• Journal of Korean Neurosurgical Society
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• 제58권2호
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• pp.93-100
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• 2015

Objective : Optimal treatment decision and estimation of the prognosis in traumatic brain injury (TBI) is currently based on demographic and clinical predictors. But sometimes, there are limitations in these factors. In this study, we analyzed three central nervous system biomarkers in TBI patients, will discuss the roles and clinical applications of biomarkers in TBI. Methods : From July on 2013 to August on 2014, a total of 45 patients were included. The serum was obtained at the time of hospital admission, and biomarkers were extracted with centrifugal process. It was analyzed for the level of S-100 beta (S100B), glial fibrillary acidic protein (GFAP), and ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1). Results : This study included 33 males and 12 females with a mean age of 58.5 (19-84) years. TBI patients were classified into two groups. Group A was severe TBI with Glasgow Coma Scale (GCS) score 3-5 and Group B was mild TBI with GCS score 13-15. The median serum concentration of S100B, GFAP, and UCH-L1 in severe TBI were raised 5.1 fold, 5.5 fold, and 439.1 fold compared to mild injury, respectively. The serum levels of these markers correlated significantly with the injury severity and clinical outcome (p<0.001). Increased level of markers was strongly predicted poor outcomes. Conclusion : S100B, GFAP, and UCH-L1 serum level of were significantly increased in TBI according to severity and associated clinical outcomes. Biomarkers have potential utility as diagnostic, prognostic, and therapeutic adjuncts in the setting of TBI.

• Journal of Korean Neurosurgical Society
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• 제66권4호
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• pp.400-408
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• 2023

Objective : Nicotinamide mononucleotide adenylyl transferase 2 (NMNAT2) is a crucial factor for the survival of neuron. The role of NMNAT2 in damage following traumatic brain injury (TBI) remains unknown. This study was designed to investigate the role of NMNAT2 in TBI-induced neuronal degeneration and neurological deficits in rats. Methods : The TBI model was established in Sprague-Dawley rats by a weight-dropping method. Real-time polymerase chain reaction, western blot, immunofluorescence, Fluoro-Jade C staining, and neurological score analyses were carried out. Results : NMNAT2 mRNA and protein levels were increased in the injured-side cortex at 6 hours and peaked 12 hours after TBI. Knocking down NMNAT2 with an injection of small interfering RNA in lateral ventricle significantly exacerbated neuronal degeneration and neurological deficits after TBI, which were accompanied by increased expression of BCL-2-associated X protein (Bax). Conclusion : NMNAT2 expression is increased and NMNAT2 exhibits neuroprotective activity in the early stages after TBI, and Bax signaling pathway may be involved in the process. Thus, NMNAT2 is likely to be an important target to prevent secondary damage following TBI.

• Journal of Korean Neurosurgical Society
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• 제29권4호
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• pp.461-470
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• 2000

Objective : Many investigators have demonstrated the protective effects of hypothermia following traumatic brain injury(TBI) in both animals and humans. It has long been recognized that mild to moderate hypothermia improves neurologic outcomes as well as reduces histologic and biochemical sequelae after TBI. In this study, two immunohistochemical staining using terminal deoxynucleotidyl-transferase-mediated biotin dUTP nick end labeling(TUNEL), staining of apoptosis, and ${\beta}$-amyloid precursor protein(${\beta}$-APP), a marker of axonal injury, were done and the authors evaluated the protective effects of hypothermia on axonal and neuronal injury after TBI in rats. Material and Method : The animals were prepared for the delivery of impact-acceleration brain injury as described by Marmarou and colleagues. TBI is achieved by allowing of a weight drop of 450gm, 1 m height to fall onto a metallic disc fixed on the intact skull of the rats. Fourty Sprague-Dawley rats weighing 400 to 450g were subjected to experimental TBI induced by an impact-acceleration device. Twenty rats were subjected to hypothermia after injury, with their rectal temperatures maintained at $32^{\circ}C$ for 1 hour. After this 1-hour period of hypothermia, rewarming to normothermic levels was accomplished over 30-minute period. Following 12 hours, 24 hours, 1 week and 2 weeks later the animals were killed and semiserial sagittal sections of the brain were reacted for visualization of the apoptosis and ${\beta}$-APP. Results : The density of ${\beta}$-APP marked damaged axons within the corticospinal tract at the pontomedullary junction and apoptotic cells at the contused cerebral cortex were calculated for each animal. In comparison with the untreated controls, a significant reduction in ${\beta}$-APP marked damaged axonal density and apoptotic cells were found in all hypothermic animals(p<0.05). Conclusion : This study shows that the posttraumatic hypothermia result in substantial protection in TBI, at least in terms of the injured axons and neurons.

• 생물정신의학
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• 제7권1호
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• pp.55-63
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• 2000

Avariety of symptoms can occur following traumatic brain injury(TBI) or other types of acquired brain injury. These symptoms can include problems with short-term memory, attention, planning, problem solving, impulsivity, disinhibition, poor motivation, and other behavioral and cognitive deficit. These symptoms may respond to certain drugs, such as dopaminergic agents. Amantadine may protect patients from secondary neuronal damage after brain injury as a effect of NMDA receptor antagonists and may improve functioning of brain-injured patients as a dopaminergic agonist. Clinically, based on current evidence, amantadine may provide a potentially effective, safe, and inexpensive option for treating the cognitive, mood, and behavioral disorders of individuals with brain injury. The rationales for using amantadine are discussed, and pertinent literatures are reviewed.

• Journal of Trauma and Injury
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• 제20권2호
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• pp.138-143
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• 2007

Purpose: $S100{\beta}$, a marker of traumatic brain injury (TBI), has been increasingly focused upon during recent years. $S100{\beta}$, is easily measured not only in cerebrospinal fluid (CSF) but also in serum. After TBI, serum S 10019, has been found to be increased at an early stage. The purpose of this study was to evaluate the clinical correlations between serum $S100{\beta}$, and neurologic outcome, and severity in traumatic brain injury. Methods: From August 2006 to October 2006, we made a protocol and studied prospectively 42 patients who visited the emergency room with TBI. Venous blood samples for $S100{\beta}$, protein were taken within six hours after TBI and vital signs, as well as the Glasgow Coma Scale (GCS), were recorded. The final diagnosis and the severity were evaluated using the Abbreviated Injury Score (AIS), and the prognosis of the patients was evaluated using the Glasgow Outcome Score (GOS). Results: Thirty-eight patients showed a favorable prognosis (discharge, recovery, transfer), and four showed an unfavorable prognosis. Serum $S100{\beta}$, was higher in patients with an unfavorable prognosis than in patients with a favorable prognosis, and a significant difference existed between the two groups ($0.74{\pm}1.50\;{\mu}g/L$ vs $7.62{\pm}6.53\;{\mu}g/L$ P=0.002). A negative correlation existed between serum $S100{\beta}$, and the Revised Traumatic Score (R2=-0.34, P=0.03), and a positive correlation existed between serum $S100{\beta}$, and the Injury Severity Score (R2=0.33, P=0.03). Furthermore, the correlation between serum $S100{\beta}$, and the initial GCS and the GCS 24 hours after admission to the ER were negative (R2=-0.62, P<0.001; R2=-0.47, P=0.005). Regarding the GOS, the mean serum concentration of $S100{\beta}$, was $7.62\;{\ss}{\partial}/L$ (SD=${\pm}6.53$) in the expired patients, $1.15\;{\mu}g/L$ in the mildly disable patient, and $0.727\;{\mu}g/L$ (SD=${\pm}0.73$) in the recovered patients. These differences are statistically significant (p<0.001). Conclusion: In traumatic brain injury, a higher level of serum concentration of $S100{\beta}$, has a poor prognosis for neurologic outcome.

• Journal of Trauma and Injury
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• 제30권4호
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• pp.140-144
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• 2017

Purpose: The optic nerve sheath diameter (ONSD) measured by ultrasonography is among the indicators of intracranial pressure (ICP) elevation. However, whether ONSD measurement is useful for initial treatment remains controversial. Thus, this study aimed to investigate the relationship between ONSD measured by computed tomography (CT) and ICP in patients with traumatic brain injury (TBI). Methods: A total of 246 patients with severe trauma from January 1, 2015 until December 31, 2015 were included in the study. A total of 179 patients with brain damage with potential for ICP elevation were included in the TBI group. The remaining 67 patients comprised the non-TBI group. A comparison was made between the two groups. Receiver operating characteristic (ROC) curve analysis was performed to determine the accuracy of ONSD when used as a screening test for the TBI group including those with TBI with midline shift (with elevated ICP). Results: The mean injury severity score (ISS) and glasgow coma scale (GCS) of all patients were $24.2{\pm}6.1$ and $5.4{\pm}0.8$, respectively. The mean ONSD of the TBI group ($5.5{\pm}1.0mm$) was higher than that of the non-TBI group ($4.7{\pm}0.6mm$). Some significant differences in age ($55.3{\pm}18.1$ vs. $49.0{\pm}14.8$, p<0.001), GCS ($11.7{\pm}4.1$ versus $13.3{\pm}3.0$, p<0.001), and ONSD ($5.5{\pm}1.0$ vs. $4.7{\pm}0.6$, p<0.001) were observed between the TBI and the non-TBI group. An ROC analysis was used to assess the correlation between TBI and ONSD. Results showed an area under the ROC curve (AUC) value of 0.752. The same analysis was used in the TBI with midline shift group, which showed an AUC of 0.912. Conclusions: An ONSD of >5.5 mm, measured on CT, is a good indicator of ICP elevation. However, since an ONSD is not sensitive enough to detect an increased ICP, it should only be used as one of the parameters in detecting ICP along with other screening tests.

• 한국콘텐츠학회논문지
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• 제11권4호
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• pp.253-262
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• 2011

외상성 뇌손상 및 우반구 손상 환자의 인지-의사소통 능력은 다른 신경학적 장애군과 다른 양상을 띤다. 따라서, 이들의 진단 시 실어증 평가도구 등을 활용하는 것은 바람직하지 않다. 본 연구에서는 두 장애군의 인지-의사소통 능력을 평가할 수 있는 문항을 개발하기에 앞서, 이와 관련된 국외 문헌 및 평가도구를 살펴보고자 하였다. 연구 결과, 외상성 뇌손상 환자의 평가 시에는 주의력, 기억력, 조직화 능력, 추론력, 기능적 의사소통 능력 등을 포괄적으로 고려하는 것이 유용함을 알 수 있었다. 또한, 우반구 손상 이후에는 주의력 등 여러 인지 영역과 함께 고차원적 언어 능력을 평가할 필요성이 제기되었다. 요컨대, 두 장애군의 인지-의사소통 능력을 평가하기 위해서는 다양한 인지-의사소통 영역 간의 영향을 반드시 고려해야 한다. 아울러, 두 장애군을 실어증 등 다른 신경학적 장애군으로부터 변별하고, 치료 시 영역별 지침서로서 활용할 수 있는 평가도구의 개발이 필요하다.

• Journal of Korean Neurosurgical Society
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• 제60권3호
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• pp.355-361
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• 2017

Objective : The aim of this study to investigate the normal values of erythropoietin (EPO) and neuroprotective effects of quercetin and mannitol on EPO and hematocrit levels after acute severe traumatic brain injury (TBI) in rat model. Methods : A weight-drop impact acceleration model of TBI was used on 40 male Wistar rats. The animals were divided into sham (group I), TBI (group II), TBI+quercetin (50 mg/kg intravenously) (group III), and TBI+mannitol (1 mg/kg intravenously) (group IV) groups. The malondialdehyde, glutathione peroxidase, catalase, EPO, and hematocrit levels were measured 1 and 4 hour after injury. Two-way repeated measures analysis of variance and Tukey's test were used for statistical analysis. Results : The malondialdehyde levels decreased significantly after administration of quercetin and mannitol compared with those in group II. Catalase and glutathione peroxidase levels increased significantly in groups III and IV. Serum EPO levels decreased significantly after mannitol but not after quercetin administration. Serum hematocrit levels did not change significantly after quercetin and mannitol administration 1 hour after trauma. However, mannitol administration decreased serum hematocrit levels significantly after 4 hour. Conclusion : This study suggests that quercetin may be a good alternative treatment for TBI, as it did not decrease the EPO levels.

• The Korean Journal of Physiology and Pharmacology
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• 제24권2호
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• pp.165-171
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• 2020

Ischemic and traumatic brain injuries are the major acute central nervous system disorders that need to be adequately diagnosed and treated. To find biomarkers for these acute brain injuries, plasma levels of some specialized pro-resolving mediators (SPMs, i.e., lipoxin A4 [LXA4], resolvin [Rv] E1, RvE2, RvD1 and RvD2), CD59 and interleukin (IL)-6 were measured at 0, 6, 24, 72, and 168 h after global cerebral ischemic (GCI) and traumatic brain injuries (TBI) in rats. Plasma LXA4 levels tended to increase at 24 and 72 h after GCI. Plasma RvE1, RvE2, RvD1, and RvD2 levels showed a biphasic response to GCI; a significant decrease at 6 h with a return to the levels of the sham group at 24 h, and again a decrease at 72 h. Plasma CD59 levels increased at 6 and 24 h post-GCI, and returned to basal levels at 72 h post-GCI. For TBI, plasma LXA4 levels tended to decrease, while RvE1, RvE2, RvD1, and RvD2 showed barely significant changes. Plasma IL-6 levels were significantly increased after GCI and TBI, but with different time courses. These results show that plasma LXA4, RvE1, RvE2, RvD1, RvD2, and CD59 levels display differential responses to GCI and TBI, and need to be evaluated for their usefulness as biomarkers.

• Journal of Korean Neurosurgical Society
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• 제66권1호
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• pp.63-71
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• 2023

Objective : Traumatic brain injury (TBI) is one of the most common injuries in patients with multiple trauma, and it associates with high post-traumatic mortality and morbidity. A trauma center was established to provide optimal treatment for patients with severe trauma. This study aimed to compare the treatment outcomes of patients with severe TBI between non-trauma and trauma centers based on data from the Korean Neuro-Trauma Data Bank System (KNTDBS). Methods : From January 2018 to June 2021, 1122 patients were enrolled in the KNTDBS study. Among them, 253 patients from non-traumatic centers and 253 from trauma centers were matched using propensity score analysis. We evaluated baseline characteristics, the time required from injury to hospital arrival, surgery-related factors, neuromonitoring, and outcomes. Results : The time from injury to hospital arrival was shorter in the non-trauma centers (110.2 vs. 176.1 minutes, p=0.012). The operation time was shorter in the trauma centers (156.7 vs. 128.1 minutes, p=0.003). Neuromonitoring was performed in nine patients (3.6%) in the non-trauma centers and 67 patients (26.5%) in the trauma centers (p<0.001). Mortality rates were lower in trauma centers than in non-trauma centers (58.5% vs. 47.0%, p=0.014). The average Glasgow coma scale (GCS) at discharge was higher in the trauma centers (4.3 vs. 5.7, p=0.011). For the Glasgow outcome scale-extended (GOSE) at discharge, the favorable outcome (GOSE 5-8) was 17.4% in the non-trauma centers and 27.3% in the trauma centers (p=0.014). Conclusion : This study showed lower mortality rates, higher GCS scores at discharge, and higher rates of favorable outcomes in trauma centers than in non-trauma centers. The regional trauma medical system seems to have a positive impact in treating patients with severe TBI.