• Journal of Acupuncture Research
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• v.23 no.6
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• pp.221-227
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• 2006

Objectives : The purpose of this case is to report the improvement after treatment about tonic spasm of a transverse myelitis patient. Methods : We treated the patient with acupuncture therapy and herbal medicine from the 19th July 2006 to the 4th October 2006. At first we used Ssanghwa-tang until the 24th July 2006. After that we used Samul-tang until 2nd August. Lastly we used Yukmigihwang-tang until the 4th October 2006. And we used acupuncture at Asi points and used Sheng Ge of Liver from beginning to end. We checked the patient with frequency of tonic spasm and other symptoms. Results : After two months of treatments, frequency of tonic spasm decreased and abdominal muscle rigidity, visual disturbance, ocular discomfort and oppressed feeling in the chest were improved.

• The Journal of Internal Korean Medicine
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• v.39 no.2
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• pp.130-138
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• 2018

Neuromyelitis optica (NMO) is an autoimmune inflammatory disorder of the central nervous system characterized by optic neuritis and longitudinally extensive myelitis. Painful tonic spasm is a common complication of NMO, but there have been no reports about it in Korean medicine studies. In this case, we treated a 53-year-old woman diagnosed with NMO with paraplegia, painful tonic spasm, and decreased visual acuity using Korean medicine treatment, including acupuncture, herbal medicine, cupping, and moxibustion. We measured changes in clinical symptoms using the manual muscle testing (MMT), the numeric rating scale (NRS), the modified Barthel Index (MBI), and the Functional Independence Measure (FIM). After treatment, clinical symptoms were improved. The results indicate that Korean medicine treatment may be effective in the treatment of an NMO patient with paraplegia and painful tonic spasm.

• Journal of Korean Neurosurgical Society
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• v.42 no.5
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• pp.355-362
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• 2007

Hemifacial spasm (HFS) is characterized by tonic clonic contractions of the muscles innervated by the ipsilateral facial nerve. Compression of the facial nerve by an ectatic vessel is widely recognized as the most common underlying etiology. HFS needs to be differentiated from other causes of facial spasms, such as facial tic, ocular myokymia, and blepharospasm. To understand the overall craniofacial abnormalities and to perform the optimal surgical procedures for HFS, we are to review the prevalence, pathophysiology, differential diagnosis, details of each treatment modality, usefulness of brainstem auditory evoked potentials monitoring, debates on the facial EMG, clinical course, and complications from the literature published from 1995 to the present time.

• The Journal of Dong Guk Oriental Medicine
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• v.7 no.2
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• pp.69-79
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• 1999

Hemifacial spasm including blepharospasm is characterized by spontaneous clonic an d tonic muscle spasm on one side of the face with synkinesis. Though the etiology of hemifacial spasm is not entirely understood, generally there are two. One is nuclear hypothesis and the other is peripheral hypothesis. There are two ways of treatment of hemifacial spasm. One is internal medicine and the other is operative method. In oriental medicine, hemifacial spasm is very similar to diseases such as Anpojindo (眼胞振跳), Poryunjindo(胞輪振跳), or Aunido(眼眉跳) in symptoms. The diseases such as Anpojindo(眼胞振跳), Poryunjindo(胞輪振跳), Anmido(眼眉跳) is related to the function of liver(肝) and risk factors are regarded as Pung(風). The acupuncture therapy of hemifacial spasm is based on Liver meridian(LV), Gallbladder meridian(GB). And ear-acupuncture is recommended as a good method for hemifacial spasm.

• Journal of Genetic Medicine
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• v.18 no.1
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• pp.44-47
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• 2021

Cerebral creatine deficiency syndrome (CCDS) is a disorder where a defect is present in transport of creatine in the brain. Creatine plays an essential role in the energy metabolism of the brain. This is a genetic disorder, autosomal recessive or X linked, characterized by intellectual disability, speech and language delay, epilepsy, hypotonia, etc. Until recently very few number of cases have been reported. Here we report a case of 1.5-year-old boy who had epilepsy (epileptic spasm and generalized tonic clonic seizure), intellectual disability, microcephaly, hypotonia and speech delay. His magnetic resonance imaging of brain showed cortical atrophy and electroencephalography showed burst suppression pattern. The diagnosis was confirmed by clinical exome sequencing which showed novel mutation of SLC6A8+ in exon 9, suggestive of X linked recessive CCDS. The patient was then treated with glycine, L-arginine and creatine monohydrate with multiple antiepileptic drugs.

• Clinical and Experimental Pediatrics
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• v.46 no.1
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• pp.95-99
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• 2003

Krabbe disease is a rare autosomal recessive disorder clinically characterized by retardation in motor development, prominent spasticity, seizures, and optic atrophy. Pathologically, there are many globoid cells in the white matter, in addition to the lack of myelin and the presence of severe gliosis. Hence Krabbe disease is known as globoid cell leukodystrophy. Biochemically, the primary enzymatic deficiency in Krabbe disease is galactocerebroside beta-galactosidase. Patients with Krabbe disease can be subdivided into the early-onset type and late-onset type, according to the onset of clinical manifestations. Most patients with early-onset type die before their second birthday. We describe a girl with Krabbe disease associated with uncontrolled seizures, which was confirmed with biochemical study and MRI. The clinical findings of this patient included hyperirritability, scissoring of the legs, flexion of arm, and clenching of the fists, and generalized tonic seizures. EEG showed hypsarrhythmia, and MRI demonstrated degenerative white matter changes in bilateral periventricular white matter, posterior rim of internal capsule, basal ganglia and brain stem on T2W1 and FLAIR image. The diagnosis was based on clinical features of progressive neurologic deterioration in conjunction with low galactocerebroside beta-galactosidase activity.

• The Journal of Korean Obstetrics and Gynecology
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• v.23 no.4
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• pp.57-66
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• 2010

Purpose: To provide basic informations for guidelines of Ginseng usage during lactation. Method: Based on a regulation of scope and preparation of herbal prescriptions by Ministry of health and welfare of Korea, we selected the formulae for postpartum care and disease in 7 Korean Medical Classics. And we searched the number of formulae including Ginseng, dosage and indications of Ginseng in formulae in those books. Results: The range of Ginseng dosage during lactation from medical classics is 1.5-18.75g/day for medical purposes. Indications of Ginseng are lethargy, excessive bleeding, asthma, fever, cold, pain, dizziness, mental disorder, spasm, digestive problem, constipation, diarrhea, urinary incontinence, edema, breast engorgement, lack of breastmilk, breast ulcer, etc. But Ginseng had not been used in the case of stroke, epistaxis, beginning of mastitis, tumor of lower abdomen. Conclusions: Ginseng should be recommended less than 1.5g/d as a nutritional supplement. If breastfeeding woman wants to take Ginseng as a medication or as a tonic, she should consult with a official specialist about proper prescription and dosage instead of risky random medication.

• Clinical and Experimental Pediatrics
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• v.59 no.sup1
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• pp.29-31
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• 2016

Glucose transport 1 (GLUT-1) deficiency is a rare syndrome caused by mutations in the glucose transporter 1 gene (SLC2A1) and is characterized by early-onset intractable epilepsy, delayed development, and movement disorder. De novo mutations and several hot spots in N34, G91, R126, R153, and R333 of exons 2, 3, 4, and 8 of SLC2A1 are associated with this condition. Seizures, one of the main clinical features of GLUT-1 deficiency, usually develop during infancy. Most patients experience brief and subtle myoclonic jerk and focal seizures that evolve into a mixture of different types of seizures, such as generalized tonic-clonic, absence, myoclonic, and complex partial seizures. Here, we describe the case of a patient with GLUT-1 deficiency who developed infantile spasms and showed delayed development at 6 months of age. She had intractable epilepsy despite receiving aggressive antiepileptic drug therapy, and underwent a metabolic workup. Cerebrospinal fluid (CSF) examination showed CSF-glucose-to-blood-glucose ratio of 0.38, with a normal lactate level. Bidirectional sequencing of SLC2A1 identified a missense mutation (c.1198C>T) at codon 400 (p.Arg400Cys) of exon 9.

• The Journal of Korean Physical Therapy
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• v.11 no.3
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• pp.37-44
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• 1999

Delayed onset muscle soreness is a sensation of discomfort that occurs 24h after exercise, and it is associated with the performance of unfamiliar and high force muscle wor, such as eccentric contractions. The injury to the muscle has been well described but the mechanism underlying the injury is not fully understood. Although the pathophysiological processes underlying delayed onset muscle soreness are not completely understood, many researchers have investigated various treatments in a attempt to reduce the soreness. These treatments have focused on reducing the inflammation, or edema, consequent to tissue damage, and breaking up the cycle which is thought provoke tonic muscle spasm or pain. Physical therapy is the most importance thechniques to reduce delayed onset muscle soreness. Physical therapy on delayed onset muscle soreness includes massage, exercise, therapeutic ultrasound, TENS, stretching and cryotherapy, this investigation should encourage physical therapists to experiment further with various techniques to reduce delayed onset muscle soreness.