| Project/Area Number |
12671464
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Osaka University |
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Principal Investigator |
SHIBATA Masahiko Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科学, 助手 (50216016)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIYA Ikuto Osaka University, Graduate School of Medicine, Professor, 医学系研究科学, 教授 (80028505)
MASHIMO Takashi Osaka University, Graduate School of Medicine, Professor, 医学系研究科学, 教授 (60157188)
SHIMIZU Tadao Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科学, 助手 (40303961)
MIYAUCH Satoru Brain Function Research Group, Kansai Advanced Research Center, Chief Researcher, 関西先端研究センター・知覚機構研究室, 室長(研究職) (80190734)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2000: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | alllodynia / complex regional pain syndrome / FMRI / neuro-imaging / capsokin / neuro imaging |
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| Research Abstract |
We demonstrated the anatomical area of cerebral activation triggered by non-nociceptive stimulation in a single patient with allodynia using functional MRI evaluations. Cerebral activation with non-nociceptive stimulus was measured for both the painful right foot and the healthy left foot. The same measurements were carried out 3 month later, after confirming that the alludynia triggered an increase in activity in the primary and second somatosensory area, inferior parietal lobe, insula, medial prefrontal cortex, anterior cingulated cortex and supplementary motor area, whereas stimulation to the healthy side only resulted n activity in the primary somatosensory area and inferior parietal lobe. Three months later, after the symptoms of allodynia had disappeared, the same stimuli to the right foot showed a decrease in activation of only the primary and second somatosensory area.
Allodynia is secondary to nerve injury or tissue damage. The mechanism of how allodynia is perceived is essentially unknown. In our case the patient presented signs which fit the criteria for CRPS type I. Although these symptoms ceased naturally, the allodynia seen in our patient was common to that of CRPS type I. We believe that our findings are significant for understanding the pathophysiology of allodynia seen in CRP type I.
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