Kim, Sung Tae;Jin, Sung-Chul;Jeong, Hae Woong;Seo, Jung Hwa;Ha, Sam Yeol;Pyun, Hae Wook
Journal of Korean Neurosurgical Society
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v.56
no.6
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pp.463-468
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2014
Objective : Unexpected Solitaire stent detachment can occur during mechanical Solitaire thrombectomy. The purpose of this study was to retrospectively evaluate the influencing factors causing unexpected Solitaire stent detachment and the clinical outcomes. Methods : Between October 2011 to December 2013, 232 cases of mechanical Solitaire thrombectomy for acute ischemic stroke were performed in 3 stroke centers. During this period, we encountered unexpected Solitaire stent detachments during mechanical Solitaire thrombectomies in 9 cases. Results : Solitaire stents unexpectedly detached in 9 cases (3.9%) during the retrieval of Solitaire stents. The median patient age was 76 years. The occlusion sites of the unexpected stent detachment were the proximal middle cerebral artery (MCA) in 7 cases and the internal carotid artery in 2 cases. The sizes of the stents that unexpectedly detached were $6{\times}30$ mm in 7 cases, $5{\times}30$ mm in 1 case, and $4{\times}20$ mm in 1 case. Four patients had unexpected detachment at the first retrieval, 1 patient at the second, 3 patients at the third, and 1 patient at the fifth. In all of the cases of unexpected detachment at the first retrieval, the stent deployment site was the proximal MCA. After detachment, a proximal marker of the Solitaire stent was observed in 3 patients. However, no marker was visible in the remaining 6 patients. Conclusion : Unexpected Solitaire stent detachment should be considered in the first instance of stent retrieval for a relatively large-diameter stent, especially in elderly patients with MCA occlusions.
Objective : To evaluate the feasibility and clinical and angiographic outcomes of stent-assisted embolization for complex middle cerebral artery (MCA) aneurysms. Methods : The records of 23 consecutive patients with 24 MCA aneurysms, who underwent stent-assisted embolization of the aneurysm, were retrospectively evaluated. Results : Fifteen aneurysms were treated with one stent and 8 were treated using more than two stents (5 a stent-within-a-stent, 1 triple stents, and two Y-stent). Angiographically, complete or near complete occlusion was achieved in 15 aneurysms (65.2%), residual neck in five (21.7%), and residual aneurysm in three (13.1%). Five aneurysms demonstrated thrombosis within the stent during the procedure and hospitalization, and were resolved by intraarterial and intravenous Tirofiban injection. Symptomatic thromboembolic complications were developed in five patients and permanent deficits demonstrated in two patients with modified Rankin Scale 1 and 2, respectively. Treatment-related permanent morbidity and mortality rates were 8.3% and 0% with relatively high complication rate. Angiographic follow-up was available in 17 aneurysms at 6-31 months (mean, 13.2 months) and showed stable or improved in 15 (88.2%) and major and minor recurrence in one, respectively. Conclusion : Complex MCA aneurysms could be treated by stent-assisted coiling and showed lower recanalization rate during mid-term follow-up by effective flow diversion due to various stent-assisted techniques. Our results warrant further study with a longer follow-up period in a larger sample.
This study demonstrates the effects of Yanggyuksanhwa-Tang, Sasang constitutional herb prescription reported its clinical effect on the stroke of the So-yang In(少陽人), on the cerebral blood flow changes induced by nitro L-arginine methyl ester (L-NAME) treatment and ischemic brain damage induced by the middle cerebral artery occlusion (MCAO) in the rats. The changes of the arterial blood pressure, cerebral blood flow, and the diameter of the pial artery were measured in rats treated with L-NAME. And the changes of the infarct size, volume, and plasma tumor necrosis factor alpha ($TNF-{\alpha}$) levels were measured in the rats that the middle cerebral artery has been occluded by the intraluminal suture thread method. Yanggyuksanhwa-Tang was administered by the i.v. injection on the L-NAME treated rats, by the i.o. administration on the MCAO rats. The results is 1. The changes of the arterial blood pressure was not different statistically between in the L-NAME treated control group and in the Yanggyuksanhwa-Tang administered group. 2. Increase in the cerebral blood flow induced by L-NAME treatment was attenuated in the Yanggyuksanhwa-Tang administered group significantly (P<0.05) as compared with the L-NAME treated control group. 3. Decrease in the diameter of the pial artery induced by L-NAME treatment was attenuated about 18% in the Yanggyuksanhwa-Tang administered group as compared with the L-NAME treated control group. 4. Ischemic damaged infarct areas were decreased significantly (P<0.05) in the interaural 12mm, 10mm, and 6mm brain sections of the Yanggyuksanhwa-Tang administered group as compared the MCA occluded control group. 5. Total ischemic infarct volume was decreased significantly (P<0.05) in the Yanggyuksanhwa-Tang administered group as compared the MCA occluded control group. 6. Plasma $TNF-{\alpha}$ levels were decreased significantly (P<0.01) in the Yanggyuksanhwa-Tang administered group as compared the MCA occluded control group.
The present study examined influence of various ischemic duration on extent of focal ischemic brain injury induced by middle cerebral artery occlusion (MCAO) in rats. The MCAO was produced by insertion of a 17 mm silicone-coated 4-0 nylon surgical thread to the origin of MCA through the internal carotid artery for 30, 60, 90, 120 min (transient) or 24 hr (permanent) in male Sprague-Dawley rats under isoflurane anesthesia. Reperfusion in transient MCAO models was achieved by pulling the thread out of the internal carotid artery. Only rats showing neurological deficits characterized by left hemiparesis and/or circling to the left, were included in cerebral ischemic groups. The rats were sacrificed 24 hr after MCAO and seven serial coronal slices of the brain were stained with 2,3,5-triphenyltetrazolium chloride. Infarct size was measured using a computerized image analyzer. Ischemic damage was common in the frontoparietal cortex (somatosensory area) and the lateral segment of the striatum while damage to the medial segment of the striatum depended on the duration of the occlusion. In the 30-min MCAO grouts, however, infarcted region was primarily confined to the striatum and it was difficult to clearly delineate the region since there was mixed population of live and dead cells in the nucleus. Infarct volume was generally increased depending on the duration of MCAO, showing the most severe damage in the permanent MCAO group. However, there was no significant difference in infarct size between the 90-min and 120-min MCAO groups. % Edema also tended to increase depending on the duration of MCAO. The results suggest that the various focal ischemic rat models established in the present study can be used to evaluate in vivo neuroprotective activities of candidate compounds or to elucidate pathophysiological mechanisms of ischemic neuronal cell death.
The purpose of this study was to utilize Magnetic Resonance Imaging (MRI) and Magnetic Resonance Angiography (MRA) to analyze intracerebral regional distributions (hot spot) of ischemic cerebrovascular diseases which were characterized by stenosis and occlusion cerebral vasculature, except for cerebrovascular diseases induced by rupture of cerebral vasculature in terms of Korean people's cerebrovascular diseases, so that it could apply the findings of analysis to clinical practices. This study focused only on analyzing intracerebral regional distributions of ischemic cerebrovascular diseases that are characterized by stenosis and occlusion cerebral vasculature, because there are different etiologic mechanisms of ischemic cerebrovascular diseases like hemorrhagic cerebrovascular diseases (caused by rupture of cerebral vasculature) and cerebral infarction (induced by atheromatous arteriosclerosis). As a result, this study could come to the following findings of analysis: 1. According to sex ratio analysis, it was found that male group comprised larger portion of total 626 subjects in this study than female one (55.0% > 45.0%). 2. According to analysis on actual intracerebral regional distributions of ischemic cerebrovascular diseases, it was found that most subjects (37.5 %) were attacked by such diseases on the right side of cerebral vasculature, which was followed by left side of cerebral vasculature (35.1%) and bilateral cerebral vasculature (27.3%) respectively. 3. According to analysis on actual intracerebral regional distributions of ischemic cerebrovascular diseases, it was found that internal carotid artery (ICA) comprised the largest portion (38.9%) of those distributions, which was followed by middle cerebral artery (MCA, 35.7%), posterior cerebral artery (PCA, 13.4%), anterior cerebral artery (ACA, 6.0%) and vertebral artery (VA, 3.3%) respectively. 4. It was found that there was no subject attacked by any disease on A-com region, and there was only one male subject attacked by cerebrovascular diseases on P-com region. 5. It was found that female group was more susceptible to the attack of cerebrovascular diseases on MCA region than male one (54.6% > 42.2%), which means significant differences depending upon sex on statistical basis ($x^2$ = 9.64, p < .01). 6. It was found that male group was more susceptible to the attack of cerebrovascular diseases on ICA region (56.4% > 46.8%), which means significant differences depending upon sex on statistical basis ($x^2$ = 5.71, p < .05). 7. Moreover, it was also found that male group was more susceptible to the attack of cerebrovascular diseases on BA region (2.3% > 0.4%), which means significant differences depending upon sex on statistical basis ($x^2$ = 4.25, p < .05). 8. However, it was found that there was not any significant difference in intracerebral vasculature-specific distributions of cerebrovascular diseases depending on age of subjects, and stenosis comprised larger portion of cerebrovascular diseases than occlusion.
Kwak, Dong Hoon;Kim, Sung Min;Lee, Dea Hoon;Kim, Ji Su;Kim, Sun Mi;Lee, Seo Ul;Jung, Kyu Yong;Seo, Byoung Boo;Choo, Young Kug
Molecules and Cells
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v.20
no.3
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pp.354-360
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2005
Neuronal damage subsequent to transient cerebral ischemia is a multifactorial process involving several overlapping mechanisms. Gangliosides, sialic acid-conjugated glycosphingolipids, reduce the severity of acute brain damage in vitro. However their in vivo effects on the cerebral cortex damaged by ischemic infarct are unknown. To assess the possible protective role of gangliosides we examined their expression in the cerebral cortex damaged by ischemic infarct in the rat. Ischemia was induced by middle cerebral artery (MCA) occlusion, and the resulting damage was observed by staining with 2, 3, 5-triphenylterazolium chloride (TTC). High-performance thin-layer chromatography (HPTLC) showed that gangliosides GM3 and GM1 increased in the damaged cerebral cortex, and immunofluorescence microscopy also revealed a significant change in expression of GM1. In addition, in situ hybridization demonstrated an increase in the mRNA for ganglioside GM3 synthase. These results suggest that gangliosides GM1 and GM3 may be synthesized in vivo to protect the cerebral cortex from ischemic damage.
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.
Objectives : In this study, the neuroprotective effects of modified Boyanghwano-Tang (mBHT) and the major medicinal plants, Astragali Radix(AR) and Salviae Miltiorrhizae Radix(SMR) were investigated in transient middle cerebral artery occlusion (tMCAO)-induced ischemic stroke of rats. Methods : mBHT(400 mg/kg) and AR(154 mg/kg) or SMR(62 mg/kg) water extract orally injected in rats after 90 min occlusion of MCA and then allow reperfusion to 24 h. Brain infarction was measured by TTC staining and the expressions of NOS isoforms and apoptotic molecules were determined in ischemic brain by Western blot. Results : The results showed that mBHT has stronger neuropreotective property through inhibitions of the PARP cleaved and caspase-3 activation in ischemic rats, and could reduced infarction volumes comparison of those of AR or SMR, respectively. While, AR extract has an angiogenic property through increasing the expressions of eNOS and VEGF, and SMR extract has a strong anti-inflammatory effects through inhibition of iNOS expression in ischemic brains. Conclusions : These results suggest that mBHT has multifactorial therapeutic advantages through anti-apoptosis, anti-inflammation and angiogenesis for ischemic stroke based on a synergistic combination of ingradients rather than monotherapy.
Objective : Diagnosing acute cerebral infarction is crucial in determining prognosis of stroke patients. Although many serologic tests for prompt diagnosis are available, the clinical application of serologic tests is currently limited. We investigated whether $S100{\beta}$, matrix metalloproteinase-9 (MMP-9), D-dimer, and heat shock protein 70 (HSP70) can be used as biomarkers for acute cerebral infarction. Methods : Focal cerebral ischemia was induced using the modified intraluminal filament technique. Mice were randomly assigned to 30-minute occlusion (n=10), 60-minute occlusion (n=10), or sham (n=5) groups. Four hours later, neurological deficits were evaluated and blood samples were obtained. Infarction volumes were calculated and plasma $S100{\beta}$, MMP-9, D-dimer, and HSP70 levels were measured using enzyme-linked immunosorbent assay. Results : The average infarction volume was $12.32{\pm}2.31mm^3$ and $46.9{\pm}7.43mm^3$ in the 30- and 60-minute groups, respectively. The mean neurological score in the two ischemic groups was $1.6{\pm}0.55$ and $3.2{\pm}0.70$, respectively. $S100{\beta}$, MMP-9, and HSP70 expressions significantly increased after 4 hours of ischemia (p=0.001). Furthermore, $S100{\beta}$ and MMP-9 expressions correlated with infarction volumes (p<0.001) and neurological deficits (p<0.001). There was no significant difference in D-dimer expression between groups (p=0.843). The area under the receiver operating characteristic curve (AUC) showed high sensitivity and specificity for MMP-9, HSP70 (AUC=1), and $S100{\beta}$ (AUC=0.98). Conclusion : $S100{\beta}$, MMP-9, and HSP70 can complement current diagnostic tools to assess cerebral infarction, suggesting their use as potential biomarkers for acute cerebral infarction.
To assess the relationship between the severity of stenosis in MCA territory and the differentiation of syndromes in oriental medical aspects, the general characteristics, the scores of stroke-pattern identification, and the findings of MRA were compared in 18 acute cerebral infarction patientshospitalized in Dept. of Internal Medicine, Pundang CHA Oriental Medicine Hospital from 1998 sep. 1 to 1999 sep. 31. We compared the scores of stroke-pattern identification with the severity of stenosis by Kruskall-Wallis test, and analyzed the relationship by Pearson correlation test. The P value under 0.05 was regarded as significant. The results are as follows: The incidence of stenosis(mild to complete occlusion) was 83.3%. There were significant difference of the mean scores according to the severity of stenosis in Yin deficiency pattern. We could also observe a strong relationship between the severity of stenosis and Yin deficiency pattern, whose Pearson correlation coefficient was 0.655 (P<0.05). These results showed that Yin deficiency pattern could be a major cause of cerebral infarction.
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