• The Journal of Internal Korean Medicine
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• v.21 no.4
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• pp.661-665
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• 2000

Amyotrophic Lateral Sclerosis(ALS) is a fatal neuromuscular disease characterized by progressive muscle weakness resulting in paralysis. ALS is characterized by both upper and lower motor neuron damage. Diagnostic tests include magnetic resonance imaging(MRI) electromyogram(EMG), muscle biopsy, and blood tests. In order for a definitive diagnosis of ALS to be made, damage must be evident in both upper and lower motor neurons. When three limbs are sufficiently affected, the diagnosis is ALS. There is no cure for ALS. We recently experienced one case of ALS, The patients was diagnosed as ALS by EMG and Symptoms. We diagnosed her as Wea jeung and treated by Herbal-medication based on the differentiation of symtoms. we report change of his symptoms through both western medical treatment and oriental medical treatment.

• Journal of Korean Physical Therapy Science
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• v.10 no.1
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• pp.65-73
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• 2003

The purpose of this study was to determine whether neuromuscular electrical stimulation(NMES), applied over the antagonist or the agonist, would alter the H reflex. Attention was focused on the roles of stimulus location. We used normal eight subjects without neuromuscular disease which were divided into 3 groups; the subjects were diveded into group of antagonist, agonist, antagonist-agonist. All groups were meted of eight subjects. Neuromuscular electrical stimulation was administered for 15 minutes. All subjects were subjected to three tests, including a pre-test, post-test and post-20 minute test. The data were analyzed by repeated measures ANOVA and paired t-test. The results were as follows; 1. H latencies were significantly increased in agonist and antagonist-agonist group (p<.01). 2. H/M intervals were significantly increased in agonist and antagonist-agonist group (p<.01). 3. H amplitudes were significantly increased in agonist (p<.001) and antagonist-agonist group (p<.01). 4. H/M ratios were significantly decreased in agonist and antagonist-agonist group (p<.01). In agonist group. H-reflex amplitudes and H/M ratios were more significantly decreased than antagonist group. Future studies will need to determine what influence NMES may have on the excitability of spinal motor neurons in people having UMN syndrome.

• Annals of Clinical Neurophysiology
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• v.15 no.2
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• pp.59-62
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• 2013

Man-in-the-barrel syndrome (MIBS) is a clinical syndrome of bilateral upper limb weakness with normal lower extremity function. It can be caused by various neurological conditions such as bilateral cerebral hypoperfusion, syringomyelia, motor neuron disease, or cervical myelopathies. We report a patient with MIBS after cervical spinal cord ischemia. It is postulated to be caused by ischemic insults of anterior spinal artery from repeated and prolonged neck extension.

• The Journal of Korea Institute of Information, Electronics, and Communication Technology
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• v.12 no.4
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• pp.413-418
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• 2019

Studies are now actively underway to confirm the degree of treatment and rehabilitation of patients with brain-related diseases (dementia, schizophrenia, depression, Parkinson's disease). Among them, Transcranial magnetic stimulation (TMS) is widely used in treatment because it is a technique that is used for noninvasive brain neuron control in patients with brain disorders. It can be seen that muscle fatigue of normal people increases during Transcranial magnetic stimulation. Therefore, in this paper, our purpose is to build an EMG measurement system to measure motor neuron-induced response during transcranial magnetic stimulation and We identify a motor-neutral response system using tendency in the RMS graph. As an experimental method, the Raw Data received through the surface EMG device and analyzed by RMS technique, after the contraction and relaxation movement of the biceps brachii. As a result of the experiment, we confirmed the trend of rising RMS graph, and it will can be used to determine the self-stimulation intensity for each individual in consideration of the data of the motor-neutral response.

• Journal of the Korean Society of Physical Medicine
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• v.2 no.2
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• pp.205-212
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• 2007

Purpose : Herpes zoster is a common dermatologic disorder and is caused by reactivation of varicella zoster virus lying dormant in the ganglion of the dorsal root Methods : The aim of this study is to elucidate the clinical characteristics of herpes zoster and it's nature of pain, and is to review the method of physical therapy for pain control. Results : Herpes zoster is characterized by segmental rash, pain, and sensory symptoms, For most patients skin healing and pain resolution occur within 3-4 weeks, However, pain can continue after the rash has healed. Pain and paresthesia often the eruption of herpes zoster and vary from itching to stabbing. The preeruptive pain may simulate other diseases and may lead to misdiagnosis and misdirected interventions. Motor symptomatology is less well known and is most often related to central nervous system disease, although true lower motor neuron application is also thought to exist Subclinical motor involvement is relatively more common than clinical motor weakness and is easily detected by using electromyography. Higher incidences of herpes zoster were observed in female and in the elderly. Conclusion : The nature of pain associated with herpes zoster varied from a superficial itching to server stabbing or bursting, and paresthesia occurred most frequently. Therefore, the study of herpes zoster will be more research and comprehend, and the approach of physical therapy should be need positively.

• Biomolecules & Therapeutics
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• v.29 no.5
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• pp.498-505
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• 2021

Amyotrophic lateral sclerosis (ALS) is a lethal neurological disorder characterized by the deterioration of motor neurons. The aim of this study was to investigate alteration of cationic amino acid transporter (CAT-1) activity in the transport of lysine and the pretreatment effect of lysine on pro-inflammatory states in an amyotrophic lateral sclerosis cell line. The mRNA expression of cationic amino acid transporter 1 was lower in NSC-34/hSOD1^G93A (MT) than the control cell line (WT), lysine transport is mediated by CAT-1 in NSC-34 cell lines. The uptake of [³H]L-lysine was Na⁺-independent, voltage-sensitive, and strongly inhibited by inhibitors and substrates of cationic amino acid transporter 1 (system y⁺). The transport process involved two saturable processes in both cell lines. In the MT cell line, at a high-affinity site, the affinity was 9.4-fold higher and capacity 24-fold lower than that in the WT; at a low-affinity site, the capacity was 2.3-fold lower than that in the WT cell line. Donepezil and verapamil competitively inhibited [³H]L-lysine uptake in the NSC-34 cell lines. Pretreatment with pro-inflammatory cytokines decreased the uptake of [³H]L-lysine and mRNA expression levels in both cell lines; however, the addition of L-lysine restored the transport activity in the MT cell lines. L-Lysine exhibited neuroprotective effects against pro-inflammatory states in the ALS disease model cell lines. In conclusion, studying the alteration in the expression of transporters and characteristics of lysine transport in ALS can lead to the development of new therapies for neurodegenerative diseases.

• Journal of Korean Neurosurgical Society
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• v.67 no.5
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• pp.510-520
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• 2024

Objective : Parkinson's disease (PD) is one of the most prevalent neurodegenerative diseases, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. The treatment of PD aims to alleviate motor symptoms by replacing the reduced endogenous dopamine. Currently, there are no disease-modifying agents for the treatment of PD. Zebrafish (Danio rerio) have emerged as an effective tool for new drug discovery and screening in the age of translational research. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is known to cause a similar loss of dopaminergic neurons in the human midbrain, with corresponding Parkinsonian symptoms. L-type calcium channels (LTCCs) have been implicated in the generation of mitochondrial oxidative stress, which underlies the pathogenesis of PD. Therefore, we investigated the neuro-restorative effect of LTCC inhibition in an MPTP-induced zebrafish PD model and suggested a possible drug candidate that might modify the progression of PD. Methods : All experiments were conducted using a line of transgenic zebrafish, Tg(dat:EGFP), in which green fluorescent protein (GFP) is expressed in dopaminergic neurons. The experimental groups were exposed to 500 μmol MPTP from 1 to 3 days post fertilization (dpf). The drug candidates : levodopa 1 mmol, nifedipine 10 μmol, nimodipine 3.5 μmol, diethylstilbestrol 0.3 μmol, luteolin 100 μmol, and calcitriol 0.25 μmol were exposed from 3 to 5 dpf. Locomotor activity was assessed by automated tracking and dopaminergic neurons were visualized in vivo by confocal microscopy. Results : Levodopa, nimodipine, diethylstilbestrol, and calcitriol had significant positive effects on the restoration of motor behavior, which was damaged by MPTP. Nimodipine and calcitriol have significant positive effects on the restoration of dopaminergic neurons, which were reduced by MPTP. Through locomotor analysis and dopaminergic neuron quantification, we identified the neuro-restorative effects of nimodipine and calcitriol in zebrafish MPTP-induced PD model. Conclusion : The present study identified the neuro-restorative effects of nimodipine and calcitriol in an MPTP-induced zebrafish model of PD. They restored dopaminergic neurons which were damaged due to the effects of MPTP and normalized the locomotor activity. LTCCs have potential pathological roles in neurodevelopmental and neurodegenerative disorders. Zebrafish are highly amenable to high-throughput drug screening and might, therefore, be a useful tool to work towards the identification of disease-modifying treatment for PD. Further studies including zebrafish genetic models to elucidate the mechanism of action of the disease-modifying candidate by investigating Ca2+ influx and mitochondrial function in dopaminergic neurons, are needed to reveal the pathogenesis of PD and develop disease-modifying treatments for PD.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.18 no.12
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• pp.352-358
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• 2017

Frontotemporal dementia, the second most common cause of early onset dementia, is a neurodegenerative clinical syndrome characterized by progressive deficits in behavior, executive function and language. Although motor symptoms in frontotemporal dementia are represented by motor neuron disease, parkinsonism and progressive supranuclear palsy syndrome, there have been no reports of motor weakness caused by the direct involvement of central motor nervous systems in frontotemporal dementia. Moreover, no association between clinical dementia groups and complex regional pain syndrome has been reported. We diagnosed a rare case with motor weakness and complex regional pain syndrome of lower limbs due to central nervous system lesion in a patient with frontotemporal dementia by magnetic resonance imaging, electrodiagnostic study and three phase bone scan. Following steroid therapy for complex regional pain syndrome, pain was improved. Functional improvement was noted after rehabilitation therapy, including functional electrical stimulation, muscle strengthening exercise and gait training during hospitalization. This case report suggests that rehabilitation therapy for motor weakness in frontotemporal dementia could be effective for improving overall function.

• Biomolecules & Therapeutics
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• v.32 no.1
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• pp.154-161
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• 2024

Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disorder that causes progressive paralysis. L-Citrulline is a nonessential neutral amino acid produced by L-arginine via nitric oxide synthase (NOS). According to previous studies, the pathogenesis of ALS entails glutamate toxicity, oxidative stress, protein misfolding, and neurofilament disruption. In addition, L-citrulline prevents neuronal cell death in brain ischemia; therefore, we investigated the change in the transport of L-citrulline under various pathological conditions in a cell line model of ALS. We examined the uptake of [¹⁴C]L-citrulline in wild-type (hSOD1wt/WT) and mutant NSC-34/ SOD1^G93A (MT) cell lines. The cell viability was determined via MTT assay. A transport study was performed to determine the uptake of [¹⁴C]L-citrulline. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis was performed to determine the expression levels of rat large neutral amino acid transported 1 (rLAT1) in ALS cell lines. Nitric oxide (NO) assay was performed using Griess reagent. L-Citrulline had a restorative effect on glutamate induced cell death, and increased [¹⁴C]L-citrulline uptake and mRNA levels of the large neutral amino acid transporter (LAT1) in the glutamate-treated ALS disease model (MT). NO levels increased significantly when MT cells were pretreated with glutamate for 24 h and restored by co-treatment with L-citrulline. Co-treatment of MT cells with L-arginine, an NO donor, increased NO levels. NSC-34 cells exposed to high glucose conditions showed a significant increase in [¹⁴C]L-citrulline uptake and LAT1 mRNA expression levels, which were restored to normal levels upon co-treatment with unlabeled L-citrulline. In contrast, exposure of the MT cell line to tumor necrosis factor alpha, lipopolysaccharides, and hypertonic condition decreased the uptake significantly which was restored to the normal level by co-treating with unlabeled L-citrulline. L-Citrulline can restore NO levels and cellular uptake in ALS-affected cells with glutamate cytotoxicity, pro-inflammatory cytokines, or other pathological states, suggesting that L-citrulline supplementation in ALS may play a key role in providing neuroprotection.

• Annals of Clinical Neurophysiology
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• v.15 no.2
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• pp.53-58
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• 2013

Background: The autophagy is the major route for lysosomal degradation of misfolded protein aggregates and oxidative cell components. We hypothesized that rapamycin (autophagy enhancer) would prolong the survival of motor neuron and suppress the disease progression in amyotrophic lateral sclerosis (ALS). Methods: A total of 24 transgenic mice harboring the human G93A mutated SOD1 gene were used. The clinical status involving rotarod test and survival, and biochemical study of ALS mice model were evaluated. Results: The onset of symptoms was significantly delayed in the rapamycin administration group compared with the control group. However, after the clinical symptom developed, the rapamycin exacerbated the disease progression and shortened the survival of ALS mice model, and apoptosis signals were up-regulated compared with control group. Conclusions: Even though further detailed studies on the relevancy between autophagy and ALS will be needed, our results revealed that the rapamycin administration was not effective for being novel promising therapeutic strategy in ALS transgenic mice and exacerbated the apoptosis.