Background: Panic disorder (PD) is a common and often chronic psychiatric condition that can lead to considerable disability in daily life. Using [18F]fluorodeoxyglucose-PET, we examined brain baseline glucose metabolism in PD patients in comparison with normal controls and the changes in glucose metabolism after 12 weeks of escitalopram treatment. Methods: Fifteen patients with PD were compared to 20 normal controls using [18F]FDG-PET at baseline and brain metabolism after 12 weeks of escitalopram treatment was compared to pretreatment in the patient group using voxel-based statistical analysis and post hoc region-of-interest analysis. Results: Patients with PD showed decreased metabolism in both the frontal, right temporal, and left posterior cingulate gyruses. After 12 weeks of escitalopram treatment, treatment responders showed metabolic increases in global neocortical areas as well as limbic areas whereas nonresponders did not. Conclusion: Abnormal neocortical function appears to be associated with the pathophysiology of PD and escitalopram exerts its therapeutic action by modulating brain activity at the level of the neocortex and limbic system, notably the amygdala and parahippocampal gyrus.
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