Rigidity decreases resting tremor intensity in Parkinson's disease: A [123I]β‐CIT SPECT study in early, nonmedicated patients
Identifieur interne : 000944 ( Istex/Curation ); précédent : 000943; suivant : 000945Rigidity decreases resting tremor intensity in Parkinson's disease: A [123I]β‐CIT SPECT study in early, nonmedicated patients
Auteurs : Ania Winogrodzka [Pays-Bas] ; Robert C. Wagenaar [Pays-Bas] ; Paul Bergmans [Pays-Bas] ; Astrid Vellinga [Pays-Bas] ; Jan Booij [Pays-Bas] ; Eric A. Van Royen [Pays-Bas] ; Richard E. A. Van Emmerik [États-Unis] ; Johannes C. Stoof [Pays-Bas] ; Erik Ch. Wolters [Pays-Bas]Source :
- Movement Disorders [ 0885-3185 ] ; 2001-11.
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Abstract
Tremor is one of the clinical hallmarks of Parkinson's disease (PD). Although it is accepted that other classic symptoms of PD such as rigidity and bradykinesia result from a degeneration of the nigrostriatal system and subsequent reduction in striatal dopamine, the pathophysiology of resting tremor remains unclear. The majority of recent single photon emission computed tomography (SPECT) and positron emission tomography (PET) studies, using various radioligands, demonstrated significant correlation between striatal radioligand bindings and the degree of parkinsonian symptoms such as rigidity and bradykinesia, but not tremor. We investigate the relationship between the degeneration of the nigrostriatal pathway and the appearance of resting tremor, taking into account the possible interference of rigidity with the resting tremor. Thirty early and drug‐naïve PD patients were examined. Tremor and rigidity of the arms were assessed using UPDRS, and the power of tremor was estimated using spectral analysis of tremor peaks. [123I]β‐CIT SPECT was used to assess degeneration of the dopaminergic system in PD patients. A comparison between asymmetry indices showed that in terms of both tremor and rigidity, the most affected arm corresponded significantly with the contralateral striatum, having the largest reduction in radioligand binding. Furthermore, tremor power accounted for a significant part of variance in the contralateral striatum, suggesting a relationship between this PD symptom and the degeneration of the dopaminergic system. Further, the degree of tremor was reduced with increasing rigidity. However, correcting for the influence of rigidity, the significant contribution of tremor in the variance in the contralateral striatal [123I]β‐CIT binding disappeared. When the confounding influence of rigidity is taken into account, no significant direct relationship between dopaminergic degeneration and the degree of tremor could be found. Other pathophysiological mechanisms should be similarly investigated in order to further our understanding of the origin of resting tremor in PD. © 2001 Movement Disorder Society.
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DOI: 10.1002/mds.1205
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Wagenaar</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology, University Hospital Vrije Universiteit, Amsterdam, The Netherlands</mods:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, University Hospital Vrije Universiteit, Amsterdam</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Department of Physical Therapy, University Hospital Vrije Universiteit, Amsterdam, The Netherlands</mods:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Physical Therapy, University Hospital Vrije Universiteit, Amsterdam</wicri:regionArea></affiliation></author><author><name sortKey="Bergmans, Paul" sort="Bergmans, Paul" uniqKey="Bergmans P" first="Paul" last="Bergmans">Paul Bergmans</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology, University Hospital Vrije Universiteit, Amsterdam, The Netherlands</mods:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, University Hospital Vrije Universiteit, Amsterdam</wicri:regionArea></affiliation></author><author><name sortKey="Vellinga, Astrid" sort="Vellinga, Astrid" uniqKey="Vellinga A" first="Astrid" last="Vellinga">Astrid Vellinga</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology, University Hospital Vrije Universiteit, Amsterdam, The Netherlands</mods:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, University Hospital Vrije Universiteit, Amsterdam</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Department of Physical Therapy, University Hospital Vrije Universiteit, Amsterdam, The Netherlands</mods:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Physical Therapy, University Hospital Vrije Universiteit, Amsterdam</wicri:regionArea></affiliation></author><author><name sortKey="Booij, Jan" sort="Booij, Jan" uniqKey="Booij J" first="Jan" last="Booij">Jan Booij</name><affiliation wicri:level="1"><mods:affiliation>Department of Nuclear Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands</mods:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Nuclear Medicine, Academic Medical Center, University of Amsterdam, Amsterdam</wicri:regionArea></affiliation></author><author><name sortKey="Van Royen, Eric A" sort="Van Royen, Eric A" uniqKey="Van Royen E" first="Eric A." last="Van Royen">Eric A. Van Royen</name><affiliation wicri:level="1"><mods:affiliation>Department of Nuclear Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands</mods:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Nuclear Medicine, Academic Medical Center, University of Amsterdam, Amsterdam</wicri:regionArea></affiliation></author><author><name sortKey="Van Emmerik, Richard E A" sort="Van Emmerik, Richard E A" uniqKey="Van Emmerik R" first="Richard E. A." last="Van Emmerik">Richard E. A. Van Emmerik</name><affiliation wicri:level="1"><mods:affiliation>Department of Exercise Sciences, University of Massachusetts, Amherst, Massachusetts, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Exercise Sciences, University of Massachusetts, Amherst, Massachusetts</wicri:regionArea></affiliation></author><author><name sortKey="Stoof, Johannes C" sort="Stoof, Johannes C" uniqKey="Stoof J" first="Johannes C." last="Stoof">Johannes C. Stoof</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology, University Hospital Vrije Universiteit, Amsterdam, The Netherlands</mods:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, University Hospital Vrije Universiteit, Amsterdam</wicri:regionArea></affiliation></author><author><name sortKey="Wolters, Erik Ch" sort="Wolters, Erik Ch" uniqKey="Wolters E" first="Erik Ch." last="Wolters">Erik Ch. Wolters</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology, University Hospital Vrije Universiteit, Amsterdam, The Netherlands</mods:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, University Hospital Vrije Universiteit, Amsterdam</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-11">2001-11</date><biblScope unit="vol">16</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1033">1033</biblScope><biblScope unit="page" to="1040">1040</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">F13D0A856F0A7BCA11D6767BCFC19D4C8490D9B8</idno><idno type="DOI">10.1002/mds.1205</idno><idno type="ArticleID">MDS1205</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>SPECT</term><term>resting tremor</term><term>rigidity</term><term>spectral analysis</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Tremor is one of the clinical hallmarks of Parkinson's disease (PD). Although it is accepted that other classic symptoms of PD such as rigidity and bradykinesia result from a degeneration of the nigrostriatal system and subsequent reduction in striatal dopamine, the pathophysiology of resting tremor remains unclear. The majority of recent single photon emission computed tomography (SPECT) and positron emission tomography (PET) studies, using various radioligands, demonstrated significant correlation between striatal radioligand bindings and the degree of parkinsonian symptoms such as rigidity and bradykinesia, but not tremor. We investigate the relationship between the degeneration of the nigrostriatal pathway and the appearance of resting tremor, taking into account the possible interference of rigidity with the resting tremor. Thirty early and drug‐naïve PD patients were examined. Tremor and rigidity of the arms were assessed using UPDRS, and the power of tremor was estimated using spectral analysis of tremor peaks. [123I]β‐CIT SPECT was used to assess degeneration of the dopaminergic system in PD patients. A comparison between asymmetry indices showed that in terms of both tremor and rigidity, the most affected arm corresponded significantly with the contralateral striatum, having the largest reduction in radioligand binding. Furthermore, tremor power accounted for a significant part of variance in the contralateral striatum, suggesting a relationship between this PD symptom and the degeneration of the dopaminergic system. Further, the degree of tremor was reduced with increasing rigidity. However, correcting for the influence of rigidity, the significant contribution of tremor in the variance in the contralateral striatal [123I]β‐CIT binding disappeared. When the confounding influence of rigidity is taken into account, no significant direct relationship between dopaminergic degeneration and the degree of tremor could be found. Other pathophysiological mechanisms should be similarly investigated in order to further our understanding of the origin of resting tremor in PD. © 2001 Movement Disorder Society.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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