• Therapeutic Science for Rehabilitation
• /
• v.7 no.1
• /
• pp.11-26
• /
• 2018

Objective : This case study was to verify effects of cognitive rehabilitation and swallowing rehabilitation on Hypoxic-Ischemic Brain Injury patient by Suicidal Attempt. Methods : The subject was a 32-year old Hypoxic-ischemic brain injury patient by suicidal attempt. He received treatment once a day five times a week, for a half an hour for each session from September 8th to December 16th, 2016. Treatment were cognitive and swallowing rehabilitation. He was assessed based on Mini-Mental State Examination-Korean (MMSE-K), Korean-Modified Barthel Index (K-MBI), Computerized Neurocognitive Function Test (CNT), Videofluoroscopic Dysphagia Scale (VDS), American Speech-Language-Hearing Association National Outcomes Measurements System (ASHA-NOMS). Results : The patient's total MMSE-K score increased from 25 to 27. His K-MBI score increased from 74 to 88. His memory, attention span, and executive function (DST, VST, SWCT, WCST) by CNT scores were improved. VDS score has no changes to 34, 44.5 and 34. ASHA-NOMS score also has no change to 6, 2 and 6. Conclusion : The study showed that the application of the treatment of cognitive and swallowing in hypoxic-ischemic brain injury patient by suicidal attempt results has positive effects on cognitive functions, and swallowing function.

• Clinical and Experimental Pediatrics
• /
• v.45 no.6
• /
• pp.732-742
• /
• 2002

Purpose : In order to evaluate the hypoxia-ischemia(H-I) induced neurotoxicity and the protective effect of xanthine oxidase(XO) inhibitor(allopurinol), cell number, cell viability, lactate dehydrogenase(LDH), protein synthesis(PS) and protein kinase C(PKC) activity were measured in cerebral neurons and astrocytes. Methods : Cytotoxic effect was measured by in vitro assay at 12-72 hours after H-I on cerebral neurons and astrocytes derived from 7-day old neonatal rats which were subjected to unilateral common carotid artery occlusion and exposed to hypoxic condition for 3 hours. The protective effect of XO inhibitor was examined by the cell number, cell viability, LDH and PS on 14 days after H-I with allopurinol intraperitoneal injection 15 minutes prior to H-I. In addition, the effect of allopurinol on PKC activity in hypoxic conditions was examined in neurons. Results : 72 hours from H-I, the cell numbers and viability were decreased significantly in time-dependent manner on neurons and those of astrocytes also decreased slightly, compared with control. In neonatal rats treated with H-I, the cell number, cell viability, and PS in neurons were decreased, but LDH was increased significantly compared with control. In neonatal rats pretreated with allopurinol, the cell number and viability, and PS in neurons were increased and LDH was decreased significantly compared with H-I. PKC was increased remarkably after hypoxic condition. But PKC was decreased significantly against hypoxic condition after allopurinol pretreatment. Conclusion : From these results, it is suggested that H-I is more toxic in neurons than astrocytes and allopurinol is very protective with increasing of PS, and decreasing of LDH and PKC in neurons from hypoxic-ischemic condition.

• Clinical and Experimental Pediatrics
• /
• v.49 no.2
• /
• pp.198-202
• /
• 2006

Purpose : Fas is a cell surface receptor that transduces apoptotic death signals. Interaction of extracelluar domain of Fas with Fas ligand(FasL) triggers the apoptotic process in many diseases. We investigated the expression of Fas and FasL in the hippocampus of 7-day-old newborn rat brains following hypoxia-ischemia injury. Methods : The 7-days-old newborn rats were exposed to 8 percent oxygen for two hours after the ligation of right common carotid arteries. The newborn rats were killed and their brains were removed at 12, 14 and 48 hours after hypoxic-ischemic injury. The expressions of Fas and FasL of the right hippocampus were observed by western blotting and immunofluorescent staining. Results : Fas and FasL were strongly expressed in the right hippocampus ipsilateral to the ligation of the common carotid artery by western blotting at 12 hours following hypoxic-ischemic injury, and then slowly decreased. The immunofluorescent expressions of Fas and FasL strongly increased in the CA1 area of the right hippocampus at 12 and 24 hours following hypoxic-ischemic injury. The immunofluorescent expression of Fas decreased at 48 hours, but the expression of FasL persisted strongly at 48 hours following hypoxic-ischemic injury. Conclusion : The interaction of Fas with FasL on the cell surface may be involved in neuronal injury following hypoxic-ischemic injury in the developing brain.

• Clinical and Experimental Pediatrics
• /
• v.52 no.12
• /
• pp.1337-1347
• /
• 2009

Purpose:Taurine (2-aminoethanesulfonic acid) is a simple sulfur-containing amino acid. It is abundantly present in tissues such as brain, retina, heart, and skeletal muscles. Current studies have demonstrated the neuroprotective effects of taurine, but limited data are available for such effects during neonatal period. The aim of this study was to determine whether taurine could reduce hypoxic-ischemic (HI) cerebral injury via anti-apoptosis mechanism. Methods:Embryonic cortical neurons isolated from Sprague-Dawley (SD) rats at 18 days gestation were cultured in vitro. The cells were divided into hypoxia group, taurine-treated group before hypoxic insult, and taurine-treated group after HI insult. In the in vivo model, left carotid artery ligation was performed in 7-day-old SD rat pups. The pups were exposed to hypoxia, administered an injection of 30 mg/kg of taurine, and killed at 1 day, 3 days, 1 week, 2 weeks, and 4 weeks after the hypoxic insult. We compared the expressions of Bcl-2, Bax, and caspase-3 among the 3 groups by using real- time polymerase chain reaction (PCR) and western blotting. Results:The cells in the taurine-treated group before hypoxic insult, although similar in appearance to those in the normoxia group, were lesser in number. In the taurine-treated group, Bcl-2 expression increased, whereas Bax and caspase-3 expressions reduced. Conclusion:Taurine exerts neuroprotective effects onperinatal HI brain injury due to its anti-apoptotic effect. The neuroprotective effect was maximal at 1-2 weeks after the hypoxic injury.

• Clinical and Experimental Pediatrics
• /
• v.50 no.7
• /
• pp.686-693
• /
• 2007

Purpose : Mycophenolic acid (MPA), the active metabolite of mycophenolate mofetil (MMF), is a potent inhibitor of inosine-monophosphate dehydrogenase (IMPDH), a new immunosuppressive drug used. It was reported that MPA protected neurons after excitotoxic injury, induced apoptosis in microglial cells. However, the effects of MPA on hypoxic-ischemic (HI) brain injury has not been yet evaluated. Therefore, we examined whether MPA could be neuroprotective in perinatal HI brain injury using Rice-Vannucci model (in vivo) and in rat brain cortical cell culture induced by hypoxia (in vitro). Methods : Cortical cells were cultured using a 18-day-pregnant Sprague-Dawley (SD) rats and incubated in 1% $O_2$ incubator for hypoxia. MPA ($10{\mu}g/mL$) before or after a HI insult was treated. Seven-day-old SD rat pups were subjected to left carotid occlusion followed by 2 hours of hypoxic exposure (8% $O_2$). MPA (10 mg/kg) before or after a HI insult were administrated intraperitoneally. Apoptosis was measured using western blot and real-time PCR for Bcl-2, Bax, caspase-3. Results : H&E stain revealed increased brain volume in the MPA-treated group in vivo animal model of neonatal HI brain injury. Western blot and real-time PCR showed the expression of caspase-3 and Bax/Bcl-2 were decreased in the MPA-treated group In in vitro and in vivo model of perinatal HI brain injury, Conclusion : These results may suggest that the administration of MPA before HI insult could significantly protect against perinatal HI brain injury via anti-apoptotic mechanisms, which offers the possibility of MPA application for the treatment of neonatal HI encephalopathy.

• 월간산업보건
• /
• s.295
• /
• pp.50-57
• /
• 2012

• Tuberculosis and Respiratory Diseases
• /
• v.39 no.4
• /
• pp.299-303
• /
• 1992

• The Journal of Korean Physical Therapy
• /
• v.15 no.4
• /
• pp.199-207
• /
• 2003

This review describes the neurophathological mechanisms that are implicated in perinatal brain injury. Perinatal brain injury is the most important cause of morbidity and mortality to infants, often leading to spastic motor deficits, mental retardation, seizures, and learning impairments. The immature brain injury is usually caused by cerebral hypoxia-ischemia, hemorrhage, or infection. The important form of perinatal brain injury is the hypoxic-ischemic injury and the cerebral hemorrhage. The pathology of hypoxic-ischemic injury include delayed energy failure by mitochondrial dysfunction, neuronal excitotoxicity and vulnerability of white matter in developing brain. The immature brain has the fragile vascular bed of germinal matrix and can not effectively centralize their circulation. Therefore, the cerebral hemorrhage process is considered to be involved in the periventricular leukomalacia.

• Childhood Kidney Diseases
• /
• v.11 no.1
• /
• pp.32-40
• /
• 2007

Purpose : We performed this study to determine the incidence of acute renal failure(ARF) in birth asphyxia and to correlate the severity of asphyxia and hypoxic-ischemic encephalopathy (HIE) and ARF in asphyxiated neonates. Methods : Data was retrospectively collected from the medical records of 33 patients with neonatal asphyxia and of 33 neonates with no asphyxia. On the basis the 5-minute Apgar score, the asphyxiated neonates were further grouped into mild(6 or 7), moderate(4 or 5), and severe asphyxia(3 or less). Asphyxiated neonates with HIE were staged by the Sarnat and Sarnat scoring system. We compared serum creatinine, blood urea nitrogen, electrolytes, and urine output on day 3 of life and the incidence and severity of intraventricular hemorrhage(IVH) between each group. Results : ARF occurred in 8(24.2%) asphyxiated neonates. Of these, 3(37.5%) were oliguric, while 1(10.0%) patient with mild asphyxia, 2(18.2%) of moderate asphyxia, and 5(41.7%) with of severe asphyxia had ARF(P>0.05). One(25%) patient with stage I HIE, 4(50%) with stage II HIE, and 3(75%) of HIE with stage III HIE developed ARF(P<0.01). There was no statistical correlation between the severity of asphyxia and HIE stage. One(7.7%) patient with grade 1 IVE, 0(0.0%) with grade 2 IVH, 2(66.7%) with grade 3 IVH, and 2(100.0%) with grade 4 IVH had ARF(P<0.01). Mortality was higher in asphyxiated neonates with ARF(P<0.05). There was no significant difference between the oliguric and non-oliguric renal failure. Conclusion : We found that the greater the degree of HIE, the higher was the incidence of ARF. Asphyxiated neonates with ARF had a poorer prognosis.

• Neonatal Medicine
• /
• v.17 no.2
• /
• pp.181-192
• /
• 2010

Purpose: Current studies have demonstrated the neuroprotective effects of dizocilpine (MK-801) in many animal models of brain injury, including hypoxic-ischemic (HI) encephlopathy, trauma and excitotoxicity, but limited data are available for those during the neonatal periods. Here we investigated whether dizocilpine can protect the developing rat brain from HI injury via anti-apoptosis. Methods: In an in vitro model, embryonic cortical neuronal cell culture of Sprague-Dawley (SD) rats at 18-day gestation was done. The cultured cells were divided into three groups: normoxia (N), hypoxia (H), and hypoxia treated with dizocilpine (HD). The N group was prepared in 5% $CO_2$ incubators and the other groups were placed in 1% $O_2$ incubators (94% N2, 5% $CO_2$) for 16 hours. In an in vivo model, left carotid artery ligation was done in 7-day-old SD rat pups. The animals were divided into six groups; hypoxia (N), hypoxia (H), hypoxia with sham-operation (HS), hypoxia with operation (HO), HO treated with vehicle (HV), and HO treated with dizocilpine (HD). Hypoxia was made by exposure to a 2 hour period of hypoxic incubator (92% N2, 8% $O_2$). Results: In the in vitvo and in vivo models, the expressions of Bcl-2 in the hypoxia groups were reduced compared to the normoxia group. whereas those in the dizocilpine-treated group were increased compared to the hypoxia group. However. the expressions of Bax and caspase-3 and the ratio of Bax/Bcl-2 were revealed reversely. Conclusion: Dizocilpine has neuroprotective property over perinatal HI brain injury via anti-apoptosis.