• Annals of Clinical Neurophysiology
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• v.9 no.1
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• pp.26-28
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• 2007

Miller Fisher syndrome (MFS) is a variant of Guillian-Barre syndrome (GBS) characterized by the triad of ophthalmoplegia, ataxia, and areflexia. Although recurrent GBS is a well known entity, the recurrence of MFS is extremely rare. Here we report an unusual case of recurrent MFS. Initially, the patient had presented with ophthalmoplegia, ataxia, areflexia, and tingling sensation of all extremities. After resolution of the first episode, the patient presented with atypical MFS characterized by ataxia, areflexia, and tingling sensation without ophthalmoplegia.

• The Journal of Korean Medicine
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• v.20 no.4
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• pp.98-105
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• 2000

Miller Fisher syndrome is characterized by acute external ophthalmoplegia, ataxia and areflexia in the abscence of significant motor or sensory deficit in the limbs and usually results in a complete recovery. Most cases have anteceding events like upper respiratory infection or other viral infections. Its accurate anatomic lesion sites and pathogenesis is still unknown. Recently we experienced a 47 year-old man who had a sudden onset of complete total ophthalmoplegia, ataxia, diplopia and whose condition was improved through Oriental medical treatment.

• 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 Academy of Child and Adolescent Psychiatry
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• v.8 no.1
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• pp.133-138
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• 1997

Prader Willi Syndrome(PWS) was first recognized and reported by Prader-Willi. The etiology of the syndrome is not fully understood, but 50-70% of the patients show small deletion in chromosome 15. Manifested symtoms vary according to developmental age. In early life, hypotonia, areflexia, feeding difficulties, hypothermia, microgenitalia, hypoplastic scrotum, cryptochordism were observed. But in several years, hypotonia disappears, and polyphagia, decreased satiety, psychomotor retardation, obesity, hypogonadism and short stature become main problems. Behavioural problems including temper and aggressive outbursts, stealing food, hoarding food, and self excoriating skin picking, trichotillomania are more prominent during adolescence and young adulthood. Also, irritable, depressed mood are described. Lots of psychological and behavioural problems explain the reason why psychiatrists have managed and reported this syndrome. However, there has been no official report of PWS in our country. So authors report the clinical characteristics and issues in management of a patient with PWS.

• 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.8 no.1
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• pp.71-73
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• 2006

Many neurologic signs are found in Miller Fisher syndrome (MFS) especially including pupillary abnormalities. But when internal ophthalmoparesis is first manifestation in MFS, diagnosis may be difficult in acute phase of illness. We report two cases of MFS presenting with internal ophthalmoplegia. Pupillary areflexia may be involved in acute phase of MFS. When acute bilateral internal ophthalmoparesis is encounted in clinical practice, initial manifestation of MFS should be included in differential diagnosis.

• Annals of Clinical Neurophysiology
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• v.5 no.1
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• pp.11-15
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• 2003

Backgrounds: Kennedy disease is a X-linked recessive disease characterized by bulbar symptoms, proximal muscle weakness, and gynecomastia. Methods: We analyzed clinical symptoms and performed electrodiagnostic studies on 6 patients. Results: We found following features: 1) proximal muscle weakness 2) bulbar symptoms, as dysarthria, facial and tongue atrophy 3) hyporeflexia or areflexia 4) fasciculations, predominantly on face, and proximal upper extremities 5) decreased sensory nerve action potentials(SNAPs) 6) chronic neurogenic changes in needle EMG. Conclusions: Kennedy disease is characterized by degenerative process of anterior horn cell and dorsal root ganglion without upper motor neuron dysfunction. Increased triple nucleotide CAG repeats(>38) in androgen receptor gene of Xp21 will confirm early stage of this disease.

• Annals of Clinical Neurophysiology
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• v.9 no.1
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• pp.19-22
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• 2007

Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) occur commonly in the patients who have been on mechanical ventilation for more than 1 week. Even in some patients diagnosed with CIP, an underlying myopathy may be the primary cause of the muscle weakness. The cormorbid status of CIP and CIM is called as critical illness polyneuropathy and critical illness myopathy (CIPNM). We describe a 56-year-old man with acute quadriparesis and areflexia after systemic inflammatory response syndrome. The diagnosis of CIPNM is important to avoid unnecessary investigations and unreasonably pessimistic prognosis. Electrophysiologic studies are essential for the diagnosis and for planning further clinical management.

• Annals of Clinical Neurophysiology
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• v.22 no.2
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• pp.117-120
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• 2020

Miller Fisher syndrome (MFS) is characterized by the acute ophthalmoparesis, ataxia and areflexia. We describe the case of 70-year-old man with cardinal symptom of MFS and active pulmonary tuberculosis (Tb). A thorough evaluation led to the diagnosis of MFS and treatment with intravenous immunoglobulin (IVIg) was started. The complete resolution of ophthalmoparesis and ataxia was observed from the fourth day of IVIg treatment. This is the first report to describe a case of MFS that developed in patient pulmonary tuberculosis.

• Annals of Clinical Neurophysiology
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• v.9 no.2
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• pp.89-92
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• 2007

A 33-year-old women developed weakness in all limbs 3 days prior to admission. Motor examination showed decreased strength in all limbs, but sensory examination was normal. Deep tendon reflexes were areflexia. Electrophysiological examination showed conduction blocks with nearly normal conduction velocities and terminal latencies in motor nerves and normal amplitudes and velocities in sensory nerves. Her serum was positive for IgG antibodies to gangliosides GM1, GD1b, and galactocerebroside. Acute motor conduction block neuropathy may be another variant of Guillain-Barre syndrome.