OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE
Identifieur interne : 002428 ( Istex/Corpus ); précédent : 002427; suivant : 002429OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE
Auteurs : Owen B. White ; Jean A. Saint-Cyr ; James A. SharpeSource :
- Brain [ 0006-8950 ] ; 1983-09.
Abstract
Horizontal vestibulo-ocular reflex (VOR) function was quantified in 14 parkinsonian patients and compared with that of 10 age-matched normals. Eight patients had mild and 6 had advanced rigidity and akinesia. In advanced disease VOR gains were subnormal in darkness during sinusoidal whole-body rotation at frequencies from 0.3 to 3.0 Hz. When fixating a stationary target, patients enhanced VOR gains to near unity, but gains of patients with advanced disease were significantly lower than controls. Visual suppression of the VOR by fixating a target moving with the head was defective in all stages of the disease. Advanced patients also exhibited defective voluntary control of the reflex in darkness: both voluntary enhancement, by imagining a stationary target, and voluntary suppression, by imagining a target moving with the head, were abnormal. This disordered voluntary control of the VOR was independent of defective visually mediated smooth pursuit. Attempted visual and voluntary suppression of the reflex produced a rise in VOR gain, above the hypoactive values recorded in darkness in advanced disease. This inappropriate activation of the VOR implied structural integrity of brainstem smooth eye movement pathways, despite vestibulo-ocular hyporeflexia. Unrecognized degeneration in brainstem VOR circuits, or defective cerebral hemisphere control of the reflex caused by the nigrostriatal or cerebral cortical dysfunction of Parkinson's disease, may explain subnormal ocular responses to passive head motion. We attribute the abnormal visual and voluntary modulation of smooth eye movements to disordered long-loop cerebral control of the VOR and suggest that it is analogous to the defective long-loop cerebral regulation of spinal reflexes that occurs in Parkinson's disease.
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DOI: 10.1093/brain/106.3.555
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE</title><author><name sortKey="White, Owen B" sort="White, Owen B" uniqKey="White O" first="Owen B." last="White">Owen B. White</name><affiliation><mods:affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</mods:affiliation></affiliation></author><author><name sortKey="Saint Cyr, Jean A" sort="Saint Cyr, Jean A" uniqKey="Saint Cyr J" first="Jean A." last="Saint-Cyr">Jean A. Saint-Cyr</name><affiliation><mods:affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</mods:affiliation></affiliation></author><author><name sortKey="Sharpe, James A" sort="Sharpe, James A" uniqKey="Sharpe J" first="James A." last="Sharpe">James A. Sharpe</name><affiliation><mods:affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:BC1823C9E8EA86FB804007104B5F038BBEE036E4</idno><date when="1983" year="1983">1983</date><idno type="doi">10.1093/brain/106.3.555</idno><idno type="url">https://api-v5.istex.fr/document/BC1823C9E8EA86FB804007104B5F038BBEE036E4/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">002428</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002428</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE</title><author><name sortKey="White, Owen B" sort="White, Owen B" uniqKey="White O" first="Owen B." last="White">Owen B. White</name><affiliation><mods:affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</mods:affiliation></affiliation></author><author><name sortKey="Saint Cyr, Jean A" sort="Saint Cyr, Jean A" uniqKey="Saint Cyr J" first="Jean A." last="Saint-Cyr">Jean A. Saint-Cyr</name><affiliation><mods:affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</mods:affiliation></affiliation></author><author><name sortKey="Sharpe, James A" sort="Sharpe, James A" uniqKey="Sharpe J" first="James A." last="Sharpe">James A. Sharpe</name><affiliation><mods:affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1983-09">1983-09</date><biblScope unit="volume">106</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="555">555</biblScope><biblScope unit="page" to="570">570</biblScope></imprint><idno type="ISSN">0006-8950</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Horizontal vestibulo-ocular reflex (VOR) function was quantified in 14 parkinsonian patients and compared with that of 10 age-matched normals. Eight patients had mild and 6 had advanced rigidity and akinesia. In advanced disease VOR gains were subnormal in darkness during sinusoidal whole-body rotation at frequencies from 0.3 to 3.0 Hz. When fixating a stationary target, patients enhanced VOR gains to near unity, but gains of patients with advanced disease were significantly lower than controls. Visual suppression of the VOR by fixating a target moving with the head was defective in all stages of the disease. Advanced patients also exhibited defective voluntary control of the reflex in darkness: both voluntary enhancement, by imagining a stationary target, and voluntary suppression, by imagining a target moving with the head, were abnormal. This disordered voluntary control of the VOR was independent of defective visually mediated smooth pursuit. Attempted visual and voluntary suppression of the reflex produced a rise in VOR gain, above the hypoactive values recorded in darkness in advanced disease. This inappropriate activation of the VOR implied structural integrity of brainstem smooth eye movement pathways, despite vestibulo-ocular hyporeflexia. Unrecognized degeneration in brainstem VOR circuits, or defective cerebral hemisphere control of the reflex caused by the nigrostriatal or cerebral cortical dysfunction of Parkinson's disease, may explain subnormal ocular responses to passive head motion. We attribute the abnormal visual and voluntary modulation of smooth eye movements to disordered long-loop cerebral control of the VOR and suggest that it is analogous to the defective long-loop cerebral regulation of spinal reflexes that occurs in Parkinson's disease.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>OWEN B. WHITE</name><affiliations><json:string>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</json:string></affiliations></json:item><json:item><name>JEAN A. SAINT-CYR</name><affiliations><json:string>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</json:string></affiliations></json:item><json:item><name>JAMES A. SHARPE</name><affiliations><json:string>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</json:string></affiliations></json:item></author><subject><json:item><value>Articles</value></json:item></subject><articleId><json:string>106.3.555</json:string></articleId><language><json:string>unknown</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>Horizontal vestibulo-ocular reflex (VOR) function was quantified in 14 parkinsonian patients and compared with that of 10 age-matched normals. Eight patients had mild and 6 had advanced rigidity and akinesia. In advanced disease VOR gains were subnormal in darkness during sinusoidal whole-body rotation at frequencies from 0.3 to 3.0 Hz. When fixating a stationary target, patients enhanced VOR gains to near unity, but gains of patients with advanced disease were significantly lower than controls. Visual suppression of the VOR by fixating a target moving with the head was defective in all stages of the disease. Advanced patients also exhibited defective voluntary control of the reflex in darkness: both voluntary enhancement, by imagining a stationary target, and voluntary suppression, by imagining a target moving with the head, were abnormal. This disordered voluntary control of the VOR was independent of defective visually mediated smooth pursuit. Attempted visual and voluntary suppression of the reflex produced a rise in VOR gain, above the hypoactive values recorded in darkness in advanced disease. This inappropriate activation of the VOR implied structural integrity of brainstem smooth eye movement pathways, despite vestibulo-ocular hyporeflexia. Unrecognized degeneration in brainstem VOR circuits, or defective cerebral hemisphere control of the reflex caused by the nigrostriatal or cerebral cortical dysfunction of Parkinson's disease, may explain subnormal ocular responses to passive head motion. We attribute the abnormal visual and voluntary modulation of smooth eye movements to disordered long-loop cerebral control of the VOR and suggest that it is analogous to the defective long-loop cerebral regulation of spinal reflexes that occurs in Parkinson's disease.</abstract><qualityIndicators><score>10</score><pdfWordCount>5435</pdfWordCount><pdfCharCount>34239</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>16</pdfPageCount><pdfPageSize>492 x 701 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractWordCount>259</abstractWordCount><abstractCharCount>1793</abstractCharCount><keywordCount>1</keywordCount></qualityIndicators><title>OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE</title><genre><json:string>research-article</json:string></genre><host><title>Brain</title><language><json:string>unknown</json:string></language><issn><json:string>0006-8950</json:string></issn><eissn><json:string>1460-2156</json:string></eissn><publisherId><json:string>brainj</json:string></publisherId><volume>106</volume><issue>3</issue><pages><first>555</first><last>570</last></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>neurosciences</json:string><json:string>clinical neurology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix></categories><publicationDate>1983</publicationDate><copyrightDate>1983</copyrightDate><doi><json:string>10.1093/brain/106.3.555</json:string></doi><id>BC1823C9E8EA86FB804007104B5F038BBEE036E4</id><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/BC1823C9E8EA86FB804007104B5F038BBEE036E4/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api-v5.istex.fr/document/BC1823C9E8EA86FB804007104B5F038BBEE036E4/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api-v5.istex.fr/document/BC1823C9E8EA86FB804007104B5F038BBEE036E4/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE</title><title level="a" type="sub">I. THE HORIZONTAL VESTIBULO-OCULAR REFLEX AND ITS REGULATION</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>© Oxford University Press</p></availability><date>1983</date></publicationStmt><notesStmt><note>Reprint requests to Dr J. A. Sharpe, Toronto Western Hospital, 399 Bathurst St., Toronto, Ontario M5T 2S8, Canada.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE</title><title level="a" type="sub">I. THE HORIZONTAL VESTIBULO-OCULAR REFLEX AND ITS REGULATION</title><author xml:id="author-0000"><persName><forename type="first">OWEN B.</forename><surname>WHITE</surname></persName><affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</affiliation></author><author xml:id="author-0001"><persName><forename type="first">JEAN A.</forename><surname>SAINT-CYR</surname></persName><affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</affiliation></author><author xml:id="author-0002"><persName><forename type="first">JAMES A.</forename><surname>SHARPE</surname></persName><affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</affiliation></author><idno type="istex">BC1823C9E8EA86FB804007104B5F038BBEE036E4</idno><idno type="DOI">10.1093/brain/106.3.555</idno><idno type="ArticleID">106.3.555</idno></analytic><monogr><title level="j">Brain</title><idno type="pISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><idno type="PublisherID">brainj</idno><idno type="PublisherID-hwp">brain</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1983-09"></date><biblScope unit="volume">106</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="555">555</biblScope><biblScope unit="page" to="570">570</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1983</date></creation><abstract><p>Horizontal vestibulo-ocular reflex (VOR) function was quantified in 14 parkinsonian patients and compared with that of 10 age-matched normals. Eight patients had mild and 6 had advanced rigidity and akinesia. In advanced disease VOR gains were subnormal in darkness during sinusoidal whole-body rotation at frequencies from 0.3 to 3.0 Hz. When fixating a stationary target, patients enhanced VOR gains to near unity, but gains of patients with advanced disease were significantly lower than controls. Visual suppression of the VOR by fixating a target moving with the head was defective in all stages of the disease. Advanced patients also exhibited defective voluntary control of the reflex in darkness: both voluntary enhancement, by imagining a stationary target, and voluntary suppression, by imagining a target moving with the head, were abnormal. This disordered voluntary control of the VOR was independent of defective visually mediated smooth pursuit. Attempted visual and voluntary suppression of the reflex produced a rise in VOR gain, above the hypoactive values recorded in darkness in advanced disease. This inappropriate activation of the VOR implied structural integrity of brainstem smooth eye movement pathways, despite vestibulo-ocular hyporeflexia. Unrecognized degeneration in brainstem VOR circuits, or defective cerebral hemisphere control of the reflex caused by the nigrostriatal or cerebral cortical dysfunction of Parkinson's disease, may explain subnormal ocular responses to passive head motion. We attribute the abnormal visual and voluntary modulation of smooth eye movements to disordered long-loop cerebral control of the VOR and suggest that it is analogous to the defective long-loop cerebral regulation of spinal reflexes that occurs in Parkinson's disease.</p></abstract><textClass><keywords scheme="keyword"><list><item><term>Articles</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1983-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/BC1823C9E8EA86FB804007104B5F038BBEE036E4/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">brain</journal-id><journal-id journal-id-type="publisher-id">brainj</journal-id><journal-id journal-id-type="pmc">brain</journal-id><journal-title>Brain</journal-title><issn pub-type="epub">1460-2156</issn><issn pub-type="ppub">0006-8950</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">106.3.555</article-id><article-id pub-id-type="doi">10.1093/brain/106.3.555</article-id><article-categories><subj-group><subject>Articles</subject></subj-group></article-categories><title-group><article-title>OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE</article-title><subtitle>I. THE HORIZONTAL VESTIBULO-OCULAR REFLEX AND ITS REGULATION</subtitle></title-group><contrib-group><contrib contrib-type="author"><name><surname>WHITE</surname><given-names>OWEN B.</given-names></name></contrib><contrib contrib-type="author"><name><surname>SAINT-CYR</surname><given-names>JEAN A.</given-names></name></contrib><contrib contrib-type="author"><name><surname>SHARPE</surname><given-names>JAMES A.</given-names></name></contrib><aff><institution>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital</institution> <addr-line>399 Bathurst Street, Toronto M5T 2S8</addr-line> <institution>Departments of Medicine, Ophthalmology and Anatomy, University of Toronto</institution> <addr-line>Canada</addr-line></aff></contrib-group><author-notes><corresp>Reprint requests to Dr J. A. Sharpe, Toronto Western Hospital, 399 Bathurst St., Toronto, Ontario M5T 2S8, Canada.</corresp></author-notes><pub-date pub-type="ppub"><month>9</month><year>1983</year></pub-date><volume>106</volume><issue>3</issue><fpage>555</fpage><lpage>570</lpage><history><date date-type="received"><day>07</day><month>7</month><year>1982</year></date><date date-type="rev-recd"><day>23</day><month>11</month><year>1982</year></date></history><copyright-statement>© Oxford University Press</copyright-statement><copyright-year>1983</copyright-year><abstract><p>Horizontal vestibulo-ocular reflex (VOR) function was quantified in 14 parkinsonian patients and compared with that of 10 age-matched normals. Eight patients had mild and 6 had advanced rigidity and akinesia. In advanced disease VOR gains were subnormal in darkness during sinusoidal whole-body rotation at frequencies from 0.3 to 3.0 Hz. When fixating a stationary target, patients enhanced VOR gains to near unity, but gains of patients with advanced disease were significantly lower than controls. Visual suppression of the VOR by fixating a target moving with the head was defective in all stages of the disease. Advanced patients also exhibited defective voluntary control of the reflex in darkness: both voluntary enhancement, by imagining a stationary target, and voluntary suppression, by imagining a target moving with the head, were abnormal. This disordered voluntary control of the VOR was independent of defective visually mediated smooth pursuit.</p><p>Attempted visual and voluntary suppression of the reflex produced a rise in VOR gain, above the hypoactive values recorded in darkness in advanced disease. This inappropriate activation of the VOR implied structural integrity of brainstem smooth eye movement pathways, despite vestibulo-ocular hyporeflexia. Unrecognized degeneration in brainstem VOR circuits, or defective cerebral hemisphere control of the reflex caused by the nigrostriatal or cerebral cortical dysfunction of Parkinson's disease, may explain subnormal ocular responses to passive head motion. We attribute the abnormal visual and voluntary modulation of smooth eye movements to disordered long-loop cerebral control of the VOR and suggest that it is analogous to the defective long-loop cerebral regulation of spinal reflexes that occurs in Parkinson's disease.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE</title><subTitle>I. THE HORIZONTAL VESTIBULO-OCULAR REFLEX AND ITS REGULATION</subTitle></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE</title><subTitle>I. THE HORIZONTAL VESTIBULO-OCULAR REFLEX AND ITS REGULATION</subTitle></titleInfo><name type="personal"><namePart type="given">OWEN B.</namePart><namePart type="family">WHITE</namePart><affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JEAN A.</namePart><namePart type="family">SAINT-CYR</namePart><affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JAMES A.</namePart><namePart type="family">SHARPE</namePart><affiliation>From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital, 399 Bathurst Street, Toronto M5T 2S8, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>Articles</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">1983-09</dateIssued><copyrightDate encoding="w3cdtf">1983</copyrightDate></originInfo><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Horizontal vestibulo-ocular reflex (VOR) function was quantified in 14 parkinsonian patients and compared with that of 10 age-matched normals. Eight patients had mild and 6 had advanced rigidity and akinesia. In advanced disease VOR gains were subnormal in darkness during sinusoidal whole-body rotation at frequencies from 0.3 to 3.0 Hz. When fixating a stationary target, patients enhanced VOR gains to near unity, but gains of patients with advanced disease were significantly lower than controls. Visual suppression of the VOR by fixating a target moving with the head was defective in all stages of the disease. Advanced patients also exhibited defective voluntary control of the reflex in darkness: both voluntary enhancement, by imagining a stationary target, and voluntary suppression, by imagining a target moving with the head, were abnormal. This disordered voluntary control of the VOR was independent of defective visually mediated smooth pursuit. Attempted visual and voluntary suppression of the reflex produced a rise in VOR gain, above the hypoactive values recorded in darkness in advanced disease. This inappropriate activation of the VOR implied structural integrity of brainstem smooth eye movement pathways, despite vestibulo-ocular hyporeflexia. Unrecognized degeneration in brainstem VOR circuits, or defective cerebral hemisphere control of the reflex caused by the nigrostriatal or cerebral cortical dysfunction of Parkinson's disease, may explain subnormal ocular responses to passive head motion. We attribute the abnormal visual and voluntary modulation of smooth eye movements to disordered long-loop cerebral control of the VOR and suggest that it is analogous to the defective long-loop cerebral regulation of spinal reflexes that occurs in Parkinson's disease.</abstract><note type="author-notes">Reprint requests to Dr J. A. 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