| Project/Area Number |
11470297
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | DOKKYO UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
KAWANOTO Toshiki DOKKYO UNIVERSITY, SCHOOL OF MEDICINE, Instructor, 医学部, 助手 (50301461)
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| Co-Investigator(Kenkyū-buntansha) |
OKUHATA Soshi DOKKYO UNIVERSITY, SCHOOL OF MEDICINE, Lecturer, 医学部, 講師 (20194508)
KIM Phyo DOKKYO UNIVERSITY, SCHOOL OF MEDICINE, Professor, 医学部, 教授 (90231290)
渡辺 邦彦 獨協医科大学, 医学部, 講師 (00230954)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥15,500,000 (Direct Cost: ¥15,500,000)
Fiscal Year 2000: ¥5,200,000 (Direct Cost: ¥5,200,000)
Fiscal Year 1999: ¥10,300,000 (Direct Cost: ¥10,300,000)
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| Keywords | chronic cord compression / spinal cord / neuronal loss / rat / apoptosis / microvascular anatomy / compression myelopathy |
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| Research Abstract |
A novel experimental model for cervical myelopathy was developed in the rat. A thin expanding polymer was inserted under the cervical laminae without cord injury. After the insertion (cord compression), voluntary exercise activity and locomotion capability were monitored for 25 weeks. Although voluntary exercise activity was not changed, locomotion capability deteriorated with a latency of 17 weeks after cord compression and worsened progressively. Those characteristics were resembled to clinical spondylotic myelopathy. Motor neuron was counted at 1, 3, 9 and 25 weeks after cord compression. The neuron count decreased in 9 weeks and 25 weeks significantly. The count of 25 weeks after compression was only 66% compared with control groups. We also investigated the changes microvasculature of the spinal cord in this compression model using silicone rubber perfusion technique. At 25 weeks after compression, vein in the white matter and gray matter were dilated and vessels of cord surface were compressed. This suggest that the disturbance of microcirculation in- and/or extramedullary was caused clinical symptom and delayed neuronal loss.
We believe the present model is to help advancement of the neuropathological and neurophysiological studies of the mechanism of cervical myelopathy.
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