• Annals of Clinical Neurophysiology
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• 제16권1호
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• pp.27-31
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• 2014

Thiamine deficiency can cause peripheral polyneuropathy and Wernicke's encephalopathy. Wernicke's encephalopathy is characterized by ataxia, ophthalmoplegia, nystagmus, and confusion, and typically presents acute and rapidly progressive course, whereas peripheral neuropathy associated with thiamine deficiency manifests chronic and slowly progressive one. However, acute and rapidly progressive axonal polyneuropathy combined with Wernicke's encephalopathy is quite rare and unusual. Here, we describe a patient with Wernicke's encephalopathy who presented with acute bilateral axonal neuropathy.

• Annals of Clinical Neurophysiology
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• 제3권2호
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• pp.115-121
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• 2001

The occurrence of muscle weakness in patients with sepsis or multiple organ failure managed in the intensive care unit has been recognized with increasing frequency in the last two decades. The difficulty in examining critically ill patients may explain why this complication has been only recently recognized. This weakness is due to an axonal polyneuropathy which is called critical illness polyneuropathy(CIP). It must be differentiated from myopathy or neuromuscular junction disturbance that can also occur in the intensive care setting. Neither the cause nor the exact mechanism of CIP has been elucidated. Electrophysiological studies demonstrated an acute axonal damage of the peripheral nerves. Before the recognition of CIP, these cases were usually misdiagnosed as Guillain-$Barr{\acute{e}}$ syndrome. Clinical recovery from the neuropathy is rapid and nearly complete in those patients who survive. Thus, neuropathy acquired during critical illness, although causing a delayed in weaning from ventilatory support and hospital discharge, does not worsen long-term prognosis.

• Annals of Clinical Neurophysiology
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• 제6권1호
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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.

• Annals of Clinical Neurophysiology
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• 제4권2호
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• pp.91-97
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• 2002

The field of critical care medicine has flourished, but an unfortunate result of improved patient survival in the intensive care unit is the occurrence of certain acquired neuromuscular disorders. During the last two decades, various neuromuscular disorders were recognized as common causes of weakness occurring in critically ill patients. The two most common disorders are an acute quadriplegic myopathy predominantly associated with the use of intravenous corticosteroids and neuromuscular junction blocking agents and severe systemic illness termed critical illness myopathy(CIM), and an axonal sensorimotor polyneuropathy termed critical illness polyneuropathy. I will review briefly about general components of the CIM.

• Annals of Clinical Neurophysiology
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• 제7권1호
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• pp.31-33
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• 2005

Segmental zoster paresis (SZP) is a clinically rare complication of herpes zoster. But it has not been reported that acute cerebral motor cortical infarction coincidentally occurred in SZP. A 86-year-old woman was admitted due to pain, tingling sensation, and weakness of left arm. She had an acute onset of pain and tingling sensation in left arm at first day, shoulder weakness at second day, and multifocal vesicles at fourth day. Deep tendon reflexes of left arm were decreased than right. Electromyography showed an axonal polyneuropathy at superior trunk level of left brachial plexus. Median and ulnar sensory evoked potential tests were normal. Brain MRI showed a high signal in right primary motor cortex on diffusion weighted image. We report a case of acute cerebral motor cortical infarction coincidentally occurred in SZP.

• Annals of Clinical Neurophysiology
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• 제3권1호
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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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• 제15권2호
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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.

• 대한한방소아과학회지
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• 제17권2호
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• pp.199-211
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• 2003

저자는 경희대학교(慶熙大學校) 한의과대학(韓醫科大學) 부속한방(附屬韓方) 병원(病院)에 내원한 Guillain-Barre syndrome 환자를 한약(韓藥)과 간접염(間接炎) 및 침치료(鍼治療를) 사용하여 환자의 증상이 호전되었음을 확인하였으므로 이에 문헌고찰과 함께 보고하는 바이다.