• Annals of Clinical Neurophysiology
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• v.6 no.1
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• pp.52-56
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• 2004

Acute motor axonal neuropathy (AMAN) is a subtype of Guillain-Barre syndrome and characterized by selective involvement of motor fibers. Acute disseminated encephalomyelitis (ADEM) is a demyelinating disease of central nervous system. The coincidence of central and peripheral nervous system involvement has been reported rarely. We described a 37-year-old male patient presented with fever and altered consciousness. The examination of cerebrospinal fluid and brain magnetic resonance imaging was compatible with acute disseminated encephalomyelitis. Several days after admissionb his mentality was improved but quadriparesis, multiple cranial neuropathies, and areflexia were detected. Electrophysiologic studies suggested axonal form of motor dominant polyneuropathy. We report a case of acute motor axonal neuropathy combined with ADEM. We consider that this case is an example of simultaneous immunologic process to the common pathogenic epitope of central nervous system and peripheral nervous system.

• Journal of Sasang Constitutional Medicine
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• v.33 no.3
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• pp.171-180
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• 2021

Objectives This case report is about a Taeyangin patient with Acute Motor Axonal Neuropathy identified as Hae-Yeok pattern using Ogapijangchuk-tang. In this study, we report the significant improvement of lower extremity weakness and pain of this patient after Sasang Constitutional medicine treatment. Methods The patient was identified as Taeyangin Hae-Yeok pattern and treated with Ogapijangchuk-tang. Guillain-Barre Syndrome disability scale was used to assess the overall function of the patient. The Numeral Rating Scale was used to assess the change of lower extremity pain. Also the change of lower extremity weakness was measured by patient's expression and graded by Manual Muscle Test. Result and Conclusion After treatment with Ogapijangchuk-tang, patient's symptoms were improved. And there was not any side effect. In conclusion, this study shows that Sasang Constitutional medicine can be effective treatment for Taeyangin patient with Acute Motor Axonal Neuropathy.

• Annals of Clinical Neurophysiology
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• v.2 no.1
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• pp.1-7
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• 2000

From among the group of patients diagnosed clinically to have Guillain-Barre syndrome(GBS), subgroups with pure motor involvement have been identified. Some of such patients appear to have an axonal neuropathy by eletrophysiology. Such cases have been termed acute motor axonal neuropathy(AMAN). Many of these patients are found clinically to have normal sensation and to have electrodiagnostic patterns consistent with selective degeneration of motor axons. A serological survey showed some of individuals with AMAN had evidence of antecedent Campylobacter jejuni(CJ) infection. And AMAN has an association with the presence of anti-ganglioside antibodies. This article reviewed briefly the AMAN and their relationship to CJ infection and anti-ganglioside antibodies.

• Annals of Clinical Neurophysiology
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• v.20 no.1
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• pp.49-52
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• 2018

Reversible conduction block (RCB) was rare in patients with acute motor sensory axonal neuropathy (AMSAN). A-46-year-old man presented with paresthesia, weakness, diplopia, and dysarthria. Nerve conduction study (NCS) exhibited axonal changes with conduction block in motor and sensory nerves. His symptoms were rapidly progressed and recovered. Conduction block was disappeared in the follow-up NCS performed after 2 weeks. The AMSAN case with RCB showed rapid progress and rapid recovery of clinical symptoms as acute motor axonal neuropathy patients with RCB.

• Annals of Clinical Neurophysiology
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• v.3 no.1
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• pp.43-46
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• 2001

Acute pandysautonomic neuropathy(APN) is an uncommon clinical entitiy involving vasomotor, sudomotor, pupilomotor, secretomotor and other autonomic systems. Both sympathetic or parasympathetic fibers are involved with relative preservation of somatic sensory and motor function. Although APN shares several clinical features with GBS, it is not clear whether APN is a subvariety of GBS. We report two young patients with APN. Patient 1 was a 18-year-old girl with recurrent fainting spells. Patient 2 was a 23-year-old man sufferring from unexplained nausea and vomiting. Both had a history of previous upper respiratory infection. They presented with gastroparesis, anhydrosis and orthostatic hypotension. Mild numbness and tingling sense was present, but motor power was intact. Neurologic examination showed bilateral tonic pupil, decreased pain and vibration sense, and absent tendon reflexes. Nerve conduction study indicated diffuse sensorimotor polyneuropathy. Nerve biopsy in patient 2 revealed axonal degeneration. After conservative management, gastrointestinal symptoms were improved in patient 2, however, patient 1 suffered from the symptoms lasting more than several months. These cases suggest that post-infectious dysautonomic symptoms in young patient may indicate the diagnosis of APN. Although the natural course is generally benign, accurate diagnosis and proper management may be mandatory for the better clinical outcome.

• Annals of Clinical Neurophysiology
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• v.2 no.2
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• pp.81-88
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• 2000

Background : Guillain-$Barr{\acute{e}}$ syndrome(GBS) is characterized clinically by acute flaccid paralysis, areflexia, and albumino-cytologic dissociation. Based on electrophysiology and pathology, GBS can be divided into either predominantly demyelinating or predominantly axonal patterns. Objectives : The clinical and laboratory status of probable acute axonal GBS occurring at a mental hospital was evaluated. Methods : Eight schizophrenia patients with probable acute axonal GBS were analyzed. Results : The mean age of the patients was 38 years old. Most of the patients were men. All patients showed an acute ascending paraparesis and/or quadriparesis with areflexia, and all have a history of schizophrenia for 3~20 years. The diseases occurred predominantly in the summer and electrodiagnostic studies revealed axonal patterns. The patients were treated by supportive care, except one patient with intravenous immunoglobulin. The prognosis was improved in 3 ; no change in 4 and 1 became aggravated. One patient with acute motor-sensory axonal neuropathy had a recurrence after 10 months of the first attack. Conclusions : Axonal GBS has been considered uncommon clinically or electrophysiologically, but 8 probable acute axonal GBSs occurring at a mental hospital have been diagnosed in 3.5 years.

• Journal of The Korean Society of Clinical Toxicology
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• v.13 no.1
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• pp.46-49
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• 2015

Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. Following are brief statements describing the motor peripheral neuropathy involved bilateral lower extremities of a patient who recovered following acute carbon monoxide poisoning. After inhalation of smoke from a fire, a 60-year-old woman experienced bilateral leg weakness without edema or injury. Neurological examination showed diplegia and deep tendon areflexia in lower limbs. There was no sensory deficit in lower extremities, and no cognitive disturbances were detected. Creatine kinase was normal. Electroneuromyogram patterns were compatible with the diagnosis of bilateral axonal injury. Clinical course after normobaric oxygen and rehabilitation therapy was marked by complete recovery of neurological disorders. Peripheral neuropathy is an unusual complication of CO intoxication. Motor peripheral neuropathy involvement of bilateral lower extremities is exceptional. Various mechanisms have been implicated, including nerve compression secondary to rhabdomyolysis, nerve ischemia due to hypoxia, and direct nerve toxicity of carbon monoxide. Prognosis is commonly excellent without sequelae. Emergency physicians should understand the possible-neurologic presentations of CO intoxication and make a proper decision regarding treatment.

• Annals of Clinical Neurophysiology
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• v.7 no.2
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• pp.65-74
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• 2005

Charcot-Marie-Tooth (CMT) disease was described by Charcot and Marie in France and, independently, by Tooth in England in 1886. CMT is the most common form of inherited motor and sensory neuropathy, and is a genetically heterogeneous disorder of the peripheral nervous system. Therefore, many genes have been identified as CMT-causative genes. Traditionally, subclassification of CMT have been divided into autosomal dominant inherited demyelinating (CMT1) and axonal (CMT2) neuropathies, X-linked neuropathy (CMTX), and autosomal recessive inherited neuropathy (CMT4). Recently, intermediate type (CMT-Int) with NCVs between CMT1 and CMT2 is considered as a CMT type. There are several related peripheral neuropathies, such as $D{\acute{e}}j{\acute{e}}rine$-Sottas neuropathy (DSN), congenital hypomyelination (CH), hereditary neuropathy with liability to pressure palsies (HNPP) and giant axonal neuropathy (GAN). Great advances have been made in understanding the molecular basis of CMT, and 17 distinct genetic causes of CMT have been identified. The number of newly discovered mutations and identified genetic loci is rapidly increasing, and this expanding list has proved challenging for physicians trying to keep up with the field. Identifying the genetic cause of inherited neuropathies is often important to determine at risk family members as well as diagnose the patient. In addition, the encouraging studies have been published on rational potential therapies for the CMT1A. Now, we develop a model of how the various genes may interact in the pathogenesis of CMT disorder.

• Annals of Clinical Neurophysiology
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• v.24 no.2
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• pp.101-106
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• 2022

Neurological complications attributed to coronavirus disease-19 (COVID-19) infection have been reported including acute disseminated encephalomyelitis, Guillain-Barré syndrome, and so on. Herein, we report a 49-year-old woman presented with acute encephalopathy and paraplegia simultaneously after COVID-19 infection. Brain magnetic resonance imaging (MRI) showed symmetric hyperintense basal ganglia lesions on T2-weighted imaging. Cerebrospinal fluid pleocytosis, motor axonal neuropathy and enhancement of conus medullaris nerve roots on spine MRI were observed. We treated her with high-dose corticosteroid and intravenous immunoglobulin.

• Annals of Clinical Neurophysiology
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• v.19 no.2
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• pp.148-150
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• 2017

Peripheral neuropathy associated with hyper-IgE-emia have been rarely reported. Here we present a 72-year-old man with acute motor axonal neuropathy who had relatively poor prognosis. The serum was weakly positive for IgG GQ1b and GT1a, and serum IgE was significantly elevated. He was transferred to a rehabilitation center with Medical Research Council grade 3 lower extremity weakness on admission day 65. We would suggest that hyper-IgE-emia may increase the magnitude and rate of neural damage in this case.