TY - JOUR
T1 - Changes in cerebral glucose utilization in patients with panic disorder treated with cognitive-behavioral therapy
AU - Sakai, Yojiro
AU - Kumano, Hiroaki
AU - Nishikawa, Masami
AU - Sakano, Yuji
AU - Kaiya, Hisanobu
AU - Imabayashi, Etsuko
AU - Ohnishi, Takashi
AU - Matsuda, Hiroshi
AU - Yasuda, Asako
AU - Sato, Atsushi
AU - Diksic, Mirko
AU - Kuboki, Tomifusa
N1 - Funding Information:
This study was supported by a grant-in-aid from the Ministry of Health, Labor, and Welfare of Japan awarded to the second (H.K.) and last authors (T.K.) and by a grant-in-aid for Scientific Research ((B)(2)15330150) from the Japan Society for the Promotion of Science awarded to the fourth author (Y.S.).
PY - 2006/10/15
Y1 - 2006/10/15
N2 - Several neuroanatomical hypotheses of panic disorder have been proposed focusing on the significant role of the amygdala and PAG-related "panic neurocircuitry." Although cognitive-behavioral therapy is effective in patients with panic disorder, its therapeutic mechanism of action in the brain remains unclear. The present study was performed to investigate regional brain glucose metabolic changes associated with successful completion of cognitive-behavioral therapy in panic disorder patients. The regional glucose utilization in patients with panic disorder was compared before and after cognitive-behavioral therapy using positron emission tomography with 18F-fluorodeoxyglucose. In 11 of 12 patients who showed improvement after cognitive-behavioral therapy, decreased glucose utilization was detected in the right hippocampus, left anterior cingulate, left cerebellum, and pons, whereas increased glucose utilization was seen in the bilateral medial prefrontal cortices. Significant correlations were found between the percent change relative to the pretreatment value of glucose utilization in the left medial prefrontal cortex and those of anxiety and agoraphobia-related subscale of the Panic Disorder Severity Scale, and between that of the midbrain and that of the number of panic attacks during the 4 weeks before each scan in all 12 patients. The completion of successful cognitive-behavioral therapy involved not only reduction of the baseline hyperactivity in several brain areas but also adaptive metabolic changes of the bilateral medial prefrontal cortices in panic disorder patients.
AB - Several neuroanatomical hypotheses of panic disorder have been proposed focusing on the significant role of the amygdala and PAG-related "panic neurocircuitry." Although cognitive-behavioral therapy is effective in patients with panic disorder, its therapeutic mechanism of action in the brain remains unclear. The present study was performed to investigate regional brain glucose metabolic changes associated with successful completion of cognitive-behavioral therapy in panic disorder patients. The regional glucose utilization in patients with panic disorder was compared before and after cognitive-behavioral therapy using positron emission tomography with 18F-fluorodeoxyglucose. In 11 of 12 patients who showed improvement after cognitive-behavioral therapy, decreased glucose utilization was detected in the right hippocampus, left anterior cingulate, left cerebellum, and pons, whereas increased glucose utilization was seen in the bilateral medial prefrontal cortices. Significant correlations were found between the percent change relative to the pretreatment value of glucose utilization in the left medial prefrontal cortex and those of anxiety and agoraphobia-related subscale of the Panic Disorder Severity Scale, and between that of the midbrain and that of the number of panic attacks during the 4 weeks before each scan in all 12 patients. The completion of successful cognitive-behavioral therapy involved not only reduction of the baseline hyperactivity in several brain areas but also adaptive metabolic changes of the bilateral medial prefrontal cortices in panic disorder patients.
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U2 - 10.1016/j.neuroimage.2006.06.017
DO - 10.1016/j.neuroimage.2006.06.017
M3 - Article
C2 - 16889985
AN - SCOPUS:33748699979
SN - 1053-8119
VL - 33
SP - 218
EP - 226
JO - NeuroImage
JF - NeuroImage
IS - 1
ER -