• Journal of Veterinary Clinics
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• v.30 no.2
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• pp.107-110
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• 2013

A 6-year-old, castrated male Shih-tzu dog was presented due to left side facial paralysis with head tilt. Neurological examination revealed absence of facial sensation, menance response, and palpebral reflex on the left side. On magnetic resonance imaging (MRI), intracranial intra-arachnoid cyst (IIAC) was noted. The dog was poor response to steroid and dieuretic therapy. Based on characteristic historical and clinical findings, and excluding of other causes of acute facial nerve dysfunction, the dog was tentatively diagnosed as idiopathic facial paralysis. The clinical signs were improved gradually after acupuncture therapy with bee venom. Eight weeks after initial acupuncture with bee venom, the patient recovered sensory and neurological facial signs. This case report demonstrates that bee venom acupuncture for an idiopathic facial paralysis could be useful in a dog.

• Journal of the Korean neurological association
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• v.36 no.4
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• pp.337-340
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• 2018

Human immunodeficiency virus (HIV) infection can result in ischemic stroke via several mechanisms, including opportunistic infection, vasculopathy, cardioembolism, and coagulopathy. HIV-vasculopathy is related to endothelial dysfunction, stenosis and aneurysm formation, infectious vasculitis, dissection and accelerated atherosclerosis during highly active antiretroviral therapy (HAART). We represent a case of HIV infection manifested as an acute ischemic stroke attack. After 4 months during HAART, our patient experienced a recurrent ischemic stroke with progression of middle cerebral artery stenosis.

• Physical Therapy Korea
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• v.29 no.2
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• pp.147-155
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• 2022

Background: Although various conventional approaches have been employed to reduce spasticity in neurological rehabilitation, only a few studies have shown scientific evidence for its effectiveness. Thus, we introduced a different concept (Ueda method) of rehabilitation therapy that can complement the limitations of conventional therapy. Objects: This study aimed to investigate the immediate effects of the application of the Ueda method on patients with spasticity after stroke via an electrophysiological study. Methods: We conducted a randomized double-blind pilot study in two rehabilitation hospitals involving 30 stroke patients who were randomly allocated to the Ueda (n = 15) and convention (n = 15) groups. Electromyographic data of six examined muscles in both upper extremities of all patients were recorded. The A-ApA index and activation ratios of upper extremity muscles were evaluated and compared between the groups to confirm post-intervention changes in upper-extremity flexor spasticity and flexion synergies. Repeated-measures analysis of variance was conducted to confirm the therapeutic effect (2 × 2) as a function of group (Ueda vs. convention) and time (pre-/post-intervention) on all outcome measures (p < 0.05). Results: In the Ueda group, the mean A-ApA index values differed significantly before and after the intervention (p = 0.041), indicating a weak evidence level; however, the effect size was medium (d = -0.503). The interaction effects of the A-ApA index between the Ueda and convention groups and between pre-intervention and post-intervention stages were significant (p = 0.012). The effect size was large (n_p² = 0.220). In the Ueda group, the activation ratios of the anterior deltoid fiber significantly decreased after the intervention in all reaching tasks. Conclusion: The Ueda method reduces upper-extremity flexor spasticity and changes its synergy in stroke patients and should be considered a rehabilitation therapy for spastic stroke patients.

• Animal cells and systems
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• v.15 no.4
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• pp.279-286
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• 2011

Hypoxic ischemia injury is a common cause of functional brain damage, resulting from a decrease in cerebral blood flow and oxygen supply to the brain. The main problems associated with hypoxic ischemia to the brain are memory impairment and dopamine dysfunction. Hypothermia has been suggested to ameliorate the neurological impairment induced by various brain insults. In this study, we investigated the effects of hypothermia on memory function and dopamine synthesis following hypoxic ischemia to the brain in rats. For this purpose, a step-down avoidance task, a radial eight-arm maze task, and immunohistochemistry for tyrosine hydroxylase (TH) and 5-bromo-2'-deoxyuridine (BrdU) were performed. The present results indicated that the hypoxic ischemia-induced disturbance of the animal's performances and spatial working memory was associated with a decrement in TH expression in the substantia nigra and striatum, and an increase in cell proliferation in the hippocampal dentate gyrus. Hypothermia treatment improved the animals' performance and spatial working memory by suppressing the decrement in TH expression in the substantia nigra and striatum and the increase in cell proliferation in the dentate gyrus. We suggest that hypothermia can be an efficient therapeutic modality to facilitate recovery following hypoxic ischemia injury to the brain, presumably by modulating the dopaminergic cell loss.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.8 no.2
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• pp.217-231
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• 1997

This paper first reviewed the current neurological theories concerning the etiology of ADHD and secondly, examined results of studies that applied neuropsychological assessment methods in the examination of ADHD children both here in Korea and abroad. ADHD children were found to exhibit characteristic responses indicating deficits in vigilance, sustained attention, distractibility, allocation and regulation of attention in many assessments of attention, in addition to deficits in executive functioning, working and associative memory. Such neuropsychological assessment results suggest that in addition to dysfunction in the frontal lobe and the reticular activation system, dysfunction may exist in other neural pathways involving many areas of the brain. However, because a substantial number of neuropsychological assessment tools being employed in Korea for ADHD children had been developed abroad, a Korean standardization project involving ADHD and normal control children, in addition to other child psychiatric population pools must be conducted in order to obtain appropriate age norms and test validity, and in order to make possible a more accurate and precise comparison and interpretation in the assessment of ADHD children.

• Safety and Health at Work
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• v.3 no.4
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• pp.257-267
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• 2012

Occupational neurotoxic diseases have become increasingly common in Taiwan due to industrialization. Over the past 40 years, Taiwan has transformed from an agricultural society to an industrial society. The most common neurotoxic diseases also changed from organophosphate poisoning to heavy metal intoxication, and then to organic solvent and semiconductor agent poisoning. The nervous system is particularly vulnerable to toxic agents because of its high metabolic rate. Neurological manifestations may be transient or permanent, and may range from cognitive dysfunction, cerebellar ataxia, Parkinsonism, sensorimotor neuropathy and autonomic dysfunction to neuromuscular junction disorders. This study attempts to provide a review of the major outbreaks of occupational neurotoxins from 1968 to 2012. A total of 16 occupational neurotoxins, including organophosphates, toxic gases, heavy metals, organic solvents, and other toxic chemicals, were reviewed. Peer-reviewed articles related to the electrophysiology, neuroimaging, treatment and long-term follow up of these neurotoxic diseases were also obtained. The heavy metals involved consisted of lead, manganese, organic tin, mercury, arsenic, and thallium. The organic solvents included n-hexane, toluene, mixed solvents and carbon disulfide. Toxic gases such as carbon monoxide, and hydrogen sulfide were also included, along with toxic chemicals including polychlorinated biphenyls, tetramethylammonium hydroxide, organophosphates, and dimethylamine borane. In addition we attempted to correlate these events to the timeline of industrial development in Taiwan. By researching this topic, the hope is that it may help other developing countries to improve industrial hygiene and promote occupational safety and health care during the process of industrialization.

• Journal of Ginseng Research
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• v.42 no.3
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• pp.379-388
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• 2018

Background: Ginsenosides are the main ingredients of Korean Red Ginseng. They have extensively been studied for their beneficial value in neurodegenerative diseases such as Parkinson's disease (PD). However, the multitarget effects of Korean Red Ginseng extract (KRGE) with various components are unclear. Methods: We investigated the multitarget activities of KRGE on neurological dysfunction and neurotoxicity in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD. KRGE (37.5 mg/ kg/day, 75 mg/kg/day, or 150 mg/kg/day, per os (p.o.)) was given daily before or after MPTP intoxication. Results: Pretreatment with 150 mg/kg/day KRGE produced the greatest positive effect on motor dysfunction as assessed using rotarod, pole, and nesting tests, and on the survival rate. KRGE displayed a wide therapeutic time window. These effects were related to reductions in the loss of tyrosine hydroxylase-immunoreactive dopaminergic neurons, apoptosis, microglial activation, and activation of inflammatory factors in the substantia nigra pars compacta and/or striatum after MPTP intoxication. In addition, pretreatment with KRGE activated the nuclear factor erythroid 2-related factor 2 pathways and inhibited phosphorylation of the mitogen-activated protein kinases and nuclear factor-kappa B signaling pathways, as well as blocked the alteration of blood-brain barrier integrity. Conclusion: These results suggest that KRGE may effectively reduce MPTP-induced neurotoxicity with a wide therapeutic time window through multitarget effects including antiapoptosis, antiinflammation, antioxidant, and maintenance of blood-brain barrier integrity. KRGE has potential as a multitarget drug or functional food for safe preventive and therapeutic strategies for PD.

• Molecules and Cells
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• v.37 no.11
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• pp.767-776
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• 2014

Alzheimer's disease (AD) is clinically characterized with progressive memory loss and cognitive decline. Synaptic dysfunction is an early pathological feature that occurs prior to neurodegeneration and memory dysfunction. Mounting evidence suggests that aggregation of amyloid-${\alpha}$ ($A{\alpha}$) and hyperphosphorylated tau leads to synaptic deficits and neurodegeneration, thereby to memory loss. Among the established genetic risk factors for AD, the ${\varepsilon}4$ allele of apolipoprotein E (APOE) is the strongest genetic risk factor. We and others previously demonstrated that apoE regulates $A{\alpha}$ aggregation and clearance in an isoform-dependent manner. While the effect of apoE on $A{\alpha}$ may explain how apoE isoforms differentially affect AD pathogenesis, there are also other underexplored pathogenic mechanisms. They include differential effects of apoE on cerebral energy metabolism, neuroinflammation, neurovascular function, neurogenesis, and synaptic plasticity. ApoE is a major carrier of cholesterols that are required for neuronal activity and injury repair in the brain. Although there are a few conflicting findings and the underlying mechanism is still unclear, several lines of studies demonstrated that apoE4 leads to synaptic deficits and impairment in long-term potentiation, memory and cognition. In this review, we summarize current understanding of apoE function in the brain, with a particular emphasis on its role in synaptic plasticity and the underlying cellular and molecular mechanisms, involving low-density lipoprotein receptor-related protein 1 (LRP1), syndecan, and LRP8/ApoER2.

• Toxicological Research
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• v.30 no.4
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• pp.267-276
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• 2014

Exposures to lead (Pb) are associated with neurological problems including psychiatric disorders and impaired learning and memory. Pb can be absorbed by iron transporters, which are up-regulated in hereditary hemochromatosis, an iron overload disorder in which increased iron deposition in various parenchymal organs promote metal-induced oxidative damage. While dysfunction in HFE (High Fe) gene is the major cause of hemochromatosis, the transport and toxicity of Pb in Hfe-related hemochromatosis are largely unknown. To elucidate the relationship between HFE gene dysfunction and Pb absorption, H67D knock-in Hfe-mutant and wild-type mice were given drinking water containing Pb 1.6 mg/ml ad libitum for 6 weeks and examined for behavioral phenotypes using the nestlet-shredding and marble-burying tests. Latency to nestlet-shredding in Pb-treated wild-type mice was prolonged compared with non-exposed wild-types (p < 0.001), whereas Pb exposure did not alter shredding latency in Hfe-mutant mice. In the marble-burying test, Hfe-mutant mice showed an increased number of marbles buried compared with wild-type mice (p = 0.002), indicating more repetitive behavior upon Hfe mutation. Importantly, Pb-exposed wild-type mice buried more marbles than non-exposed wild-types, whereas the number of marbles buried by Hfe-mutant mice did not change whether or not exposed to Pb. These results suggest that Hfe mutation could normalize Pb-induced behavioral alteration. To explore the mechanism of repetitive behavior caused by Pb, western blot analysis was conducted for proteins involved in brain dopamine metabolism. The levels of tyrosine hydroxylase and dopamine transporter increased upon Pb exposure in both genotypes, whereas Hfe-mutant mice displayed down-regulation of the dopamine transporter and dopamine D1 receptor with D2 receptor elevated. Taken together, our data support the idea that both Pb exposure and Hfe mutation increase repetitive behavior in mice and further suggest that these behavioral changes could be associated with altered dopaminergic neurotransmission, providing a therapeutic basis for psychiatric disorders caused by Pb toxicity.

• Proceedings of the KAIS Fall Conference
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• 2011.12a
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• pp.170-173
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• 2011

Therapeutic hypothermia(TH) improves neurological outcomes and reduces mortality among survivors of out-of-hospital cardiac arrest. Animal and human studies have shown that TH results in improved salvage of the myocardium, reduced infarct size, reduced left ventricular remodeling and better long-term left ventricular function in settings of regional myocardial ischemia. This study is to investigate the effect of TH on post-resuscitation myocardial dysfunction and survival time after cardiac arrest and resuscitation in a rat model of myocardial infarction (MI). Thoracotomies were performed in 10 Male Sprague-Dawley rats weighing 450-550 g. MI was induced by ligation of the left anterior descending coronary artery (LAD). Ninety min after LAD ligation, ventricular fibrillation induction and subsequent cardiopulmonary resuscitation was performed before defibrillation attempts. Animals were randomized to two groups: a) Acute MI-Normothermia b) Acute MI-Hypothermia ($32^{\circ}C$ for 4 h). Myocardial functions, including cardiac output, left ventricular ejection fraction, and myocardial performance index were measured echocardiographically together with duration of survival. Ejection fraction, cardiac output and myocardial performance index were $54.74{\pm}9.16$, $89.00{\pm}8.89$, $1.30{\pm}0.09$ respectively and significantly better in the TH group than those of the normothermic group at the first 4 h after resuscitation($32.20{\pm}1.85$,$41.60{\pm}8.62$,$1.77{\pm}0.19$)(p=0.00). The survival time of the hypothermic group ($31.8{\pm}14.8$ h) was greater than that of the normothermic group($12.3{\pm}6.5$ h, p<0.05). This study suggested that TH attenuated post resuscitation myocardial dysfunction in acute MI and would be a potential strategy in post resuscitation care.