- 著者
- Eiichi SUEHIRO Tatsuya TANAKA Masatou KAWASHIMA Akira MATSUNO
- 出版者
- The Japan Neurosurgical Society
- 雑誌
- Neurologia medico-chirurgica (ISSN:04708105)
- 巻号頁・発行日
- pp.2022-0276, (Released:2022-11-25)
- 参考文献数
- 21
The Japan Neurotrauma Data Bank is a source of epidemiological data for patients with severe traumatic brain injury (TBI) and is sponsored by the Japan Society of Neurotraumatology. In this report, we examined the changes in the treatment of severe TBI in Japan based on data of the Japan Neurotrauma Data Bank. Controlling and decreasing intracranial pressure (ICP) are the primary objective of severe TBI treatment. Brain-oriented whole-body control or neurocritical care, including control of cerebral perfusion pressure, respiration, and infusion, are also increasingly considered important because cerebral tissues require oxygenation to improve the outcomes of patients with severe TBI. The introduction of neurocritical care in Japan was delayed compared with that in Western countries. However, the rate of ICP monitoring increased from 28.0% in 2009 to 36.7% in 2015 and is currently likely to be higher. Neurocritical care has also become more common, but the functional prognosis of patients has not significantly improved in Japan. Changes in the background of patients with severe TBI suggest the need for improvement of acute-phase treatment for elderly patients. Appropriate social rehabilitation from the subacute to chronic phases and introduction of cellular therapeutics are also needed for patients with TBI.
- 著者
- Eiichi SUEHIRO Yuichi FUJIYAMA Miwa KIYOHIRA Yukari MOTOKI Junzo NOJIMA Michiyasu SUZUKI
- 出版者
- The Japan Neurosurgical Society
- 雑誌
- Neurologia medico-chirurgica (ISSN:04708105)
- 巻号頁・発行日
- vol.59, no.2, pp.63-67, 2019 (Released:2019-02-15)
- 参考文献数
- 25
- 被引用文献数
- 3 12
d-dimer is a potential biomarker for the detection of traumatic brain injury (TBI). However, the mechanisms that trigger elevation of d-dimer in TBI remain unclear. The purpose of this study was to evaluate the reliability of d-dimer in blood as a biomarker for TBI and to determine the mechanisms involved in regulating its blood levels. Nine patients with moderate to severe isolated TBI (Glasgow Coma Scale [GCS] score 7–13) were admitted to our hospital from May 2013 to June 2014. Blood samples were collected from systemic arteries on arrival and at 1, 3, 5, and 7 days after injury. Blood levels of neuron specific enolase (NSE), d-dimer, and soluble tissue factor (sTF) were measured. NSE (33.4 ng/ml: normal <12.0 ng/ml) and d-dimer (56.1 μg/ml: normal <1.0 μg/ml) were elevated at admission and declined on day 1 after injury. At admission, there were significant correlations of d-dimer levels with NSE (R = 0.727, P = 0.026) and sTF (R = 0.803, P = 0.009) levels. The blood level of d-dimer accurately reflects the degree of brain tissue damage indicated by NSE levels. Our data suggest that release of sTF induced by brain tissue damage may activate the coagulation cascade, leading to elevation of d-dimer.