|Hyun-Bo Sim;Eun-Ho Kang; and Bum-Hee Yu
Department of Psychiatry, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
Objective : 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 [18F]
Fluorodeoxy-glucose-positron emission tomography (FDG-PET) before and after 12
weeks of paroxetine treatment.
Methods : We assessed the brain glucose metabolism of 5 PD patients, using the
[18F]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).
Results : 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).
Conclusion : 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.
Brain imaging;Positron emission tomography;Panic disorder;Paroxetine.