• Title/Summary/Keyword: Brain damage

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Ipsilateral Motor Deficit during Three Different Specific Task Following Unilateral Brain Damage (편측 뇌손상 환자에서 특정 과제에 한정된 동측 상지의 운동 결함 분석)

  • Kwon, Yong-Hyun;Kim, Chung-Sun
    • The Journal of Korean Physical Therapy
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    • v.17 no.2
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    • pp.67-87
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    • 2005
  • Impaired sensorimotor function of the hand ipsilateral to a unilateral brain damage has been reported in a variety of motor task. however, it is still the controversial issue because of the difficulty of detection in clinical situation, patients' variability(time after onset, contralateral upper extremity severity, other cognitive functions including apraxia), and the performed various motor task. The purpose of this study is to determine the presence of ipsilateral motor deficit following unilateral brain damage in three different specific tasks(hand tapping, visual tracking and coin rotation) compared with healthy age-sex matched control group using the same hand and to investigate the lateralized motor control in each hemispheric function. Findings revealed that stroke patients with unilateral brain damage experienced difficulties with rapid-simple repetitive movement, visuomotor coordination, complex sequencing movement on ipsilateral side. Also, Comparison of the left-hemispheric stroke groups and the right-hemispheric stroke groups revealed that patients with a left-hemisphere damage tended to be more variable in performing all of the three tasks. These results show that stroke patient with left hemisphere damage has more ipsilateral motor deficit, and the left hemisphere contributes to the processing of motor control that necessary for the executing actions with ipsilateral hand.

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Analysis of Traumatic Brain Injury Using a Finite Element Model

  • Suh Chang-Min;Kim Sung-Ho;Oh Sang-Yeob
    • 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.

Protective Effects of Gamiheechum-tang(Jiaweixiqian-tang) on Hypertension and Brain Damage (가미치첨탕이 고혈압 및 뇌손상에 미치는 효과)

  • Ryu, Jong-Sam;Kim, Dong-Hee;Park, Jong-O;Namgung, UK;Hong, Seok
    • The Journal of Korean Medicine
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    • v.24 no.3
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    • pp.72-83
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    • 2003
  • Objective : The goal of the present study was to investigate the protective effect of Gamiheechum-tang (Jiaweixiqian-tang; GHCT) on brain tissue damage from chemical or ischemic insults. Methods : Levels of cultured cortical neuron death caused by toxic chemicals were measured by LDH release assay. Neuroprotective effects of GHCT on brain tissues were examined in vivo by ischemic model of middle cerebral artery (MCA) occlusion. Results : Animal groups treated with GBCT showed significantly decreased hypertension, and reduced levels of aldosterone, dopamine, and epinephrine in the plasma. GHCT treatments ($l0-200\mu\textrm{g}/ml$) significantly decreased cultured cortical neuron death mediated by AMPA, kainate, BSO, or Fe2+ when measured by LDH release assay. Yet, cell death mediated by NMDA was effectively protected by GHCT at the highest concentration examined ($200\mu\textrm{g}/ml$). In the in vivo experiment examining brain damage by MCA occlusion, affected brain areas by ischemic damage and edema were significantly less in animal groups administered with GHCT compared to the non-treated control group. Neurological examinations of forelimbs and hindlimbs showed that GHCT treatment improved animals' recovery from ischemic injury. Moreover, the extent of injury in cortical and hippocampal pyramidal neurons in ischemic rats was much reduced by GHCT, whose morphological features were similarly observed in non-ischemic animals. Conclusion : The present data suggest that GBCT may play an important role in protecting brain tissues from chemical or ischemic injuries.

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Effects of Purgative Action with Natrii Sulfas on Bax and HSP72 Expressions of the MCAO Rat Brain (망초(芒硝)의 사하작용(瀉下作用)이 MCAO 흰쥐 뇌조직의 Bax 및 HSP72 발현에 미치는 영향)

  • Kim, Kon-Sik;Kim, Bum-Hoi;Lee, Dong-Eun;Yang, Kee-Young;Kim, Seong-Joon;Kang, Hee;Sohn, Nak-Won
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.23 no.4
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    • pp.818-824
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    • 2009
  • This study aimed to evaluate the effect of purgation therapy with Natrii sulfas, a therapy for stroke patients with constipation in the oriental medicine, on the ischemic brain damage of the rats. The ischemic brain damage was induced by the middle cerebral artery occlusion (MCAO), Natrii sulafas was administered once after the MCAO. After 48 hours, expressions of Bax, Bcl-2, c-Fos, and HSP72 on the brain tissues were observed by immunohistochemistrical methods or technique. Purgation therapy with Natrii sulfas attenuated the excess of Bax expression caused by the ischemic brain damage. It was significant statistically in the penumbra of cerebral cortex, but not in the caudate putamen, of the MCAO rats. Purgation therapy with Natrii sulfas did not attenuate the excess of Bcl-2 expression caused by the ischemic brain damage. Purgation therapy with Natrii sulfas did not attenuate the excess of c-Fos expression caused by the ischemic brain damage. Purgation therapy with Natrii sulfas attenuated the excess of HSP72 expression caused by the ischemic brain damage. It was significant statistically in the penumbra of cerebral cortex, but not in the caudate putamen, of the MCAO rats. These results suggest that purgation therapy with Natrii sulfas has a neuroprotective effect on the ischemic brain damage and an anti-apoptotic effect.

An Introduction to Luria-Nebraska Neuropsychological Battery (Luria-Nebraska 신경심리검사의 소개)

  • Kim, Young-Chul
    • Sleep Medicine and Psychophysiology
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    • v.1 no.1
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    • pp.29-35
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    • 1994
  • Overall purposes of neuropsychological tests are summarized as follows: 1) Indentifying brain damage in individuals who have symptoms of uncertain etiology; 2) Assessing the extent and nature of deficits for forensic purposes and planning appropriate intervention; 3) Evaluating the effects of intervention or rehabilitation; 4) Examining the effects of various types of brain damage across different populations; and 5) Testing theoretical propositions about brain-behavior relationship. Of the neuropsychological tests, the Luria-Nebraska Neuropsychological Battery(LNNB) is easily transportable, relatively inexpensive, and performable by trained technician. The Korean version of LNNB is now being designed and will be used clinically in the near future. Localization and equipotential theories of brain function had been prevalent until Luria's theory of brain function. Brain, composed of three brain units in the theory, is the functional system in which each brain area has specific function and produce the function-related behavior. LNNB consists of 11 clinical scales, 5 summary scales, 8 localization scales, and 28 factor scales.

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The Study of the Subjective Symptoms according to Frontal Lobe Damage and Change in Neurocognitive Function in Traumatic Head Injury Patients (두부외상 환자에서 전두엽 손상과 신경인지기능 변화에 따른 주관적인 증상 연구)

  • Kim, Jun-Won;Han, Doug-Hyun;Kee, Baik-Seok;Park, Doo-Byung
    • Anxiety and mood
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    • v.8 no.1
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    • pp.31-40
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    • 2012
  • Objective : The purpose of this study was to analyze the correlation between symptom severity and neurocognitive factors in traumatic head injury patients. In addition, the effect of frontal lobe damage on these parameters was examined. Methods : We selected 18 patients who had brain damage for the moderate to severe traumatic brain injury (MSTBI) group, and 17 patients who met the diagnostic criteria for post-traumatic stress disorder (PTSD) without the finding of brain damage for the comparison group. For the evaluation of neurocognitive function, K-WAIS, Rey-Kim Memory Test, K-FENT, WCST, and MMPI-2 were used. Results : The results of the comparison (using the malingering scale) revealed that the values of PDS and PK, which express the severity of symptoms, and the values of the validity scale F, F (B), and F (P) were significantly higher in the overly-expressed group. F (B) in overly-expressed group and PK, Pt, and Sc in the properly-expressed group had significant correlation with the severity of symptoms. F (B), S, and Stroop error inhibition in PTSD, and PK, Pt, Sc, and MQ in MSTBI had significant correlation with the severity of symptoms. The results of the comparison based on the finding of frontal lobe damage revealed that PDS, EIQ, and MQ ware significantly higher in the group without brain damage. Conclusions : It was revealed that each neurocognitive factor was correlated with the severity of symptoms. There was a decrease in complaints or symptoms reported by the frontal lobe injury group, and this is believed to be due to degenerative change in the personality and emotional functioning of these patients following frontal lobe damage.

Study on the Effect of Gamiyukmijihwang-tang on the Brain damage (가미육미지황탕이 뇌신경세포 손상 및 뇌허혈 병태 모델에 미치는 영향)

  • Kim Jin hyung;Kim Yun Sik;Seol In Chan;Kim Dong Hee
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.17 no.2
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    • pp.467-475
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    • 2003
  • This studt was investigated to prove the effect of GMYM on the brain damage. The results were as follows; 1. GMYM showed significantly inhibitory effect on LDH release by NMDA. AMPA and Kinate. 2. GMYM showed significantly inhibitory effect on LDH release by BSO and Fe2+. 3. GMYM decreased coma duration time in a infatal dose of KCN and showed 30% of survival rate in a fatal dose. 4. GMYM showed improvement of forelimb and hindlimb test after MCA occulusion in neurological exemination. 5. GMYM decreased ischemic area and edema incited by the MCA blood flow block. These results indicate that GMYM can be used in the brain damage sujected to brain ischemia. Further study will be needed about the functional mechanism and etc.

Study on the Effect of Gamisihotang(GSHT) on Glutamate Receptor, Free Radical and Brain Damage in Rats Subjected to Brain Ischemia (가미시호탕이 뇌허혈시 Glutamate receptor, free radical 및 뇌손상 보호에 미치는 영향)

  • Oh Byung-Yul;Kim Min-Sang;Yu Byeong-Chan;Choi Young;Seol In-Chan
    • The Journal of Korean Medicine
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    • v.25 no.3
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    • pp.32-44
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    • 2004
  • Objectives : This study was undertaken to prove the effect of GSHT on the glutamate receptor, free radical and brain damage in rats subjected to brain ischemia Methods : Levels of cultured cortical neuron death caused by toxic chemicals were measured by LDH release assay. Neuroprotective effects of GSHT on brain tissues were examined in vivo by ischemic model of middle cerebral artery (MCA) occlusion. Results : GSHT showed significant inhibitory effect on LDH release induced by NMDA-kinate-Fe/sup 2+/. GSHT remarkably decreased coma duration time in a nonfatal dose of KCN and showed higher survival rate in a fatal dose. GSHT remarkably decreased ischemic area and edema induced by the MCA blood flow block. GSHT showed high improvement of forelimb and hind limb test after MCA occlusion in neurological examination. GSHT showed no significant change after MCA occlusion in pathological observation of the normal group. Conclusions : These results indicate that GSHT can be used to treat the brain damage caused by brain ischemia. Further study will be needed about the functional mechanism, etc.

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Astrogliosis Is a Possible Player in Preventing Delayed Neuronal Death

  • Jeong, Hey-Kyeong;Ji, Kyung-Min;Min, Kyoung-Jin;Choi, Insup;Choi, Dong-Joo;Jou, Ilo;Joe, Eun-Hye
    • Molecules and Cells
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    • v.37 no.4
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    • pp.345-355
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    • 2014
  • Mitigating secondary delayed neuronal injury has been a therapeutic strategy for minimizing neurological symptoms after several types of brain injury. Interestingly, secondary neuronal loss appeared to be closely related to functional loss and/or death of astrocytes. In the brain damage induced by agonists of two glutamate receptors, N-ethyl-D-aspartic acid (NMDA) and kainic acid (KA), NMDA induced neuronal death within 3 h, but did not increase further thereafter. However, in the KA-injected brain, neuronal death was not obviously detectable even at injection sites at 3 h, but extensively increased to encompass the entire hemisphere at 7 days. Brain inflammation, a possible cause of secondary neuronal damage, showed little differences between the two models. Importantly, however, astrocyte behavior was completely different. In the NMDA-injected cortex, the loss of glial fibrillary acidic protein-expressing ($GFAP^+$) astrocytes was confined to the injection site until 7 days after the injection, and astrocytes around the damage sites showed extensive gliosis and appeared to isolate the damage sites. In contrast, in the KA-injected brain, $GFAP^+$ astrocytes, like neurons, slowly, but progressively, disappeared across the entire hemisphere. Other markers of astrocytes, including $S100{\beta}$, glutamate transporter EAAT2, the potassium channel Kir4.1 and glutamine synthase, showed patterns similar to that of GFAP in both NMDA- and KA-injected cortexes. More importantly, astrocyte disappearance and/or functional loss preceded neuronal death in the KA-injected brain. Taken together, these results suggest that loss of astrocyte support to neurons may be a critical cause of delayed neuronal death in the injured brain.

Experimental Study of Fraction of Citri Reticulatae Viride Pericarpium extract on the Brain Damage in Cerebral Ischemia (청파활성분획이 허혈성 뇌손상에 미치는 실험적 연구)

  • Rho Young Ho;Jeong Hyun Woo;Lee Won Suk
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.16 no.5
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    • pp.893-898
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    • 2002
  • Citri Reticulatae Viride Pericarpium extract(CRVP) have been used in oriental medicine for many centuries as a therapeutic agent for smoothing the liver and regulating the circulation of qi, and promoting digestion and removing stagnated food. The effects of CRVP on the inhibition of brain damage in cerebral ischemia is not known. Therefore, this Study was designed to investigate the cerebral protective effects of CRVP on the transient cerebral ischemia using modern techniques, and further to provide the possibility of scientification of oriental medicine. The size of cerebral infarct size was measured by morphometry, and brain edema was measured by morphometry and brain water content determination. The results were a$ follows ; 1. Water fraction of CRVP was reduced infect area of rats brain slices which were subjected to a transient cerebral ischemia in a dose-dependent manner. 2. Methylene chloride fraction and hexane fraction of CRVP was significantly reduced infarct area of rats brain slices which were subjected to a transient cerebral ischemia in a dose-dependent manner. 3. Methylene chloride fraction and hexane fraction of CRVP was significantly reduced infarct volume of rats brain which was subjected to a transient cerebral ischemia in a dose-dependent manner. 4. Methylene Chloride fraction and hexane fraction of CRVP was significantly decreased brain edema induced by a transient cerebral ischemia in a dose-dependent manner. 5. Methylene chloride fraction and hexane fraction of CRVP was significantly decreased brain water content of rats which were subjected to a transient cerebral ischemia. It is suggested that CRVP has an anti-ischemic effect through the inhibition of brain damage in a transient cerebral ischemia, and that in future further development of main effective constituent in CRVP can provide a novel therapeutic strategy for cerebral ischemia.