• Annals of Clinical Neurophysiology
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• v.24 no.1
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• pp.26-29
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• 2022

Immune checkpoint inhibitors (ICIs) have emerged as one of the most promising therapeutic options for advanced cancers. While ICIs have improved survival in multiple cancers, their increased use is restricted by various immune-related adverse events. In this report we describe a patient with renal cell carcinoma who received a combination of ICIs, nivolumab plus ipilimumab, and who developed lumbosacral polyradiculoneuropathy. Corticosteroid use was an effective treatment for this patient.

• Journal of Korean Neurosurgical Society
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• v.37 no.1
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• pp.70-72
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• 2005

Primary spinal cord lymphomas are rare, and are either extra-/intradural masses with leptomeningeal infiltration or intramedullary in nature. The authors present a patient with a diffuse large B-cell lymphoma involving the sacral nerve root, extension to extradural space, and the cranial nerve.

• Annals of Clinical Neurophysiology
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• v.15 no.2
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• pp.63-67
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• 2013

Multiple cranial and peripheral neuropathies as a delayed sequellae of ethylene glycol poisoning is a less well known clinical entity and its information about long-term electrophysiological and clinical outcomes is limited. We report a 45-year-old male who presented with acute renal failure and subsequently developed multiple cranial neuropathy, respiratory failure, and flaccid tetraparesis. Through sequential electrophysiological studies, we would like suggest that the main pathophysiology of ethylene glycol-related neuropathy is a demyelinating polyradiculoneuropathy with secondary axonal degeneration.

• The Journal of Internal Korean Medicine
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• v.24 no.4_2
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• pp.975-986
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• 2003

Introduction: Guillain-Barre syndrome(GBS) is defined as a recognizable clinical entity that is characterized by rapidly evolving symmetric limb weakness, a loss of tendon reflexes, absent or mild sensory signs, and variable autonomic dysfunctions. Recently there is an opinion that Acute Inflammatory Demyelinating Polyradiculoneuropathy'(AIDP) is more effective than 'GBS' for the symptoms. These symptoms are applicable to rheumatic arthritis(痺), flaccid paralysis of limb(?) caused by wind, cold and dampness(風, 寒, 濕) from an oriental medical view point. On this, we reported one case that diagnosed as 'complex of rheumatic arthritis(痺) and flaccid paralysis of limb(?)' at our oriental medical hospital. Result: we considered these symptoms as 'complex of rheumatic arthritis(痺), flaccid paralysis of limb(?)'. In accordance with the result, we treated the patient with Chung-Sang Tong-Jung On-Ha(淸上通中溫下). We concluded that external factors such as wind, cold and dampness(風, 寒, 濕) and internal factors like vital energy's disharmony(生氣不調和) affected the patient.

• Annals of Clinical Neurophysiology
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• v.10 no.1
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• pp.70-73
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• 2008

By definition, the time to reach nadir in Guillain-Barre syndrome (GBS) is within four weeks. This is in contrast to the chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), which progress for at least two months. However, CIDP can take a relapsing and remitting form and could mimic treatment related fluctuations of GBS (GBS-TRFs) especially during the early phase of disease. We report a patient with CIDP who initially presented with a rapidly progressive limb weakness mimicking GBS, but finally showed good recovery after long term corticosteroid therapy.

• Annals of Clinical Neurophysiology
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• v.7 no.1
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• pp.17-19
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• 2005

Polyneuropathy that is associated with monoclonal gammopathy of undetermined significance (MGUS) similar to chronic inflammatory demyelinating polyneuropathy (CIDP) has been reported before, whereas a connection to acute inflammatory demyelinating polyneuropathy (AIDP) has not been. A 52 year-old man was presented with ascending paralysis beginning 1 day ago. Neurological examinations showed facial diplegia and decreased motor power and deep tendon reflexes in all extremities. On electrophysiologic study, sensorimotor polyneuropathy was observed. Protein-and immunoelectrophoresis revealed IgA $\lambda$ monoclonal gammopathy. High dose steroid therapy was given and the symptoms improved slightly.

• Annals of Clinical Neurophysiology
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• v.7 no.1
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• pp.25-27
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• 2005

The Guillain-Barre syndrome (GBS) is an acute polyradiculoneuropathy marked by flaccid areflexic paralysis. Although the pathogenesis of GBS remains incompletely defined, considered as an autoimmune disease most frequently triggered by an previous infection. Antecedent infections with Campylobacter jejuni, cytomegalovirus, Ebstein-Barr virus, Mycoplasma pneumoniae, Haemophilus influenzae, human immunodeficiency virus, enterovirus, rotavirus are common. But, it is rare that GBS following typhoid fever. We present a case of typical GBS after antecedent Salmonella typhi infection.

• Annals of Clinical Neurophysiology
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• v.19 no.1
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• pp.50-53
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• 2017

An infection is less likely to elicit chronic inflammatory demyelinating polyneuropathy (CIDP) than Guillain-$Barr{\acute{e}}$ syndrome. We here report a case of acute-onset CIDP following hepatitis A virus infection and briefly comment on the potential mechanisms regarding the induction and chronicity of autoimmunity after a viral infection.

• Annals of Clinical Neurophysiology
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• v.19 no.1
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• pp.54-57
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• 2017

Distal acquired demyelinating symmetric (DADS) neuropathy is a variant form of chronic inflammatory demyelinating polyradiculoneuropathy. A 54-year-old man presented with gait disturbance owing to weakness in both legs. Nerve conduction studies showed demyelinating sensorimotor polyneuropathy, and laboratory studies demonstrated anti-GM1 and anti-GD1b IgG antibodies, but no anti-myelin associated glycoprotein activity. We suggest that an antiganglioside antibodies assay needs to be applied when DADS neuropathy is suspected in order to improve the classification of dysimmune neuropathies.

• Journal of The Korean Society of Clinical Toxicology
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• v.16 no.1
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• pp.57-59
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• 2018

Severe systemic responses including neurologic complications such as myasthenia gravis, myeloradiculopathy, optic neuropathy, parkinsonism, stroke and Guillain-$barr{\acute{e}}$ syndrome can occur after bee stings. This case describes a 78-year-old female who presented with symptoms of acute progressive bilateral symmetrical weakness in both lower legs after multiple bee stings. Nerve conduction study findings were consistent with acute sensorimotor axonal neuropathy and recovered by treatment with intravenous immunoglobulin. This case highlights that bee stings can result in acute onset Guillain-$barr{\acute{e}}$ syndrome, although the pathophysiologies of bee venoms need to be investigated accurately.