• Journal of Korean Neurosurgical Society
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• 제60권4호
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• pp.391-396
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• 2017

Objective : To investigate the neuroprotective effects of Ginkgolide B (GB) against ischemic stroke-induced injury in vivo and in vitro, and further explore the possible mechanisms concerned. Methods : Transient middle cerebral artery occlusion (tMCAO) mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated N2a cells were used to explore the neuroprotective effects of GB. The expression of brain-derived neurotrophic factor (BDNF) was detected via Western blot and qRT-PCR. Results : GB treatment (4 mg/kg, i. p., bid) significantly reduced neurological deficits, water content, and cerebral infarct volume in tMCAO mice. GB also significantly increased Bcl-2/Bax ratio, reduced the expression of caspase-3, and protected against OGD/R-induced neuronal apoptosis. Meanwhile, GB caused the up-regulation of BDNF protein in vivo and in vitro. Conclusion : Our data suggest that GB might protect the brain against ischemic insult partly via modulating BDNF expression.

• Laboraroty Animal Research
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• 제33권3호
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• pp.244-250
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• 2017

${\alpha}$-Synuclein is abundantly expressed in neuronal tissue, plays an essential role in the pathogenesis of neurodegenerative disorders, and exerts a neuroprotective effect against oxidative stress. Cerebral ischemia causes severe neurological disorders and neuronal dysfunction. In this study, we examined ${\alpha}$-synuclein expression in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury and neuronal cells damaged by glutamate treatment. MCAO surgical operation was performed on male Sprague-Dawley rats, and brain samples were isolated 24 hours after MCAO. We confirmed neurological behavior deficit, infarction area, and histopathological changes following MCAO injury. A proteomic approach and Western blot analysis demonstrated a decrease in ${\alpha}$-synuclein in the cerebral cortices after MCAO injury. Moreover, glutamate treatment induced neuronal cell death and decreased ${\alpha}$-synuclein expression in a hippocampal-derived cell line in a dose-dependent manner. It is known that ${\alpha}$-synuclein regulates neuronal survival, and low levels of ${\alpha}$-synuclein expression result in cytotoxicity. Thus, these results suggest that cerebral ischemic injury leads to a reduction in ${\alpha}$-synuclein and consequently causes serious brain damage.

• 대한신경과학회지
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• 제36권4호
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• pp.341-344
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• 2018

It is uncommon for Fabry's disease (FD) patient to present with an isolated ischemic stroke without other typical symptoms or signs of FD. A 48-year-old woman presented with recurrent limb weakness and her brain magnetic resonance imaging revealed multiple ischemic brain lesions. Ten years ago, the patient had been diagnosed with heterozygote FD by the genetic test, but she had not shown any typical symptoms or sign of FD so far. Isolated organ involvement could occur in heterozygote FD.

• 약학회지
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• 제32권5호
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• pp.343-350
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• 1988

Recent hypothesis suggested that intracellular accumulation of calcium is a common denominator of ischemic celullar damage. Flunarizine, a calcium entry blocker, posses vasodilating properties in cerebral vascular beds and clinically used in circulatory disorders. The present study was designed to evaluate the effect of flunarizine on ischemic and hypoxic brain damage. An ischemic model was made by bilateral carotid artery ligation (BCAL) in Wistar strain rat. Hypoxic model was made by intravenous injection(i.v.) of KCN to rats and mice. In mice, flunarizine not only reduced the mortality of KCN, but also delayed the onset time of convulsion. The contents of ATP, creatine phosphate and glucose, cerebral energy metabolite, decreased 30 minutes after BCAL and KCN i, v, while that of lactate increased. But these variations were suppressed by flunarizine. Furthermore, increase in the dosage of flunarizne generally promoted the recovery of cerebral energy metabolites in hypoxic animals. The results suggest that flunarizine had a protective effect against ischemic and hypoxic brain damage due to its ameliorating action on the cerebral energy metabolism.

• Journal of Korean Neurosurgical Society
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• 제39권4호
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• pp.300-302
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• 2006

"Stunning" represents prolonged contractile depression of any muscular component after alleviation of severe ischemia, as shown in reperfusion following acute myocardial ischemia or ischemic stroke. Clinically, it presents with no or delayed recovery past to thrombolytic therapy but its pathogenic mechanism is not fully uncovered yet. We describe a unique case of a 63-year-old woman, who was undertaken endovascular coiling for the aneurysms, deteriorated several hours later without known cause, and showed delayed clinical improvement over the next 3 days following thrombolysis. Immediate post-thrombolysis magnetic resonance imaging scan showed no apparent abnormality except for high signal intensity within the corresponding hemisphere. Reversible but delayed nature of " brain stunning" can be explained by these images and it seems to be caused by a certain type of reperfusion injury.

• Journal of Korean Neurosurgical Society
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• 제65권4호
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• pp.603-608
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• 2022

Vertebral artery (VA) occlusion is frequently encountered, usually without acute ischemic injury of the brain. However, when it is accompanied by hypoplasia or stenosis of the opposite VA, brain ischemia may develop due to insufficient collateral supply. Both hemodynamic instability and embolic infarction can occur in VA occlusion, which may cause severe symptoms in a patient. Extracranial carotid-VA bypass should be considered for symptomatic VA occlusion patients, especially when the patient has repeated ischemic brain injuries. In this report, the cases of three extracranial carotid-VA bypass patients are introduced, along with a brief description of the surgical techniques. All three cases were treated with different bypass methods according to their disease location.

• Journal of Korean Neurosurgical Society
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• 제58권1호
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• pp.22-29
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• 2015

Objective : Perinatal hypoxic-ischemic encephalopathy (HIE) and prolonged febrile seizures (pFS) are common neurologic problems that occur during childhood. However, there is insufficient evidence from experimental studies to conclude that pFS directly induces hippocampal injury. We studied cognitive function and histological changes in a rat model and investigated which among pFS, HIE, or a dual pathologic effect is most detrimental to the health of children. Methods : A rat model of HIE at postnatal day (PD) 7 and a pFS model at PD10 were used. Behavioral and cognitive functions were investigated by means of weekly open field tests from postnatal week (PW) 3 to PW7, and by daily testing with the Morris water maze test at PW8. Pathological changes in the hippocampus were observed in the control, pFS, HIE, and HIE+pFS groups at PW9. Results : The HIE priming group showed a seizure-prone state. The Morris water maze test revealed a decline in cognitive function in the HIE and HIE+pFS groups compared with the pFS and control groups. Additionally, the HIE and HIE+pFS groups showed significant hippocampal neuronal damage, astrogliosis, and volume loss, after maturation. The pFS alone induced minimal hippocampal neuronal damage without astrogliosis or volume loss. Conclusion : Our findings suggest that pFS alone causes no considerable memory or behavioral impairment, or cellular change. In contrast, HIE results in lasting memory impairment and neuronal damage, gliosis, and tissue loss. These findings may contribute to the understanding of the developing brain concerning conditions caused by HIE or pFS.

• 대한의생명과학회지
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• 제11권3호
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• pp.355-363
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• 2005

This study aimed to investigate the cerebroprotective effect of vascular endothelial growth factor (VEGF) on permanent focal cerebral ischemia in Sprague-Dawley rats. Right middle cerebral artery (MCA) was occluded for 6 and 24 hours by an intraluminal monofilament technique. An open cranial window was made on the right parietal bone for determination of continuous changes in regional cerebral blood flow (rCBF) by laser-Doppler flowmetry. The infarct size was morphometrically determined using the 2,3,5-triphenyltetrazolium chloride technique. Brain edema was determined by measuring brain water content. In normal rats, rCBF was significantly increased by intravenous infusion of VEGF for 10 minutes. The VEGF-induced increase in rCBF was significantly inhibited by pretreatment with suramin, a heparin-binding growth factor inhibitor as well as $N^{\omega}-nitro-L-arginine$, a nitric oxide synthase inhibitor. In focal cerebral ischemic rats, the amplitude of decrease in rCBF during ischemic period was significantly less in VEGF-treated group, compared with that in vehicle-treated group. The cerebral infarct size was reduced by VEGF in a dose-dependent manner. The brain edema formation was dose-dependently reduced by VEGF in 24-hour MCA occlusion group but not in 6-hour MCA occlusion group. It is suggested that VEGF not only improves the rCBF during cerebral ischemic period but also reduces the brain edema formation, and thereby exert a protective effect on focal cerebral ischemia in rats.

• 한국콘텐츠학회논문지
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• 제11권4호
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• pp.273-282
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• 2011

본 연구는 국소 허혈성 뇌손상 흰쥐 모델에서 tDCS의 자극 적용시간을 달리하였을 때, 앞다리 운동감각 기능변화와 신경영양인자(GAP-43)발현에 미치는 영향을 알아보고자 하였다. 뇌손상 모델은 Sprague -Dawley계 흰쥐 80마리를 'Longa'방법을 이용하여 중대뇌동맥(middle cerebral artery)을 폐색하여 유발하였고, 실험군을 4개로 나누었다; 실험군I은 허혈성 뇌손상 유발군(n=20), 실험군II는 허혈성 뇌손상 유발 후 tDCS(10분) 적용군(n=20), 실험군III은 허혈성 뇌손상 유발 후 tDCS(20분) 적용군(n=20), 실험군IV는 허혈성 뇌손상 유발 후 tDCS(30분) 적용군(n=20)으로 나누었다. 앞다리운동감각 기능검사를 위해 수정된 앞다리배치 검사와 단일 팰릿 닿기 검사를 실시하였으며, 신경가소성에 대한 면역조직화학적 검사로 운동감각 영역에서의 GAP-43 단백질 발현을 관찰하였다. 앞다리운동감각 검사는 14일에서 실험군III (p<0.05)이 다른 군들에 비해 유의한 차이를 보였으며, 단일 팰릿 닿기 검사는 14일에서 실험군III(p<0.01)과 실험군IV(p<0.05)에서 유의한 차이를 보였다. 또한, 면역조직학적 검사는 14일에 실험군III이 다른 군들에 비해 현저한 면역양성반응의 증가를 보였다. 따라서, 0.1 mA의 강도로 20분간 적용했을 때가 앞다리운동감각 기능과 신경가역성 인자 GAP-43 발현에 가장 좋은 조건임을 알 수 있었다.

• 재활치료과학
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• 제7권1호
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• pp.11-26
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• 2018

목적 : 본 사례연구는 자살시도로 인한 저산소성 허혈성 뇌손상 환자의 특징적 증상과 신경학적 회복 양상을 고려한 인지 및 연하 재활 중심의 작업치료 중재를 소개하고 중재 효과로 인한 회복 양상에 대해 알아보고자 하였다. 연구방법 : 연구 대상은 자살시도로 인한 저산소성 허혈성 뇌손상을 진단받은 32세 남성으로 치료기간은 2016년 9월 8일부터 12월 6일까지이며, 주 5회 하루 한 번 재활치료를 받았다. 작업치료는 신경학적 기전으로 인한 저산소 허혈성 뇌손상의 특징과 자살이라는 정신 건강학적 특징을 바탕으로 이루어 졌으며, 인지와 연화 재활 중심의 프로그램이었다. 인지기능은 Mini Mental State Examination-Korean(MMSE-K), Computerized Neurocognitive Function Test(CNT), 일상생활활동 수준은 Korean-Modified Barthel Index(K-MBI), 연하기능은 Videofluoroscopic Dysphagia Scale(VDS), American Speech-Language-Hearing Association National Outcomes Measurements System (ASHA-NOMS)로 평가하였다. 결과 : 저산소성 허혈성 뇌손상 환자의 지연성 뇌손상 기전에 따라 인지기능 평가인 MMSE-K, CNT와 일상생활활동 수준을 평가하는 K-MBI, 연하기능을 평가하는 VDS, ASHA NOMS 결과에서 초기 평가 결과에 비해 모든 기능에서 저하가 나타났으나 회복 기전과 함께 재활 치료가 병행되며 모든 기능이 회복되어 초기 평가 수준으로 호전되었다. 결론 : 본 연구 결과 자살시도로 인한 심리적 요인과 저산소성 허혈성 뇌손상으로 인한 인지 및 연하적 요인을 고려한 일반적인 작업치료 프로그램은 환자에게 긍정적 회복 양상을 나타냈다. 이를 바탕으로 저산소성 허혈성 뇌손상으로 인한 지연성 뇌손상이 발생한 환자에게 작업치료의 개입은 필요한 부분이며, 정신건강과 인지 및 연하기능의 중심 프로그램이 개발되어야할 것이다.