About: Panic Disorder Severity Scale is a research topic. Over the lifetime, 174 publications have been published within this topic receiving 8117 citations.
TL;DR: Combining imipramine and CBT appeared to confer limited advantage acutely but more substantial advantage by the end of maintenance, and each treatment worked well immediately following treatment and during maintenance;CBT appeared durable in follow-up.
Abstract: ContextPanic disorder (PD) may be treated with drugs, psychosocial intervention,
or both, but the relative and combined efficacies have not been evaluated
in an unbiased fashion.ObjectiveTo evaluate whether drug and psychosocial therapies for PD are each
more effective than placebo, whether one treatment is more effective than
the other, and whether combined therapy is more effective than either therapy
alone.Design and SettingRandomized, double-blind, placebo-controlled clinical trial conducted
in 4 anxiety research clinics from May 1991 to April 1998.PatientsA total of 312 patients with PD were included in the analysis.InterventionsPatients were randomly assigned to receive imipramine, up to 300 mg/d,
only (n=83); cognitive-behavioral therapy (CBT) only (n=77); placebo only
(n=24); CBT plus imipramine (n=65); or CBT plus placebo (n=63). Patients were
treated weekly for 3 months (acute phase); responders were then seen monthly
for 6 months (maintenance phase) and then followed up for 6 months after treatment
discontinuation.Main Outcome MeasuresTreatment response based on the Panic Disorder Severity Scale (PDSS)
and the Clinical Global Impression Scale (CGI) by treatment group.ResultsBoth imipramine and CBT were significantly superior to placebo for the
acute treatment phase as assessed by the PDSS (response rates for the intent-to-treat
[ITT] analysis, 45.8%, 48.7%, and 21.7%; P=.05 and P=.03, respectively), but were not significantly different
for the CGI (48.2%, 53.9%, and 37.5%, respectively). After 6 months of maintenance,
imipramine and CBT were significantly more effective than placebo for both
the PDSS (response rates, 37.8%, 39.5%, and 13.0%, respectively; P=.02 for both) and the CGI (37.8%, 42.1%, and 13.0%, respectively).
Among responders, imipramine produced a response of higher quality. The acute
response rate for the combined treatment was 60.3% for the PDSS and 64.1%
for the CGI; neither was significantly different from the other groups. The
6-month maintenance response rate for combined therapy was 57.1% for the PDSS
(P=.04 vs CBT alone and P=.03
vs imipramine alone) and 56.3% for the CGI (P=.03
vs imipramine alone), but not significantly better than CBT plus placebo in
either analysis. Six months after treatment discontinuation, in the ITT analysis
CGI response rates were 41.0% for CBT plus placebo, 31.9% for CBT alone, 19.7%
for imipramine alone, 13% for placebo, and 26.3% for CBT combined with imipramine.ConclusionsCombining imipramine and CBT appeared to confer limited advantage acutely
but more substantial advantage by the end of maintenance. Each treatment worked
well immediately following treatment and during maintenance; CBT appeared
durable in follow-up.
TL;DR: Medications, particularly those that influence the serotonin system, are hypothesized to desensitize the fear network from the level of the amygdala through its projects to the hypothalamus and the brainstem, and effective psychosocial treatments may also reduce contextual fear and cognitive misattributions.
Abstract: OBJECTIVE: In a 1989 article, the authors provided a hypothesis for the neuroanatomical basis of panic disorder that attempted to explain why both medication and cognitive behavioral psychotherapy are effective treatments. Here they revise that hypothesis to consider developments in the preclinical understanding of the neurobiology of fear and avoidance. METHOD: The authors review recent literature on the phenomenology, neurobiology, and treatment of panic disorder and impressive developments in documenting the neuroanatomy of conditioned fear in animals. RESULTS: There appears to be a remarkable similarity between the physiological and behavioral consequences of response to a conditioned fear stimulus and a panic attack. In animals, these responses are mediated by a “fear network” in the brain that is centered in the amygdala and involves its interaction with the hippocampus and medial prefrontal cortex. Projections from the amygdala to hypothalamic and brainstem sites explain many of the observed signs ...
TL;DR: 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 ofpanic disorder patients and with a broader range of convergent and discriminant validity measures is needed.
Abstract: 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 discrimi...
TL;DR: Although the major societal burden of panic is caused by PD and PA-AG, isolated PAs also have high prevalence and meaningful role impairment, and 4 subgroups are significantly comorbid with other lifetime DSM-IV disorders.
Abstract: 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.
TL;DR: In this article, the authors developed an expanded measure of anxiety sensitivity (ASI-R), which consists of 36 items with subscales assessing each of the major domains of AS suggested by previous studies.