Ophthalmology · 2001
Acute ophthalmoparesis (without ataxia) associated with anti-GQ1b IgG antibody: clinical features.
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Yuki N, Odaka M, Hirata K
Аннотация
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-Barré syndrome.
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-Barré syndrome.