| Project/Area Number |
13671460
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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 |
Cerebral neurosurgery
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| Research Institution | DOKKYO UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
KAWAMOTO Toshiki SCHOOL OF MEDICINE, Assistant Professor, 医学部, 講師 (50301461)
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| Co-Investigator(Kenkyū-buntansha) |
ASAKUNO Keizo SCHOOL OF MEDICINE, Instructor, 医学部, 助手 (00316548)
OGINO Masahiro SCHOOL OF MEDICINE, Assistant Professor, 医学部, 講師 (80224137)
KIM Phyo SCHOOL OF MEDICINE, Professor, 医学部, 教授 (90231290)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2002: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2001: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | chronic cord compression / spinal cord / neuronal loss / rat / central cord injury / microvascular anatomy / compression myelopathy / acute spinal injury / acute spinal injury / chronic spinal cord compression / central cord injury / neuronal loss / apoptosis / compressive myclopathy / MEP |
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| Research Abstract |
A novel experimental model for central cord injury was not developed in the animal model. A thin expanding polymer was inserted under the cervical laminae without cord injury. We have studied the chronic spinal compression model of rat. We use the model of the rat; we tried studying the mechanism of central cord injury. In our model, the motor neuron count decreased in 9 weeks and 25 weeks significantly. The count of 25 weeks after compression was only 66% compared with control group. Then, the hyperextension of hyperflexion injury was given; a motor weakness of upper extremity will happen or not. Some of our model, there were the individual like a central cord injury. The fact will give us the possibility of central cord injury model of the rat. We also investigated the timing of decompression of the compressed spinal cord. At 8 to 12 weeks after compression (the time was the motor neuron count were decreased), if the decompression was not achieved, the capability of locomotion was not improved. In clinical, the fact suggested the timing of decompression surgery. We will continue the study of central cord injury using the model and clinical material. We believe the present model is to help advancement of the neuropathological and neurophysiological studies of the mechanism of central cord injury.
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