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Jack M Gorman - One of the best experts on this subject based on the ideXlab platform.
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evidence based guidelines for interpretation of the Panic Disorder severity scale
Depression and Anxiety, 2009Co-Authors: Toshi A Furukawa, Katherine M Shear, David H Barlow, Roy Money, Scott W Woods, Jack M Gorman, Eva Etschel, Rolf R Engel, Stefan LeuchtAbstract:BACKGROUND: The Panic Disorder Severity Scale (PDSS) is promising to be a standard global rating scale for Panic Disorder. In order for a clinical scale to be useful, we need a guideline for interpreting its scores and their changes, and for defining clinical change points such as response and remission. METHODS: We used individual patient data from two large randomized controlled trials of Panic Disorder (total n=568). Study participants were administered the PDSS and the Clinical Global Impression (CGI)--Severity and --Improvement. We applied equipercentile linking technique to draw correspondences between PDSS and CGI-Severity, numeric changes in PDSS and CGI-Improvement, and percent changes in PDSS and CGI-Improvement. RESULTS: The interpretation of the PDSS total score differed according to the presence or absence of agoraphobia. When the patients were not agoraphobic, score ranges 0-1 corresponded with "Normal," 2-5 with "Borderline," 6-9 with "Slightly ill," 10-13 with "Moderately ill," and 14 and above with "Markedly ill." When the patients were agoraphobic, score ranges 3-7 meant "Borderline ill," 8-10 "Slightly ill," 11-15 "Moderately ill," and 16 and above "Markedly ill." The relationship between PDSS change and CGI-Improvement was more linear when measured as percentile change than as numeric changes, and was indistinguishable for those with or without agoraphobia. The decrease by 75-100% was considered "Very much improved," that by 40-74% "Much improved," and that by 10-39% "Minimally improved." CONCLUSION: We propose that "remission" of Panic Disorder be defined by PDSS scores of five or less and its "response" by 40% or greater reduction.
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cost efficacy of individual and combined treatments for Panic Disorder
The Journal of Clinical Psychiatry, 2007Co-Authors: Kathryn R Mchugh, Katherine M Shear, David H Barlow, Jack M Gorman, Michael W Otto, Scott W WoodsAbstract: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.
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Neuroanatomical Hypothesis of Panic Disorder, Revised
American Journal of Psychiatry, 2000Co-Authors: Jack M Gorman, Justine M. Kent, Gregory M. Sullivan, Jeremy D. CoplanAbstract: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 ...
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multicenter collaborative Panic Disorder severity scale
American Journal of Psychiatry, 1997Co-Authors: Katherine M Shear, Timothy A Brown, David H Barlow, Roy Money, Diane E Sholomskas, Scott W Woods, Jack M Gorman, Laszlo A PappAbstract: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...
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carbon dioxide hypersensitivity hyperventilation and Panic Disorder
American Journal of Psychiatry, 1993Co-Authors: Laszlo A Papp, Donald F Klein, Jack M GormanAbstract: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.
Martin E Keck - One of the best experts on this subject based on the ideXlab platform.
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regulation of the hypothalamic pituitary adrenocortical system in patients with Panic Disorder
Neuropsychopharmacology, 2006Co-Authors: Angelika Erhardt, Florian Holsboer, Marcus Ising, Paul G Unschuld, N Kern, Susanne Lucae, Benno Putz, Manfred Uhr, Elisabeth B Binder, Martin E KeckAbstract:Regulation of the Hypothalamic–Pituitary–Adrenocortical System in Patients with Panic Disorder
Katherine M Shear - One of the best experts on this subject based on the ideXlab platform.
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evidence based guidelines for interpretation of the Panic Disorder severity scale
Depression and Anxiety, 2009Co-Authors: Toshi A Furukawa, Katherine M Shear, David H Barlow, Roy Money, Scott W Woods, Jack M Gorman, Eva Etschel, Rolf R Engel, Stefan LeuchtAbstract:BACKGROUND: The Panic Disorder Severity Scale (PDSS) is promising to be a standard global rating scale for Panic Disorder. In order for a clinical scale to be useful, we need a guideline for interpreting its scores and their changes, and for defining clinical change points such as response and remission. METHODS: We used individual patient data from two large randomized controlled trials of Panic Disorder (total n=568). Study participants were administered the PDSS and the Clinical Global Impression (CGI)--Severity and --Improvement. We applied equipercentile linking technique to draw correspondences between PDSS and CGI-Severity, numeric changes in PDSS and CGI-Improvement, and percent changes in PDSS and CGI-Improvement. RESULTS: The interpretation of the PDSS total score differed according to the presence or absence of agoraphobia. When the patients were not agoraphobic, score ranges 0-1 corresponded with "Normal," 2-5 with "Borderline," 6-9 with "Slightly ill," 10-13 with "Moderately ill," and 14 and above with "Markedly ill." When the patients were agoraphobic, score ranges 3-7 meant "Borderline ill," 8-10 "Slightly ill," 11-15 "Moderately ill," and 16 and above "Markedly ill." The relationship between PDSS change and CGI-Improvement was more linear when measured as percentile change than as numeric changes, and was indistinguishable for those with or without agoraphobia. The decrease by 75-100% was considered "Very much improved," that by 40-74% "Much improved," and that by 10-39% "Minimally improved." CONCLUSION: We propose that "remission" of Panic Disorder be defined by PDSS scores of five or less and its "response" by 40% or greater reduction.
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cost efficacy of individual and combined treatments for Panic Disorder
The Journal of Clinical Psychiatry, 2007Co-Authors: Kathryn R Mchugh, Katherine M Shear, David H Barlow, Jack M Gorman, Michael W Otto, Scott W WoodsAbstract: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.
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reliability of the self report version of the Panic Disorder severity scale
Depression and Anxiety, 2002Co-Authors: Patricia R Houck, Katherine M Shear, David A Spiegel, Paola RucciAbstract:The interview-administered Panic Disorder Severity Scale (PDSS) has been demonstrated to be a reliable and valid measurement of Panic Disorder severity. The purpose of this paper is to report on the reliability and usefulness of the self-report form (PDSS-SR). The PDSS and PDSS-SR were administered to 108 psychiatric outpatients with and without Panic Disorder. The internal consistency of the instruments was analyzed with Cronbach's alpha. Test-retest reliability was assessed on 25 of these subjects by using intraclass correlation coefficient (ICC). In addition, decrease in Panic symptoms was measured after cognitive-behavioral treatment (CBT) treatment on 27 subjects. Cronbach's alpha was.917 for PDSS-SR and.923 for the PDSS. The PDSS-SR had good test-retest reliability (ICC=0.81) and was sensitive to change with treatment, with a mean decrease of 7.3 (S.D.=5.1). The self-report version of the PDSS is a reliable format, which could be useful in clinical and research settings.
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reliability and validity of the Panic Disorder severity scale replication and extension
Journal of Psychiatric Research, 2001Co-Authors: Katherine M Shear, Paola Rucci, Jenna Williams, Ellen Frank, Victoria J Grochocinski, Joni Vander Bilt, Patricia R Houck, Tracey WangAbstract:Abstract The Panic Disorder Severity Scale (PDSS) is a recently developed seven-item instrument to rate overall severity of Panic Disorder. The scale has previously shown good psychometric properties in a sample of Panic Disorder patients with no more than mild agoraphobia. The purpose of this paper is to confirm reliability and validity, to provide an estimate of a cut-score discriminating the presence or absence of current DSM-IV Panic Disorder, and to determine the factor structure of the instrument. Procedures : 104 psychiatric outpatients, including 54 with current Panic Disorder, underwent structured diagnostic assessment and the PDSS interview. The PDSS was repeated within 3–17 days. Results : we confirmed reliability and validity of the instrument and found a one-factor solution fit the data. A cut-off score of eight identifies patients with current Panic with a sensitivity of 83.3%, and a specificity of 64%. Conclusion : the PDSS is a simple, reliable instrument for use in Panic Disorder studies. A cut-score of eight may be useful as a tool to screen patients in settings such as primary care, for diagnosis-level symptoms.
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multicenter collaborative Panic Disorder severity scale
American Journal of Psychiatry, 1997Co-Authors: Katherine M Shear, Timothy A Brown, David H Barlow, Roy Money, Diane E Sholomskas, Scott W Woods, Jack M Gorman, Laszlo A PappAbstract: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...
Jürgen Fritze - One of the best experts on this subject based on the ideXlab platform.
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gender differences in associations of glutamate decarboxylase 1 gene gad1 variants with Panic Disorder
PLOS ONE, 2012Co-Authors: Heike Weber, Christian Jacob, Jürgen Fritze, Katharina Domschke, Benedikt Klauke, Claus Jurgen Scholz, Christian Baumann, Wolfgang Maier, Borwin BandelowAbstract:Background: Panic Disorder is common (5% prevalence) and females are twice as likely to be affected as males. The heritable component of Panic Disorder is estimated at 48%. Glutamic acid dehydrogenase GAD1, the key enzyme for the synthesis of the inhibitory and anxiolytic neurotransmitter GABA, is supposed to influence various mental Disorders, including mood and anxiety Disorders. In a recent association study in depression, which is highly comorbid with Panic Disorder, GAD1 risk allele associations were restricted to females. Methodology/Principal Findings: Nineteen single nucleotide polymorphisms (SNPs) tagging the common variation in GAD1 were genotyped in two independent gender and age matched case-control samples (discovery sample n=478; replication sample n=584). Thirteen SNPs passed quality control and were examined for gender-specific enrichment of risk alleles associated with Panic Disorder by using logistic regression including a genotype6gender interaction term. The latter was found to be nominally significant for four SNPs (rs1978340, rs3762555, rs3749034, rs2241165) in the discovery sample; of note, the respective minor/risk alleles were associated with Panic Disorder only in females. These findings were not confirmed in the replication sample; however, the genotype6gender interaction of rs3749034 remained significant in the combined sample. Furthermore, this polymorphism showed a nominally significant association with the Agoraphobic Cognitions Questionnaire sum score. Conclusions/Significance: The present study represents the first systematic evaluation of gender-specific enrichment of risk alleles of the common SNP variation in the Panic Disorder candidate gene GAD1. Our tentative results provide a possible explanation for the higher susceptibility of females to Panic Disorder.
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chromosome 4q31 34 Panic Disorder risk locus association of neuropeptide y y5 receptor variants
American Journal of Medical Genetics, 2008Co-Authors: Katharina Domschke, Christian Jacob, Jürgen Fritze, Christa Hohoff, Wolfgang Maier, Borwin Bandelow, Petra Krakowitzky, Florian Kastner, Matthias Rothermundt, Volker AroltAbstract:There is strong evidence for a genetic contribution to the pathogenesis of Panic Disorder, with a recent linkage study pointing toward a risk locus on chromosome 4q31-q34 [Kaabi et al., 2006]. Since the neuropeptide Y (NPY) system has been reported to be involved in the pathophysiology of anxiety and in particular Panic Disorder and the genes coding for NPY Y1, Y2, and Y5 receptors are located in the suggested risk region (4q31-q32), variants in the NPY, NPY Y1, Y2, and Y5 genes were investigated for association with Panic Disorder in a sample of 230 German patients with Panic Disorder and matched healthy controls. A synonymous (Gly-426-Gly) NPY Y5 coding variant (rs11946004) as well as haplotypes including rs11946004 and an intronic NPY Y5 variant (rs11724320) were significantly associated with Panic Disorder (P = 0.027), with the effect originating from the subgroup of female patients (P = 0.030), particularly with concurrent agoraphobia (P = 0.002–0.019). No association was observed for any variants located in the genes coding for NPY, NPY Y1, or Y2. The present results provide preliminary support for an influence of NPY Y5 receptor variants on the etiology of Panic Disorder in a potentially gender-specific manner further strengthening the evidence for a risk locus on chromosome 4q31-q34 in anxiety Disorders. However, in order to allow for conclusive evaluation of the present finding and to exclude a false positive result, further studies in larger, independent, preferably family based samples are warranted. © 2007 Wiley-Liss, Inc.
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association of a functional 1019c g 5 ht1a receptor gene polymorphism with Panic Disorder with agoraphobia
The International Journal of Neuropsychopharmacology, 2004Co-Authors: Claudia Rothe, Petra Franke, Christine M Freitag, Jürgen Fritze, Lise Gutknecht, Ralf Tauber, Rainald Mossner, Gerd Wagner, G Peikert, Berit WendaAbstract:Panic Disorder is a common anxiety Disorder which frequently co-occurs with agoraphobia. A functional promoter polymorphism in the serotonin receptor 1A (5-HT1A) gene has been found to be associated with major depression as well as anxiety- and depression-related personality traits. We investigated a possible association between this 5-HT1A gene promoter polymorphism and Panic Disorder by genotyping the −1019C>G single nucleotide polymorphism in 134 Panic-Disorder patients with and without agoraphobia and matched 134 controls. In our sample no significant evidence of allelic association in the combined Panic-Disorder group was found. However, our results show a significant association with the G allele in patients with Panic Disorder with agoraphobia ( p =0.03, n =101). In conclusion, our findings do not support a major contribution of this polymorphism to the pathogenesis of Panic Disorder, but provide evidence for a possible role in the subgroup with agoraphobia.
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cholecystokinin and cholecystokinin b receptor gene polymorphisms in Panic Disorder
Journal of Neural Transmission-supplement, 2004Co-Authors: V G Hosing, Philipp G Sand, C Schlesiger, Petra Franke, Anja Schirmacher, Christine M Freitag, Christian Jacob, Gregor Kuhlenbäumer, Jürgen Fritze, Marcella RietschelAbstract:Panic Disorder like other neuropsychiatric Disorders is believed to be caused by multiple psychosocial and biological factors. Several lines of evidence point to a role for the peptide neurotransmitter cholecystokinin in the pathogenesis of Panic Disorder. We therefore determined the allele and genotype frequencies of a single nucleotide polymorphism in the CCK gene (−36C > T) and one CT repeat polymorphism in the CCK-B-receptor gene in a German Panic Disorder sample (n = 115 for CCK gene polymorphism, n = 111 for CCK-B-receptor polymorphism) and compared them with gender and age matched controls . The length of the polymorphic CT repeat alleles varies between 146bp and 180bp. We first analysed the results by a permutation test which provided evidence for heterogeneity between patients and controls (p = 0.002). We then analysed the data as a di-allelic polymorphism with a short (146-162 bp) and a long (l64-180bp) allele and as a tetra-allelic polymorphism with 4 alleles (146–154 bp, 156–162 bp, 164–170 bp, 172–180 bp). In the di-allelic analysis as well as in the tetra-allelic analysis there was an excess of the longer allele (p = 0.001) or the two longer alleles (p = 0.041) respectively in patients with Panic Disorder. No difference between groups was observed for the − 36C > T polymorphism. Our findings are consistent with the notion that genetic variation in the CCK neurotransmitter system contributes to the pathogenesis of Panic Disorder.
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excess of high activity monoamine oxidase a gene promoter alleles in female patients with Panic Disorder
Human Molecular Genetics, 1999Co-Authors: Jurgen Deckert, Petra Franke, Marco Catalano, Yana V Syagailo, Monica Bosi, Olga Okladnova, Daniela Di Bella, Markus M Nothen, Piermario Maffei, Jürgen FritzeAbstract:A genetic contribution to the pathogenesis of Panic Disorder has been demonstrated by clinical genetic studies. Molecular genetic studies have focused on candidate genes suggested by the molecular mechanisms implied in the action of drugs utilized for therapy or in challenge tests. One class of drugs effective in the treatment of Panic Disorder is represented by monoamine oxidase A inhibitors. Therefore, the monoamine oxidase A gene on chromosome X is a prime candidate gene. In the present study we investigated a novel repeat polymorphism in the promoter of the monoamine oxidase A gene for association with Panic Disorder in two independent samples (German sample, n = 80; Italian sample, n = 129). Two alleles (3 and 4 repeats) were most common and constituted >97% of the observed alleles. Functional characterization in a luciferase assay demonstrated that the longer alleles (3a, 4 and 5) were more active than allele 3. Among females of both the German and the Italian samples of Panic Disorder patients (combined, n = 209) the longer alleles (3a, 4 and 5) were significantly more frequent than among females of the corresponding control samples (combined, n = 190, chi2 = 10.27, df = 1, P = 0.001). Together with the observation that inhibition of monoamine oxidase A is clinically effective in the treatment of Panic Disorder these findings suggest that increased monoamine oxidase A activity is a risk factor for Panic Disorder in female patients.
J. C. Duro - One of the best experts on this subject based on the ideXlab platform.
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Association Between Joint Hypermobility Syndrome and Panic Disorder
The American journal of psychiatry, 1998Co-Authors: Rocío Martín-santos, Antonio Bulbena, Miquel Porta, Jordi Gago, Lluis Molina, J. C. DuroAbstract:Objective:The purpose of this study was to assess whether joint hypermobility syndrome is more frequent in patients with Panic Disorder, agoraphobia, or both than in control subjects and, if so, to determine whether mitral valve prolapse modifies or accounts in part for the association.Method:A case-control study was conducted in a general teaching hospital outpatient clinic. Subjects were 99 patients, newly diagnosed and untreated, with Panic Disorder, agoraphobia, or both and two groups of age- and sex-matched control subjects: 99 psychiatric patients and 64 medical patients who had never suffered from any anxiety Disorder. Measures consisted of the Structured Clinical Interview for DSM-III-R, Beighton’s criteria for joint hypermobility syndrome, and two-dimensional and M-mode echocardiogram. The presence of mitral valve prolapse and joint hypermobility syndrome was explored by raters who were blind to subjects’ psychiatric status.Results:Joint hypermobility syndrome was found in 67.7% of patients with ...
