• Journal of Korean Neurosurgical Society
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• v.54 no.2
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• pp.100-106
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• 2013

Objective : To investigate the cases of intracranial abnormal brain MRI findings even in the negative brain CT scan after mild head injury. Methods : During a 2-year period (January 2009-December 2010), we prospectively evaluated both brain CT and brain MRI of 180 patients with mild head injury. Patients were classified into two groups according to presence or absence of abnormal brain MRI finding even in the negative brain CT scan after mild head injury. Two neurosurgeons and one neuroradiologist validated the images from both brain CT scan and brain MRI double blindly. Results : Intracranial injury with negative brain CT scan after mild head injury occurred in 18 patients (10.0%). Headache (51.7%) without neurologic signs was the most common symptom. Locations of intracranial lesions showing abnormal brain MRI were as follows; temporal base (n=8), frontal pole (n=5), falx cerebri (n=2), basal ganglia (n=1), tentorium (n=1), and sylvian fissure (n=1). Intracranial injury was common in patients with a loss of consciousness, symptom duration >2 weeks, or in cases of patients with linear skull fracture (p=0.00013), and also more frequent in multiple associated injury than simple one (35.7%>8.6%) (p=0.105). Conclusion : Our investigation showed that patients with mild head injury even in the negative brain CT scan had a few cases of intracranial injury. These findings indicate that even though the brain CT does not show abnormal findings, they should be thoroughly watched in further study including brain MRI in cases of multiple injuries and when their complaints are sustained.

• Journal of Mechanical Science and Technology
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• v.19 no.7
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• pp.1424-1431
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• 2005

In this study, head injury by impact force was evaluated by numerical analysis with 3-dimensional finite element (FE) model. Brain deformation by frontal head impact was analyzed to evaluate traumatic brain injury (TBI). The variations of head acceleration and intra-cranial pressure (ICP) during the impact were analyzed. Relative displacement between the skull and the brain due to head impact was investigated from this simulation. In addition, pathological severity was evaluated according to head injury criterion (HIC) from simulation with FE model. The analytic result of brain damage was accorded with that of the cadaver test performed by Nahum et al.(1977) and many medical reports. The main emphasis of this study is that our FE model was valid to simulate the traumatic brain injury by head impact and the variation of the HIC value was evaluated according to various impact conditions using the FE model.

• Child Health Nursing Research
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• v.17 no.4
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• pp.281-287
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• 2011

Purpose: The study was done to explore growth variation in head circumference (HC) in extremely premature infants (EPI) with brain injury. Methods: A retrospective cohort study was conducted with 79 cohort samples from the archives of the catch-up growth project. Mean age of the infants was 29.2 weeks of gestation and mean HC, 27.1 cm at birth. Their HC measurements were retrieved from the archives up to 6 month of corrected age (CA) and analyzed against history of brain injury during hospitalization. Results: Overall growth retardation in HC was observed in the cohort sample compared to longer gestation premature infants. EPI with brain injury showed decreased HC compared to infants without brain injury, and resulting growth variation across 6 month of CA. Highest retardation in HC growth was observed in male infants with brain injury. Conclusion: Extreme preterm birth itself may function as a major obstacle against HC growth toward term age in EPI. Sustainability of brain injury could be observed with higher HC growth retardation after term. Evolutionary favor to female infants may exist in HC growth of EPI. Intensive education on HC monitoring is highly suggested for parents of EPI, particularly with children with brain injury.

• Kidney Research and Clinical Practice
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• v.37 no.4
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• pp.315-322
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• 2018

The high mortality rates associated with acute kidney injury are mainly due to extra-renal complications that occur following distant-organ involvement. Damage to these organs, which is commonly referred to as multiple organ dysfunction syndrome, has more severe and persistent effects. The brain and its sub-structures, such as the hippocampus, are vulnerable organs that can be adversely affected. Acute kidney injury may be associated with numerous brain and hippocampal complications, as it may alter the permeability of the blood-brain barrier. Although the pathogenesis of acute uremic encephalopathy is poorly understood, some of the underlying mechanisms that may contribute to hippocampal involvement include the release of multiple inflammatory mediators that coincide with hippocampus inflammation and cytotoxicity, neurotransmitter derangement, transcriptional dysregulation, and changes in the expression of apoptotic genes. Impairment of brain function, especially of a structure that has vital activity in learning and memory and is very sensitive to renal ischemic injury, can ultimately lead to cognitive and functional complications in patients with acute kidney injury. The objective of this review was to assess these complications in the brain following acute kidney injury, with a focus on the hippocampus as a critical region for learning and memory.

• Korean Journal of Biological Psychiatry
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• v.7 no.1
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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.

• Clinical and Experimental Pediatrics
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• v.64 no.8
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• pp.422-429
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• 2021

Background: Carnosine has antioxidative and neuroprotective properties against hypoxic-ischemic (HI) brain injury. Hypothermia is used as a therapeutic tool for HI encephalopathy in newborn infants with perinatal asphyxia. However, the combined effects of these therapies are unknown. Purpose: Here we investigated the effects of combined carnosine and hypothermia therapy on HI brain injury in neonatal rats. Methods: Postnatal day 7 (P7) rats were subjected to HI brain injury and randomly assigned to 4 groups: vehicle; carnosine alone; vehicle and hypothermia; and carnosine and hypothermia. Carnosine (250 mg/kg) was intraperitoneally administered at 3 points: immediately following HI injury, 24 hours later, and 48 hours later. Hypothermia was performed by placing the rats in a chamber maintained at 27℃ for 3 hours to induce whole-body cooling. Sham-treated rats were also included as a normal control. The rats were euthanized for experiments at P10, P14, and P35. Histological and morphological analyses, in situ zymography, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assays, and immunofluorescence studies were conducted to investigate the neuroprotective effects of the various interventional treatments. Results: Vehicle-treated P10 rats with HI injury showed an increased infarct volume compared to sham-treated rats during the triphenyltetrazolium chloride staining study. Hematoxylin and eosin staining revealed that vehicle-treated P35 rats with HI injury had decreased brain volume in the affected hemisphere. Compared to the vehicle group, carnosine and hypothermia alone did not result in any protective effects against HI brain injury. However, a combination of carnosine and hypothermia effectively reduced the extent of brain damage. The results of in situ zymography, TUNEL assays, and immunofluorescence studies showed that neuroprotective effects were achieved with combination therapy only. Conclusion: Carnosine and hypothermia may have synergistic neuroprotective effects against brain damage following HI injury.

• Sleep Medicine and Psychophysiology
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• v.6 no.2
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• pp.97-101
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• 1999

Sleep disorders are relatively common occurrence after traumatic brain injury. Sleep disturbances often resulted in difficulties in sleep onset and sleep maintenance, nonrestorative after sleep, poor daytime performances and poor individual sense of wellbeing. Unfortunately, there has been minimal attention paid to this common and disabling sequela of brain injury. Better undertanding about problem, pathophysiology and treatment of sleep disorder after traumatic brain injury will improve the cognitive function, social adjustment and rehabilitation for injured patients. Also it may be helpful to reduce traumatic brain injury in patients with sleep apnea.

• Journal of Trauma and Injury
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• v.34 no.4
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• pp.270-278
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• 2021

Purpose: The purpose of the study is to analyze the results of surgical treatment of patients with brain and torso injury for 5 years in a single regional trauma center. Methods: We analyzed multiple trauma patients who underwent brain surgery and torso surgery for chest or abdominal injury simultaneously or sequentially among all 14,175 trauma patients who visited Dankook University Hospital Regional Trauma Center from January 2015 to December 2019. Results: A total of 25 patients underwent brain surgery and chest or abdominal surgery, with an average age of 55.4 years, 17 men and eight women. As a result of surgical treatment, there were 14 patients who underwent the surgery on the same day (resuscitative surgery), of which five patients underwent surgery simultaneously, four patients underwent brain surgery first, and one patient underwent chest surgery first, four patients underwent abdominal surgery first. Among the 25 treated patients, the 10 patients died, which the cause of death was five severe brain injuries and four hemorrhagic shocks. Conclusions: In multiple damaged patients require both torso surgery and head surgery, poor prognosis was associated with low initial Glasgow Coma Scale and high Injury Severity Score. On the other hand, patients had good prognosis when blood pressure was maintained and operation for traumatic brain injury was performed first. At the same time, patients who had operation on head and torso simultaneously had extremely low survival rates. This may be associated with secondary brain injury due to low perfusion pressure or continuous hypotension and the traumatic coagulopathy caused by massive bleeding.

• The Journal of Korean Physical Therapy
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• v.16 no.2
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• pp.90-98
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• 2004

Traumatic brain injury is an insult to the brain caused by an external physical force, that may product a diminished or altered state of consciousness, which results in impairment of cognitive abilities or physical function. The purposes of this study were to overview injury mechanism and neural plasticity of traumatic brain injury. Injury mecanism includes exitotoxicity, production free radical, inflammation and apoptosis. Furthermore traumatic brain injury has protective mechanisms includes production of neural growth factor, heat shock protein, anti-inflammatory cytokines.

• Clinical and Experimental Pediatrics
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• v.52 no.1
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• pp.105-110
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• 2009

Purpose : Perinatal asphyxia is an important cause of neonatal mortality and subsequent lifelong neurodevelopmental handicaps. Although many treatment strategies have been tested, there is currently no clinically effective treatment to prevent or reduce the harmful effects of hypoxia and ischemia in humans. Erythropoietin (Epo) has been shown to exert neuroprotective effects in various brain injury models although the exact mechanisms through which Epo functions are not completely understood. This study investigates the effect of Epo on hypoxic-ischemic (HI) brain injury and the possibility that its neuroprotective actions may be associated with iron-mediated metabolism. Methods : HI brain injury was produced in 7-day-old rats by unilateral carotid artery ligation followed by hypoxia with 8% oxygen for 2 h. At the end of HI brain injury, the rats received an intraperitoneal injection of 5,000 units/kg erythropoietin. Random premedication with iron, deferoxamine, iron-deferoxamine, or saline were performed 23 d before HI brain injury. The severity of the brain injury was assessed at 7 d after HI. Results : Single Epo treatment post-HI brain injury reduced the gross and histopathological findings of brain injury. Iron premedication did not increase the incidence or severity of the injury as measured by the damage score. Deferoxamine administration before HI brain injury improved the brain injury as compared to no treatment or Epo treatment. Conclusion : These findings indicate that Epo provides neuroprotective benefits after HI in the developing brain. These findings suggest that Epos neuroprotective actions may involve reducing iron in tissues that mediate the formation of free radicals.