Torticollis due to disinhibition of the vestibulo‐collic reflex in a patient with Steele‐Richardson‐Olszewski syndrome
Identifieur interne : 002880 ( Istex/Corpus ); précédent : 002879; suivant : 002881Torticollis due to disinhibition of the vestibulo‐collic reflex in a patient with Steele‐Richardson‐Olszewski syndrome
Auteurs : Bisdorff ; Bronstein ; C. Wolsley ; A. J. LeesSource :
- Movement Disorders [ 0885-3185 ] ; 1997-05.
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- KwdEn :
Abstract
A patient with the clinical picture of Steele‐Richardson‐Olszewski syndrome and an unusual intermittent neck twisting is reported. He had virtually no voluntary ocular movements and only very slow, low‐amplitude voluntary head movements. However, in response to optokinetic or vestibular stimulation, he developed full eye deviations in the direction of the slow phase of the expected nystagmus. No quick phases were observed, and the deviation outlasted the duration of the vestibular stimuli because of defective saccades. The head also turned fully during these stimuli, quicker than on attempted voluntary movements, and remained derivated similarly to the eyes. This suggests that the neck deviations in this patient were due to a disinhibited vestibulo‐collic reflex and a disturbed head position resetting mechanism. Neck electromyographic responses in response to whole‐body rotation indicated that the vestibulocollic reflex responsible for the torticollis in this patient had a short latency of ∼ 30 ms.
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DOI: 10.1002/mds.870120311
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He had virtually no voluntary ocular movements and only very slow, low‐amplitude voluntary head movements. However, in response to optokinetic or vestibular stimulation, he developed full eye deviations in the direction of the slow phase of the expected nystagmus. No quick phases were observed, and the deviation outlasted the duration of the vestibular stimuli because of defective saccades. The head also turned fully during these stimuli, quicker than on attempted voluntary movements, and remained derivated similarly to the eyes. This suggests that the neck deviations in this patient were due to a disinhibited vestibulo‐collic reflex and a disturbed head position resetting mechanism. Neck electromyographic responses in response to whole‐body rotation indicated that the vestibulocollic reflex responsible for the torticollis in this patient had a short latency of ∼ 30 ms.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Bisdorff</name><affiliations><json:string>MRC Human Movement and Balance Unit, Section of Neuro‐Otology, Institute of Neurology, London, England</json:string><json:string>Current Address: Hopital de la Ville, Esch/Alzette, Luxembourg</json:string></affiliations></json:item><json:item><name>Dr. Bronstein</name><affiliations><json:string>MRC Human Movement and Balance Unit, Section of Neuro‐Otology, Institute of Neurology, London, England</json:string></affiliations></json:item><json:item><name>C. Wolsley</name><affiliations><json:string>MRC Human Movement and Balance Unit, Section of Neuro‐Otology, Institute of Neurology, London, England</json:string></affiliations></json:item><json:item><name>A. J. Lees</name><affiliations><json:string>National Hospital for Neurology and Neurosurgery, London, England</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Vestibular reflexes</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Torticollis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Movement disorders</value></json:item></subject><language><json:string>eng</json:string></language><abstract>A patient with the clinical picture of Steele‐Richardson‐Olszewski syndrome and an unusual intermittent neck twisting is reported. He had virtually no voluntary ocular movements and only very slow, low‐amplitude voluntary head movements. However, in response to optokinetic or vestibular stimulation, he developed full eye deviations in the direction of the slow phase of the expected nystagmus. No quick phases were observed, and the deviation outlasted the duration of the vestibular stimuli because of defective saccades. The head also turned fully during these stimuli, quicker than on attempted voluntary movements, and remained derivated similarly to the eyes. This suggests that the neck deviations in this patient were due to a disinhibited vestibulo‐collic reflex and a disturbed head position resetting mechanism. 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Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1997-05"></date><biblScope unit="vol">12</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="328">328</biblScope><biblScope unit="page" to="336">336</biblScope></imprint></monogr><idno type="istex">C1BAAD65DE6BCE2B1C1A4133D42446FBAC8CECC2</idno><idno type="DOI">10.1002/mds.870120311</idno><idno type="ArticleID">MDS870120311</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>A patient with the clinical picture of Steele‐Richardson‐Olszewski syndrome and an unusual intermittent neck twisting is reported. He had virtually no voluntary ocular movements and only very slow, low‐amplitude voluntary head movements. However, in response to optokinetic or vestibular stimulation, he developed full eye deviations in the direction of the slow phase of the expected nystagmus. No quick phases were observed, and the deviation outlasted the duration of the vestibular stimuli because of defective saccades. The head also turned fully during these stimuli, quicker than on attempted voluntary movements, and remained derivated similarly to the eyes. This suggests that the neck deviations in this patient were due to a disinhibited vestibulo‐collic reflex and a disturbed head position resetting mechanism. 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He had virtually no voluntary ocular movements and only very slow, low‐amplitude voluntary head movements. However, in response to optokinetic or vestibular stimulation, he developed full eye deviations in the direction of the slow phase of the expected nystagmus. No quick phases were observed, and the deviation outlasted the duration of the vestibular stimuli because of defective saccades. The head also turned fully during these stimuli, quicker than on attempted voluntary movements, and remained derivated similarly to the eyes. This suggests that the neck deviations in this patient were due to a disinhibited vestibulo‐collic reflex and a disturbed head position resetting mechanism. Neck electromyographic responses in response to whole‐body rotation indicated that the vestibulocollic reflex responsible for the torticollis in this patient had a short latency of ∼ 30 ms.</abstract><note type="content">*A videotape accompanies this article.</note><subject lang="en"><genre>Keywords</genre><topic>Vestibular reflexes</topic><topic>Torticollis</topic><topic>Movement disorders</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. 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