• Journal of Korean Neurosurgical Society
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• v.50 no.5
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• pp.434-440
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• 2011

Objective : The goals of surgical intervention for metastatic spinal cord compression (MSCC) are prolonging survival and improving quality of life. Non-ambulatory paraplegic patients, either at presentation or after treatment, have a much shorter life expectancy than ambulatory patients. We therefore analyzed prognostic factors for survival and postoperative ambulation in patients surgically treated for MSCC. Methods : We assessed 103 patients with surgically treated MSCC who presented with lower extremity weakness between January 2001 and December 2008. Factors prognostic for overall survival (OS) and postoperative ambulation, including surgical method, age, sex, primary tumor site, metastatic spinal site, surgical levels, Tokuhashi score, and treatment with chemo- or radiation therapy, were analyzed retrospectively. Results : Median OS was significantly longer in the postoperatively ambulatory group [11.0 months; 95% confidence interval (CI), 9.29-12.71 months] than in the non-ambulatory group (5.0 months; 95% CI, 1.80-8.20 months) ($p$=0.035). When we compared median OS in patients with high (9-11) and low (0-8) Tokuhashi scores, they were significantly longer in the former (15.0 months; 95% CI, 9.29-20.71 months vs. 9.0 months; 95% CI, 7.48-10.52 months; $p$=0.003). Multivariate logistic regression analysis showed that preoperative ambulation with or without aid [odds ratio (OR) 5.35; 95% CI 1.57-18.17; $p$=0.007] and hip flexion power greater than grade III (OR 6.23; 95% CI, 1.29-7.35; $p$=0.038) were prognostic of postoperative ambulation. Conclusion : We found that postoperative ambulation and preoperative high Tokuhashi score were significantly associated with longer patient survival. In addition, preoperative hip flexion power greater than grade III was critical for postoperative ambulation.

• Biomolecules & Therapeutics
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• v.25 no.3
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• pp.272-278
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• 2017

Fucoidan has been reported to exhibit various beneficial activities ranging from to antivirus and anticancer properties. However, little information is available about the effects of fucoidan on cerebral ischemia-reperfusion injury (IRI). Our study aimed to explore the effects of fucoidan on cerebral IRI, as well as the underlying mechanisms. Sprague-Dawley (SD) rats were randomly subjected to four groups: Sham, IRI+saline (IRI+S), IRI+80 mg/kg fucoidan (IRI+F80), and IRI+160 mg/kg fucoidan (IRI+F160). Fucoidan (80 mg/kg or 160 mg/kg) was intraperitoneally injected from 7 days before the rats were induced to cerebral IRI model with middle cerebral artery occlusion (MCAO) method. At 24 h after reperfusion, neurological deficits and the total infarct volume were determined. The levels of inflammation-associated cytokines (interleukin (IL)-$1{\beta}$, IL-6, myeloperoxidase (MPO), and tumor necrosis factor (TNF)-${\alpha}$), oxidative stress-related proteins (malondialdehyde (MDA) and superoxide dismutase (SOD)) in the ischemic brain were measured by enzyme-linked immunosorbent assay (ELISA). Besides, the levels of apoptosis-related proteins (p-53, Bax, and B-cell lymphoma (Bcl)-2) and mitogen-activated protein kinase (MAPK) pathway (phosphorylation-extracellular signal-regulated kinase (p-ERK), p-c-Jun N-terminal kinase (JNK), and p-p38) were measured. Results showed that administration of fucoidan significantly reduced the neurological deficits and infarct volume compared to the IRI+S group in a dose-dependent manner. Also, fucoidan statistically decreased the levels of inflammation-associated cytokines, and oxidative stress-related proteins, inhibited apoptosis, and suppressed the MAPK pathway. So, Fucoidan plays a protective role in cerebral IRI might be by inhibition of MAPK pathway.

• The Korean Journal of Food & Health Convergence
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• v.5 no.6
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• pp.1-4
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• 2019

Wernicke korsakoff syndrome is caused by thiamine deficiency in the body. Thiamine not available in the body, is a substance to be taken from outside with foods. There are some conditions that reduce the metabolism of thiamine taken from the body and cause a vital risk. The most important factor is alcoholism. Wernicke Korsakoff syndrome produces both neurological and vestibular symptoms. At the same time, the damage of these symptoms to the patient psychology cannot be ignored. The aim of this study is to investigate the damage and mechanism of the syndrome in the vestibular system. In this study, we investigated vestibular symptoms of Wernicke Korsakoff syndrome due to thiamine deficiency, differences of vestibular system according to individuals and mechanism of damage caused by syndrome in vestibular system. Thiamine deficiency is caused by Wernicke Karsokoff syndrome with some external factors. This syndrome shows the most important effects of alcoholism. It causes neurological, vestibular and psychological symptoms. In this context, we can say that thiamine deficiency is a disease that causes damage in the vestibular system due to nystagmus formation and imbalance. The most important detail in the treatment stage is the detailed evaluation of symptoms associated with each other.

• Journal of Korean Academic Society of Home Health Care Nursing
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• v.19 no.1
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• pp.37-45
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• 2012

Purpose: This study was conducted in order to identify the brain injury patients's disability degree and educational needs of family caregivers. Methods: A convenience sample of 94 families with brain injury patients, who have been receiving treatment at the neurological intensive care unit and neurosurgery ward, were used. Data was collected with a self-report questionnaire from September 5 to November 28, 2011, and was analyzed using SAS program. Results: 'Defecation/urination' disability was the highest score of patient's physical disability and the next ranking was 'paralysis'. 'Memory impairment' disability was the highest score of patient's cognitive disability, and the next ranking was 'personality changes'. Overall, educational needs of family caregivers scored 4.15 out of the perfect score of 5. The factor, which scored highest, was 'information related with disease'. In addition, educational needs of family caregivers were positively related with patient's degree of. Conclusion: Educational needs of family caregivers are distinct, according to the disability degree of brain injury patient. Therefore, the study suggests the development of individualized educational program for family with brain injury patient.

• Journal of Korean Neurosurgical Society
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• v.63 no.2
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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 Neurosurgical Society
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• v.60 no.4
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• pp.433-440
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• 2017

Objective : Although minimally invasive posterior cervical foraminotomy (MI-PCF) is an established approach for motion preservation, the outcomes are variable among patients. The objective of this study was to identify significant factors that influence motion preservation after MI-PCF. Methods : Forty-eight patients who had undergone MI-PCF between 2004 and 2012 on a total of 70 levels were studied. Cervical parameters measured using plain radiography included C2-7 plumb line, C2-7 Cobb angle, T1 slope, thoracic outlet angle, neck tilt, and disc height before and 24 months after surgery. The ratios of the remaining facet joints after MI-PCF were calculated postoperatively using computed tomography. Changes in the distance between interspinous processes (DISP) and the segmental angle (SA) before and after surgery were also measured. We determined successful motion preservation with changes in DISP of ${\leq}3mm$ and in SA of ${\leq}2^{\circ}$. Results : The differences in preoperative and postoperative DISP and SA after MI-PCF were $0.03{\pm}3.95mm$ and $0.34{\pm}4.46^{\circ}$, respectively, fulfilling the criteria for successful motion preservation. However, the appropriate level of motion preservation is achieved in cases in which changes in preoperative and postoperative DISP and SA motions are 55.7 and 57.1%, respectively. Based on preoperative and postoperative DISP, patients were divided into three groups, and the characteristics of each group were compared. Among these, the only statistically significant factor in motion preservation was preoperative disc height (Pearson's correlation coefficient=0.658, p<0.001). The optimal disc height for motion preservation in regard to DISP ranges from 4.18 to 7.08 mm. Conclusion : MI-PCF is a widely accepted approach for motion preservation, although desirable radiographic outcomes were only achieved in approximately half of the patients who had undergone the procedure. Since disc height appears to be a significant factor in motion preservation, surgeons should consider disc height before performing MI-PCF.

• Korean Journal of Clinical Laboratory Science
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• v.54 no.3
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• pp.201-208
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• 2022

Neuroinflammation is defined as a neurological inflammation within the brain and the spinal cord. In neuroinflammation, microglia are the tissue-resident macrophages of the central nervous system, which act as the first line of defense against harmful pathogens. Dexmedetomidine (Dex) has an anti-inflammatory effect in many neurological conditions. Additionally, the microRNA-30a-5p (miR-30a-5p) mimic has been proven to be effective in macrophages in inflammatory conditions. This study aimed to investigate the synergistic anti-inflammatory effects of both miR-30a-5p and Dex in lipopolysaccharide (LPS)-induced BV2 cells. This study showed that miR-30a-5p and Dex decreased nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) translocation in LPS-induced BV2 cells. MiR-30a-5p and Dex alleviated tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), LPS-induced phosphorylation c-Jun N-terminal kinases (JNK), extracellular signal-regulated kinase (ERK) and p38. Also, the expression of the NOD-like receptor pyrin domain containing 3 inflammasome (NLRP3), cleaved caspase-1, and ASC was inhibited. Furthermore, LPS-stimulated nitric oxide (NO) production, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) expression were attenuated by Dex and miR-30a-5p. Our results indicate that a combination of Dex and miR-30a-5p, attenuates NF-κB activation, the mitogen-activated protein kinase (MAPK) signaling pathway, and inflammatory mediators involved in LPS-induced inflammation and inhibits the activation of the NLRP3 inflammasome in LPS-activated BV2 cells.

• Journal of Korean Neurosurgical Society
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• v.57 no.2
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• pp.73-76
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• 2015

Objective : Tumor necrosis factor alpha (TNF-${\alpha}$) have proven effects in pathogenesis of neuroinflammation after spinal cord injury (SCI). Current study is designed to evaluate the effects of an anti-TNF-${\alpha}$ agent, adalimumab, on spinal cord clip compression injury in rats. Methods : Thirty two male adult Wistar rats were divided into four groups (sham, trauma, infliximab, and adalimumab groups) and SCI was introduced using an aneurysm clip. Animals in treatment groups received 5 mg/kg subcutaneous adalimumab and infliximab right after the trauma. Malondialdehyde (MDA) levels were studied in traumatized spinal cord tissues 72 hours after the injury as a marker of lipid peroxidation. Results : Animals that received anti-TNF-${\alpha}$ agents are found to have significantly decreased MDA levels. MDA levels were significantly different between the trauma and infliximab groups (p<0.01) and trauma and adalimumab groups (p=0.022). There was no significant difference in neurological evaluation of the rats using Tarlov scale. Conclusion : These results suggest that, like infliximab, adalimumab has favorable effects on lipid peroxidation induced by spinal cord trauma in rats.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.5
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• pp.475-485
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• 2017

The present study aimed to explore the neuroprotective effect and possible mechanisms of rhGLP-1 (7-36) against transient ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in type 2 diabetic rats. First, diabetic rats were established by a combination of a high-fat diet and low-dose streptozotocin (STZ) (30 mg/kg, intraperitoneally). Second, they were subjected to MCAO for 2 h, then treated with rhGLP-1 (7-36) (10, 20, $40{\mu}g/kg$ i.p.) at the same time of reperfusion. In the following 3 days, they were injected with rhGLP-1 (7-36) at the same dose and route for three times each day. After 72 h, hypoglycemic effects were assessed by blood glucose changes, and neuroprotective effects were evaluated by neurological deficits, infarct volume and histomorphology. Mechanisms were investigated by detecting the distribution and expression of the nuclear factor erythroid-derived factor 2 related factor 2 (Nrf2) in ischemic brain tissue, the levels of phospho-PI3 kinase (PI3K)/PI3K ratio and heme-oxygenase-1 (HO-l), as well as the activities of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA). Our results showed that rhGLP-1 (7-36) significantly reduced blood glucose and infarction volume, alleviated neurological deficits, enhanced the density of surviving neurons and vascular proliferation. The nuclear positive cells ratio and expression of Nrf2, the levels of P-PI3K/PI3K ratio and HO-l increased, the activities of SOD increased and the contents of MDA decreased. The current results indicated the protective effect of rhGLP-1 (7-36) in diabetic rats following MCAO/R that may be concerned with reducing blood glucose, up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD.

• The Journal of Korean Physical Therapy
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• v.13 no.2
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• pp.281-292
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• 2001

This study was performed to investigate the effect of therapeutic exercise on brain-derived neurotrophic factor manifestation after global brain ischemia in rats. Nine rats with global ischemia were divided at random into two group. In the control group, three rats remained in cage. But, in the end, two rats were alive. In the therapeutic exercise group, six rats remained. The five rats of this group was swam for 30 minutes everyday for a week. The brain-derived neurotrophic factor expression was identified from immunohistochemistry. The results of this study were as follows : 1. In the control group, a little expression of brain-derived neurotrophic factor was observed at cortex and hippocampus layer, but cell body and axon was observed obscurely. 2. In the experimental group, a much expression of brain-derived neurotrophic factor was observed at cortex and hippocampus layer, and cell body and axon was observed clearly. In the neurological examination(beam-walking test). experimental group was obtained higher 1.4 points than control group. BDNF expression was increased by swimming for 30 minutes everyday for a week. Therefore, therapeutic exercise contribute to brain plasticity after brain ischemia.