• Annals of Clinical Neurophysiology
• /
• 제3권2호
• /
• pp.172-175
• /
• 2001

Guillain-$Barr{\acute{e}}$ syndrome(GBS) is a common demyelinating disease of the peripheral nervous system. But recently, the axonal types are also reported. Acute transverse myelitis(ATM) is also a common inflammatory disease of the spinal cord. Generally, it is difficult to identify the etiology of GBS and ATM. I guess the occurrence of the 2 diseases at once is hard to take the place. A 63-year-old woman showed an acute motor axonal GBS and a cervical-upper thoracic ATM occurring at the same time. She was treated by intravenous immunoglobulin and solumedrol therapy. Her sensory symptoms were improved rapidly but motor symptoms showed only mild improvement.

• 대한임상독성학회지
• /
• 제16권1호
• /
• pp.57-59
• /
• 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.

• Annals of Clinical Neurophysiology
• /
• 제2권2호
• /
• pp.81-88
• /
• 2000

한 정신병원에 장기입원한 정신분열증환자에서 계속 발생한 8명의 급성 축삭성 GBS로 추정되는 환자들의 평균연령은 38세였으며 7명이 남자였다. 모든 환자들은 급성 상행성 양쪽하지 마비나 사지마비를 보이면서 심부 건반사가 소실되었다. 이 병은 주로 여름철에 많이 발생 하였으며 전기생리학적 검사상 축삭이 주로 손상된 소견을 보였다. IVIG치료를 한 1명을 제외한 나머지 환자들은 경제적 사정상 대증요법으로 치료하였다. AMAN형태의 환자 3명 중 1명에서 임상적 호전을 보였고, AMSAN형태의 환자 5명 중 2명에서 임상적 호전을 보였다. AMSAN형태의 환자중 1명에선 10개월 뒤 같은 증상이 재발하였다.

• Annals of Clinical Neurophysiology
• /
• 제2권2호
• /
• pp.135-138
• /
• 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
• /
• 제22권1호
• /
• pp.13-18
• /
• 2020

The electrodiagnostic findings in Guillain-Barré syndrome (GBS) play important roles in both understanding its pathophysiology and its diagnosis. Only demyelinating neuropathies were thought to be present when GBS patients were first diagnosed in Western countries, but the concept changed when many axonal GBS patients were reported in Asia. Reversible conduction failure was subsequently revealed, and it was recognized as a pathophysiologic continuum of axonal GBS. Thus, the electrodiagnostic findings in GBS have had a profound effect on the history of this disease.

• Annals of Clinical Neurophysiology
• /
• 제19권2호
• /
• pp.148-150
• /
• 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.

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