• Korean Journal of Clinical Laboratory Science
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• v.45 no.3
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• pp.124-129
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• 2013

Separating of the facial nerve caused by compression near the blood vessels that cause the blood vessels and surgery when the hemifacial spasm, facial spasms, will disappear. These impacts have occurred very rarely and seen in this paper as facial spasms due to a brain tumor. The size of a brain tumor grows, which will put pressure on the surrounding facial spasm. Treated hemifacial spasm symptoms disappear through the removal of a brain tumor that occurs because saw.

• 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.

• Annals of Clinical Neurophysiology
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• v.9 no.1
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• pp.39-41
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• 2007

• Annals of Clinical Neurophysiology
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• v.20 no.1
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• pp.44-48
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• 2018

Neurolymphomatosis (NL) is a rare disease characterized by lymphomatous invasion of the cranial or peripheral nerves by lymphoma. A high suspicion is important due to the various presenting symptoms mandating consideration of many differential diagnoses. We report a case of NL of the cranial nerves and plexus presenting as diplopia, facial palsy, and weakness of the upper and lower limbs in sequence.

• Annals of Clinical Neurophysiology
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• v.2 no.2
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• pp.135-138
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• 2000

Both myasthenia gravis and Guillain-$Barr{\acute{e}}$ syndrome are autoimmune disorder, but it is very rare that both of them occur together. A 53-year old woman with history of myathenia gravis complained of weakness of extremities, worsening progressively for several days. Electrophysiologic study showed findings of motor axonal neuropathy without sensory involvement. She became improved in aspect of clinical symtoms and electrophysiologic findings after infusion of immunoglobulin. This is a case of Guillain-$Barr{\acute{e}}$ syndrome in a patient with myasthenia gravis.

• Annals of Clinical Neurophysiology
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• v.5 no.2
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• pp.210-213
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• 2003

POEMS syndrome is a multisystem disorder associated with polyneuropathy, organomegaly, endocrinopathy, a monoclonal protein(M-protein), and skin change. Recently we have had the opportunity to attend one patient with clinical features similar to this syndrome. He was a 46-year-old man who had a progressive polyneuropathy, swallowing difficulty, hepatosplenomegaly, hypothyroidism, IgA ${\lambda}type$ monoclonal gammapathy, specific skin change and ascites. His symptoms such as low extrimity pain and weakness, swallowing difficulty were improved by high-dose 7S-IgG. Thus, we report a case with a review of the literature.

• Annals of Clinical Neurophysiology
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• v.3 no.2
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• pp.160-163
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• 2001

Mirror movements in adult is usually accompanied with various clinical syndromes. But the pathogenesis of mirror movement is not clearly understood. A 20-year-old man visited with complaining of mirror movements in both hands, ophthalmoplegia and sensorineural hearing loss. He underwent through electromyography, transcranial magnetic stimulation, and functional magnetic resonance image. And we concluded that the mechanisms of his mirror movements were both ipsilateral innervated corticospinal tract and simultaneous activation of both motor cortex.

• Annals of Clinical Neurophysiology
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• v.7 no.1
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• pp.20-21
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• 2005

Myoclonus may originate from the cerebral cortex, subcortical structures, brainstem, spinal cord or peripheral nerve. But unilateral upper limb myoclonus related to cortical infarct is an unusual clinical picture. We report a 67-year-old man presented with myoclonus, associated with primary motor cortex infarction.

• Annals of Clinical Neurophysiology
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• v.18 no.1
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• pp.25-27
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• 2016

• Annals of Clinical Neurophysiology
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• v.23 no.1
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• pp.53-55
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• 2021

Congenital myasthenic syndromes (CMSs) are rare genetic disorders characterized by weakness and fatigue resulting from impaired neuromuscular transmission. Genetic testing can confirm the diagnosis for some types of CMS; however, variations in genotype, clinical phenotypes, age at disease onset, and responses to treatment make diagnosis very difficult. Here we present two adult patients who had significant decremental responses in repetitive nerve stimulation testing and multi-minicore pathology, and who responded to treatment with a cholinesterase inhibitor.