• Journal of Trauma and Injury
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• 제22권2호
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• pp.134-141
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• 2009

Purpose: Patients with traumatic brain injury (TBI) were referred from other hospitals for further management. In addition, patients routinely underwent computed tomography examinations of the head (HCT) in the referral hospitals. The purpose of this study was to evaluate retrospectively the utility of routine HCT scans according to the severity of TBI. Methods: Patients with TBI referred to our hospital between December 2005 and July 2008 were included in this study. We investigated HCT findings, indications for repeat HCT examinations (routine versus a neurological change), and neurosurgical interventions. The head injury severity was divided into three categories according to the Glasgow Coma Scale (GCS) score, including mild, moderate, and severe TBI. The use of neurosurgical interventions between patients who underwent routine HCT scans and patients who underwent HCT scans for a neurological change were compared according to the severity of TBI. Results: A total of 81 patients met the entry criteria for this study. Among these patients, 67%(n=54) of the patients underwent HCT scans on a routine basis, whereas 33%(n=27) of the patients underwent HCT scans for a neurological change. A total of 21 patients showed signs of a worsening condition on the HCT scans. Neurosurgical intervention was required for 23(28.4%) patients. For patients who underwent routine HCT examinations, no patient with mild TBI underwent a neurosurgical intervention. However, one patient with moderate TBI and three(13%) patients with severe TBI underwent neurosurgical interventions. The kappa index, the level of agreement for HCT indications of intervention and referral reasons for intervention, was 0.65 for high hierarchy hospitals and 0.06 for low hierarchy hospitals. Conclusion: Routine serial HCT examinations in the referred hospitals would be useful for patients with severe head injury and for patients from low hierarchy hospitals where no emergency physicians or neurosurgeons are available.

• Journal of Korean Neurosurgical Society
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• 제65권5호
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• pp.680-687
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• 2022

Objective : The influence of moderate-to-severe traumatic brain injury (TBI) on acute pulmonary injury is well established, but the association between acute pulmonary injury and mild TBI has not been well studied. Here, we evaluated the histological changes and fluctuations in inflammatory markers in the lungs to determine whether an acute pulmonary inflammatory response occurred after mild TBI. Methods : Mouse models of mild TBI (n=24) were induced via open-head injuries using a stereotaxic impactor. The brain and lungs were examined 6, 24, and 72 hours after injury and compared to sham-operated controls (n=24). Fluoro-Jade B staining and Astra blue and hematoxylin staining were performed to assess cerebral neuronal degeneration and pulmonary histological architecture. Quantitative real-time polymerase chain reaction analysis was done to measure inflammatory cytokines. Results : Increased neuronal degeneration and the mRNA expression of interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-10, and transforming growth factor (TGF)-β were observed after mild TBI. The IL-6, TNF-α, and TGF-β levels in mice with mild TBI were significantly different compared to those of sham-operated mice 24 hours after injury, and this was more pronounced at 72 hours. Mild TBI induced acute pulmonary interstitial edema with cell infiltration and alveolar morphological changes. In particular, a significant infiltration of mast cells was observed. Among the inflammatory cytokines, TNF-α was significantly increased in the lungs at 6 hours, but there was no significant difference 24 and 72 hours after injury. Conclusion : Mild TBI induced acute pulmonary interstitial inflammation and alveolar structural changes, which are likely to worsen the patient's prognosis.

• 생물정신의학
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• 제2권2호
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• pp.157-168
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• 1995

The neuropsychiatric sequelae of traumatic brain unjury(TBI) are effects on complex aspect of behavior, cognition and emotional expression. They include psychiatric disorders such as depression, psychosis, personality change, dementia, and postconcussion syndrome. The damage is done not only to the cortex of the brain but also to subcortical and axial structures. The diffuse degeneration of cerebral white mailer is axonal damage that is caused by mechanical forces shearing the neuronal fiber at the moment of impact(diffuse axonal injury, DAI). The DAI and the changed receptor-agonist mechanism ore the most important mechanisms in genesis of neuropsychiatric sequalae by mild TBI. The most important instrument for diagnosis of neuropsychiatric sequalae of TBI is a physician or psychiatrist with experience and knowledge. The most effective therapeutic tool is a professional who understands the nature of the problem.

• Journal of Trauma and Injury
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• 제33권4호
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• pp.227-235
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• 2020

Purpose: Alcohol intoxication is commonly associated with traumatic brain injury (TBI), but the influence of alcohol on the Glasgow Coma Scale (GCS) score remains unclear. This study investigates the effects of blood alcohol concentration (BAC) on the GCS score in head trauma patients with alcohol intoxication. Methods: In total, 369 head trauma patients with alcohol intoxication in a 1-year period were retrospectively analyzed. The patients underwent head computed tomography and had a BAC ≥80 mg/dL. Patients were divided into TBI and non-TBI groups. Brain injury severity was further classified using the head Abbreviated Injury Score (AIS). The effects according to 5 BAC groups were examined. Results: The TBI group consisted of 64 patients (16.2%). The mean BAC was significantly higher in the non-TBI group (293.4±87.3 mg/dL) than in the TBI group (242.8±89.9 mg/dL). The mean GCS score was significantly lower in the TBI group (10.3±4.6) than in the non-TBI group (13.0±2.5). A higher BAC showed a significant association with a lower mean GCS score in the TBI group, but not in the non-TBI group. Above ≥150 mg/dL, higher BACs showed significant odds ratios for a lower GCS score. Conclusions: The influence of alcohol in patients with head trauma depended on the presence of a brain injury. An association between a higher BAC and a lower GCS score was only observed in patients with TBI. Therefore, if a severe brain injury is suspected based on a GCS evaluation in patients with alcohol intoxication, prompt diagnosis and intensive care should be performed without delay.

• 생물정신의학
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• 제7권1호
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• pp.46-54
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• 2000

외상성 뇌손상으로 외상 후 스트레스 장애, 범불안장애, 공황장애, 강박장애, 공포장애 등의 불안장애가 비교적 흔히 발생할 수 있다. 그러나 빈발하는 불안장애인데 비해 의사들로부터 적절하게 관심을 받지도 못했으며 치료받지도 못하였다. 외상성 뇌손상 후 불안장애는 뇌손상 자체에 의해, 뇌손상과 기능상실에 대한 환자 또는 간호인의 반응에 의해 증상이 발생하기도 하고 지속되기도 한다. 의사는 이들 환자들을 진단하고 치료하기 위해서는 우선 뇌손상의 기전과 양상에 대해 지식이 있어야 하며, 불안증상을 호소하는 외상성 뇌손상 환자를 이해하고 수용하고 지지해주는 태도를 취해야 하며, 불안증상이 뇌손상에 의한 것인지 통상적인 불안 증상인지 확인해야 한다. 이들 뇌손상 환자들은 약물의 부작용에 아주 취약하기 때문에 약물치료시에는 약물의 작용기전은 말할 것도 없고 부작용에 대해 잘 알고 있어야 한다.

• Applied Microscopy
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• 제48권4호
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• pp.102-109
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• 2018

Multiple synaptic boutons (MSBs) have been reported to be synapse with two or more postsynaptic terminals in one presynaptic terminal. These MSBs are known to be increased by various brain stimuli. In the motor cortex, increased number of MSB was observed in both acrobat training (AC) model and traumatic brain injury (TBI) model. Interestingly one is a physiological stimuli and the other is pathological insult. The purpose of this study is to compare the connectivity of MSBs between AC model and TBI model in the cerebral motor cortex, based on the hypothesis that the connectivity of MSBs might be different according to the models. The motor cortex was dissected from perfused brain of each experimental animal, the samples were prepared for routine transmission electron microscopy. The 60~70 serial sections were mounted on the one-hole grid and MSB was analyzed. The 3-dimensional analysis revealed that 94% of MSBs found in AC model synapse two postsynaptic spines from same dendrite. But, 28% MSBs from TBI models synapse two postsynaptic spines from different dendrite. This imply that the MSBs observed in motor cortex of AC model and TBI model might have different circuits for the processing the information.

• Journal of Korean Neurosurgical Society
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• 제65권3호
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• pp.334-341
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• 2022

Traumatic brain injury (TBI) is one of the leading causes of death in the pediatric population in Korea. In addition, it can cause disability in children and adolescents, with physical and mental consequences. This causes a substantial burden on the health care system and occurs globally and not just in Korea. We searched and reviewed current data on the epidemiologic characteristics of pediatric TBI in Korea. Our review provides the recent epidemiological trend mainly focusing on incidence and mortality along with worldwide reported data. This review will be helpful to understand the global epidemiology of pediatric TBI and its differences between countries.

• Journal of Korean Neurosurgical Society
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• 제55권4호
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• pp.190-194
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• 2014

Objective : Post-traumatic stress disorder (PTSD) is a group of diseases that are observed in patients who had experienced a serious trauma or accident. However, some experienced it even after only a mild traumatic brain injury (TBI), and they are easily ignored due to the relatively favorable course of mild TBI. Herein, the authors investigated the incidence of PTSD in mild TBI using brief neuropsychological screening test (PTSD checklist, PCL). Methods : This study was conducted on patients with mild TBI (Glasgow coma scale ${\geq}13$) who were admitted from January 2012 to December 2012. As for PCL, it was done on patients who showed no difficulties in communication upon admission and agreed to participate in this study. By using sum of PCL, the patients were divided into high-risk group and low-risk group. PTSD was diagnosed as the three major symptoms of PTSD according to the Diagnostic and Statistical Manual of Mental Disorders, fourth-edifion. Results : A total of 314 TBI patients were admitted and 71 of them met the criteria and were included in this study. The mean age was 52.9 years-old (range : 15--94). The mean PCL score was 28.8 (range : 17--68), and 10 patients were classified as high-risk group. During follow-up, 2 patients (2.7%) of high risk group, were confirmed as PTSD and there was no patient who was suspected of PTSD in the low-risk group (p=0.017). Conclusion : PTSD is observed 2.8% in mild TBI. Although PTSD after mild TBI is rare, PCL could be considered as a useful tool for screening of PTSD after mild TBI.

• The Korean Journal of Physiology and Pharmacology
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• 제19권6호
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• pp.491-497
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• 2015

Traumatic brain injury (TBI) is a major cause of mortality and long-term disability, which can decrease quality of life. In spite of numerous studies suggesting that Epigallocatechin-3- gallate (EGCG) has been used as a therapeutic agent for a broad range of disorders, the effect of EGCG on TBI remains unknown. In this study, a weight drop model was established to evaluate the therapeutic potential of EGCG on TBI. Rats were administered with 100 mg/kg EGCG or PBS intraperitoneally. At different times following trauma, rats were sacrificed for analysis. It was found that EGCG (100 mg/kg, i.p.) treatment significantly reduced brain water content and vascular permeability at 12, 24, 48, 72 hour after TBI. Real-time PCR results revealed that EGCG inhibited TBI-induced IL-$1{\beta}$ and TNF-${\alpha}$ mRNA expression. Importantly, CD68 mRNA expression decreasing in the brain suggested that EGCG inhibited microglia activation. Western blotting and immunohistochemistry results showed that administering of EGCG significantly inhibited the levels of aquaporin-4 (AQP4) and glial fibrillary acidic protein (GFAP) expression. TBI-induced oxidative stress was remarkably impaired by EGCG treatment, which elevated the activities of SOD and GSH-PX. Conversely, EGCG significantly reduced the contents of MDA after TBI. In addition, EGCG decreased TBI-induced NADPH oxidase activation through inhibition of $p47^{phox}$ translocation from cytoplasm to plasma membrane. These data demonstrate that EGCG treatment may be an effective therapeutic strategy for TBI and the underlying mechanism involves inhibition of oxidative stress.

• Journal of Trauma and Injury
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• 제36권4호
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• pp.354-361
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• 2023

Purpose: Ketamine has historically been contraindicated in traumatic brain injury (TBI) due to concern for raising intracranial pressure. However, it is increasingly being used in TBI due to the favorable respiratory and hemodynamic properties. To date, no studies have evaluated whether ketamine administered in subjects with TBI is associated with patient survival or disability. Methods: We performed a retrospective analysis of data from the multicenter Prehospital Tranexamic Acid Use for Traumatic Brain Injury trial, comparing ketamine-exposed and ketamine-unexposed TBI subjects to determine whether an association exists between ketamine administration and mortality, as well as secondary outcome measures. Results: We analyzed 841 eligible subjects from the original study, of which 131 (15.5%) received ketamine. Ketamine-exposed subjects were younger (37.3±16.9 years vs. 42.0±18.6 years, P=0.037), had a worse initial Glasgow Coma Scale score (7±3 vs. 8±4, P=0.003), and were more likely to be intubated than ketamine-unexposed subjects (88.5% vs. 44.2%, P<0.001). Overall, there was no difference in mortality (12.2% vs. 15.5%, P=0.391) or disability measures between groups. Ketamine-exposed subjects had significantly fewer instances of elevated intracranial pressure (ICP) compared to ketamine-unexposed subjects (56.3% vs. 82.3%, P=0.048). In the very rare outcomes of cardiac events and seizure activity, seizure activity was statistically more likely in ketamine-exposed subjects (3.1% vs. 1.0%, P=0.010). In the intracranial hemorrhage subgroup, cardiac events were more likely in ketamine-exposed subjects (2.3% vs. 0.2%, P=0.025). Ketamine exposure was associated with a smaller increase in TBI protein biomarker concentrations. Conclusions: Ketamine administration was not associated with worse survival or disability despite being administered to more severely injured subjects. Ketamine exposure was associated with reduced elevations of ICP, more instances of seizure activity, and lower concentrations of TBI protein biomarkers.