• Journal of Korean Neurosurgical Society
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• v.66 no.2
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• pp.205-210
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• 2023

Delayed cerebral ischemia (DCI) remains a devastating complication in subarachnoid hemorrhage (SAH), however, there were no present reports that is associated with a ruptured spinal arteriovenous fistula (sAVF). We would like to present a rare case of DCI following embolization of a ruptured perimedullary sAVF. Initially, the patient clinical symptoms mimic a SAH caused by a ruptured intracranial aneurysm. Further evaluation revealed that the SAH was caused by a ruptured perimedullary sAVF and the patient's condition improved following the embolization procedure. Three days later, the patient developed an acute left-sided facial and motor weakness, which persisted until the patient was discharged on the day-15 onset. A magnetic resonance imaging and angiography is performed 1.5 years after discharge and revealed no signs of cerebral infarction and hemorrhage. In this paper, we reported DCI after embolization in a ruptured sAVF with SAH, supported by evidence from the current literature. We would like to also stress the importance of complete spinal and cerebral vessel imaging to reveal the underlying abnormalities and determine the most appropriate intervention.

• The Korean Journal of Pharmacology
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• v.29 no.1
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• pp.1-8
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• 1993

To elucidate involvement of platelet-activating factor (PAF) in cerebral ischemia-reperfusion injury, male Sprague-Dawley rats and albino mice of either sex were subjected to a 10-min bilateral carotid artery occlusion and 6-hr recirculation. The McGraw stroke index in mice was markedly inhibited by PAF antagonists, BN 52021 and CV 6209 (1 mg/kg, i.p., each) When they were administered 10 min before bilateral carotid artery occlusion or 1 hr after reperfusion. The increases in brain water content were significantly attenuated by treatment with BN 52021 or CV 6209 in both animals. BN 52021 exhibited a significant improvement in the postischemic blood pressure change in association with a beneficial effect on the delayed dilatation of pial arterioles after 10 min of ischemia. Thus it is suggested that PAF plays an important role as an endogenous mediator in development of cerebral ischemia-reperfusion injury, and further, specific antagonists to PAF will be able to prevent or reverse the pathological sequelae of cerebral ischemia.

• Journal of Korean Neurosurgical Society
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• v.65 no.1
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• pp.4-12
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• 2022

Objective : We reported the differentially methylated genes in patients with subarachnoid hemorrhage (SAH) using bioinformatics analyses to explore the biological characteristics of the development of delayed cerebral ischemia (DCI). Methods : DNA methylation profiles obtained from 40 SAH patients from an epigenome-wide association study were analyzed. Functional enrichment analysis, protein-protein interaction (PPI) network, and module analyses were carried out. Results : A total of 13 patients (32.5%) experienced DCI during the follow-up. In total, we categorized the genes into the two groups of hypermethylation (n=910) and hypomethylation (n=870). The hypermethylated genes referred to biological processes of organic cyclic compound biosynthesis, nucleobase-containing compound biosynthesis, heterocycle biosynthesis, aromatic compound biosynthesis and cellular nitrogen compound biosynthesis. The hypomethylated genes referred to biological processes of carbohydrate metabolism, the regulation of cell size, and the detection of a stimulus, and molecular functions of amylase activity, and hydrolase activity. Based on PPI network and module analysis, three hypermethylation modules were mainly associated with antigen-processing, Golgi-to-ER retrograde transport, and G alpha (i) signaling events, and two hypomethylation modules were associated with post-translational protein phosphorylation and the regulation of natural killer cell chemotaxis. VHL, KIF3A, KIFAP3, RACGAP1, and OPRM1 were identified as hub genes for hypermethylation, and ALB and IL5 as hub genes for hypomethylation. Conclusion : This study provided novel insights into DCI pathogenesis following SAH. Differently methylated hub genes can be useful biomarkers for the accurate DCI diagnosis.

• Journal of Korean Neurosurgical Society
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• v.67 no.2
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• pp.177-185
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• 2024

Objective : Delayed cerebral ischemia (DCI) is a major cause of disability in patients who survive aneurysmal subarachnoid hemorrhage (aSAH). Systemic inflammatory markers, such as peripheral leukocyte count and systemic immune-inflammatory index (SII) score, have been considered predictors of DCI in previous studies. This study aims to investigate which systemic biomarkers are significant predictors of DCI. Methods : We conducted a retrospective, observational, single-center study of 170 patients with SAH admitted between May 2018 and March 2022. We analyzed the patients' clinical and laboratory parameters within 1 hour and 3-4 and 5-7 days after admission. The DCI and non-DCI groups were compared. Variables showing statistical significance in the univariate logistic analysis (p<0.05) were entered into a multivariate regression model. Results : Hunt-Hess grade "4-5" at admission, modified Fisher scale grade "3-4" at admission, hydrocephalus, intraventricular hemorrhage, and infection showed statistical significance (p<0.05) on a univariate logistic regression. Lymphocyte and monocyte count at admission, SII scores and C-reactive protein levels on days 3-4, and leukocyte and neutrophil counts on days 5-7 exhibited statistical significance on the univariate logistic regression. Multivariate logistic regression analysis revealed that monocyte count at admission (odds ratio [OR], 1.64; 95% confidence interval [CI], 1.04-2.65; p=0.036) and SII score at days 3-4 (OR, 1.55; 95% CI, 1.02-2.47; p=0.049) were independent predictors of DCI. Conclusion : Monocyte count at admission and SII score 3-4 days after rupture are independent predictors of clinical deterioration caused by DCI after aSAH. Peripheral monocytosis may be the primer for the innate immune reaction, and the SII score at days 3-4 can promptly represent the propagated systemic immune reaction toward DCI.

• Journal of Korean Neurosurgical Society
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• v.59 no.2
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• pp.154-157
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• 2016

A continuous electroencephalography (cEEG) can be helpful in detecting vasospasm and delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage (SAH). We describe a patient with an aneurysmal SAH whose symptomatic vasospasm was detected promptly by using a real-time cEEG. Patient was immediately treated by intraarterial vasodilator therapy. A 50-year-old woman without any significant medical history presented with a severe bifrontal headache due to acute SAH with a ruptured aneurysm on the anterior communicating artery (Fisher grade 3). On bleed day 6, she developed a sudden onset of global aphasia and left hemiparesis preceded by cEEG changes consistent with vasospasm. A stat chemical dilator therapy was performed and she recovered without significant neurological deficits. A real-time and protocol-based cEEG can be utilized in order to avoid any delay in detection of vasospasm in aneurysmal SAH and thereby improve clinical outcomes.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.1
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• pp.246-253
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• 2005

This study was designed to investigate the neuroprotective effects of Guh-Poong-Chung-Sim-Hwan(GCH) on ischemia induced by middle cerebral artery occlusion(MCAO) in Sprague-Dawley rats. The effects of GCH administration on the size of the brain infarct and the functional status of the rats after ischemia were examined, as well as the expression of COX-2 in acute phase. The recovery of motor functions for 7 days and the brain infarct were examined to find out the delayed effects of daily GCH-administration as well. In conclusion, we found that GCH reduced both functional deficits and brain damage in the MCAO rat model of stroke. In addition, high doses of GCH reduced COX-2 expression in the penumbra. It is well known that herbal medication including GCH is very safe for humans. Accordingly, our results support the clinical use of this GKM for the treatment of stroke and offer the possibility that a potent neuroprotective agent could be developed from Korean herbal medicines.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.3
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• pp.279-286
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• 1998

It has been well documented that transient forebrain global ischemia causes selective neuronal degeneration in hippocampal CA1 pyramidal neurons with a delay of a few days. The mechanism of this delayed hippocampal CA1 pyramidal neuronal death (DND) is still controversial. To delineate the mechanisms of the DND, the effects of treatment with MK-801, an NMDA receptor antagonist, kynurenic acid, a NMDA/non-NMDA receptor antagonist, and/or cycloheximide, a protein synthesis inhibitor, on the DND were investigated in male Wistar rats. To examine the participation of apoptotic neuronal death in the DND, TUNEL staining was performed in ischemic brain section. Global ischemia was induced by 4-vessel occlusion for 20 min. All animals in this study showed the DND 3 and 7 days after the ischemic insult. The DND that occured 3 days and 7 days after the ischemia were not affected by pretreatment with MK-801 (1 mg/kg), but markedly attenuated by the pretreatment with kynurenic acid (500 mg/kg). Treatment with cycloheximide (1 mg/kg) also markedly inhibited the DND. The magnitudes of attenuation by the two drugs were similar. The magnitude of attenuation by co-treatments with kynurenic acid and cycloheximide was not greater than that with any single treatment. TUNEL staining was negative in the sections obtained 1 or 2 days after the ischemic insults, but it was positive at hippocampal CA1 pyramidal cells in sections collected 3 days after the ischemia. These results suggested that the DND should be mediated by the activation of non-NMDA receptor, not by the activation of NMDA receptor and that the activation of AMPA receptor should induce the apoptotic process in the DND.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.205.1-205.1
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• 2003

Several lines of recent evidences have shown that several pro-inflammatory genes or mediators, such as inducible nitric oxide synthase (iNOS)are strongly expressed in the ischemic brain. Inflammation is now recognized as a significant contributing mechanism in cerebral ischemia because anti-inflammatory compounds or inhibitors of iNOS have been proven to reduce ischemic brain damage. In iNOS assay, hexane fraction of M61 inhibited NO (iNOS IC50, 0.7${\mu}$g/ml). In vivo study was carried out to evaluate neuroprotective effect of hexane fraction of M61 after transient global ischemia using Mongolian gerbil ischemia model. (omitted)

• The Korean Journal of Pain
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• v.21 no.2
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• pp.119-125
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• 2008

Background: Cerebral blood vessels are innervated by sympathetic nerves from the superior cervical ganglia (SCG), and these nerves may influence the cerebral blood flow. The purpose of the present study was to evaluate the neuroprotective effect of superior cervical sympathetic ganglion block in rats that were subjected to focal cerebral ischemia/reperfusion injury. Methods: Eighty male Sprague-Dawley rats (270-320 g) were randomly assigned to one of two groups (the ropivacaine group and a control group). In all the animals, brain injury was induced by middle cerebral artery (MCA) reperfusion that followed MCA occlusion for 2 hours. The animals of the ropivacaine group received $30{\mu}l$ of 0.75% ropivacaine, and their SCG. Neurologic score was assessed at 1, 3, 7 and 14 days after brain injury. Brain tissue samples were then collected. The infarct ratio was measured by 2.3.5-triphenyltetrazolium chloride staining. The terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeled (TUNEL) reactive cells and the cells showing caspase-3 activity were counted as markers of apoptosis at the caudoputamen and frontoparietal cortex. Results: The death rate, the neurologic score and the infarction ratio were significantly less in the ropivacaine group 24 hr after ischemia/reperfusion injury. The number of TUNEL positive cells in the ropivacaine group was significantly lower than those values of the control group in the frontoparietal cortex at 3 days after injury, but the caspase-3 activity was higher in the ropivacaine group than that in the control group at 1 day after injury. Conclusions: The study data indicated that a superior cervical sympathetic ganglion block may reduce the neuronal injury caused by focal cerebral ischemia/reperfusion, but it may not prevent the delayed damage.

• Journal of Pharmacopuncture
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• v.7 no.2
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• pp.29-41
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• 2004

Objective : This experimental studies were performed in order to prove the effect of Hirudin Herbal-acupuncture by using rats that had neuronal damage due to the Middle Cerebral Artery Occulsion(MCAO). Method : We observed the change of extracellular concentrations(${\mu}M$) of dopamine, DOPAC, HVA, HIAA, glutamate, aspartate, GABA, glysine, taurine, alanine, and tyrosine as extracted by vivo microdialysis, in the Hirudin Herbal-acupuncture administrated rats($240{\sim}260g$, Sprague-Dawley) subjected to the MCAO. The dialysates were extracted three times before the MCAO and six times after the MCAO every 20 minutes, and analysed by highperformance liquid chromatography(HPLC). Results : Hirudin Herbal-acupuncture significantly inhibited glutamate, aspartate, and tyrosine which are stimulant neurotransmitters at brain ischemia, and it significantly decreased glycine, GABA, taurine, and alanine which are inhibitory neurotransmitters at brain ischemia. Conclusion : Hirudin Herbal-acupuncture may prevent delayed neuronal death(DND) in selectively vulnerable focal areas of the brain effectively.