• Annals of Clinical Neurophysiology
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• 제7권1호
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• pp.20-21
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• 2005

Myoclonus may originate from the cerebral cortex, subcortical structures, brainstem, spinal cord or peripheral nerve. But unilateral upper limb myoclonus related to cortical infarct is an unusual clinical picture. We report a 67-year-old man presented with myoclonus, associated with primary motor cortex infarction.

• The Korean Journal of Pain
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• 제21권1호
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• pp.33-37
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• 2008

Background: Cerebral blood vessels are innervated by sympathetic nerves from the superior cervical ganglion (SCG). The purpose of the present study was to evaluate the neuroprotective effect of superior cervical sympathetic ganglion block in rats subjected to permanent focal cerebral ischemia. Methods: Thirty male Sprague-Dawley rats (270-320 g) were randomly assigned to one of three groups (control, lidocaine and ropivacaine). A brain injury was induced in all rats by middle cerebral artery occlusion with a nylon thread. The animals of the local anesthetic group received $30{\mu}l$ of 2% lidocaine or 0.75% ropivacaine in the SCG. Neurologic scores were assessed 24 hours after brain injury. Brain samples were then collected. The infarct and edema ratios were measured by 2.3.5-triphenyltetrazolium chloride staining. Results: There were no differences in the death rates, neurologic scores, or infarction and edema ratios between the three groups. Conclusions: These findings suggest that superior cervical sympathetic ganglion block may not influence the brain damage induced by permanent focal cerebral ischemia in rats.

• Journal of Korean Neurosurgical Society
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• 제63권2호
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• pp.163-170
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• 2020

Objective : Milk fat globule-epidermal growth factor VIII (MFG-E8) may play a key role in inflammatory responses and has the potential to function as a neuroprotective agent for ameliorating brain injury in cerebral infarction. This study aimed to determine the role of MFG-E8 in brain injury in the subacute phase of cerebral ischemia in a rat model. Methods : Focal cerebral ischemia was induced in rats by occluding the middle cerebral artery with the modified intraluminal filament technique. Twenty-four hours after ischemia induction, rats were randomly assigned to two groups and treated with either recombinant human MFG-E8 or saline. Functional outcomes were assessed using the modified Neurological Severity Score (mNSS), and infarct volumes were evaluated using histology. Anti-inflammation, angiogenesis, and neurogenesis were assessed using immunohistochemistry with antibodies against ionized calcium-binding adapter molecule 1 (Iba-1), rat endothelial cell antigen-1 (RECA-1), and bromodeoxyuridine (BrdU)/doublecortin (DCX), respectively. Results : Our results showed that intravenous MFG-E8 treatment did not reduce the infarct volume; however, the mNSS test revealed that neurobehavioral deficits were significantly improved in the MFG-E8-treated group than in the vehicle group. Immunofluorescence staining revealed a significantly lower number of Iba-1-positive cells and higher number of RECA-1 in the periinfarcted brain region, and significantly higher numbers of BrdU- and DCX-positive cells in the subventricular zone in the MFG-E8-treated group than in the vehicle group. Conclusion : Our findings suggest that MFG-E8 improves neurological function by suppressing inflammation and enhancing angiogenesis and neuronal proliferation in the subacute phase of cerebral infarction.

• Journal of Korean Biological Nursing Science
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• 제4권2호
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• pp.19-40
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• 2002

The purpose of this study was to determine the effect of DHEA on Type I(soleus) and II muscles(plantaris, gastrocnemius) in a focal brain ischemia model rat. Thirty-seven male Sprague-Dawley rats with $200{\sim}250g$ body weights were randomly divided into four groups : CINS(cerebral ischemia + normal saline), CIDH(cerebral ischemia + DHEA), SHNS(sham + normal saline), SHDH (sham + DHEA). Both the CINS and CIDH groups were undergone a transient right middle cerebral artery occlusion operation. In the SHNS and SHDH groups, a sham operation was done. DHEA was administered daily at a dose of 0.34mmol/kg, and normal saline was administered daily at the same dose by intraperitoneal injection for 7days after operation. Cerebral infarction in the CINS and CIDH groups was identified by staining with 2% triphenyltetrazolium chloride solution for 60 minutes. The data were analyzed by Kruskal-Wallis test and Mann-Whitney U test using the SPSSWIN 9.0 program. The results were summarized as follows: 1) The muscle weights of soleus(Type I), plantaris and gastrocnemius(Type II) in CINS group were significantly less than those of the SHNS group(p<.01). The muscle fiber cross-sectional area of the CINS group was significantly less than that of the SHNS group in Type I muscle fiber of the soleus and Type II muscle fiber of the plantaris and gastrocnemius(p<.05). The myofibrillar protein content of the CINS group was significantly less than that of the SHNS group in the left gastrocnemius and right soleus(p<.05). 2) The muscle weights of the soleus, plantaris and gastrocnemius except the unaffected side of the plantaris in the CIDH significantly increased compared to those of the CINS group(p<.05). The muscle fiber cross-sectional area of the CIDH group significantly increased compared to that of the CINS group in Type II muscle fiber of the plantaris and gastrocnemius(p<.05). The myofibrillar protein content of the CIDH group significantly increased compared to that of the CINS group in the left soleus(p<.05). 3) On the post-op 8 day, the body weight of the CINS group was significantly less than that of the CIDH, SHNS and SHDH groups(p<.01). Total diet intake of the CINS and CIDH groups was significantly less than that of the SHNS and SHDH groups(p<.01). Based on these results, it was identified that muscle atrophy could be induced during the 7 days after cerebral infarction, and DHEA administration during the early stage of cerebral infarction might attenuate muscle atrophy.

• Nutritional Sciences
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• 제9권4호
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• pp.240-247
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• 2006

In this study we investigated the neuroprotective, antioxidative, and hypocholestrolemic effects of dietary soy protein and soy isoflavone in a rat focal brain ischemia model. Weaning Sprague-Dawley rats were fed a 20% casein-based diet (CA), 20% soy protein-based diet (SP), or 0.2% soy isoflavones-supplemented diet (ISO) for 6 weeks. The cortical infarction volume of the ISO group was significantly lower than that of the SP group. The thiobarbituric acid reactive substances (TBARS) were considerably lower in the ISO group than the CA group. Glutatbione peroxidase activities of the SP group were notably higher than those of the CA group. Acetylcholinesterase (AchE) activities of the SP group were significantly decreased compared to the CA group. LDL cholesterol levels and LDL/HDL ratios of the ISO group were lower than those of the CA and SP groups. Our results collectively suggest that soy isoflavones may contribute to neuroprotection by reducing the TBARS and serum LDL/HDL ratio, whereas soy protein may be associated with the regulation of cognitive functions by modulating AchE activity.

• 대한의생명과학회지
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• 제29권4호
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• pp.263-273
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• 2023

This study aimed to investigate effect of scalp acupuncture (SA) and repetitive transcranial magnetic stimulation (rTMS) intervention on neuromotor function in photothrombotic cerebral infarction (PCI) rat model. Sixty male SD rats were used. PCI was induced on M1 cortex of right frontal lobe. SA was performed at the Qianding (GV21), Xuanli (GB6) acupoints of ipsilesional M1. Low-frequency rTMS was delivered to contralesional M1. All rats were randomly divided into 4 groups: group A, normal (n, 15); group B, PCI without any stimulation intervention (n, 15); group C, PCI with SA (n, 15); group D, PCI with rTMS (n, 15). Rota-rod test and Ladder rung walking test (LWT) were done weekly for 8 weeks after PCI. SA or rTMS was started from post-PCI 4^th day as protocol for 8 weeks. H/E stain and IHC were done. Western blot and qRT-PCR study were performed for MAP2 and BDNF from ipsilesional M1 peri-infarction tissue. Brain MRI study was conducted to quantify the volume of cerebral infarction. As a result, left forelimb and hindlimb function significantly improved more in group C and D than control group, with expressed more BDNF and MAP2. And brain MRI showed focal infarction of right M1 after PCI, and infarction volume progressively decreased in group C and D than group B from post-PCI 5^th to 8^th week. SA or rTMS was more effective than no intervention group on neuromotor function of PCI rat model. The functional recovery was associated with stimulation intervention-related neurogenesis.

• Journal of Korean Neurosurgical Society
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• 제40권3호
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• pp.189-192
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• 2006

Spontaneous dissection of the anterior cerebral artery is an unusual cause of subarachnoid hemorrhage. We present a case of a dissecting aneurysm of the anterior cerebral artery presenting with subarachnoid hemorrhage. A 51-year-old woman presented to our hospital with severe headache. Neurological examination demonstrated neck stiffness, decreased visual acuity of the left eye, and left ankle weakness. Computed tomographic scans showed subarachnoid hemorrhage. The initial cerebral angiogram demonstrated a slightly narrowed caliber and mild poststenotic dilation of the right A1 segment. A second cerebral angiogram 14 days later revealed no change in the focal narrowing of the proximal A1 segment but marked progression of the dilatation of the distal A1 segment. Right pterional craniotomy was performed. A sausage-like dilation of the right A1 segment was found with no definite mural hematoma. This abnormal right A1 segment was wrapped with a Sundt clip. A postoperative computed tomographic scan revealed Infarction of the right head of the caudate nucleus and the anterior limb of the right internal capsule. If a dissecting aneurysm is suspected, serial angiographic studies should be performed because of the possibility of dynamic changes over a short period.

• Journal of Korean Neurosurgical Society
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• 제29권2호
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• pp.167-179
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• 2000

Objective : We studied to clarify the effective time zone of mild hypothermic neural protection during ischemia and/or reperfusion after middle cerebral artery occlusion. Methods : In a reversible cerebral infarct model which maintained reperfusion of blood flow after middle cerebral artery occlusion for two hours, the size of cerebral infarction, cerebral edema and the extent of neurological deficit were observed and analyzed for comparison between the control and the experimental groups under hypothermia($33.5^{\circ}C$). The temporalis muscle temperature was reduced to $33.5^{\circ}C$ by surface cooling for two hours during middle cerebral artery occlusion for study group I. The following groups applied hypothermia for two-hour periods after reperfusion : group II(0-2 hours), group III(2-4 hours), and group IV(4-6 hours). They were rewarmed to $36.5^{\circ}C$ until sacrified at 2, 4, 6, 12, and 24 hours after reperfusion. Control group was maintained at normothermia without hypothermia. Results : In the experimental groups with hypothermia, the average value of the size of cerebral infarction($mean{\pm}SD$) was $1.97{\pm}1.65%$, which was a remarkable reduction over that of the control, $4.93{\pm}3.79%$. In the control, a progressive increase was shown in the size of infarction from point of reperfusion to 6 hours after reperfusion without further changes in size afterward. Intra-ischemic hypothermia(group I) prevented ischemic injury but did not prevent reperfusion injury. Group II examplified the most neural protective effect in comparison to the control group and group IV(p<0.05). The cortex was more vulnerable to reperfusion injury than the subcortex. Mild hypothermia showed more neural protective effects on the cortex than subcortex. Conclusion : The most appropriate time zone for application of mild hypothermia was defined to be within four hours following reperfusion.

• The Korean Journal of Pain
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• 제21권2호
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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 Medicine and Life Science
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• 제19권2호
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• pp.74-77
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• 2022

We present a fatal case of cerebral arterial thrombosis after corona virus disease 19 (COVID-19) vaccination with ChAdOx1 nCOV-19. The deceased was a 63-year-old woman with no relevant medical history. She presented symptoms of nausea, fatigue, and headache immediately after vaccination. Ten days after vaccination, she suddenly started vomiting and developed high blood pressure. The patient eventually died 23 days after vaccination. Autopsy findings showed that the cerebral arteries and internal carotid arteries were fully enlarged and were compacted with thrombi. The brain stem showed ischemic necrosis, and extravasation from this necrotic lesion led to focal subarachnoid hemorrhage around the brain stem where large blood clots still remained. No aneurysms or atherosclerotic changes were found in these arteries. We note the following three facts. Firstly, all symptoms occurred immediately after vaccination; secondly, the main cause of death was consistent with known side effects of the vaccine; and lastly, the mechanism of thrombus formation in this case goes beyond the general category of thrombogenesis known so far. While the authors know that this case does not fall into known categories of vaccine side effects, we presenting this case to demonstrate that a comprehensive review of various possibilities related to vaccine side effects is needed to establish a COVID-19 defense system.