| Project/Area Number |
18591612
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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 | Jikei University School of Medicine |
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Principal Investigator |
SATOSHI Sawauchi Jikei University School of Medicine, School of Medicine, Assistant Professor (80235457)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥2,170,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Traumatic Brain Iniury / Acute Subdural Hematoma / S-100 protein / Neuron Snecifie Ennlase / Brain Swelling |
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| Research Abstract |
The high mortality of acute subdural hematoma (SDH) is largely explained by its frequent association with primary brain damage consisting of contusion and brain swelling. However, the nature and causes of brain swelling after traumatic brain injury are multifactorial and poorly understood. S-100B proteins and neuron specific enolase (NSE) are considered to be neurobiochemical markers for the brain damage. Serum concentration and kinetics of S-100B protein and NSE provide the assessment of the primary brain damage after acute SDH. In the present study, we examined serum concentration and kinetics of S-100B protein and NSE on the physiological consequence and brain edema formation in the experimental animal model of SDH alone, SDH associated with diffuse brain injury (DBI), and SDH + DBI + hypoxemia. Serum S-100B protein and NSE were significantly correlated with injury severity. The significant correlation was found between the initial S-100B and NSE. In the group of SDH + DBI + hypoxia, the serum value of S-100B protein and NSE was significantly higher compared with SDH alone and SDH + DBI. Secondary increase of serum markers was associated with the presence of secondary insult such as hypoxia or hypotension. Given our findings, it is possible that the poor outcome of acute SDH depends not only on the characteristics of the hematoma itself, but also on the presence of additional cerebral parenchymal injury and secondary insult. Thus, it is possible that the brain swelling associated with acute SDH is mainly caused by cytotoxic brain edema aggravated by an additional secondary insult. In the future, S100B and NSE measurements might reliably predict secondary brain injury and also be used to monitor the efficacy of treatments.
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