ophthalmoplegia/hnačka

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Role of anti-GQ1B antibody in differential diagnosis of acute ophthalmoparesis.

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Miller Fisher syndrome (MFS) is a triad of total external ophthalmoplegia, ataxia, and areflexia, while botulism has the usual clinical presentation of involvement of cranial muscles and palsies with blurred vision, diplopia, ptosis, dilated pupils, and facial paralysis, caused by a bacterial

Ataxia, ophthalmoplegia, and impairment of consciousness in a 19-month-old American boy.

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A 19-month-old, white, Pennsylvanian boy, with an unremarkable medical history, presented to our hospital with a 3-week history of nonbloody, nonbilious emesis up to 5 times a day and nonbloody diarrhea. Ten days before admission, his gait became progressively unsteady, until he finally refused to

[Internal ophthalmoplegia in acute oropharyngeal palsy with anti-GQ1b and anti-GT1a IgG antibodies].

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A patient with acute oropharyngeal palsy associated with internal ophthalmoplegia was reported. A 13-year-old boy had fever and diarrhea for two days. Ten days after resolution of these symptoms, he noticed difficulty in speaking (day 1). Neurological findings on day 4 included bilateral mydriasis,

Ophthalmoplegia, demyelinating neuropathy, leukoencephalopathy, myopathy, and gastrointestinal dysfunction with multiple deletions of mitochondrial DNA: a mitochondrial multisystem disorder in search of a name.

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This article describes a 37-year-old woman with progressive external ophthalmoplegia, peripheral neuropathy, and chronic intractable diarrhea. Laboratory studies disclosed lactic acidosis, ragged red fibers lacking cytochrome c oxidase, high-normal muscular mitochondrial enzymes, demyelinating

Mitochondrial neurogastrointestinal encephalomyopathy: an autosomal recessive disorder due to thymidine phosphorylase mutations.

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Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is an autosomal recessive disorder defined clinically by severe gastrointestinal dysmotility; cachexia; ptosis, ophthalmoparesis, or both; peripheral neuropathy; leukoencephalopathy; and mitochondrial abnormalities. The disease is caused

[Fisher's syndrome following Campylobacter jejuni enteritis--a case report and review of the literature].

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A 13-year-old boy presented with ophthalmoplegia, cerebella ataxia and areflexia subsequent to watery diarrhea and pyrexia. Campylobacter jejuni (PEN 2: LIO 4) was isolated from the stools. The patient had a high titer of IgG anti-GQ1b IgG antibody titers which decreased during the clinical course.

[A case of multiple cranial neuropathy after Campylobacter jejuni infection].

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We report a patient who developed overlapping symptoms of ophthalmoplegia and oropharyngeal palsy after Campylobacter jejuni infection. A 15-year-old man had diarrhea and fever, and developed dysarthria, diplopia and ptosis two weeks later. He did not show ataxia, weakness or abnormal tendon

Antecedent symptoms in Guillain-Barré syndrome: an important indicator for clinical and serological subgroups.

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OBJECTIVE To examine whether Guillain-Barré syndrome (GBS) can be classified in clinical and immunological subgroups based on the type of prior illness. Background - The existence of antecedent symptoms supports the diagnosis of GBS in patients who experience acute muscle weakness progression.

[Intestinal pseudoobstructions and gastric necrosis in mitochondrial myopathy].

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METHODS A 24-year-old female patient suffered for 4 months from recurrent abdominal pain, vomiting and diarrhea. Signs of an acute abdomen were the initial reason for admitting the patient to our hospital. The slim, pale patient had a complete bloated abdomen. Neurological status was

[A case of atypical Miller Fisher syndrome associated with antiphospholipid antibodies].

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We report a 56-year-old man with external ophthalmoplegia and ataxic gait following a diarrhea, being diagnosed atypical Miller Fisher syndrome (FS). On admission, he had severe diplopia and bilateral external ophthalmoplegia were observed. The deep tendon reflexes were decreased on the right upper

[Immunoadsorption therapy with TR-350 (tryptophan column) for Guillain-Barré syndrome: investigation including serum antiganglioside antibody assay].

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Immunoadsorption therapy (IAT) using TR-350 was performed for 14 patients with Guillain-Barré syndrome (GBS). Presence of serum antiganglioside antibodies (AGA) was investigated in all the patients in the acute phase. In 14 patients studied, 6 men and 8 women, ages from 24 to 74 years(mean, 42.5

Mitochondrial neurogastrointestinal encephalomyopathy.

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Mitochondrial neurogastrointestinal encephalomyopathy is an autosomal recessive disorder in which a nuclear mutation of the thymidine phosphorylase gene leads to mitochondrial genomic dysfunction. Herein, we report a 29-year-old Iranian man with abdominal pain, diarrhea, hearing loss,

Relationships between anti-ganglioside antibodies and clinical characteristics of Guillain-Barré syndrome.

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We studied relationships between anti-ganglioside antibodies and the clinical characteristics of Guillain-Barré syndrome (GBS) using multivariate analysis. Serum anti-ganglioside antibodies were measured by enzyme-linked immunosorbent assay (ELISA) in 42 GBS patients and 47 controls. Relationships

Atypical Descending Paralysis in Miller Fisher Syndrome: A Rare Variant of Guillain-Barre Syndrome.

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Miller Fisher syndrome (MFS) is a rare variant of Guillain-Barre syndrome (GBS) which usually presents with descending paralysis. Common symptoms are ophthalmoplegia, ataxia, and areflexia. Our case presented with an atypical presentation. A 52-year old lady presented to the neurology outpatient

[Acute peritonitis and small bowel diverticula in a patient with mitochondrial neurogastrointestinal encephalomyopathy].

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BACKGROUND Jejunal and ileal diverticula are acquired lesions that are often associated with intestinal motility disturbances like those occurring in myopathies and neuropathies with visceral affection. Mitochondrial neurogastrointestinal encephalomyopathy is characterized by gastrointestinal

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