• Annals of Clinical Neurophysiology
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• v.6 no.1
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• pp.57-60
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• 2004

The sixty two-year-old woman was admitted with facial diplegia and ataxic gait. Neurological examination revealed areflexia and sensory ataxia with decreased sensation of position and vibration in both lower extremities. Electrophysiologic study suggest motor dominant demyelinating polyneuropathy and bilateral facial neuropathy. CSF study revealed no cells and increased proteins. After intravenous immunoglobulin therapy, sensory ataxia and electrophysiological study had markedly improved for 3 months.

• The Journal of the Society of Stroke on Korean Medicine
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• v.24 no.1
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• pp.55-66
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• 2023

■Objective The aim of this study is to report the effects of Korean medicine treatment on patients complaining of sensory disorder of Lateral medullary syndrome caused by lateral medullary infarction. ■Method The patient received Sogyeonghwalhyeoltang, acupuncture, electroacupuncture, TENS and Jungsongouhyul pharmacopuncture treatment for 18 days. Abnormal sensation was evaluated using the Numerical Rating Scale (NRS), and sensory ataxia was evaluated using quantitative sensory evaluation for light touch, pain, and temperature, and then the sensation was evaluated using % compared with sensation felt when normal was 100%. Symptoms were evaluated over a total of 3 weeks on 2/7, 2/14, and 2/21. ■Results After treatment, NRS scores decreased both when the abnormal sensation was stable and when stimulated. The recovery score for sensory ataxia increased, with more pronounced recovery in the trunk area and slower recovery in the peripheral area. ■Conclusion This case shows that combined Oriental medicine treatment helps recover from sensory disorder in Lateral medullary syndrome.

• The Journal of the Society of Stroke on Korean Medicine
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• v.15 no.1
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• pp.39-49
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• 2014

This report is about a case of an ataxia patient with sensory loss diagnosed with thalamic Infarction. The patient had symtoms of gait disturbances and dysmetria. We used Korean medicine treatment modalities including acupunture, electroacupuncture, moxibustion and herb medicines. The improvement of ataxia was evaluated by International Cooperative Ataxia Rating Scale and Balance master^Ⓡ system. After treatment, decreased scores of International Cooperative Ataxia Rating Scale and change of the trace of Balance master^Ⓡ system showed that symtoms of ataxia were improved. Sensory deficits and other conditions were also getting better. This report suggests that Korean medicine could have a therapeutic effect for Thalamic ataxia.

• The Journal of Korean Medicine
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• v.20 no.4
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• pp.98-105
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• 2000

Miller Fisher syndrome is characterized by acute external ophthalmoplegia, ataxia and areflexia in the abscence of significant motor or sensory deficit in the limbs and usually results in a complete recovery. Most cases have anteceding events like upper respiratory infection or other viral infections. Its accurate anatomic lesion sites and pathogenesis is still unknown. Recently we experienced a 47 year-old man who had a sudden onset of complete total ophthalmoplegia, ataxia, diplopia and whose condition was improved through Oriental medical treatment.

• Journal of Genetic Medicine
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• v.14 no.2
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• pp.71-74
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• 2017

Mutations in the DNA methyltransferase 1 gene (DNMT1) were reported to cause two phenotypes: OMIM 604121 and OMIM 614116. The first phenotype includes autosomal dominant cerebellar ataxia, deafness, and narcolepsy, which were reported to be caused by mutations in exon 21. The second phenotype includes hereditary sensory and autonomic neuropathy type 1E, which was suggested to be caused by mutations in exon 20 and 21. In this article, we report a novel heterozygous missense variant c.898A>C, p.(Lys300Gln) in exon 12 of DNMT1 in a young woman who presented with pure cerebellar ataxia. This report indicates that a mutation in exon 12 may lead to pure cerebellar ataxia. Another possibility is that the patient is currently in an early stage of the disease, and as the disease progresses, she will have more manifestations. To confirm or exclude this possibility, a subsequent follow-up study reporting the disease progression in this patient may be needed. Further reports of cases with the same mutation are needed to confirm the phenotype of this mutation.

• Annals of Clinical Neurophysiology
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• v.10 no.1
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• pp.74-78
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• 2008

Pyridoxine has been known as an essential cofactor in many important biological reactions of tissue metabolism including blood, skin, and central nervous system. Nowadays, vitamins are widely consumed because of the belief that they provide health benefits with no harm. We report a patient with sensory ataxia who had a 3-year history of excessive vitamin $B_6$ intake. Her clinical and electrodiagnostic findings were characteristic of sensory neuronopathy, which were probably caused by pyridoxine intoxication. Physicians should be aware of the toxicities of megavitamin therapy.

• Annals of Clinical Neurophysiology
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• v.3 no.2
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• pp.156-159
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• 2001

Miller Fisher syndrome(MFS) has been the focus of conflicting opinions regarding the peripheral versus the central nature of the site of major neural injury. We present our electrophysiological findings in one case of MFS to help clarify the pattern of peripheral nerve injury in this syndrome. A 45-year-old man visited our hospital due to sudden diplopia. Initial examination revealed internuclear opthalmoplegia. The next day, his symptoms rapidly aggravated to complete external ophthalmoplegia, ataxia, and areflexia with hand and foot numbness. Serial electrophysiological studies were performed. The results of brainstem evoked potential(BAEP) and blink reflex were normal in the serial studies. Motor and sensory nerve conduction study(NCS) were normal findings in second hospital day, but ulnar sensory nerve shows no sensory nerve action potential(SNAP) and sural sensory conduction velocity was delayed in 7th hospital day. Our patient's clinical presentation began to improve on 15th hospital day, and his electrophysiologic study showed improvement on 29th hospital day. We believe that all the manifestations of MFS can be explained by the involvement of peripheral nerves without brainstem or cerebellar lesion with the serial electrophysiological studies.

• Annals of Clinical Neurophysiology
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• v.4 no.1
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• pp.70-73
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• 2002

Acute autonomic neuropathy is a rare disease. Since the first case was reported by Young et.al., in 1969, a number of similar cases have been described, with some variation of the accompanied neurologic deficits. Acute autonomic and sensory neuropathy(AASN) is characterized by the acute onset of autonomic dysfunction and sensory disturbances. A 16-year-old girl experienced high fever($40^{\circ}C$) and erythematous rash on whole trunk and face followed by pain and sensory loss over the whole body, dysphagia, ataxia, urinary retention, and postural hypotension. There was no evidence of limb weakness. The electrophysiologic studies of this patient revealed sensory polyneuropathy and the various autonomic function test showed autonomic dysfunction. The recovery of her autonomic and sensory symptoms is incomplete, three months after the onset of the symptoms. The etiology of the acute autonomic and sensory neuropathy is not known. Most previous authors have suggested the dysautonomia may be an acute immunological damage to peripheral fibers of the autonomic nervous system. We report a case of acute autonomic and sensory neuropathy.

• Annals of Clinical Neurophysiology
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• v.17 no.1
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• pp.31-34
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• 2015

We report a case with squamous cell lung cancer with concomitant Guillain-Barre syndrome (GBS) as a paraneoplastic syndrome. A 67-year-old patient who was previously diagnosed as metastatic squamous cell lung cancer developed mild symmetrical weakness, paresthesia and sensory ataxia. Nerve conduction study showed sensorimotor polyneuropathy. Analysis of cerebrospinal fluid showed high tilter for monospecific anti-GD1b IgG antibody without onconeuronal antibodies. After treatment with intravenous immunoglobulin, the patient's symptoms improved.

• Journal of Oriental Neuropsychiatry
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• v.12 no.1
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• pp.219-229
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• 2001

The brainstem include midbrain, pons & medulla. In acute stage of brainstem infarction, neurologic symptoms may be progressive. So we must pay special attention to Wallenberg's syndrome. In other words, Wallenberg's syndrome is dorsolateral medullary syndrome. A-54-years-old woman was admitted because of vertigo, ataxia & somatic sensory loss of left face and right half-body. Brain MRI showed high SI in T2W, low SI in T1W lesion left medullary infarction. We diagnosed the case as Shin-heo type Oriental medically and prescribed Gihwangemjakamibang. Diabetes mellitus was found out. So We have controlled diabetes mellitus by Occidental medical therapy. In the end, The symptoms of the patient became better. We know that cooperative(oriental & occidental) medical therapy is better than one medical therapy.Here we present one case of Wallenberg's syndrome who was admitted at Kunpo Wonkwang University Hospital Oriental Neuropsychiatry from 14th March to 6th April. 2001.