrater reliability. Internal consistency, convergent and discriminant validity, and sensitivity to change were also determined. RESULTS: The Panic Disorder Severity Scale was associated with excellent interrater reliability, moderate internal consistency, and favorable levels of validity and sensitivity to change. Individual items showed good convergent and discriminant validity. Analysis suggested a two-factor model fit the data best. CONCLUSIONS: The Panic Disorder Severity Scale is a simple, efficient way for clinicians to rate severity in patients with established diagnoses of panic disorder. However, further research with more diverse groups of panic disorder patients and with a broader range of convergent and discriminant validity measures is needed.

Agoraphobia↗
PubMed1997

Clomipramine treatment of panic disorder: pros and cons.

BACKGROUND: Controlled trials suggest that clomipramine may be a highly effective antipanic drug. Lowering the starting dose may alleviate troublesome initial side effects and increase acceptability and compliance. METHOD: Fifty-eight patients with DSM-III-R panic disorder with or without agoraphobia underwent 13 weeks of clomipramine treatment. Starting at 10 mg/day, the dose was gradually increased to a mean dose of 97 mg/day. RESULTS: While completers showed highly significant improvement, the benefits were severely limited by a high dropout rate due to adverse reactions occurring mostly during the first 2 weeks of treatment. CONCLUSION: Given the alternatives, clomipramine should not be used as a first-line antipanic medication.

Adult↗
PubMed1996

Ventilatory effects of tryptophan depletion in panic disorder: a preliminary report.

On the basis of preclinical studies, we hypothesized that deficient serotonin neurotransmission may be associated with the respiratory hyperactivity and carbon dioxide sensitivity seen in panic disorder. We used the tryptophan depletion method to investigate the effects of transient reductions in serotonin on respiration in five patients with panic disorder and seven normal control subjects. During room air breathing, the patients showed significantly increased ventilation when tryptophan-depleted, while the normal subjects showed no significant changes in respiration. These preliminary data suggest that serotonergic manipulation may affect ventilatory indices, with panic disorder patients being particularly sensitive to the effect of tryptophan depletion.

Adult↗
PubMed1996

Ambulatory monitoring of respiration in anxiety.

An ambulatory monitor, body suit, and calibration procedure were developed to compare the respiration of seven patients with panic disorder and twelve normal volunteers. Subjects wore a body suit with Respitrace bands, connected to a portable respiratory monitor for a period of 24 hours. Breath by breath values for respiratory rate and tidal volume were computed every two minutes. There was a significant difference between patients and controls in their patterns of minute ventilation during sleep. Tidal volume, rather that respiratory rate increases characterized the periods of anxiety and limited symptom attacks.

Adult↗
PubMed1995

Instructional set does not alter outcome of respiratory challenges in panic disorder.

In an attempt to reproduce the findings of Rapee et al (1986) that instructional set could alter the anxiogenic effects of carbon dioxide inhalation, 45 patients with panic disorder received two sets of instructions and then underwent a series of respiratory challenges (room air hyperventilation, 5% and 7% CO2 inhalation). The instructions failed to alter the anxiogenic response to any of the interventions.

Administration, Inhalation↗
PubMed1995

Rebreathing tests in panic disorder.

In order to compare the ventilatory response of panic patients and normal controls, 21 panic disorder patients with agoraphobia and 21 normal controls underwent the Read rebreathing test. Panic patients panicked significantly more during the test, responded with more respiratory rate and less tidal volume, but showed no hypersensitivity to inhaled carbon dioxide compared to normal controls.

Adult↗
PubMed1995

Persistence of blunted human growth hormone response to clonidine in fluoxetine-treated patients with panic disorder.

OBJECTIVE: The authors determined the effects of antipanic treatment with fluoxetine on human growth hormone (GH) response to the alpha 2 agonist clonidine. METHOD: Seventeen patients with panic disorder and 15 healthy volunteers were challenged with clonidine. Thirteen of the patients and 12 of the volunteers were given a second challenge with clonidine 12 weeks later. The patients received open fluoxetine and the healthy subjects received no treatment between challenges. Subjects with high baseline human GH levels (greater than 2 ng/ml) at the first and second challenges were excluded from further analysis. RESULTS: The patients with panic disorder (N = 13 for the first challenge and N = 9 for the second) had significantly lower human GH responses to clonidine than the healthy subjects (N = 14 during the first challenge and N = 9 for the second) during both challenges, despite clinical improvement in eight of the nine patients at the time of the second challenge. CONCLUSIONS: Blunted secretion of human GH in response to clonidine in patients with panic disorder persists despite clinical recovery.

Clonidine↗
PubMed1995

Adinazolam-SR in panic disorder with agoraphobia: relationship of daily dose to efficacy.

BACKGROUND: We report the results from a multicenter, double-blind, randomized, fixed-dose study designed to evaluate the relationship between daily dose and efficacy of adinazolam-SR in patients with panic disorder with agoraphobia. METHOD: Patients (N = 315) were randomized to one of four treatment groups (placebo, N = 83; 30-mg group, N = 79; 60-mg group, N = 81; and 90-mg group, N = 72) and then treated twice daily for 4 weeks. All treatment groups were comparable demographically. Primary efficacy measures included total number of panic attacks, global improvement score using the Clinical Global Impressions (CGI) scale, phobic anxiety dimension of the Symptom Checklist-90 phobic cluster, overall phobia state using the Phobia Scale, and severity of illness on the CGI. RESULTS: The 60- and 90-mg/day adinazolam-SR treatment groups showed superior results when compared with the placebo group at Week 4 while the 30-mg group did not. Treatment with adinazolam-SR was well tolerated, with sedation the only treatment-emergent symptom that occurred more frequently in patients treated with adinazolam-SR than placebo. CONCLUSION: These results suggest that adinazolam-SR at doses of 60-mg/day or greater administered twice daily is a safe and effective treatment in selected patients with panic disorder with agoraphobia.

Adolescent↗
PubMed1994

Anxiogenic effects of CO2 and hyperventilation in patients with panic disorder.

OBJECTIVE: Previous studies have indicated that patients with panic disorder are more likely than normal subjects to have acute panic attacks during inhalation of CO2, but methodological objections have been raised. In this study the authors attempted to address three of these methodological problems by ensuring that raters who assessed whether panic attacks occurred were blind to subjects' diagnoses, by randomizing the order of administration of 5% CO2 and hyperventilation, and by challenging a greater number of subjects with 7% CO2. METHOD: Patients with panic disorder and normal subjects underwent 20-minute inhalations of 5% CO2 and 7% CO2 and 15 minutes of room-air hyperventilation. Ratings of panic/no panic during each condition were made separately by an assessor blind to diagnosis and by the subject. Scores on four panic rating scales were also recorded before and after each intervention. RESULTS: Room-air hyperventilation caused panic attacks in a small number of patients; the difference in panic rate between patients and comparison subjects was statistically significant by the subjects' but not by the raters' assessment. Panic rates during 5% CO2 and 7% CO2 were significantly greater among the patients by both assessments; the panic rate was greatest during 7% CO2. Order of administration did not significantly affect panic rates for hyperventilation and 5% CO2. CONCLUSIONS: Panic patients were clearly more sensitive to the anxiogenic effects of CO2 than comparison subjects, and CO2 was a more potent anxiogenic stimulus than room-air hyperventilation. Seven percent CO2 discriminated best between patients and comparison subjects and should be the focus of further research.

Administration, Inhalation↗
PubMed1994

Augmentation strategies with tricyclic or fluoxetine treatment in seven partially responsive panic disorder patients.

BACKGROUND: Although panic disorder is generally responsive to single antidepressant pharmacotherapy, a substantial percentage of patients fail either to respond adequately or to maintain a therapeutic response. METHOD: The authors report on seven consecutive openly treated patients with panic disorder who showed inadequate antipanic responses to treatment regimens including either a tricyclic (TCA) or fluoxetine. Those patients taking a TCA had fluoxetine added and those patients taking fluoxetine had a TCA added. RESULTS: All seven patients showed an improvement in antipanic response to the combination treatment. CONCLUSION: The current case series is the first, to our knowledge, to suggest that the combination of a TCA and fluoxetine may provide a viable pharmacotherapeutic option for panic disorder patients who have failed to respond to an adequate trial of either a TCA or fluoxetine. Appropriate controlled studies are recommended.

Adult↗
PubMed1993

The effect of acetazolamide on ventilation in panic disorder patients.

OBJECTIVE: Patients with panic disorder are behaviorally hypersensitive to CO2 inhalation and may also be biologically hypersensitive. A report by Mathew et al. showed, however, that administration of the carbonic anhydrase inhibitor acetazolamide, which is believed to increase brain CO2 level, did not cause panic in panic disorder patients. The authors of the present study noted that respiratory frequency did not increase in the earlier experiment and wondered whether respiratory stimulation occurred during acetazolamide administration, as would be expected if CO2 level increases significantly. METHOD: Ten patients with panic disorder and six normal control subjects received injections of acetazolamide, 1 g i.v., as per the Mathew et al. protocol, during breath by breath measurement of both tidal volume and frequency of respiration. RESULTS: Three patients had panic attacks, one before receiving acetazolamide, one during the injection, and one 2 minutes after injection. Only the last of these attacks appeared possibly attributable to acetazolamide. None of the control subjects panicked. Neither patients nor control subjects exhibited meaningful change in tidal volume, respiratory frequency, or minute ventilation, and both groups experienced a trend toward significant decrease in overall levels of anxiety and dyspnea after acetazolamide injection. CONCLUSIONS: The authors replicated the earlier finding that acetazolamide is not panicogenic in patients with panic disorder but also showed that at the dose given, there is no meaningful effect on ventilation. If acetazolamide does affect CO2 levels it does so in a way that does not stimulate ventilation. Therefore, the acetazolamide injection results of Mathew et al. and of the present study do not challenge hypotheses linking panic attacks to hypersensitive respiratory control mechanisms.

Acetazolamide↗
PubMed1993

Diagnostic and substance specificity of carbon-dioxide-induced panic.

OBJECTIVE: The authors assessed the substance and diagnostic specificity of carbon-dioxide-induced panic since, in addition to the specific biochemical effects of inhaled carbon dioxide (CO2), simple physiologic distress is also frequently implicated as a panicogenic factor during respiratory challenge studies with CO2 in patients with anxiety disorders. METHOD: Eighteen patients with panic disorder, 20 with social phobia, and 23 psychiatrically normal subjects inhaled a mixture of 35% CO2 and 65% O2 for 30 seconds through a face mask. They also breathed for 30 seconds through a valve reducing the diameter of the airway. A double-blind, counterbalanced, randomized design was used. RESULTS: In spite of important similarities between the two interventions, including the induction of equal amounts of subjective respiratory distress, carbon dioxide inhalation was significantly more potent than increased airway resistance in provoking panic in the anxiety disorder patients. The patients with panic disorder were significantly more sensitive to CO2 than were the patients with social phobia or the normal subjects. CONCLUSIONS: Carbon dioxide inhalation appears to have a specific panicogenic effect in panic patients that goes beyond simple breathlessness.

Administration, Inhalation↗
PubMed1993

Carbon dioxide hypersensitivity, hyperventilation, and panic disorder.

OBJECTIVE: The purpose of this article is to offer a comprehensive, data-based explanation of the relationship between hyperventilation and panic disorder linking CO2 hypersensitivity, cognitive/behavioral factors, and the respiratory effects of antipanic pharmacologic and psychological treatments. METHOD: The authors conducted a computerized search of MEDLINE for relevant articles. RESULTS: Some panic patients have a chronic, subtle respiratory disturbance. Acute hyperventilation is neither necessary nor sufficient for panic to occur. Respiratory abnormalities in panic patients may adaptively aim at coping with a hypersensitive CO2 chemoreceptor system. Pharmacologic panicogens also stimulate the respiratory system, causing hyperventilation. Triggering this hypersensitive respiratory control mechanism may incite panic. Antipanic medications may reset the receptor threshold. Misattribution and catastrophic interpretation of somatic symptoms or the sense of loss of control may contribute to panic symptoms. Behavioral interventions such as desensitization or breathing retraining may block the full-blown attack. Cognitive strategies through cognitive control of respiration may supplement and accentuate these interventions. CONCLUSIONS: Panic disorder may be due to an inherently unstable autonomic nervous system, coupled with cognitive distress.

Alkalosis, Respiratory↗
PubMed1992

Exercise tolerance in panic disorder patients.

Sixteen panic patients and fifteen normal controls performed submaximal exercise testing on a bicycle ergometer. Only one patient subject panicked. Biochemical, physiological, and psychological data showed similar exercise tolerance in both patients and controls. Exercise-induced distress and lactate increment do not appear to cause panic attacks.

Adult↗
PubMed1992

Amelioration of mitral valve prolapse after treatment for panic disorder.

Twenty panic disorder patients with mitral valve prolapse showed amelioration of prolapse on repeat echocardiogram after treatment for panic disorder. This effect was significant when compared to repeat echocardiograms in eight psychiatrically normal control subjects with mitral valve prolapse.

Adult↗
PubMed1991

Cognitive-behavior therapy for panic disorder delivered by psychopharmacologically oriented clinicians.

A cognitive-behavioral treatment program for panic disorder was delivered by staff members of a psychiatric center that traditionally utilizes pharmacological methods. Psychiatrists, a nurse practitioner, and psychologists not previously exposed to behavioral techniques were trained by a behavioral psychologist to utilize a treatment program consisting of breathing control, cognitive restructuring, and exposure to panic-eliciting somatic cues. Of the 24 patients treated as part of this training in panic control therapy, 14 were panic-free after treatment and three additional patients showed moderate improvement and decreased frequency of panic. A case example is presented to demonstrate the application of behavioral techniques to individual patients. Discussion is focused on issues surrounding training in behavioral methods and problems in exporting behavioral technology to centers that emphasize psychopharmacological approaches to treatment.

Adult↗