• 대한한방성인병학회지
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• 제10권1호
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• pp.39-45
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• 2005

Objectives It is the case study of a critically ill patient with cerebral infarction and acute edematous change at femur due to a hematoma, of whom taken care with herb medicine according to the diagnosis of SCM(Sasang Constitutional Medicine). Methods The syndrome of the patient was diagnosed as a superficial disease of Taeumin. So after the on-set of the femoral edema, Jowiseungchung-tang added Castanea mollissima(Gunyul) and Maladera castanea(Jejo) was used. And we checked the change of the circumferencial size her thigh and followed up the sonography. Results and conclusions The therapy was significantly effective, and the edema was rapidly absorbed. The circumferential size was 83cm at on-set time, but got smaller to 57cm almost same to the healthy side of her thigh, and there was no more hematoma or systemic hemorrhagic sign on the body.

• Journal of Korean Neurosurgical Society
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• 제58권1호
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• pp.83-88
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• 2015

Organized hematoma is a rare complication that can develop following gamma knife radiosurgery (GKS) for cerebral arteriovenous malformation (AVM). Here, we describe 5 patients with growing organized hematomas that developed from completely obliterated AVMs several years after GKS. The patients were 15, 16, 30, 36, and 38 years old at the time of GKS, respectively, and 3 patients were female. Four AVMs were located in the lobe of the brain, and the remaining AVM were in the thalamus. Between 2-12 years after GKS, patients developed progressive symptoms such intractable headache or hemiparesis and enhancing mass lesions were identified. Follow-up visits revealed the slow expansion of the hematomas and surrounding edema. Steroids were ineffective, and thus surgery was performed. Histology revealed organized hematomas with a capsule, but there was no evidence of residual AVMs or vascular malformation. After surgery, the neurological symptoms of all patients improved and the surrounding edema resolved. However, the hematoma continued to expand and intraventricular hemorrhage developed in 1 patient whose hematoma was only partially removed. GKS for cerebral AVM can be complicated by growing, organized hematomas that develop after complete obliteration. Growing hematomas should be surgically evacuated if they are symptomatic. Radical resection of the hematoma capsule is also strongly recommended.

• 대한중풍순환신경학회지
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• 제12권1호
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• pp.1-7
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• 2011

Objectives : The purpose is to discuss the clinical applications of Orungsan(Goreisan: 五苓散) as an alternative management for increased intracranial pressure in the field of neurosurgery in Japan. Methods and Results : Attention has focused on Kampo medicine(traditional Japanese medicine) for some cerebral disease including chronic subdural hematoma(CSDH) and cerebral infarction in Japan. Orungsan and one of its classes, Sirungtang(Saireto: 柴苓湯) are well known their effects on brain edema. After some studies of Orungsan has the anti-edemic effects by the inhibition of aquaporin, this herbal medicine has been used widely in the neurosurgery field in Japan. It is high time to think about where we are and we go ahead for the progress and the integration in medicine. We have reviewed the studies using Orungsan or Sirungtang, that was reported at the 20th annual meeting of 'the Japan society for Kampo medicine and neurological surgery' was held on November 5, 2011 in Tokyo. Fifteen studies related with Orungsan or Sirungtang were reported among all 32 studies at the meeting. Orungsan in ten, and Sirungtang in five among 14 studies contained specific clinical case. In the aspects of disease, thirteen papers were related with SDH, including CSDH(11), SSDH(1), aneurism clipping for SDH prevention(1), and one was acute cerebral infarction and one was multiple metastatic brain tumor. In the report style, case control study was 7(mostly retrospective), and the case report was 8. Conclusions : Orungsan may be plausible to be an alternative method to reduce brain edema after SDH and other brain injury in the field of neurosurgery.

• Journal of Korean Neurosurgical Society
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• 제58권4호
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• pp.321-327
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• 2015

Objective : To determine whether the use of contrast enhancement (especially its extent) predicts malignant brain edema after intra-arterial thrombectomy (IAT) in patients with acute ischemic stroke. Methods : We reviewed the records of patients with acute ischemic stroke who underwent IAT for occlusion of the internal carotid artery or the middle cerebral artery between January 2012 and March 2015. To estimate the extent of contrast enhancement (CE), we used the contrast enhancement area ratio (CEAR)-i.e., the ratio of the CE to the area of the hemisphere, as noted on immediate non-enhanced brain computed tomography (NECT) post-IAT. Patients were categorized into two groups based on the CEAR values being either greater than or less than 0.2. Results : A total of 39 patients were included. Contrast enhancement was found in 26 patients (66.7%). In this subgroup, the CEAR was greater than 0.2 in 7 patients (18%) and less than 0.2 in the other 19 patients (48.7%). On univariate analysis, both CEAR ${\geq}0.2$ and the presence of subarachnoid hemorrhage were significantly associated with progression to malignant brain edema (p<0.001 and p=0.004), but on multivariate analysis, only CEAR ${\geq}0.2$ showed a statistically significant association (p=0.019). In the group with CEAR ${\geq}0.2$, the time to malignant brain edema was shorter (p=0.039) than in the group with CEAR <0.2. Clinical functional outcomes, based on the modified Rankin scale, were also significantly worse in patients with CEAR ${\geq}0.2$ (p=0.003) Conclusion : The extent of contrast enhancement as noted on NECT scans obtained immediately after IAT could be predictive of malignant brain edema and a poor clinical outcome.

• Journal of Korean Neurosurgical Society
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• 제50권2호
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• pp.147-150
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• 2011

We report a case of cerebral actinomycosis in a 69-year-old immunocompetent woman. The patient showed a progressive worsened mental status for one week. MRI examination showed an increased size of multiple enhancing nodular lesions associated with mild perilesional edema. We performed an open biopsy for the right frontal enhancing lesion. The intraoperative finding showed a yellowish friable lesion that was not demarcated with normal tissue. Pathologically, an actinomycotic lesion with sulfur granules and inflammatory cells was diagnosed. We report an unusual case of diffuse involvement of cerebral actinomycosis. The presence of the uncapsulated friable lesion that consisted mainly of foamy macrophages and lymphocytes could explain the unusual radiological features.

• 대한한방내과학회지
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• 제22권2호
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• pp.127-134
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• 2001

The purpose of this investigation is to evaluate the effects of Samwha-tang(三化湯) Extracts on reversible forebrain ischemia experimentally induced from the occlusion of middle cerebral artery. The volume of cerebral ischemia, the volume of cerebral edema, and the change of pyramidal neuron of the CA1 area in hippocampus through light microscopy were investigated. we obtained the following results. The volume of the control group, which had ischemic damage was 21%, and the volume of the sample group, which had ischemic damage, was 16%. The ratio of the volume of the right/left hemisphere was 117.2 in the control group, and 108.8 in the sample group. Also, the light microscopy revealed that the pyramidal cells of CA1 area in hippocampus had many damages like changes into discontinuous and unsystematic forms. But, in the sample group, the cells were less damaged compared with the control group.

• Biomolecules & Therapeutics
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• 제25권4호
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• pp.383-389
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• 2017

Dexmedetomidine is an ${\alpha}2$-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induced cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of $1{\mu}g/kg$ load dose, followed by $0.05{\mu}g/kg/min$ infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-$1{\beta}$, interleukin-6 and tumor nevrosis factor-${\alpha}$ as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-${\kappa}Bp65$, inhibitor of ${\kappa}B{\alpha}$ and phosphorylated of ${\kappa}B{\alpha}$ in hippocampus were assessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-${\kappa}B$ pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.

• The Korean Journal of Physiology and Pharmacology
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• 제28권3호
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• pp.239-252
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• 2024

Dexmedetomidine displays multiple mechanisms of neuroprotection in ameliorating ischemic brain injury. In this study, we explored the beneficial effects of dexmedetomidine on blood-brain barrier (BBB) integrity and neuroinflammation in cerebral ischemia/reperfusion injury. Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 1.5 h and reperfusion for 24 h to establish a rat model of cerebral ischemia/reperfusion injury. Dexmedetomidine (9 ㎍/kg) was administered to rats 30 min after MCAO through intravenous injection, and SB203580 (a p38 MAPK inhibitor, 200 ㎍/kg) was injected intraperitoneally 30 min before MCAO. Brain damages were evaluated by 2,3,5-triphenyltetrazolium chloride staining, hematoxylin-eosin staining, Nissl staining, and brain water content assessment. BBB permeability was examined by Evans blue staining. Expression levels of claudin-5, zonula occludens-1, occludin, and matrix metalloproteinase-9 (MMP-9) as well as M1/M2 phenotypes-associated markers were assessed using immunofluorescence, RT-qPCR, Western blotting, and gelatin zymography. Enzyme-linked immunosorbent assay was used to examine inflammatory cytokine levels. We found that dexmedetomidine or SB203580 attenuated infarct volume, brain edema, BBB permeability, and neuroinflammation, and promoted M2 microglial polarization after cerebral ischemia/reperfusion injury. Increased MMP-9 activity by ischemia/reperfusion injury was inhibited by dexmedetomidine or SB203580. Dexmedetomidine inhibited the activation of the ERK, JNK, and p38 MAPK pathways. Moreover, activation of JNK or p38 MAPK reversed the protective effects of dexmedetomidine against ischemic brain injury. Overall, dexmedetomidine ameliorated brain injury by alleviating BBB permeability and promoting M2 polarization in experimental cerebral ischemia/reperfusion injury model by inhibiting the activation of JNK and p38 MAPK pathways.

• Journal of Korean Neurosurgical Society
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• 제29권9호
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• pp.1171-1178
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• 2000

Objective : The purpose of the present study was to determine the appropriate time of clinical intervention by observing and analyzing the changes in the size of infarct, penumbra and cerebral edema and the extend of neurological deficit due to reperfusion damage according to time in a reversible cerebral ischemic model of reperfusing blood flow after inducing ischemia by maintaining middle cerebral artery occlusion for 2 hours(h) in rats. Methods : The rats were divided according to reperfusion time into control group(0 h reperfusion time) and experimental groups(0.5, 1, 2, 3, 4, 5, 6, 12, and 24 h of reperfusion time). Results : Changes in the size of infarction due to reperfusion damage were 0.93, 1.48 and 1.16% at 0.5, 1 and 2 h after reperfusion, respectively, and although a statistical significance was not present compared to 1.35% of the control group, damages increased drastically up to 6 h(6.64%), and the size increased were 6.65 and 6.78% at 12 and 24 h, respectively. Also there was no significant difference after 6 h up to 24 h in the size of infarction. In the areas where infarction occurred, reperfusion damage increased significantly with time in cortex than in subcortex. Accordingly, the size of penumbra area also showed a statistically significant decrease from 2 h up to 6 h after reperfusion, and 6 h after reperfusion, the area almost disappeared, becoming permanent infarction. Thus, reperfusion damage showed a significant increase from 2 h up to 6 h after reperfusion, and became steady thereafter. As for the mean ratio of the extend of cerebral edema, the control group and reperfusion 0.5 h group were 1.073 and 1.081, respectively ; up to 2 h thereafter, the ratio decreased to 1.01 but increased again with time ; and in reperfusion 12 h and reperfusion 24 h, the ratios were 1.070 and 1.075, respectively, showing similar size with that of control group. As for neurological deficit scores, the score of the control group was 2.67, that of reperfusion 2 h was 2, those of reperfusion 3 h and 6 h groups were 3.2 and 3.8, respectively, and those of reperfusion 12 h and 24 h groups were 4.2 and 4.6, respectively. Thus, as for the test results, the neurological deficit increased with time 2 h after reperfusion, and in reperfusion 12 and 24 h groups, almost all the symptoms appeared. Conclusion : As shown in these results, although the changes in the size of infarction due to reperfusion damage did not increase up to 2 h after reperfusion in the experimental groups compared to the control group, damage increased significantly thereafter up to 6 h, and the size remained about the same from 6 h to 24 h after reperfusion, becoming permanent infarction ; thus, the appropriate time of intervention according to the present study is at least 6 h before after maintaining reperfusion, including the time of cerebral artery occlusion.

• Journal of Korean Neurosurgical Society
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• 제42권4호
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• pp.331-336
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• 2007

Objective : The aim of this study was to analyze the treatment results and prognostic factors in patients with massive cerebral infarction who underwent decompressive craniectomy. Methods : From January 2000 to December 2005, we performed decompressive craniectomy in 24 patients with massive cerebral infarction. We retrospectively reviewed the medical records, radiological findings, initial clinical assessment using the Glasgow Coma Scale, serial computerized tomography (CT) with measurement of midline and septum pellucidum shift, and cerebral infarction territories. Patients were evaluated based on the following factors : the pre- and post-operative midline shifting on CT scan, infarction area or its dominancy, consciousness level, pupillary light reflex and Glasgow Outcome Scale. Results : All 24 patients (11 men, 13 women; mean age, 63 years; right middle cerebral artery (MCA) territory, 17 patients; left MCA territory, 7 patients) were treated with large decompressive craniectomy and duroplasty. The average time interval between the onset of symptoms and surgical decompression was 2.5 days. The mean Glasgow Coma Scale was 12.4 on admission and 8.3 preoperatively. Of the 24 surgically treated patients, the good outcome group (Group 2 : GOS 4-5) comprised 9 cases and the poor outcome group (Group1 : GOS 1-3) comprised 15 cases. Conclusion : We consider decompressive craniectomy for large hemispheric infarction as a life-saving procedure. Good preoperative GCS, late clinical deterioration, small size of the infarction area, absence of anisocoria, and preoperative midline shift less than 11mm were considered to be positive predictors of good outcome. Careful patient selection based on the above-mentioned factors and early operation may improve the functional outcome of surgical management for large hemispheric infarction.