Abstract
Background: Functional neuroimaging studies have implicated hyperactivity of the frontal cortex in obsessive-compulsive disorder (OCD); however, relationships between abnormal brain activity, clinical improvement, and neuropsychological function have not been clarified in OCD. To clarify the pathophysiology of this disorder, regional changes in brain function were examined during administration of cognitive and symptom provocation tasks in patients with OCD before and after treatment. Methods: Ten outpatients with OCD participated in the study. Functional magnetic resonance imaging (fMRI) was performed before and after treatment. Stroop and symptom provocation tasks were administered during fMRI. Each patient was randomly allocated to receive either pharmacotherapy with fluvoxamine 200 mg/day (n = 4) or behavior therapy (n = 6) for 12 weeks. Results: After 12-week treatment, mean (± SD) total score on the Yale-Brown Obsessive-Compulsive Scale decreased from 29.00 ± 3.59 to 14.60 ± 9.22, representing symptomatic improvement from moderate to mild. After symptom improvement, symptom provocation-related activation in the orbitofrontal, dorsolateral-prefrontal, and anterior cingulate cortices decreased. Conversely, Stroop task-related activation in the parietal cortex and cerebellum increased. Conclusions: After improvement of OCD with either fluvoxamine or behavioral therapy, hyperactivation of the frontal lobe related to a symptom-provocative state decreases, and posterior brain activity related to action-monitoring function increases.
| Original language | English |
|---|---|
| Pages (from-to) | 901-910 |
| Number of pages | 10 |
| Journal | Biological Psychiatry |
| Volume | 57 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - Apr 15 2005 |
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All Science Journal Classification (ASJC) codes
- Biological Psychiatry
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Brain activation of patients with obsessive-compulsive disorder during neuropsychological and symptom provocation tasks before and after symptom improvement : A functional magnetic resonance imaging study. / Nakao, Tomohiro; Nakagawa, Akiko; Yoshiura, Takashi; Nakatani, Eriko; Nabeyama, Maiko; Yoshizato, Chika; Kudoh, Akiko; Tada, Kyoko; Yoshioka, Kazuko; Kawamoto, Midori; Togao, Osamu; Kanba, Shigenobu.
In: Biological Psychiatry, Vol. 57, No. 8, 15.04.2005, p. 901-910.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Brain activation of patients with obsessive-compulsive disorder during neuropsychological and symptom provocation tasks before and after symptom improvement
T2 - A functional magnetic resonance imaging study
AU - Nakao, Tomohiro
AU - Nakagawa, Akiko
AU - Yoshiura, Takashi
AU - Nakatani, Eriko
AU - Nabeyama, Maiko
AU - Yoshizato, Chika
AU - Kudoh, Akiko
AU - Tada, Kyoko
AU - Yoshioka, Kazuko
AU - Kawamoto, Midori
AU - Togao, Osamu
AU - Kanba, Shigenobu
PY - 2005/4/15
Y1 - 2005/4/15
N2 - Background: Functional neuroimaging studies have implicated hyperactivity of the frontal cortex in obsessive-compulsive disorder (OCD); however, relationships between abnormal brain activity, clinical improvement, and neuropsychological function have not been clarified in OCD. To clarify the pathophysiology of this disorder, regional changes in brain function were examined during administration of cognitive and symptom provocation tasks in patients with OCD before and after treatment. Methods: Ten outpatients with OCD participated in the study. Functional magnetic resonance imaging (fMRI) was performed before and after treatment. Stroop and symptom provocation tasks were administered during fMRI. Each patient was randomly allocated to receive either pharmacotherapy with fluvoxamine 200 mg/day (n = 4) or behavior therapy (n = 6) for 12 weeks. Results: After 12-week treatment, mean (± SD) total score on the Yale-Brown Obsessive-Compulsive Scale decreased from 29.00 ± 3.59 to 14.60 ± 9.22, representing symptomatic improvement from moderate to mild. After symptom improvement, symptom provocation-related activation in the orbitofrontal, dorsolateral-prefrontal, and anterior cingulate cortices decreased. Conversely, Stroop task-related activation in the parietal cortex and cerebellum increased. Conclusions: After improvement of OCD with either fluvoxamine or behavioral therapy, hyperactivation of the frontal lobe related to a symptom-provocative state decreases, and posterior brain activity related to action-monitoring function increases.
AB - Background: Functional neuroimaging studies have implicated hyperactivity of the frontal cortex in obsessive-compulsive disorder (OCD); however, relationships between abnormal brain activity, clinical improvement, and neuropsychological function have not been clarified in OCD. To clarify the pathophysiology of this disorder, regional changes in brain function were examined during administration of cognitive and symptom provocation tasks in patients with OCD before and after treatment. Methods: Ten outpatients with OCD participated in the study. Functional magnetic resonance imaging (fMRI) was performed before and after treatment. Stroop and symptom provocation tasks were administered during fMRI. Each patient was randomly allocated to receive either pharmacotherapy with fluvoxamine 200 mg/day (n = 4) or behavior therapy (n = 6) for 12 weeks. Results: After 12-week treatment, mean (± SD) total score on the Yale-Brown Obsessive-Compulsive Scale decreased from 29.00 ± 3.59 to 14.60 ± 9.22, representing symptomatic improvement from moderate to mild. After symptom improvement, symptom provocation-related activation in the orbitofrontal, dorsolateral-prefrontal, and anterior cingulate cortices decreased. Conversely, Stroop task-related activation in the parietal cortex and cerebellum increased. Conclusions: After improvement of OCD with either fluvoxamine or behavioral therapy, hyperactivation of the frontal lobe related to a symptom-provocative state decreases, and posterior brain activity related to action-monitoring function increases.
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UR - http://www.scopus.com/inward/citedby.url?scp=20144389554&partnerID=8YFLogxK
U2 - 10.1016/j.biopsych.2004.12.039
DO - 10.1016/j.biopsych.2004.12.039
M3 - Article
C2 - 15820711
AN - SCOPUS:20144389554
VL - 57
SP - 901
EP - 910
JO - Biological Psychiatry
JF - Biological Psychiatry
SN - 0006-3223
IS - 8
ER -