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Panic disorder is a common, disabling condition that affects 3% to 5% of the world's population. Althoughit is treatable, panic disorder goes unrecognized and untreated in many patients.Patients with panic disorder have an increased risk for other psychiatricdisorders, especially other anxiety disorders, and panic disorder is associatedwith other medical conditions such as migraines, fibromyalgia, and irritablebowel syndrome. Clinicians treating panic disorder must be able to recognizethe disorder, differentiate it from other disorders in which panic attacks arepart of the symptomatology, and map out an individualized treatment plan foreach patient. This presentation discusses the importance of collaborationbetween doctor and patient and details available treatment options, includingantidepressants, benzodiazepines, and cognitive-behavioral therapy.
Because this piece has no abstract, we have provided for your benefit the first 3 sentences of the full text.
Because this piece does not have an abstract, we have provided for your benefit the first 3 sentences of the full text.
Sir: Although paradoxical effects of γ-aminobutyric acid (GABA)-ergic medications (excitation instead of sedation) are well-known, they have received no satisfactory explanation. We report the case of a 54-year-old woman with schizophrenia, in which we were able to observe this clinical pattern and its neural correlates.
Case report. The patient was in her forties, working as an assistant professor at a university, when she developed mostly negative symptoms.' ‹
Objective: The objective of this study was to examine the relative cost-efficacy of empirically supported treatments for panic disorder. As psychosocial, pharmacologic, and combined treatments have all demonstrated efficacy in the treatment of panic disorder, cost-efficacy analysis provides an additional source of information to guide clinical decision making.
Method: Cost-efficacy was examined based on results from the Multicenter Comparative Treatment Study of Panic Disorder, a randomized controlled trial of treatment for panic disorder (DSM-III-R). The trial was conducted from May 1991 to April 1998. Cost-efficacy ratios representing the cost per 1-unit improvement in Panic Disorder Severity Scale mean item score were calculated for 3 monotherapies (cognitive-behavioral therapy [CBT], imipramine, and paroxetine) and 2 combination treatments (CBT-imipramine and CBT-paroxetine) at the end of acute, maintenance, and follow-up phases.
Results: Results demonstrated consistently greater cost-efficacy for individual over combined treatments, with imipramine representing the most cost-efficacious treatment option at the completion of the acute phase (cost-efficacy ratio = $972) and CBT representing the most cost-efficacious option at the end of maintenance treatment (cost efficacy ratio = $1449) and 6 months after treatment termination (cost-efficacy ratio = $1227).
Conclusion: In the context of similar efficacy for combined treatments, but poorer cost-efficacy, current monotherapies should be considered the first-line treatment of choice for panic disorder. Additionally, CBT emerged as the most durable and cost-effective monotherapy and, hence, should be considered as a particularly valuable treatment from the perspective of cost accountability.
Objective: It is generally agreed that alcohol use disorders and panic disorder with (PD[A]) or without agoraphobia (PD) tend to occur within the same individual. However, the cause of this comorbidity remains controversial. Three main explanations are that (1) PD(A) promotes pathologic alcohol use as self-medication, (2) chronic alcohol use and alcohol withdrawal induce changes in the neurochemical system that promote panic, and (3) a third factor, such as familial transmission, promotes both conditions. The aim of this review was to survey the literature in order to determine the validity of these explanatory models.
Data Sources: A review of epidemiologic, family, and laboratory studies was performed. Studies were identified using PubMed (English-language articles published from 1960 to 2006, using the search term alcohol and panic).
Study Selection: Twenty studies were reviewed and selected according to the following criteria: PD(A) and alcohol abuse/dependence diagnosed according to the DSM, no additional comorbidity, use of adult samples, comparison with a nonclinical control group, or application of a crossover design.
Data Extraction: Nonsignificant results or trends only were reported as "no difference." Data on "anxiety disorders" or "substance abuse" in general were not included.
Data Synthesis: In PD(A), alcohol lessens anxious apprehension, thereby decreasing the likelihood of panic. In alcohol use disorders, alcohol increases CO2 sensitivity and may thereby promote panic. In both cases, a significant familial transmission contributes to the co-occurrence.
Conclusion: Findings would seem to indicate that PD(A) and alcohol use disorders can both serve to initiate the other via independent mechanisms. Further studies are warranted.
Objective: The American Psychiatric Association (APA) practice guideline for panic disorder recommends psychodynamic psychotherapy for panic disorder patients with comorbid personality disorders. No data underlie this recommendation. This exploratory study assessed the moderating effect of personality disorder on psychodynamic and non-psychodynamic psychotherapy outcome.
Method: Forty-nine subjects with primary DSM-IV panic disorder were randomly assigned to 12 weeks of twice-weekly Panic-Focused Psychodynamic Psychotherapy or Applied Relaxation Training. The primary outcome measure was the Panic Disorder Severity Scale; the moderating effect of Axis II psychopathology on the Sheehan Disability Scale was also tested. The trial was conducted between February 2000 and January 2005.
Results: Twenty-four subjects (49%) met DSM-IV criteria for a Structured Clinical Interview for DSM-IV Axis II Disorders-diagnosed personality disorder, of whom 19 (79%) had a cluster C diagnosis. Presence of a cluster C diagnosis moderated treatment outcome. Such subjects experienced greater improvements in Panic-Focused Psychodynamic Psychotherapy than subjects without cluster C comorbidity.
Conclusions: Despite its small sample size, this exploratory analysis provides initial preliminary evidence corroborating the APA practice guideline recommendation. Future panic disorder clinical trials should explore Axis II moderator effects.
Clinical Trials Registration: ClinicalTrials.gov identifier NCT00128388' ‹
Sir: Paroxetine, fluoxetine, sertraline, venlafaxine, clonazepam, and alprazolam are currently the only medications approved by the U.S. Food and Drug Administration for the treatment of panic disorder. In practice, first-line treatment usually involves selective serotonin reuptake inhibitors (SSRIs). Other treatment options might include tricyclic antidepressants (most commonly clomipramine and imipramine), venlafaxine, buspirone, nefazodone, β-blockers, and monoamine oxidase inhibitors (MAOIs).' ‹
Objective: To compare the long-term efficacy of venlafaxine extended release (ER) with placebo in preventing panic disorder relapse inoutpatient treatment responders.
Method: Outpatients aged >= 18 years who met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria for panic disorder with or without agoraphobia for at least the previous 3 months, with >= 6 full symptom panic attacks in the 2 weeks prior to screening and >= 3 in the 2 weeks before baseline and a Clinical Global Impressions-Severity of Illness rating >= 4 at screen were eligible to participate. Outpatients received flexible-dose (75-225 mg/day) venlafaxine ER for 12 weeks. Treatment responders were randomly assigned to venlafaxine ER or placebo for 26 weeks. Criteria for response were = 2 full symptom panic attacks per week for 2 consecutive weeks or discontinuation due to loss of effectiveness, was evaluated using Kaplan-Meier survival analysis. The study was conducted between December 2001 and August 2003.
Results: The intent-to-treat population had 291 patients in the open-label phase and 169 in the double-blind phase (placebo, N = 80; venlafaxine ER, N = 89; mean daily dose 165-171 mg). Time to relapse was significantly longer with venlafaxine ER than placebo (p < .001). All secondary measures of panic attack treatment efficacy, quality of life, and disability were significantly better with venlafaxine ER than placebo (p <= .005).
Conclusion: Venlafaxine ER was safe, well tolerated, and effective in preventing relapse in outpatients with panic disorder.
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