Changes in Cerebral Cortex and Limbic Brain Functions after Short-Term Paroxetine Treatment in Panic Disorder: An [18F]FDG-PET Pilot Study
1
조회
0
다운로드
2
인용
0
참고문헌
키워드
초록
ObjectiveaaPanic 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. MethodsaaWe 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). ResultsaaAfter 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). ConclusionaaIn 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.
Abstract
ObjectiveaaPanic 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. MethodsaaWe 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). ResultsaaAfter 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). ConclusionaaIn 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.
참고문헌 (29)
- Kessler RC, "The epidemiology of panic attacks, panic disorder, and agoraphobia in the National Comorbidity Survey Replication", Arch Gen Psychiatry, 63, pp.415~424 (2006)
- Kroenke K, "Anxiety disorders in primary care: prevalence, impairment, comorbidity, and detection", Ann Intern Med, 146, pp.317~325 (2007)
- Slaap BR, "The prediction of nonresponse to pharmacotherapy in panic disorder: a review", Depress Anxiety, 14, pp.112~122 (2001)
- Neumeister A, "Anxiety disorders: Neurochemical aspects in Comprehensive Textbook Of Psychiatry (8th Ed. vol 1)", pp.1739~1741 (2005), Lippincott Williams & Wilkins
- Kent JM, "Molecular targets in the treatment of anxiety", Biol Psychiatry, 52, pp.1008~1030 (2002)
- Gorman JM, "Neuroanatomical hypothesis of panic disorder, revised", Am J Psychiatry, 157, pp.493~505 (2000)
- Malhi GS, "Making sense of neuroimaging in psychiatry", Acta Psychiatr Scand, 117, pp.100~117 (2008)
- Reiman EM, "A focal brain abnormality in panic disorder, a severe form of anxiety", Nature, 310, pp.683~685 (1984)
- Bisaga A, "Cerebral glucose metabolism in women with panic disorder", Am J Psychiatry, 155, pp.1178~1183 (1998)
- Lim YJ, "Korean panic disorder severity scale: construct validity by confirmatory factor analysis", Depress Anxiety, 24, pp.95~102 (2007)
- First MB, "Structured clinical interview for DSM-IV axis I disorders" (1996), New York State Psychiatric Institute
- Hamilton M, "A rating scale for depression", J Neurol Neurosurg Psychiatry, 23, pp.56~62 (1960)
- Hamilton M, "The assessment of anxiety states by rating", Br J Med Psychol, 32, pp.50~55 (1959)
- Spielberger CD, "Manual for the state-trait anxiety inventory" (1970), Consulting Psychologists Press
- Altshuler LL, "Assessment of affective variables in clinical trials in Handbook of Clinical Trials: The Neurobehavioral Approach", pp.141~164 (1991), Netherlands Publishers
- "Practice guideline for the treatment of patients with panic disorder. Work Group on Panic Disorder", Am J Psychiatry, 155(5), pp.1~34 (1998), American Psychiatric Association
- Talairach J, "Co-Planar Stereotaxic Atlas of the Human Brain" (1988), Thieme
- Park IH, "Medial prefrontal default-mode hypoactivity affecting trait physical anhedonia in schizophrenia", Psychiatry Res, 171, pp.155~165 (2009)
- LeDoux JE, "Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear", J Neurosci, 8, pp.2517~2529 (1988)
- Davis M, "The role of the amygdala in fear and anxiety", Annu Rev Neurosci, 15, pp.353~375 (1992)
- Schaefer SM, "Modulation of amygdalar activity by the conscious regulation of negative emotion", J Cogn Neurosci, 14, pp.913~921 (2002)
- Quirk GJ, "Stimulation of medial prefrontal cortex decreases the responsiveness of central amygdala output neurons", J Neurosci, 23, pp.8800~8807 (2003)
- Boshuisen ML, "rCBF differences between panic disorder patients and control subjects during anticipatory anxiety and rest", Biol Psychiatry, 52, pp.126~135 (2002)
- Kent JM, "Clinical utility of the selective serotonin reuptake inhibitors in the spectrum of anxiety", Biol Psychiatry, 44, pp.812~824 (1998)
- Welkowitz LA, "Cognitive-behavior therapy for panic disorder delivered by psychopharmacologically oriented clinicians", J Nerv Ment Dis, 179, pp.473~477 (1991)
- Prasko J, "The change of regional brain metabolism (18FDG-PET) in panic disorder during the treatment with cognitive behavioral therapy or antidepressants", Neuro Endocrinol Lett, 25, pp.340~348 (2004)
- Allman JM, "The anterior cingulate cortex. The evolution of an interface between emotion and cognition", Ann N Y Acad Sci, 935, pp.107~117 (2001)
- Zhou L, "Evidence that serotonin reuptake modulators increase the density of serotonin innervation in the forebrain", J Neurochem, 96, pp.396~406 (2006)
- Hariri AR, "Serotonin transporter genetic variation and the response of the human amygdala", Science, 297, pp.400~403 (2002)