• Journal of Korean Neurosurgical Society
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• v.41 no.6
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• pp.411-413
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• 2007

We report on a diabetic 52-year-old man who complained ocular floating sensation, headache and dizziness, in whom a left parieto-occipital dural ateriovenous fistulas [DAVFs], fed by bilateral superficial temporal arteries and occipital artery, drained into the cortical vein of the left parieto-occipital convexity. Because the patient's chief complaint was ocular symptom for diabetic retinopathy, we initially didn't consider an DAVFs until brain magnetic resonance imaging [MRI] was done. Diffusion-weighted brain MRI revealed acute cerebral infarction and microhemorrhage in the lesion. Transarterial embolization with mixture of glue and lipiodol obliterated the DAVFs completely. Although the DAVFs fed by multi-arteries, the fistulous portion has been disappeared after embolization via an only left occipital artery Endovascular embolization of the fistula led to symptomatic improvement, except ocular discomfort.

• Journal of Chest Surgery
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• v.18 no.4
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• pp.746-752
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• 1985

A retrospective clinical observation was made of 40 patients with postoperative cerebral dysfunction among 2634 patients who underwent open-heart operations in Severance Hospital. Yonsei University between 1962, the year the first successful open heart operation was done, and June 1985. Suspected causes of brain damage were reviewed. Brain CT findings were evaluated in 24 patients. There were 15 cerebral infarcts, 4 intracerebral bleedings, 3 ischemic brain damages, 1 infarction with intracerebral hemorrhage and 1 diffuse cortical atrophy from unknown cause. The most frequent site of cerebral infarction was the middle cerebral artery area with no predilection on the right of left.

• Korean Journal of Medicinal Crop Science
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• v.19 no.1
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• pp.31-37
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• 2011

Previous work demonstrated that an ethanol extract (HS0608) of a mixture of three medicinal plants of Curcuma longae radix, Phellinus linteus, and Scutellariae radix markedly inhibits $A{\beta}$ (25-35)-induced neurotoxicity. The present study was performed to further verify the neuroprotective effect of HS0608 on oxidative and ischemic cerebral injury using cultured rat cortical neurons and rats. Exposure of cultured cortical neurons to $100\;{\mu}M$ hydrogen peroxide ($H_2O_2$) induced neuronal apoptotic death. At $10-100{\mu}g/ml$, HS0608 inhibited neuronal death, elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) induced by $H_2O_2$ in primary cultures of rat cortical neurons. In vivo, HS0608 prevented cerebral ischemic injury induced by 2-h middle cerebral artery occlusion (MCAO) and 24-h reperfusion. The ischemic infarct and edema were significantly reduced in rats that received HS0608 (200 mg/kg). These results suggest that the anti-oxidative properties of HS0608 may be responsible for its neuroprotective effect against focal cerebral ischemic injury and that HS0608 may have a therapeutic role in neurodegenerative diseases such as stroke.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.33 no.2
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• pp.171-175
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• 2011

Implant placement on the anterior mandible is considered a common and safe surgical procedure. However, severe hemorrhage can occur if branches of the sublingual artery, which run through the lingual cortical plate of the mandible, are damaged. Excessive hemorrhage caused by injury to the sublingual artery can result in life-threatening problems such as airway obstruction. A 54-year old male patient without any generalized systemic conditions was referred due to active bleeding after implant placement in the anterior mandible. Gauze compression with surgicel and bosimin were performed and hemostasis was achieved. The patient was discharged after 3 days without any supplementary bleeding.

• Korean Journal of Radiology
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• v.23 no.3
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• pp.333-342
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• 2022

Objective: Intracranial atherosclerotic stroke occurs through various mechanisms, mainly by artery-to-artery embolism (AA) or branch occlusive disease (BOD). This study evaluated the spatial relationship between middle cerebral artery (MCA) plaques and perforating arteries among different MCA territory infarction types using vessel wall magnetic resonance imaging (VW-MRI). Materials and Methods: We retrospectively enrolled patients with acute MCA infarction who underwent VW-MRI. Thirty-four patients were divided into three groups according to infarction pattern: 1) BOD, 2) both BOD and AA (BOD-AA), and 3) AA. To determine the factors related to BOD, the BOD and BOD-AA groups were combined into one group (with striatocapsular infarction [BOD+]) and compared with the AA group. To determine the factors related to AA, the BOD-AA and AA groups were combined into another group (with cortical infarction [AA+]) and compared with the BOD group. Plaque morphology and the spatial relationship between the perforating artery orifice and plaque were evaluated both quantitatively and qualitatively. Results: The plaque margin in the BOD+ group was closer to the perforating artery orifice than that in the AA group (p = 0.011), with less enhancing plaque (p = 0.030). In the BOD group, plaques were mainly located on the dorsal (41.2%) and superior (41.2%) sides where the perforating arteries mainly arose. No patient in the AA group had overlapping plaques with perforating arteries at the cross-section where the perforator arose. Perforating arteries associated with culprit plaques were most frequently located in the middle two-thirds of the M1 segment (41.4%). The AA+ group had more stenosis (%) than the BOD group (39.73 ± 24.52 vs. 14.42 ± 20.96; p = 0.003). Conclusion: The spatial relationship between the perforating artery orifice and plaque varied among different types of MCA territory infarctions. In patients with BOD, the plaque margin was closer and blocked the perforating artery orifice, and stenosis degree and enhancement were less than those in patients with AA.

• Archives of Pharmacal Research
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• v.23 no.4
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• pp.413-417
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• 2000

The effect of ischemia/reperfusion-induced neuronal damage on the memory impairment were investigated using active avoidance and Morris water maze tasks in Wistar rats. Focal ischemia was induced by 1 h occlusion of the right middle cerebral artery (MCA) of Wistar male rats. Reperfusion was induced by releasing the occlusion and restoring the blood circulation for 24 h. The acquisition and preservation memory tested by active avoidance showed a significant difference between the sham and ischemia/reperfusion group. The water maze acquisition performance was also significant difference between sham and ischemia/repefusion groups in both latency and moving distance. The infarction volume was increased by the ischemia/reperfusion. Furthermore, the cresyl violet staining of the ischemia/reperfusion brain showed severe neuronal damage (pyramidal cell loss) in the cortex in addition to the striatum lesion of brain. This study shows that pyramidal cell damage in the cortex lesion may be partially related to memorial disturbance in the ischemia/reperfusion brain injury.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.4
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• pp.167-172
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• 2006

In the present study, we developed a simple method to predict the neuronal cell death in the mouse hippocampus and striatum following transient global forebrain ischemia by evaluating both cerebral blood flow and the plasticity of the posterior communicating artery (PcomA). Male C57BL/6 mice were anesthetized with halothane and subjected to bilateral occlusion of the common carotid artery (BCCAO) for 30 min. The regional cerebral blood flow (rCBF) was measured by laser Doppler flowmetry. The plasticity of PcomA was visualized by intravascular perfusion of India ink solution. When animals had the residual cortical microperfusion less than 15% as well as the smaller PcomA whose diameter was less than one third compared with that of basilar artery, neuronal damage in the hippocampal subfields including CA1, CA2, and CA4, and in the striatum was consistently observed. Especially, when mice met these two criteria, marked neuronal damage was observed in CA2 subfield of the hippocampus. In contrast, after transient BCCAO, neuronal damage was consistently produced in the striatum, dependent more on the degree of rCBF reduction than on the plasticity of PcomA. The present study provided simple and highly reproducible criteria to induce the neuronal cell death in the vulnerable mice brain areas including the hippocampus and striatum after transient global forebrain ischemia.

• 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 Korean Neurosurgical Society
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• v.57 no.1
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• pp.54-57
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• 2015

A 66-year-old woman presented with intermittent paraparesis and generalized tonic-clonic seizure. Cerebral angiography demonstrated dural arteriovenous fistula (AVF) involving superior sagittal sinus (SSS), which was associated with SSS occlusion on the posterior one third. The dural AVF was fed by bilateral middle meningeal arteries (MMAs), superficial temporal arteries (STAs) and occipital arteries with marked retrograde cortical venous reflux. Transfemoral arterial Onyx embolization was performed through right MMA and STA, but it was not successful, which resulted in partial obliteration of dural AVF because of tortuous MMA preventing the microcatheter from reaching the fistula closely enough. Second procedure was performed through left MMA accessed by direct MMA puncture following small decortications of cranium overlying the MMA using diamond drill one week later. Microcatheter could be located far distally to the fistula through 5 F sheath placed into the MMA and complete obliteration of dural AVF was achieved using 3.9 cc of Onyx.

• The Korean Journal of Nuclear Medicine
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• v.24 no.2
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• pp.325-331
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• 1990

Radionuclide renal scintigraphies were performed in a 24-year-old man with right renal artery branch stenosis. Captopril enhanced $^{99m}Tc-DTPA$ renal scintigraphy revealed no abnormal finding in the right kidney. But, $^{99m}Tc-DMSA$ renal scintigraphy showed regional cortical photon deficient area corresponding to the area supplied by the stenotic branch artery. The defect size increased in captopril enhanced $^{99m}Tc-DMSA$ renal scintigrphy and nearly disappeared after successful transluminal renal angioplasty. This case suggests that the captopril enhanced $^{99m}Tc-DMSA$ renal scintigraphy may be a useful method in the evaluation of renovascular hypertension, especially due to branch renal srtery stenosis.