• Title, Summary, Keyword: 뇌손상

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The effect of erythropoietin in neonatal rat model of hypoxic-ischemic brain injury (Erythropoietin의 투여가 신생백서 저산소허혈뇌손상에 미치는 영향)

  • Kim, Heng-Mi;Choe, Byung-Ho;Kwon, Soon-Hak;Sohn, Yoon-Kyung
    • 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.

Neuroimaging of Traumatic Brain Injury (외상성 뇌손상의 영상진단)

  • Choi, Woo Suk
    • Korean Journal of Biological Psychiatry
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    • v.2 no.2
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    • pp.169-176
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    • 1995
  • 두부 외상은 많은 발생율과 사망율을 차지하고 있으며, 건강한 생활을 위해 큰 관심을 갖게 되었다. 신경방사선영상은 외상성 뇌손상 환자들의 진단과 치료에 필수적인 방법이다. 뇌손상의 기본 기전, 병리, 그리고 영상 소견을 이해 하는 것은 매우 중요하다. 1970년대에 Glasgow coma scale의 형상과 전산화단층촬영(CT)의 발달은 임상의사들이 두부외상에 대한 평가와 환자들의 경과를 예상하는데 극적인 변화를 주었다. 최근 자기공명영상(MRI)의 발달로 외상성 뇌손상의 형태를 더욱 이해 하게 되었고, 두부 외상의 발견율이 높아지게 되었다.

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Neurocognitive Function Assessment of Traumatic Brain Injury (외상후 뇌손상의 신경인지기능 평가)

  • Oh, Byoung Hoon
    • Korean Journal of Biological Psychiatry
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    • v.2 no.2
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    • pp.177-185
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    • 1995
  • 외상후 뇌손상은 대표적이며, 가장 중요한 신경정신계 질환의 하나이다. 더욱이 외상후 뇌손상 환자들은 각종의 사고 및 산업재해 등으로 인해 그 수가 급증하고 있으며, 특히 인지기능의 장애로 인한 다양한 기질성 정신장애로 고통을 겪게 된다. 따라서 외상후 뇌손상은 손상의 시점에서부터 정확하고 올바른 평가는 물론 손상후의 경과 및 치료대책의 수립에 있어서 체계적이며 종합적인 신경인지기능의 평가는 필수적이다. 왜냐하면 신경인지기능평가는 뇌의 손상부위와 이와 관련된 기능장애 및 행동의 변화에 대한 객관적인 자료를 제시해 주기 때문이다. 신경인지기능 평가의 영역은 지각, 운동기능은 물론 주요인지기능인 기억, 언어, 실행 및 감정조절능력에 이르기까지 다양하며, 외상후 뇌손상환자들은 손상부위 및 정도에 따라 신경인지기능의 장애를 초래하게 된다. 대표적인 신경인지기능평가 도구로는 KWIS, Halstead-Reitan, Luria-Nebraska batteries, 특히 전두엽기능검사인 Wisconsin Card Sorting Test (WCST)를 비롯하여, 현재는 PC/S Vienna Test System 및 Stim등의 각종 전산화 인지기능검사가 개발되어 임상에서 활발히 사용되고 있다. 즉 외상후 뇌손상환자를 위한 신경인지기능평가의 목적은 뇌손상과 관련된 신경인지기능장애를 정확히 평가하여, 환자 개개인에 적합한 인지재활치료 계획을 수립하는데 있다. 물론 여기에는 신경정신상태검사(neuropsychiatric mental status examination)를 통하여 외상 후 뇌손상의 경과 및 예후에 결정적인 영향을 미칠 수 있는 나이, 의식소실 및 외상후 기억 손상 시간의 정확한 측정은 물론 심리 사회 문화적인 상태와 두부외상전 환자의 지적수준 및 사회 적용기능이 함께 평가되어야 할 것이다.

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Anxiety Disorders after Traumatic Brain Injury (외상성 뇌손상 후의 불안장애)

  • Kim, Young-Chul
    • Korean Journal of Biological Psychiatry
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    • v.7 no.1
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    • pp.46-54
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    • 2000
  • Traumatic brain injury(TBI) is generally considered to be a risk factor for psychiatric disorders, especially depression and anxiety disorder. Despite the anxiety disorders are frequent sequelae after traumatic brain injury, the patients have not been payed medical attention and treated by doctors properly. The factors of precipitating and sustaining the anxiety disorders after TBI are brain injury itself, and the patient's or caregiver's response to the disability after TBI. To diagnose and treat them effectively, the knowledge about the mechanisms of and symptoms after TBI have to be needed. Psychiatrist should be a supportive and good listener to the patients who are complaining anxiety symptoms and differentiate whether the psychiatric symptoms are due to TBI or not. Because the TBI patients are very sensitive to drug side effects, doctors have to be familiar with the side effects as well as the mechanisms of action of the common psychotropics.

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Neuropathological Mechanisms of Perinatal Brain Injury (주산기 뇌손상의 신경병리적 기전)

  • Song Ju-Young;Kim Jin-Sang
    • The Journal of Korean Physical Therapy
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    • v.15 no.4
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    • pp.199-207
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    • 2003
  • This review describes the neurophathological mechanisms that are implicated in perinatal brain injury. Perinatal brain injury is the most important cause of morbidity and mortality to infants, often leading to spastic motor deficits, mental retardation, seizures, and learning impairments. The immature brain injury is usually caused by cerebral hypoxia-ischemia, hemorrhage, or infection. The important form of perinatal brain injury is the hypoxic-ischemic injury and the cerebral hemorrhage. The pathology of hypoxic-ischemic injury include delayed energy failure by mitochondrial dysfunction, neuronal excitotoxicity and vulnerability of white matter in developing brain. The immature brain has the fragile vascular bed of germinal matrix and can not effectively centralize their circulation. Therefore, the cerebral hemorrhage process is considered to be involved in the periventricular leukomalacia.

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Alterations of Calcium-binding Protein Immunoreactivities in the Hippocampus Following Traumatic Brain Injury (외상성 뇌손상 후 해마내 칼슘결합단백질 면역반응의 변화)

  • Oh, Yun-Jung;Kim, Baek-Seon;Park, Dae-Kyoon;Park, Kyung-Ho;Ko, Jeong-Sik;Kim, Duk-Soo
    • Applied Microscopy
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    • v.41 no.4
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    • pp.235-248
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    • 2011
  • Traumatic brain injury (TBI) is one of the leading causes of death and disability in children and adults and is a major risk factor for the development of posttraumatic epilepsy (PTE). Recent studies have provided significant insight into the pathophysiological mechanisms underlying the development of epilepsy. Although the link between brain trauma and epilepsy is well recognized, the complex biological mechanisms that result in PTE following TBI have not been fully elucidated. Therefore, this study investigated in order to identify whether or not the abnormal expression of calcium-binding proteins in the lesioned hippocampus plays a role in neuronal damage by brain trauma and whether or not the expressions may change in the contralateral hippocampus during the adaptive stage as early time point following TBI. During early time point following TBI, both parvalbumin (PV) and calbindin D-28k (CB) immunoreactivities were decreased with in the lesioned hippocampus. However, these expressions were recovered to control levels as depend on time courses. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced as compared to the control levels, whereas CB expression was unchanged. These findings indicate that the alterations of the calcium-binding proteins, especially PV and CB, may contribute to the neuronal death and/or damage induced by abnormal inhibitory neurotransmission at early time period following brain trauma and the development of epileptogenesis in patients with traumatic brain injury.

Cellular and Biochemical Mechanism of Perinatal Hypoxic-Ischemic Brain Injury (주산기 저산소-허혈 뇌손상의 세포 생화학적 기전)

  • Chang, Young Pyo
    • Clinical and Experimental Pediatrics
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    • v.45 no.5
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    • pp.560-567
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    • 2002
  • 주산기 뇌손상은 주로 급격한 저산소-허혈 손상에 의하는데 급격한 산소 공급의 차단은 oxidative phosphorylation을 정지 시켜서 뇌대사를 위한 에너지 공급이 차단되게 된다. 에너지 공급이 차단된 뇌세포는 뇌세포막에서 세포 내외의 이온 농도 차를 유지시키던 ATP-dependent $Na^{+}-K^{+}$ pump의 기능이 정지 되고, 세포 내외의 농도 차에 따라 $Na^{+}$, $Cl^{+}$, $Ca^{{+}{+}}$의 대규모 세포 내로 이동이 일어난다. 세포 내로 calcium 이온의 이동은 glutamate 수용체의 활성화에 의해서도 일나는데, 세포 내 calcium 이온의 증가는 protease, lipase, nuclease 등을 활성화 시켜 세포를 사망에 이르게 하는 연속적이고 다양한 생화학적 반응을 일으키게 된다. Glutamate는 대표적인 신경 전달 물질인데 저산소-허혈 손상 시 glutamate 수용체의 지나친 흥분은 미성숙 뇌에 뇌손상을 유발하는데, NMDA 또는 non-NMDA 수용체와 복합체를 형성하고 있는 calcium 이동 통로를 활성화 시켜 세포 내 calcium 이온을 증가시키고, 그 외에 metabotropic recetor는 G-protein의 활성화 등을 통해 뇌손상을 유발하는 다양한 생화학적 반응을 매개한다. 저산소-허혈 손상 후 재산소화와 재관류가 일어나면서 뇌세포의 지연성 사망(secondary neuronal death)이 일어나는데 이는 초기 손상 후 뒤이어 일어나는 다양한 생화학적 반응에 의하는데 다량의 산소 자유기 발생, nitric oxide의 생성, 염증 반응과 싸이토카인, 신경전도 물질의 과흥분 등이 관여하며, 신경 세포 사망은 세포괴사(necrosis)뿐 아니라 일부는 세포 사멸(apoptosis)로 알려진 의도된 세포 사망(programmed cell death)에 의한 것으로 생각되고 있다(Fig. 2).

Occupational Therapy in Hypoxic-Ischemic Brain Injury Patient by Suicidal Attempt: Case Report (자살시도로 인한 저산소성 허혈성 뇌손상 환자의 재활치료 - 인지 재활과 연하 재활을 중심으로: 사례연구)

  • Lee, Eui-Yun;Park, Ji-Hyuk
    • Therapeutic Science for Rehabilitation
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    • v.7 no.1
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    • pp.11-26
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    • 2018
  • Objective : This case study was to verify effects of cognitive rehabilitation and swallowing rehabilitation on Hypoxic-Ischemic Brain Injury patient by Suicidal Attempt. Methods : The subject was a 32-year old Hypoxic-ischemic brain injury patient by suicidal attempt. He received treatment once a day five times a week, for a half an hour for each session from September 8th to December 16th, 2016. Treatment were cognitive and swallowing rehabilitation. He was assessed based on Mini-Mental State Examination-Korean (MMSE-K), Korean-Modified Barthel Index (K-MBI), Computerized Neurocognitive Function Test (CNT), Videofluoroscopic Dysphagia Scale (VDS), American Speech-Language-Hearing Association National Outcomes Measurements System (ASHA-NOMS). Results : The patient's total MMSE-K score increased from 25 to 27. His K-MBI score increased from 74 to 88. His memory, attention span, and executive function (DST, VST, SWCT, WCST) by CNT scores were improved. VDS score has no changes to 34, 44.5 and 34. ASHA-NOMS score also has no change to 6, 2 and 6. Conclusion : The study showed that the application of the treatment of cognitive and swallowing in hypoxic-ischemic brain injury patient by suicidal attempt results has positive effects on cognitive functions, and swallowing function.

Taurine exerts neuroprotective effects via anti-apoptosis in hypoxic-ischemic brain injury in neonatal rats (신생 흰쥐의 저산소성 허혈성 뇌손상에서 항세포사멸사를 통한 taurine의 신경보호 효과)

  • Jeong, Ji Eun;Kim, Tae Yeol;Park, Hye Jin;Lee, Kye Hyang;Lee, Kyung Hoon;Choi, Eun Jin;Kim, Jin Kyung;Chung, Hai Lee;Seo, Eok Su;Kim, Woo Taek
    • Clinical and Experimental Pediatrics
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    • v.52 no.12
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    • pp.1337-1347
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    • 2009
  • Purpose:Taurine (2-aminoethanesulfonic acid) is a simple sulfur-containing amino acid. It is abundantly present in tissues such as brain, retina, heart, and skeletal muscles. Current studies have demonstrated the neuroprotective effects of taurine, but limited data are available for such effects during neonatal period. The aim of this study was to determine whether taurine could reduce hypoxic-ischemic (HI) cerebral injury via anti-apoptosis mechanism. Methods:Embryonic cortical neurons isolated from Sprague-Dawley (SD) rats at 18 days gestation were cultured in vitro. The cells were divided into hypoxia group, taurine-treated group before hypoxic insult, and taurine-treated group after HI insult. In the in vivo model, left carotid artery ligation was performed in 7-day-old SD rat pups. The pups were exposed to hypoxia, administered an injection of 30 mg/kg of taurine, and killed at 1 day, 3 days, 1 week, 2 weeks, and 4 weeks after the hypoxic insult. We compared the expressions of Bcl-2, Bax, and caspase-3 among the 3 groups by using real- time polymerase chain reaction (PCR) and western blotting. Results:The cells in the taurine-treated group before hypoxic insult, although similar in appearance to those in the normoxia group, were lesser in number. In the taurine-treated group, Bcl-2 expression increased, whereas Bax and caspase-3 expressions reduced. Conclusion:Taurine exerts neuroprotective effects onperinatal HI brain injury due to its anti-apoptotic effect. The neuroprotective effect was maximal at 1-2 weeks after the hypoxic injury.

Effect of Improved Forelimb Sensorimotor Function on the Transcranial Direct Current Stimulation in a Focal Ischemic Brain Injury Rat Model (국소 허혈성 뇌손상 흰쥐 모델에서 경두개직류전기자극이 앞다리 운동감각 기능 증진에 미치는 효과)

  • Kim, Gi-Do;Sim, Ki-Cheol;Kim, Kyung-Yoon
    • The Journal of the Korea Contents Association
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    • v.11 no.4
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    • pp.273-282
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    • 2011
  • This study was to investigate the effect of improve forelimb sensorimotor function and neurotrophic factor(GAP-43) expression when differing an application time of tDCS in ischemic brain injury rat model(pre, $1^{st}$, $7^{th}$, $14^{th}$). Focal ischemic brain injury was induced in 80 Sprague-Dawley rats through middle cerebral artery occlusion(MCAO) by 'Longa' method. And then experimental groups were randomly divided into four groups; GroupI: MCAO induction, GroupII: application of tDCS(10 min) after MCAO induction, GroupIII: application of tDCS(20 min) after MCAO induction, GroupIV: application of tDCS(30 min) after MCAO induction. Modified limb placing test and single pellet reaching test were performed to test forelimb sensorimotor function. And the histological examination was also observed through the immunohistochemistric response of GAP-43(growth-associated protein-43) in the cerebral cortex. In modified limb placing test, groupIII(p<0.05) showed significantly improve than the other groups on $14^{th}$). day. In single pellet reaching test, groupIII(p<0.01) and groupIV(p<0.05) significantly improved on $14^{th}$) day. And in immunohistochemistric response of GAP-43, group III showed significantly positive response than the other groups on $14^{th}$ day. These results suggest that the intensity(0.1 mA)/time(20 min) condition of tDCS application has a significant impact on the sensorimotor functional recovery in focal ischemic brain injury rat models.