• Annals of Clinical Neurophysiology
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• v.22 no.2
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• pp.51-60
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• 2020

Muscle pathology findings may guide the diagnosis of neuromuscular disorders since they are helpful for understanding the pathological processes causing muscle weakness and also provide significant clues for the diagnosis of muscle diseases. Recent advances in molecular genetics mean that a muscle biopsy can be omitted when diagnosing inherited muscle diseases. However, the muscle pathology can still play a role in those cases and its findings are also required when diagnosing inflammatory myopathies.

• Clinical and Experimental Pediatrics
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• v.46 no.2
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• pp.109-115
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• 2003

• Journal of Genetic Medicine
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• v.4 no.2
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• pp.122-127
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• 2007

• The Journal of Pediatrics of Korean Medicine
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• v.14 no.1
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• pp.197-204
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• 2000

Neuromuscular disorders are common causes of weakness and hypotonia in the infantile period and in childhood. Accurate diagnosis of specific neuromuscular disorders depends first on identification of which aspect of the peripheral neuromuscular system is affected-the motor neuron in the spinal cord, the nerve root or peripheral nerve, the neuromuscular junction, or the muscle-and then on the determination of the etiology and specific clinical entity. Spinal muscular atrophy(SMA) is the most common autosomal-recessive genetic disorder lethal to infants. The three major childhood-onset forms of SMA are now usually called type I, type II and typeⅢ. Progression of the disease is due to loss of anterior horn cells, thought to be caused by apoptosis. Diagnosis is based on the course of the illness, as well as certain changes seen on nerve and muscle biopsy and electrodiagnostic studies. More recently, our understanding of the genetics of this disorder has provided a noninvasive approach to diagnosis. We report on a 3-year-old male patient with spinal muscular atrophy type II. He had progressive muscular weakness since 18 months of age. The upper arms were slightly, and the thighs moderately atrophic. There was muscle weakness of both the upper and lower limbs, being more proximal in distribution. Electromyogram revealed a neurogenic pattern.

• Advances in Traditional Medicine
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• v.10 no.4
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• pp.239-253
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• 2010

Coenzyme $Q_{10}$ ($CoQ_{10}$, or ubiquinone) is an electron carrier of the mitochondrial respiratory chain (electron transport chain) with antioxidant properties. In view of the involvement of $CoQ_{10}$ in oxidative phosphorylation and cellular antioxidant protection a deficiency in this quinone would be expected to contribute to disease pathophysiology by causing a failure in energy metabolism and antioxidant status. Indeed, a deficit in $CoQ_{10}$ status has been determined in a number of neuromuscular and neurodegenerative disorders. Primary disorders of $CoQ_{10}$ biosynthesis are potentially treatable conditions and therefore a high degree of clinical awareness about this condition is essential. A secondary loss of $CoQ_{10}$ status following HMG-CoA reductase inhibitor (statins) treatment has been implicated in the pathophysiology of the myotoxicity associated with this pharmacotherapy. $CoQ_{10}$ and its analogue, idebenone, have been widely used in the treatment of neurodegenerative and neuromuscular disorders. These compounds could potentially play a role in the treatment of mitochondrial disorders, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, Friedreich's ataxia, and other conditions which have been linked to mitochondrial dysfunction. This article reviews the physiological roles of $CoQ_{10}$, as well as the rationale and the role in clinical practice of $CoQ_{10}$ supplementation in different neurological diseases, from primary $CoQ_{10}$ deficiency to neurodegenerative disorders. These will help in future for treatment of patients suffering from neurodegenerative disease.

• PNF and Movement
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• v.17 no.1
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• pp.145-156
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• 2019

Purpose: This study suggests clinical reasoning strategies for therapists with little experience in clinical reasoning for the evaluation and treatment of patients with neurological disorders. Methods: The suggested method was the mnemonic PT STRESS whose initials represent the body structure and functions that can affect the activity limits and the items that can cause problems at the functional level in patients with neurological disorders. Results: PT STRESS stands for pain (P), ability of the trunk (T), sensation (S), tone (T), range of motion (R), emotion and endurance (E), muscular strength (strength), and stability (S). It tests and measures problems in the body structure and functions. Conclusion: This study suggests easy clinical reasoning strategies that can be used by therapists who have insufficient experience in the evaluation or treatment of patients with neurological disorders. However, more factors need to be considered in the future with regard to clinical reasoning of the diverse problems of patients with neurological disorders.

• The Korean Journal of Pain
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• v.24 no.1
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• pp.1-6
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• 2011

Botulinum toxin has been used for the treatment of many clinical disorders by producing temporary skeletal muscle relaxation. In pain management, botulinum toxin has demonstrated an analgesic effect by reducing muscular hyperactivity, but recent studies suggest this neurotoxin could have direct analgesic mechanisms different from its neuromuscular actions. At the moment, botulinum toxin is widely investigated and used in many painful diseases such as myofascial syndrome, headaches, arthritis, and neuropathic pain. Further studies are needed to understand the exact analgesic mechanisms, efficacy and complications of botulinum toxin in chronic pain disorders.

• The Journal of the Korean dental association
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• v.49 no.2
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• pp.72-76
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• 2011

Temporomandibular disorders refer to a large group musculoskeletal disorders that originate from the masticatory structures. The AADR recognize that temporomandibular (TMDs) encompass a group of musculoskeletal and neuromuscular conditions that involve the temporomandibular joints (TMJs), the masticatory muscles, and all associated tissues. The signs and symptoms associated with these disorders are diverse, and may include difficulties with chewing, speaking, and other orofacial functions. They also are frequently associated with acute or persistent pain, and the patients often suffer from other painful disorders. The chronic forms of TMD pain may lead to absence from or impairment of work or social interactions, resulting in an overall reduction in the quality of life. However, the consensus of recent scientific literature about currently available technological diagnostic devices for TMDs is that, except for various imaging modalities, none of them shows the sensitivity and specificity required to separate normal subjects from TMD patients or to distinguish among TMD subgroups. This article reviews the various instruments to aid in the diagnosis of TMDs, and the overall validity and practical use of the Electromyography.

• Annals of Clinical Neurophysiology
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• v.8 no.1
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• pp.6-15
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• 2006

Intravenous immunoglobulin (IVIg) is the treatment of choice for many autoimmune neuropathic disorders such as Guillain-Barre syndrome (GBS), chronic inflammatory Demyelinating neuropathy (CIDP), and multifocal motor neuropathy (MMN). IVIg is preferred because the adverse reactions are milder and fewer than the other immune-modulating methods such as steroid, other immunosuppressant such as azathioprine, and plasmapheresis. IVIg also has been used in other autoimmune neuromuscular disorders (inflammatory myopathy, myasthenia gravis, and Lambert-Eaton myasthenic syndrome) and has been known as safe and efficient agent in these disorders. Since IVIg would get more indications and be used more commonly, clinicians need to know the detailed mechanism of action, side effects, and practical points of IVIg.

• PNF and Movement
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• v.16 no.3
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• pp.345-353
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• 2018

Purpose: The purpose of the present study was to compare the effects of proprioceptive neuromuscular facilitation (PNF) and static stretching on weight distribution and flexibility for trunk flexion. Method: Sixty participants who had no musculoskeletal disorders were recruited from a local university within six months of this study. The participants were randomly assigned to a PNF stretching group (N=30) and a static stretching group (N=32). For the pre-and post-measurement design, the left-right weight distribution, anterior-posterior weight distribution, and finger-to-floor distance (FFD) were measured before and after the stretching interventions. Result: The FFD results were significantly improved after the interventions, regardless of the group differentiation (p<0.05). The PNF stretching intervention significantly increased the differences between anterior and posterior weight distribution compared to the static stretching group (p<0.05). Conclusions: Both the PNF and static stretching interventions could improve flexibility for trunk flexion mobility. Although the PNF intervention improved the weight distribution in the anterior-posterior direction, further research is required to investigate the various PNF interventions on left-and-right and anterior-posterior weight distribution.