Cognitive behavior therapy for panic disorder.

Panic Disorder affects around 3.5% of the population during their lifetime, affecting twice as many women. It is often comorbid with depression and other anxiety disorders. Panic disorder can be assessed by a variety of interviews and self-report questionnaires. The theoretical model underlying CBT explains panic from both a learning perspective as well as a cognitive one. Treatment comprises of both behavioral and cognitive components. Treatment outcome studies show that CBT is an effective, acceptable and cost-effective treatment for Panic Disorder.

Long-term outcome of early interventions to prevent posttraumatic stress disorder.

BACKGROUND: Failing to prevent posttraumatic stress disorder (PTSD) has major clinical and public health consequences. This work evaluates the 3-year outcome of offering early interventions to survivors with acute PTSD. METHODS: Adults admitted consecutively to the hospital with acute DSM-IV PTSD were randomized, between June 2003 and October 2007, to 12 weeks of prolonged exposure (n = 63) or cognitive therapy (n = 40) or concealed SSRI (escitalopram; n = 23) versus placebo (n = 23). Eighty-two participants who declined treatment were followed as well. Treatment started 1 month after the traumatic event, and participants were reassessed 5 and 36 months later. Assessors were blinded to treatment allocation and acceptance. The Clinician-Administered PTSD Scale (CAPS) evaluated PTSD and PTSD symptoms. Self-reported symptoms, general functioning, and employment status were secondary outcomes. Participants lost to follow-up were missing completely at random. RESULTS: Prolonged exposure and cognitive therapy significantly reduced PTSD and PTSD symptoms between 1 and 5 months (mean CAPS total scores [95% CI] at 1 month: prolonged exposure = 73.59 [68.21-78.96] and cognitive therapy = 71.78 [66.92-78.93]; mean CAPS total scores [95% CI] at 5 months: prolonged exposure = 28.59 [21.89-35.29] and cognitive therapy = 29.48 [21.32-37.95], P < .001), and their results remained stable. At 3 years, however, the study groups had similar levels of PTSD symptoms (mean CAPS total scores [95% CI]: prolonged exposure = 31.51 [20.25-42.78]; cognitive therapy = 32.08 [20.74-43.42]; SSRI = 34.31 [16.54-52.07]; placebo = 32.13 [20.15-44.12]; and no intervention = 30.59 [19.40-41.78]), similar prevalence of PTSD (28.6%-46.2%), and similar secondary outcomes. CONCLUSION: Early prolonged exposure and cognitive therapy accelerated the recovery from acute PTSD. Their effect remained stable, however, without reducing the 3-year prevalence of the disorder. The lingering prevalence of PTSD, despite efficient interventions, illustrates a nonremitting, treatment-refractory subset of survivors and outlines a major clinical and public health challenge. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT00146900.

Prevention of posttraumatic stress disorder by early treatment: results from the Jerusalem Trauma Outreach And Prevention study.

CONTEXT: Preventing posttraumatic stress disorder (PTSD) is a pressing public health need. OBJECTIVES: To compare early and delayed exposure-based, cognitive, and pharmacological interventions for preventing PTSD. DESIGN: Equipoise-stratified randomized controlled study. SETTING: Hadassah Hospital unselectively receives trauma survivors from Jerusalem and vicinity. PARTICIPANTS: Consecutively admitted survivors of traumatic events were assessed by use of structured telephone interviews a mean (SD) 9.61 (3.91) days after the traumatic event. Survivors with symptoms of acute stress disorder were referred for clinical assessment. Survivors who met PTSD symptom criteria during the clinical assessment were invited to receive treatment. INTERVENTIONS: Twelve weekly sessions of prolonged exposure (PE; n = 63), or cognitive therapy (CT; n = 40), or double blind treatment with 2 daily tablets of either escitalopram (10 mg) or placebo (selective serotonin reuptake inhibitor/placebo; n = 46), or 12 weeks in a waiting list group (n = 93). Treatment started a mean (SD) 29.8 (5.7) days after the traumatic event. Waiting list participants with PTSD after 12 weeks received PE a mean (SD) 151.8 (42.4) days after the traumatic event (delayed PE). MAIN OUTCOME MEASURE: Proportion of participants with PTSD after treatment, as determined by the use of the Clinician-Administered PTSD Scale (CAPS) 5 and 9 months after the traumatic event. Treatment assignment and attendance were concealed from the clinicians who used the CAPS. RESULTS: At 5 months, 21.6% of participants who received PE and 57.1% of comparable participants on the waiting list had PTSD (odds ratio [OR], 0.21 [95% CI, 0.09-0.46]). At 5 months, 20.0% of participants who received CT and 58.7% of comparable participants on the waiting list had PTSD (OR, 0.18 [CI, 0.06-0.48]). The PE group did not differ from the CT group with regard to PTSD outcome (OR, 0.87 [95% CI, 0.29-2.62]). The PTSD prevalence rates did not differ between the escitalopram and placebo subgroups (61.9% vs 55.6%; OR, 0.77 [95% CI, 0.21-2.77]). At 9 months, 20.8% of participants who received PE and 21.4% of participants on the waiting list had PTSD (OR, 1.04 [95% CI, 0.40-2.67]). Participants with partial PTSD before treatment onset did similarly well with and without treatment. CONCLUSIONS: Prolonged exposure, CT, and delayed PE effectively prevent chronic PTSD in recent survivors. The lack of improvement from treatment with escitalopram requires further evaluation. Trauma-focused clinical interventions have no added benefit to survivors with subthreshold PTSD symptoms. Trial Registration clinicaltrials.gov Identifier: NCT00146900.