Cognitive-behavior therapy for panic disorder delivered by psychopharmacologically oriented clinicians
ABSTRACT 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.
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- "The hypothesis is that medications, particularly those that influence the serotonin system, desensitize the fear network, from the level of the amygdala through its projections into the hypothalamus and the brainstem.24 Effective psychosocial treatments may also reduce contextual fear and cognitive misattributions at the level of the prefrontal cortex and hippocampus.25 Prasko et al.26 examined the effects of SSRIs, as well as CBT, on PD patients in terms of basal glucose metabolism, using [18F]FDG-PET. "
ABSTRACT: Panic disorder (PD) is a common and often chronic psychiatric illness, and serotonin-specific reuptake inhibitors (SSRIs) are the drugs of choice for the treatment of PD. Previous studies suggested the cerebral cortex and limbic brain structures played a major role in the development of PD, but the therapeutic effect of SSRIs on specific brain structures remains unclear in PD. We examined the changes in PD patients' glucose metabolism using the [(18)F] Fluorodeoxy-glucose-positron emission tomography (FDG-PET) before and after 12 weeks of paroxetine treatment. We assessed the brain glucose metabolism of 5 PD patients, using the [(18)F]FDG-PET, and treated them with paroxetine (12.5-37.5 mg/day) for 12 weeks. Then, we compared before and after treatment PET images of the patients, using voxel-based statistical analysis and a post hoc regions of interest analysis. Furthermore, we measured the patients' clinical variables, including information from the Panic Disorder Severity Scale (PDSS), Clinical Global Impression for Severity (CGI-S), and Hamilton Anxiety Rating Scale (HAMA). After 12 weeks of paroxetine treatment, the patients showed significant clinical improvement in terms of PDSS, CGI-S and HAMA scores (12.8±1.8 vs. 3.8±2.3, 4.6±0.5 vs. 2.0±1.4, and 15.2±4.0 vs. 5.0±1.2, respectively; all p values<0.05). After treatment, patients' glucose metabolism increased significantly in global brain areas: the right precentral gyrus, right middle frontal gyrus, right amygdala, right caudate body, right putamen, left middle frontal gyrus, left precentral gyrus, left insula, left parahippocampal gyrus, and left inferior frontal gyrus (All areas were significant at uncorrected p<0.001 and cluster level corrected p<0.05). In these PD patients, cerebral cortex and limbic brain functions changed after short-term treatment with paroxetine. The therapeutic action of paroxetine may be related to altered glucose metabolism at both the cerebral cortex and limbic brain areas.Psychiatry investigation 09/2010; 7(3):215-9. DOI:10.4306/pi.2010.7.3.215 · 1.15 Impact Factor
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ABSTRACT: Objectives: Animal model studies may allow greater elucidation of the cerebral circuits involved in the genesis of Panic Disorder (PD), but these stu- dies have not yet been fully analyzed. Methods: The authors review recent literature on the neurobiology and neuroanatomy of PD. Results: In this update, the authors present a revision of data that demonstrates the existence of a "fear network", which has as its main point the cen- tral nucleus of the amygdale and includes the hypothalamus, the thalamus, the hippocampus, the periaqueductal gray region, the locus ceruleus and other brainstem structures. Its existence is evidenced in animal studies of emotional and behavioral states, and its presence and importance can be extrapolated to the study of PD in humans. Conclusion: This fear network can allow new progresses and studies using neuroimaging techniques and/or psychopharmacological trials, further elu- cidating the cerebral circuits of PD.
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ABSTRACT: Podeu consultar la versió anterior a: http://hdl.handle.net/2445/358 Se abordan diversos aspectos de la agorafobia y el trastorno de pánico: naturaleza, edad de comienzo y curso, frecuencia, problemas asociados, génesis y mantenimiento, métodos e instrumentos de evaluación, y eficacia y utilidad clínica del tratamiento psicológico y farmacológico. Además, se ofrecen guías para aplicar los tratamientos psicológicos más eficaces.