Cases reported "Miller Fisher Syndrome"

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1/30. miller fisher syndrome with central involvement: successful treatment with plasmapheresis.

    miller fisher syndrome is characterized by external ophthalmoplegia, ataxia, and areflexia. Most researchers favor a peripheral origin while others suggest a brainstem inflammatory lesion or a combination of central and peripheral demyelination. We report 2 cases of miller fisher syndrome with the typical triad of ataxia, areflexia, and ophthalmoplegia. Strong clinical evidence of central involvement included initial drowsiness, bilateral Babinski sign, and quadriparesis. Evoked potential studies showed prolongation of central conduction time. plasmapheresis was performed to relieve respiratory failure in Patient 1 and to shorten the duration of nasogastric tube feeding due to severe bulbar palsy in Patient 2. Significant improvement of electrophysiologic parameters was recorded after plasmapheresis. Abnormal evoked potentials, together with clinical evidence of central nervous system abnormalities, support the hypothesis that there is a combination of peripheral and central involvement in miller fisher syndrome in our patients. plasmapheresis is highly effective in relieving the profound neurological deficits of this atypical syndrome.
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ranking = 1
keywords = peripheral, nervous system
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2/30. Can immunoadsorption plasmapheresis be used as the first choice therapy for neuroimmunological disorders?

    The subjects were 31 patients in whom immunoadsorption plasmapheresis (IAPP) was performed as the first choice therapy for primary or recurrent neuroimmunological disorders. The clinical manifestations before and after IAPP and the use of corticosteroids were investigated in the present study. IAPP was clinically effective in all patients. The corticosteroids (CSs) administration was begun or CSs were increased after completion of IAPP in 11 patients. IAPP was performed as the first choice therapy, and favorable results were obtained in patients with guillain-barre syndrome and Miller-Fisher syndrome. IAPP alone was also effective in a patient with lupoid sclerosis. When IAPP was used alone in 2 patients with chronic inflammatory demyelinating polyradiculoneuropathy, it completely eliminated the clinical manifestations, but the symptoms recurred about 2 months later. Therefore, although IAPP could be performed as the first choice therapy for many neuroimmunological disorders, subsequent therapies should be carefully investigated.
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ranking = 0.21077504833073
keywords = neuropathy
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3/30. Fisher syndrome with tetraparesis and antibody to GQ1b: evidence for motor nerve terminal block.

    A Fisher syndrome (FS) patient with antibody to tetrasyaloganglioside GQ1b (GQ1b) developed late limb weakness. Serial motor conduction velocities (MCVs) showed a marked reduction of distal compound muscle action potential (CMAP) amplitudes, worse at 2-3 weeks, followed by a dramatic increase in week 5. Motor conduction velocities were always in the normal range, distal motor latencies changed only slightly, and conduction block in intermediate nerve segments was absent. These electrophysiological data might suggest an axonal neuropathy or a distal demyelinating conduction block. However, the dramatic increase of distal CMAP amplitudes over a short time without significant changes of distal motor latencies, CMAP duration, and morphology indicate that weakness in this FS patient might be due to a block of acetylcholine release from motor terminals, possibly mediated by anti-GQ1b antibodies.
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ranking = 0.46445959215707
keywords = neuropathy, nerve
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4/30. IgG anti-GQ1b positive acute ataxia without ophthalmoplegia.

    IgG anti-GQ1b antibody was present in a patient with acute ataxia and areflexia without ophthalmoplegia or elementary sensory loss. Sensory nerve conduction studies and somatosensory evoked potentials were normal, but postural body sway analysis showed dysfunction of the proprioceptive afferent system. The clinical presentation and laboratory results for this patient resemble those of miller fisher syndrome, except for the lack of ophthalmoplegia. This case may represent part of an IgG anti-GQ1b syndrome.
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ranking = 0.050736908765268
keywords = nerve
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5/30. magnetic resonance imaging enhancement of cranial nerves in inflammatory bulbar polyneuropathy.

    A patient with generalized inflammatory polyneuropathy and facial diplegia was studied with magnetic resonance imaging. Multiple cranial nerves showed signal enhancement without sensory or motor dysfunction.
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ranking = 1.30755978548
keywords = neuropathy, nerve
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6/30. Acute onset of a bilateral areflexical mydriasis in Miller-Fisher syndrome: a rare neuro-ophthalmologic disease.

    Miller-Fisher syndrome (MFS) is characterized by variable ophthalmoplegia, ataxia, and tendon areflexia. It seems to be a variant of guillain-barre syndrome (GBS), but unlike in GBS, there is a primitive involvement of the ocular motor nerves, and in some cases there is brainstem or cerebellum direct damage. The unusual case of MFS in the current study started with a bilateral areflexical mydriasis and a slight failure of accommodative-convergence. Ocular-movement abnormalities developed progressively with a palsy of the upward gaze and a bilateral internuclear ophthalmoplegia to a complete ophthalmoplegia. In the serum of this patient, high titers of an IgG anti-GQ1b ganglioside and IgG anti-cerebellum. anti-purkinje cells in particular, were found. The former autoantibody has been connected to cases of MFS, of GBS with associated ophthalmoplegia, and with other acute ocular nerve palsies. The anti-cerebellum autoantibody could explain central nervous system involvement in MFS. The role of these findings and clinical implications in MFS and in other neuro-ophthalmologic diseases are discussed.
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ranking = 0.20420122917112
keywords = nervous system, nerve
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7/30. miller fisher syndrome: an uncommon acute neuropathy.

    The syndrome of ophthalmoplegia, ataxia, and areflexia was first described in 1956 by Miller Fisher. This syndrome has long been believed to be a variant of guillain-barre syndrome (GBS), mainly because of its areflexia, cerebrospinal fluid findings, and its postinfectious presentation. The case of an 11-year-old male with miller fisher syndrome (MFS) is described. MFS differs from GBS in several key clinical features and presents an extensive and challenging differential diagnosis. It is useful to recognize MFS as both a variant of GBS and a distinct entity with its own therapeutic considerations.
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ranking = 0.84310019332292
keywords = neuropathy
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8/30. guillain-barre syndrome: perspectives with infants and children.

    An acute flaccid paraparesis or ascending quadriparesis in an infant or child constitutes a very important pediatric neurology emergency. The guillain-barre syndrome (GBS) is the most frequent cause. This is primarily an autoimmune, post-infectious, demyelinating, peripheral nervous system process. A small percentage of children develop a primary axonal process not unlike that identified more commonly in china. Because of the potential for acute respiratory compromise, any child suspected of having GBS needs immediate hospitalization. The major considerations in differential diagnosis include transverse myelitis, toxic neuropathies, tick paralysis, infantile botulism, myasthenia gravis, and dermatomyositis. On occasion, some younger children present with an acute severe pain syndrome that may mask as a pseudo-encephalopathy. Another clinical variant is the Miller-Fisher syndrome characterized by ataxia, ophthalmoparesis, and areflexia. This is associated with a high frequency of the anti-GQ-1-b antibodies. Although most children with GBS have a relatively benign clinical course, some become very ill and require intubation with intensive care monitoring. Immunomodulating treatment should be used for any child who loses the ability to walk. To date, no well-controlled study has been completed analyzing the relative merits of the two most commonly used therapies, namely plasmapheresis or intravenously administered immunoglobulin.
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ranking = 20.714268737348
keywords = peripheral nervous system, peripheral, nervous system
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9/30. Features of sensory ataxic neuropathy associated with anti-GD1b IgM antibody.

    Some reports have called sensory ataxic neuropathy (SAN) associated with IgM antibody against b-series gangliosides a chronic form of miller fisher syndrome (MFS), but this has yet to be established. We examined five patients with SAN and eight patients with IgG anti-GQ1b-positive MFS. Only one patient with SAN complained of diplopia, whose ocular movement was not limited. The other four patients had neither diplopia nor limitation of ocular movement. All the SAN patients had severe deep sense impairment, whereas one patient with MFS showed only mild vibratory sense impairment. All sera from the SAN patients had remarkably high IgM antibody titers to the b-series gangliosides GD3, GD2, GD1b, GT1b, GQ1b, GQ1b alpha, fucosyl-GD1b, and alpha galactosyl [alpha fucosyl] GD1b. An absorption study confirmed that the anti-GQ1b antibodies cross-reacted with GD3, GD2, GD1b, and GT1b. In contrast, only two samples from the MFS patients had IgG antibody to GD3, and no sample reacted with GD2, GD1b, or GT1b. SAN has different clinical or serological features from MFS, and therefore is not a chronic form of it.
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ranking = 1.0538752416536
keywords = neuropathy
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10/30. Acute ophthalmoparesis (without ataxia) associated with anti-GQ1b IgG antibody: clinical features.

    OBJECTIVE: To examine the clinical features of acute ophthalmoparesis (AO) (without ataxia) associated with anti-GQ1b immunoglobulin g (IgG) antibody. DESIGN: Retrospective observational case series. PARTICIPANTS: Twenty-one subjects with AO (without ataxia) who had anti-GQ1b IgG. methods: Clinical features of 21 subjects with AO were analyzed. RESULTS: Seventeen had symptoms of antecedent infection. Gaze limitation was bilateral in 16 subjects and unilateral in five, indicative that laterality does not always negate AO. Nine subjects showed abducens paresis, and two limitation of abduction and adduction. Eight, who initially had bilateral abducens palsy, subsequently had impairment of adduction and vertical movement. These showed that bilateral abducens palsy followed by oculomotor nerve involvement is characteristic of AO. Muscle stretch reflexes were normal in nine subjects, hypoactive in eight, absent in three, and brisk in one. Distal paresthesias were present in seven subjects. Acellular cerebrospinal fluid (CSF) associated with raised protein concentration was detected in three. CONCLUSIONS: Antecedent infectious symptoms, characteristic limitation of ocular movement, areflexia, distal paresthesias, and CSF albuminocytologic dissociation are useful markers for diagnosing AO as well as anti-GQ1b IgG. AO can be considered a mild form of miller fisher syndrome or a regional variant of guillain-barre syndrome.
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ranking = 0.050736908765268
keywords = nerve
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