• Journal of Korean Neurosurgical Society
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• v.50 no.6
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• pp.492-496
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• 2011

Objective : Direct revascularization surgery is regarded as the most effective method of treatment of adults with moyamoya disease. These patients, however, have a higher risk of perioperative ischemic complications than do patients with atherosclerotic stroke, and are at risk for ischemic complications in the hemisphere contralateral to the one operated on. We investigated the incidence and risk factors for ischemic stroke in the contralateral hemisphere after surgical treatment of adults with moyamoya disease. Methods : We retrospectively reviewed the medical records and results of neuroimaging studies on 79 hemispheres of 73 consecutive patients with adult moyamoya disease ($mean{\pm}SD$ age, $37.96{\pm}11.27$ years; range, 18-62 years) who underwent direct bypass surgery over 6 years. Results : Ischemic complications occurred in 4 of 79 (5.1%) contralateral hemispheres, one with Suzuki stage 3 and three with Suzuki stage 4. Three patients showed posterior cerebral artery (PCA) involvement by moyamoya vessels. Advanced stage of moyamoya disease (Suzuki stages 4/5/6; $p$=0.001), PCA involvement ($p$=0.001) and postoperative hypotension (mean arterial blood pressure <80% of preoperative mean arterial blood pressure) on the first ($p$<0.0001) and second ($p$=0.003) days after surgery were significantly correlated with postoperative contralateral ischemic complications. Conclusion : In patients with advanced moyamoya disease and involvement of the PCA, intentional hypotension can result in ischemic stroke in the hemisphere contralateral to the one operated on. Careful control of perioperative blood pressure is crucial for good surgical results.

• Clinical and Experimental Pediatrics
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• v.61 no.8
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• pp.245-252
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• 2018

Purpose: This study investigated patterns of ischemic injury observed in brain images from patients with neonatal group B Streptococcal (GBS) meningitis. Methods: Clinical findings and brain images from eight term or near-term newborn infants with GBS meningitis were reviewed. Results: GBS meningitis was confirmed in all 8 infants via cerebrospinal fluid (CSF) analysis, and patients tested positive for GBS in both blood and CSF cultures. Six infants (75.0%) showed early onset manifestation of the disease (<7 days); the remaining 2 (25.0%) showed late onset manifestation. In 6 infants (75%), cranial ultrasonography showed focal or diffuse echogenicity, suggesting hypoxic-ischemic injury in the basal ganglia, cerebral hemispheres, and periventricular or subcortical white matter; these findings are compatible with meningitis. Findings from magnetic resonance imaging (MRI) were compatible with bacterial meningitis, showing prominent leptomeningeal enhancement, a widening echogenic interhemisphere, and ventricular wall thickening in all infants. Restrictive ischemic lesions observed through diffusion-weighted imaging were evident in all eight infants. Patterns of ischemic injury as detected through MRI were subdivided into 3 groups: 3 infants (37.5%) predominantly showed multiple punctuate lesions in the basal ganglia, 2 infants (25.0%) showed focal or diffuse cerebral infarcts, and 3 infants (37.5%) predominantly showed focal subcortical or periventricular white matter lesions. Four infants (50%) showed significant developmental delay or cerebral palsy. Conclusion: Certain patterns of ischemic injury are commonly recognized in brain images from patients with neonatal GBS meningitis, and this ischemic complication may modify disease processes and contribute to poor neurologic outcomes.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.6
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• pp.327-332
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• 2005

The preventive effects of gene transfer of human copper/zinc superoxide dismutase (Cu/ZnSOD) on the development of cerebral vasospasm after subarachnoid hemorrhage (SAH) were examined usin a rat model of SAH. An experimental SAH was produced by injecting autologous arterial blood twice into the cisterna magna, and the changes in the diameter of the middle cerebral artery (MCA) were measured. Rats subjected to SAH exhibited a decreased diameter with an increased wall thickness of MCA that were significantly ameliorated by pretreatment with diphenyleneiodonium (DPI, $10{\mu}M$), an inhibitor of NAD(P)H oxidase. Furthermore, application of recombinant adenovirus ($100{\mu}l$ of $1{\times}10^{10}$ pfu/ml, intracisternally), which encodes human Cu/ZnSOD, 3 days before SAH prevented the development of SAH-induced vasospasm. Our findings demonstrate that SAH-induced cerebral vasospasm is closely related with NAD(P)H oxidase-derived reactive oxygen species, and these alterations can be prevented by the recombinant adenovirus-mediated transfer of human Cu/ZnSOD gene to the cerebral vasculature.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.2
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• pp.45-55
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• 2007

We elucidated the effects of various components of ischemic medium on the outcome of simulated ischemia-reperfusion injury. Hypoxia for up to 12 hours induced neither apoptotic bodies nor LDH release. However, reoxygenation after 6 or 12 hours of hypoxia resulted in a marked LDH release along with morphological changes compatible with oncotic cell death. H9c2 cells were then subjected to 6 hours of simulated ischemia by exposing them to modified hypoxic glucose-free Krebs-Henseleit buffer. Lowered pH (pH 6.4) of simulated-ischemic buffer resulted in the generation of apoptotic bodies during ischemia, with no concomitant LDH release. The degree of reperfusion-induced LDH release was not affected by the pH of ischemic buffer. Removal of sodium bicarbonate from the simulated ischemic buffer markedly increased cellular damages during both the simulated ischemia and reperfusion. Addition of lactate to the simulated ischemic buffer increased apoptotic cell death during the simulated ischemia. Most importantly, concomitant acidosis and high lactate concentration in ischemic buffer augmented the reperfusion-induced oncotic cell death. These results confirmed the influences of acidosis, bicarbonate deprivation and lactate on the progression and outcome of the simulated ischemia-reperfusion, and also demonstrated that concomitant acidosis and high lactate concentration in simulated ischemic buffer contribute to the development of reperfusion injury.

• The Journal of Internal Korean Medicine
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• v.23 no.1
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• pp.5-13
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• 2002

Purpose : Studies on stroke were conducted by using the scaling system to estimate, compare severity and to predict prognosis. National Institute of Health Stroke Scale is widely used for this purpose due to its accuracy in predicting clinical symptoms. According to previous studies, neurologic symptoms in acute stage of ischemic stroke did not disappear, and approximately 27% to 43% of them were aggravated, We conducted this study to define clinical aggravation and to improve ischemic stroke in its acute stage by using NIHSS. Methods and Subjects : Due to their acute ischemic stroke, twenty five patients visited Wonkwang Oriental Medicine in Cheonju within forty eight hours from its beginning stage. Two oriental medicine doctors checked NIHSS every six hours during the first ninety six hours and later every twenty four hours for twelve days from the beginning of the disease. Results : The Aggravated group consisted of nineteen out of twenty five cases, which is seventy six % and NIHSS on admissions were $5.88{\pm}0.63$ and it increased linearly over time by the equation of NIHSS on admissions was $8.50{\pm}2.02$ and it decreased linearly over time by the equation of NIHSS=-0.01 one hour+7.91. Conclusion : During the study, we defined the clinical courses of acute ischemic stroke. There have been no reports on this so far. Therefore, we hope that this study will be beneficial to expand the scope of oriental medicine in dealing with aggravating ischemic stroke in the acute stage.

• Journal of Veterinary Clinics
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• v.33 no.1
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• pp.10-15
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• 2016

The purpose of this study was to establish reproducible ischemic infarction model using allogenic blood clot in beagle dogs and identify induced ischemic lesion after middle cerebral artery occlusion using magnetic resonance imaging (MRI) and histopathologic findings. Twenty eight male beagle dogs with no evidence of neurologic disease were experimented. Allogenic embolus was made using a healthy beagle dog. After internal carotid artery (ICA) was exposure, 16G catheter was introduced through the ICA. The dog was administered 0.3 ml blood clot for 15 seconds followed by 3 ml of saline for 15 seconds. MRI scans were performed with 1.5T to evaluate ischemic lesion at 7 days after middle cerebral artery occlusion procedure. Evaluation parameters of MRI include location, distribution, infarction type, margin, shape, mass effect and intensity of T1-weighted imaging (T1WI), T2-weighted imaging (T2WI), fluid attenuated inversion recovery (FLAIR) sequence, diffusion weighted imaging (DWI) and apparent diffusion coefficient (ADC). On MRI, all dogs (28/28) showed focal or multifocal lesion including telencephalon and thalamus lesions, especially caudate nucleus (24/28). These lesions had well-defined margin from adjacent brain parenchyma, none or mild mass effect and various shape. Most of dogs appeared hyperintensity on T1WI, T2WI, FLAIR, and DWI/ADC, corresponding to chronic infarction. These lesions were histopathologically confirmed atrophic changes and unstained lesion. In conclusion, MRI is the useful method to provide information about ischemic infarction in dogs and the best reproducible ischemic infarction model was developed by using allogenic blood clot.

• 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.

• Journal of Veterinary Clinics
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• v.25 no.5
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• pp.355-358
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• 2008

The aim of this study was to investigate whether trophic factor supplementation (TFS) enhance the survival of kidney cell during cold ischemic storage and rewarming. The effect of TFS on the phosphorylation of p44/42 and p38 mitogen activated protein kinases (MAPK) signaling pathway was determined by Western blot. Apoptotic changes after cold ischemic storage and rewarming was determined by 4',6'-diamino-2-phenylindole (DAPI) staining. The cell viability was evaluated by live assay. TFS significantly decreased p44/42 and p38 MAPK activity induced by cold ischemic injury and rewarming (p < 0.05). The number of apoptotic cells was decreased after 5 minute rewarming in the presence of TFS. TFS significantly increased the cell viability after 5 minute rewarming (p < 0.05). Therefore, it was concluded that trophic factor supplementation protects kidney tubule cells from cold ischemic and rewarming injury via the inhibition of p44/42 and p38 MAPK activation and reducing apoptotic change.

• The Journal of Pediatrics of Korean Medicine
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• v.19 no.2
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• pp.127-136
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• 2005

Objective: There were few reports on the treatment of Wolff-Parkinson-White syndrome with Hypoxic ischemic encephalopathy. We treated a Wolff-Parkinson-White syndrome with Hypoxic ischemic encephalopathic patient with Oriental medical approach, and got a significant result. This treatment shows the possibility of healing Wolff-Parkinson-White syndrome with Hypoxic ischemic encephalopathy. So we are reporting this case. Method : Acupuncture treatment, herb medication, rehabilitation therapy were applied for treating patient's chief symptom.(involuntary movement, dystonia, aphasia, fever, perspiration) Results : Consciousness loss in acute stage of Hypoxic ischemic encephalopathy can be considered as Mental Confusion due to Phlegm(Dammisimgyu) in veiw point of Oriental medicine. Wolff-Parkinson-White syndrome can be considered as Sudden Palpitation(Gyounggye) in veiw point of Oriental medicine. After oriental medical treatment, patient's chief symptoms were improved. Conclusion: More study about oriental medical treatment on Wolff-Parkinson-White syndrome with Hypoxic ischemic encephalopathy is needed.

• The Journal of Pediatrics of Korean Medicine
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• v.19 no.2
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• pp.255-269
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• 2005

Objective : To evaluate the effect of Oriental Medical Treatment on a patient with Hypoxic Ischemic Encephalopathy followed by Cardiopulmonary Resuscitation Method : We applied various methodology of Oriental Medical Treatment including Acupuncture, Electroacupuncture, Physical treatment, Herbal Medicine, Moxibustion treatment and Western medication as well. Result: Herbal medicine was applied on the basis of the patient's history. We applied formular to remove phelgm as a pathogenic factor after Hypoxic Ischemic Encephalopathy. At the same time, considering the patient spent more than a month in ICU lacking appropriate nutrition, we used formuli on the basis of 'Deficiency of Spleen' focusing to vitalize the function of digestive system. As the condition of the patient changed, we also adapted formular accordingly. We prescribed Herbal medication to strengthen Yin and Yang equally as she got hospitalized for long time. Also we applied Acupuncture treatment and Moxibustion treatment to control Qi flow. The general condition of the patient got better with successful removal of Foley catheter and elevated Glasgow Coma scale. We used Electroacupuncture, Physical treatment and Western medication at the same to get maximized effect on relaxing the contracted muscle. According to the Modified Ashworth Scale (MAS), we have some changes in muscle spasticity but later, the effect was not that significant. Conclusion : We had a patient with Hypoxic Ischemic Encephalopathy followed by Cardiopulmonary Resuscitation. In the management of Hypoxic Ischemic Encephalopathy, Conservative treatments are the mainstream but there are not many alternatives. Therefore, We suggest that Oriental medical approach may contribute to the management of Hypoxic Ischemic Encephalopathy.