| Project/Area Number |
14571347
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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 | KURUME UNIVERSITY |
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Principal Investigator |
TOKUTOMI Takashi KURUME UNIVERSITY, Medical Department, Associate Professor, 医学部, 助教授 (90197872)
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| Co-Investigator(Kenkyū-buntansha) |
KARUKAYA Takashi KURUME UNIVERSITY, Medical Department, Assistant, 医学部, 助手 (90330844)
TAKEUCHI Yasuharu KURUME UNIVERSITY, Medical Department, Assistant, 医学部, 助手 (00299463)
MIYAGI Tomoya KURUME UNIVERSITY, Medical Department, Assistant, 医学部, 助手 (40268909)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2002: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | Trauma / Brain injury / Hypothermia / Hemodynamic / Metabolism / Intracranial pressure / Oxygen consumption / 心拍出量 / 重症頭部外傷 |
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| Research Abstract |
Patients with Glasgow Coma Scale (GCS) scores of 5 or less after resuscitation have a very high mortality rate and a low rate of favorable outcome as compared with patients with GCS scores of 6 to 8 in traumatic brain injury. Because there is no effective treatment for patients such low GCS scores, we had initiated therapeutic hypothermia (33℃ for 48 to 72 hours) from 1994 to 1999. Contrary to our expectation, improving clinical outcome from this treatment had not been obtained, despite the intracranial pressure reduction effect of hypothermia On the basis of this experience, we gained consequences that cooling to 35℃ is sufficient to control intracranial hypertension and hypothermia below 35℃ may predispose patients to persistent cumulative oxygen debt which may associated with an increasing risk of complications. Persistently high levels of C-reactive protein (CRP) after rewarming from 33℃ was also observed. Since hypothermia was very effective in controlling intracranial hypertension, if we can avoid the adverse effects of hypothermia on systemic conditions, it may be a more promising therapeutic tool. So we have altered the target temperature to 35 from 33 after 2000. The effect of 35℃ hypothermia on intracranial hypertension was similar to those of 33 hypothermia. Cerebral perfusion pressure was controlled at higher level in the 35℃ hypothermic patients rather than 33℃ hypothermic patients. 35℃ hypothermic patients exhibited significant improvement in decline of systemic oxygen consumption and increment of CRP after rewarming. Although further accumulation of the data is necessary, 35℃ seems to be the optimal temperature to control intracranial hypertension in patients with severe traumatic brain injury.
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