• Journal of Korean Neurosurgical Society
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• v.29 no.5
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• pp.659-663
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• 2000

The motality rate of acute subdural hematoma(ASDH) associated with closed head injury is high in spite of recent advances in neurosurgery. Many variables in regard to outcome of ASDH have been assessed. But among them, intracranial pressure(ICP) control and the time interval between injury and operative evacuation are the only things that can be affected by doctor. We introduced a simple method to the management of ASDH for reducing the time interval between injury and operation. When the immediate decompressive operation of ASDH was impossible by any causes, we made a burr hole at the center of hematoma, usually on 2-3cm above temporal squama and 1-2cm behind coronal suture under local anesthesia before main operation. Partial hematoma evacuation was achieved through the burr hole and it was effective in preventing further worsening of patients neurological status before main operation. Prompt hematoma evacuation through the burr hole seemed to be effective in delaying secondary ischemic brain damage and made easy to closing the dura opening and replacement of the bone flap at the end of main decompressive operation. This easy method may reduce the time interval between injury and operation. We represent surgical technique with two cases of ASDH managed with this simple method.

• Journal of Korean Neurosurgical Society
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• v.30 no.3
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• pp.325-333
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• 2001

Objective : To clarify the benefits and therapeutic effects of intra-arterial papaverine infusion on the symptomatic cerebral vasospasm, we analyzed the results of treatment in 32 patients retrospectively. Methods : A total of 510 patients underwent surgical clipping or endovascular intra-aneurysmal treatment for ruptured intracranial aneurysm between May, 1996 and June, 1999. The delayed ischemic deficit(DID) was developed in 90 of 510 patients. Of these 90 patients, 32 developed symptomatic vasospasm inspite of using modest "3H therapy". The brain CT scan was taken before the intra-arterial infusion of papaverine. The 32 patients underwent 42 intra-arterial papaverine infusion. The symptomatic vasospasm was divided into three groups : deterioration of mental status(Group 1), appearance of a focal neurologic deficit(Group 2), or both(Group 3). We measured Glasgow Coma Scale(GCS), arterial diameters, and cerebral circulation time(CCT) at the time of pre- and postangioplasty. Results : The number of patients in group 1, 2 and 3 were 26, 7, 9 respectively. Eighteen cases showed improvement of GCS more than 2 scores, 16 more than 1, and 8 showed no change of GCS. Average cerebral circulation time(CCT) was decreased ranging from 0.0%-67.5%, and arterial diameters were increased in 21 cases ranging from 1 to 4 folds. Conclusion : Intra-arterial papaverine infusion seemed to have therapeutic effects on symptomatic vasospasm by improving the neurological signs and increasing the arterial diameter. We suggest that intra-arterial papaverine infusion would be an useful adjunctive therapeutic modality in symptomatic vasospasm.

• Biomolecules & Therapeutics
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• v.25 no.4
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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.

• Korean Journal of Pharmacognosy
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• v.34 no.4 s.135
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• pp.335-338
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• 2003

It is thought that highly reactive oxygen species generated after strokes plays a key role in damaging the brain. We examined free radical scavenging activity and neuroprotective effects of several medicinal herbs in a rat model of transient ischemia. Free radical scavenging property of medicinal herbs was examined in vitro using 1,1-diphenyl-2-picrylhydrazyl stable free radical. Transient ischemia was induced by intraluminal occlusion of the right middle cerebral artery for 120 min, followed by reperfusion for 22 hr in rats. Aqueous extracts of 8 medicinal herbs (200 mg/kg) were orally administered twice to transient ischemic rat prior to reperfusion and 2 hr after reperfusion. Total infarction volume in the hemisphere ipsilateral to the ischemia-reperfusion was significantly decreased in 7 groups treated with Sophora flavescens, Lycopus lucidus, Sanguisorba officinalis, Caesalpinia sappan, Albizia julibrissin, Rubia akane, Psoralea corylifolia, or Prunella vulgaris. However, neuroprotective effects of these medicinal herbs were not correlated with their antioxidative activities. These results suggest that these medicinal herbs exert neuroprotection via antioxidative as well as unknown mechanism.

• Journal of International Academy of Physical Therapy Research
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• v.2 no.1
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• pp.193-200
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• 2011

This study is intended to examine the tDCS and Montoya stair task(MST) on sensorimotor recovery and glial scar expression in MCAo induced stroke model of rat. To achieve this goal, this study selected 80 SD rats of 8 weeks. The experiment groups were divided them into four groups, and assigned 20 rats to each group. Group I was a experimental control group; GroupII was a tDCS application group after MCAo; Group III was a MST application group after MCAo; Group IV was a tDCS and MST application group after MCAo. In each group, neurological function test measurement, motor behavior test, montoya stair task test, immunohistochemistric finding of GFAP expression finding were analyzed. In motor behavior test, the outcome of group I was significantly difference than the other group, especially from 14days. In montoya stair task test, the outcome of group I was significantly lower than the other group especially, group II were significantly different on 14days and group IV was most significantly difference than the other group. In immunohistochemistric finding, group II, III, IV were decrease GFAP expression on depend on time stream. These results throughout the MCAo due to focal ischemic brain injury rat model four weeks tDCS and MST was applied, when the neurobehavioural, upper extremity function and ability, histopathologic data suggest that sensorimotor function recovery and a positive influence on glial scar decrease and confirmed that.

• Journal of The Korean Society of Clinical Toxicology
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• v.18 no.1
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• pp.34-41
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• 2020

Purpose: This study evaluated aggressive hyperbaric oxygen therapy (HBOT) by understanding various exposure routes of acute carbon monoxide (CO) poisoning, the risk factors causing acute cardiovascular, and neurological toxicity caused by poisoning. Methods: A retrospective study was conducted based on the medical records of 417 acute CO poisoning patients who visited the emergency care unit from March 2017 to August 2019. The exposure routes, HBOT performance, age, sex, medical history (hypertension, diabetes mellitus, ischemic heart disease, heart failure), intentionality, loss of consciousness (LOC), intake with alcohol or sedatives, and initial test results (carboxyhemoglobin (COHb), troponin-I, electrocardiography, echocardiography, brain MRI) were examined. Comparative analysis of the clinical information was conducted between the groups that showed acute cardiovascular toxicity and neurological toxicity, and groups that did not. Results: Among 417 patients diagnosed with acute CO poisoning, 201 cases (48.2%) were intentional, and charcoal briquette was the most common route (169 patients (40.5%)). Two hundred sixteen cases (51.8%) were accidental, and fire was the most common route (135 patients (32.4%)). The exposure route was more diverse with accidental poisoning. Three hundred ninety-nine patients were studied for acute cardiovascular toxicity, and 62 patients (15.5%) were confirmed to be positive. The result was statistically significant in intentionality, LOC, combined sedatives, initial COHb, HTN, and IHD. One hundred two patients were studied for acute neurological toxicity, which was observed in 26 patients (25.5%). The result was statistically significant in age and LOC. Conclusion: Active HBOT should be performed to minimize damage to the major organs by identifying the various exposure routes of CO poisoning, risk factors for acute cardiovascular toxicity (intentionality, LOC, combined sedatives, initial COHb, HTN, IHD), and the risk factors for acute neurological toxicity (age, LOC).

• Journal of Chest Surgery
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• v.34 no.7
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• pp.547-551
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• 2001

The effects of deep hypothermia and circulatory arrest during aortic arch reconstruction are associated with potential neurologic and myocardial injury. We describe a surgical technique that two patients underwent a modified Norwood procedure without circulatory arrest and myocardial ischemia. One was 13-day-old female patient, weighing 3.1kg, having a variant of hypoplastic left heart syndrome and another was 38-day-old male patient, weighing 3.4 kg, diagnosed Taussig-Bing anomaly with severe aortic arch hypoplasia, coarctation of the aorta, and subaortic stenosis. The arterial cannula was inserted in innominate artery directly. During Norwood reconstruction, regional high-flow perfusion into the inominate artery and coronary perfusion were maintained and there were no neurologic, cardiac, and renal complications in two patients. This technique may help protect the brain and myocardium from ischemic injury in patients with hypoplastic left heart syndrome or other arch anomalies including coarctation or interruption.

• The Journal of Korean Medicine
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• v.23 no.4
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• pp.140-150
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• 2002

Objectives: The water extract of Omija-tang (OMIT) has traditionally been used for treatment of ischemic heart and brain damage in oriental medicine. However, little is known about the mechanism by which the water extract of OMJT rescues cells from these damages. Therefore, this study was designed to investigate the protective mechanisms of OMJT on oxidative stress-induced toxicity in H9c2 cardiomyoblast cells. Methods: Treatments of $H_2O_2$, or $ZnC_{12}$ markedly induced death of H9c2 cardiomyoblast cells in a dose-dependent manner. The characteristics of oxidative stress-induced death of H9c2 showed apparent apoptotic features such as DNA fragmentation. OMJT significantly reduced both ${H_2O_2}-induced$ cell death and chromatin fragmentation. The decrease of B치-XL expression by $H_2O_2$ were inhibited by OMJT. In addition, the increase of Bcl-XS expression was also inhibited by OMJT. In particular, Fas expression, which is generally recognized as cell death-inducing signal by Fas/FasL interaction, was markedly increased by H2O2 in a time-dependent manner. Also, the expression profile of proteins in Chang cells were screened by using two-dimensional (2-D) gel electrophoresis. Among 300 spots resolved in 2-D gels; the comparison of control versus apoptotis cells revealed that signal intensity of 6 spots decreased and 11 spots increased. Results and Conclusions: Taken together, this study suggests that the protective effects of the water extract of OMJT against oxidative damages may be mediated by the modulation of Bcl-XL/S Fas expression.

• The Journal of Korean Medicine
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• v.24 no.2
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• pp.179-192
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• 2003

Objectives : Boyanghwanoh-tang (Buyanhaiwu-tang) has been used as a prescription for stroke, senile and vascular dementia, ischemic brain and heart damage in Oriental traditional medicine. However, there is little known about the mechanism by which the water extracts of Boyanghwanoh-tang (Buyanhaiwu-tang) rescue cells fromthese damages, and little is known about the protective mechanisms of Boyanghwanoh-tang (Buyanhaiwu-tang) on oxidative stress in neuronal cells. Therefore, we have investigated the role of Boyanghwanoh-tang (Buyanhaiwu-tang) on serum and glucose deprived apoptosis in PC12 cells. Methods : PC12 Cells have been used extensively as a model for studying the cellular and molecular effects of neuronal cells. The viability of cells was measured by MIT assay. We used DNA fragmentation and caspase 1, 2, 3, 6, 9-likeproteases activation assay. Transcriptional activation of NF-kB was assessed by using electrophoretic mobility shift assay. Results : Boyanghwanoh-tang (Buyanhaiwu-tang) rescued PC12 cells from apoptotic death by serum and glucose deprivation in a dose-dependent manner. The nuclear staining of PC12 cells clearly showed that Boyanghwanoh-tang (Buyanhaiwu-tang) attenuated nuclear condensation and fragmentation, which represent typical neuronal apoptotic characteristics. Boyanghwanoh-tang (Buyanhaiwu-tang) also prevents fragmentation of genomic DNA and activation of caspase 3-like protease in serum and glucose deprived PC12 cells. Furthermore, Boyanghwanoh-tang (Buyanhaiwu-tang) reduced the activation of NF-kB by serum and glucose-deprived apoptosis. Conclusions : These findings suggest that serum and glucose deprivation induces reduced glutathione (GSH) depletion, and consequently, apoptosis through endogenously produced reactive oxygen species in PC12 cells. Also, our data indicated that Boyanghwanoh-tang (Buyanhaiwu-tang) has protective effects against the serum and glucose deprived deaths of PC12 cells, which are mediated by the generation of GSH that, in turn, can reduce oxidative stress caused by reactive oxygen species (ROS) such as hydrogen peroxide.

• Clinical and Experimental Pediatrics
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• v.55 no.7
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• pp.238-248
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• 2012

Purpose: Hypoxic-ischemic encephalopathy is an important cause of neonatal mortality, as this brain injury disrupts normal mitochondrial respiratory activity. Carnitine plays an essential role in mitochondrial fatty acid transport and modulates excess acyl coenzyme A levels. In this study, we investigated whether treatment of primary cultures of rat cortical neurons with L-carnitine was able to prevent neurotoxicity resulting from oxygen-glucose deprivation (OGD). Methods: Cortical neurons were prepared from Sprague-Dawley rat embryos. L-Carnitine was applied to cultures just prior to OGD and subsequent reoxygenation. The numbers of cells that stained with acridine orange (AO) and propidium iodide (PI) were counted, and lactate dehydrogenase (LDH) activity and reactive oxygen species (ROS) levels were measured. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and the terminal uridine deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assay were performed to evaluate the effect of L-carnitine (1 ${\mu}M$, 10 ${\mu}M$, and 100 ${\mu}M$) on OGD-induced neurotoxicity. Results: Treatment of primary cultures of rat cortical neurons with L-carnitine significantly reduced cell necrosis and prevented apoptosis after OGD. L-Carnitine application significantly reduced the number of cells that died, as assessed by the PI/AO ratio, and also reduced ROS release in the OGD groups treated with 10 ${\mu}M$ and 100 ${\mu}M$ of L-carnitine compared with the untreated OGD group (P<0.05). The application of L-carnitine at 100 ${\mu}M$ significantly decreased cytotoxicity, LDH release, and inhibited apoptosis compared to the untreated OGD group (P<0.05). Conclusion: L-Carnitine has neuroprotective benefits against OGD in rat primary cortical neurons in vitro.