Distinguishing SWEDDs patients with asymmetric resting tremor from Parkinson's disease: A clinical and electrophysiological study
Identifieur interne : 000A39 ( Istex/Corpus ); précédent : 000A38; suivant : 000A40Distinguishing SWEDDs patients with asymmetric resting tremor from Parkinson's disease: A clinical and electrophysiological study
Auteurs : Petra Schwingenschuh ; Diane Ruge ; Mark Edwards ; Carmen Terranova ; Petra Katschnig ; Fatima Carrillo ; Laura Silveira ; Susanne. Schneider ; Georg K ; Francisco. Palomar ; Penelope Talelli ; John Dickson ; Andrew Lees ; Niall Quinn ; Pablo Mir ; John Rothwell ; Kailash BhatiaSource :
- Movement Disorders [ 0885-3185 ] ; 2010-04-15.
English descriptors
- KwdEn :
Abstract
Approximately 10% of patients diagnosed clinically with early Parkinson's disease (PD) have normal dopaminergic functional imaging (Scans Without Evidence of Dopaminergic Deficit [SWEDDs]). An important subgroup of SWEDDs are those with asymmetric rest tremor resembling parkinsonian tremor. Clinical and pathophysiological features which could help to distinguish SWEDDs from PD have not been explored. We therefore studied clinical details including non‐motor symptoms in 25 tremulous SWEDDs patients in comparison to 25 tremor‐dominant PD patients. Blinded video rating was used to compare examination findings. Electrophysiological tremor parameters and also response to a cortical plasticity protocol using paired associative stimulation (PAS) was studied in 9 patients with SWEDDs, 9 with tremor‐dominant PD (with abnormal dopamine transporter single photon emission computed tomography findings), 8 with segmental dystonia, and 8 with essential tremor (ET). Despite clinical overlap, lack of true bradykinesia, presence of dystonia, and head tremor favored a diagnosis of SWEDDs, whereas re‐emergent tremor, true fatiguing or decrement, good response to dopaminergic drugs, and presence of non‐motor symptoms favored PD. A single tremor parameter could not differentiate between groups, but the combination of re‐emergent tremor and highest tremor amplitude at rest was characteristic of PD tremor. SWEDDs and segmental dystonia patients exhibited an abnormal exaggerated response to the PAS protocol, in contrast to a subnormal response in PD and a normal response in ET. We conclude that despite clinical overlap, there are features that can help to distinguish between PD and SWEDDs which may be useful in clinical practice. The underlying pathophysiology of SWEDDs differs from PD but has similarities with primary dystonia. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23019
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<front><div type="abstract" xml:lang="en">Approximately 10% of patients diagnosed clinically with early Parkinson's disease (PD) have normal dopaminergic functional imaging (Scans Without Evidence of Dopaminergic Deficit [SWEDDs]). An important subgroup of SWEDDs are those with asymmetric rest tremor resembling parkinsonian tremor. Clinical and pathophysiological features which could help to distinguish SWEDDs from PD have not been explored. We therefore studied clinical details including non‐motor symptoms in 25 tremulous SWEDDs patients in comparison to 25 tremor‐dominant PD patients. Blinded video rating was used to compare examination findings. Electrophysiological tremor parameters and also response to a cortical plasticity protocol using paired associative stimulation (PAS) was studied in 9 patients with SWEDDs, 9 with tremor‐dominant PD (with abnormal dopamine transporter single photon emission computed tomography findings), 8 with segmental dystonia, and 8 with essential tremor (ET). Despite clinical overlap, lack of true bradykinesia, presence of dystonia, and head tremor favored a diagnosis of SWEDDs, whereas re‐emergent tremor, true fatiguing or decrement, good response to dopaminergic drugs, and presence of non‐motor symptoms favored PD. A single tremor parameter could not differentiate between groups, but the combination of re‐emergent tremor and highest tremor amplitude at rest was characteristic of PD tremor. SWEDDs and segmental dystonia patients exhibited an abnormal exaggerated response to the PAS protocol, in contrast to a subnormal response in PD and a normal response in ET. We conclude that despite clinical overlap, there are features that can help to distinguish between PD and SWEDDs which may be useful in clinical practice. The underlying pathophysiology of SWEDDs differs from PD but has similarities with primary dystonia. © 2010 Movement Disorder Society</div>
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<abstract>Approximately 10% of patients diagnosed clinically with early Parkinson's disease (PD) have normal dopaminergic functional imaging (Scans Without Evidence of Dopaminergic Deficit [SWEDDs]). An important subgroup of SWEDDs are those with asymmetric rest tremor resembling parkinsonian tremor. Clinical and pathophysiological features which could help to distinguish SWEDDs from PD have not been explored. We therefore studied clinical details including non‐motor symptoms in 25 tremulous SWEDDs patients in comparison to 25 tremor‐dominant PD patients. Blinded video rating was used to compare examination findings. Electrophysiological tremor parameters and also response to a cortical plasticity protocol using paired associative stimulation (PAS) was studied in 9 patients with SWEDDs, 9 with tremor‐dominant PD (with abnormal dopamine transporter single photon emission computed tomography findings), 8 with segmental dystonia, and 8 with essential tremor (ET). Despite clinical overlap, lack of true bradykinesia, presence of dystonia, and head tremor favored a diagnosis of SWEDDs, whereas re‐emergent tremor, true fatiguing or decrement, good response to dopaminergic drugs, and presence of non‐motor symptoms favored PD. A single tremor parameter could not differentiate between groups, but the combination of re‐emergent tremor and highest tremor amplitude at rest was characteristic of PD tremor. SWEDDs and segmental dystonia patients exhibited an abnormal exaggerated response to the PAS protocol, in contrast to a subnormal response in PD and a normal response in ET. We conclude that despite clinical overlap, there are features that can help to distinguish between PD and SWEDDs which may be useful in clinical practice. The underlying pathophysiology of SWEDDs differs from PD but has similarities with primary dystonia. © 2010 Movement Disorder Society</abstract>
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<note>Austrian Science Fund (FWF) - No. J 2764;</note>
<note>Action Medical Research</note>
<note>National Institutes of Health Research (NIHR)</note>
<note>Ministerio de Educación y Ciencia de España - No. SAF2007–60700;</note>
<note>Consejería de Innovación, Ciencia y Empresa de la Junta de Andalucía - No. CVI‐02526;</note>
<note>Consejería de Salud de la Junta de Andalucía - No. PI‐0377/2007;</note>
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<p>Approximately 10% of patients diagnosed clinically with early Parkinson's disease (PD) have normal dopaminergic functional imaging (Scans Without Evidence of Dopaminergic Deficit [SWEDDs]). An important subgroup of SWEDDs are those with asymmetric rest tremor resembling parkinsonian tremor. Clinical and pathophysiological features which could help to distinguish SWEDDs from PD have not been explored. We therefore studied clinical details including non‐motor symptoms in 25 tremulous SWEDDs patients in comparison to 25 tremor‐dominant PD patients. Blinded video rating was used to compare examination findings. Electrophysiological tremor parameters and also response to a cortical plasticity protocol using paired associative stimulation (PAS) was studied in 9 patients with SWEDDs, 9 with tremor‐dominant PD (with abnormal dopamine transporter single photon emission computed tomography findings), 8 with segmental dystonia, and 8 with essential tremor (ET). Despite clinical overlap, lack of true bradykinesia, presence of dystonia, and head tremor favored a diagnosis of SWEDDs, whereas re‐emergent tremor, true fatiguing or decrement, good response to dopaminergic drugs, and presence of non‐motor symptoms favored PD. A single tremor parameter could not differentiate between groups, but the combination of re‐emergent tremor and highest tremor amplitude at rest was characteristic of PD tremor. SWEDDs and segmental dystonia patients exhibited an abnormal exaggerated response to the PAS protocol, in contrast to a subnormal response in PD and a normal response in ET. We conclude that despite clinical overlap, there are features that can help to distinguish between PD and SWEDDs which may be useful in clinical practice. The underlying pathophysiology of SWEDDs differs from PD but has similarities with primary dystonia. © 2010 Movement Disorder Society</p>
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</name>
<name type="personal"><namePart type="given">Diane</namePart>
<namePart type="family">Ruge</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation>
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</role>
</name>
<name type="personal"><namePart type="given">Mark J.</namePart>
<namePart type="family">Edwards</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation>
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</role>
</name>
<name type="personal"><namePart type="given">Carmen</namePart>
<namePart type="family">Terranova</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Petra</namePart>
<namePart type="family">Katschnig</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation>
<affiliation>Department of Neurology, Medical University Graz, Graz, Austria</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Fatima</namePart>
<namePart type="family">Carrillo</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Unidad de Trastornos del Movimiento, Servicio de Neurología, Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, CIBERNED, Seville, Spain</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Laura</namePart>
<namePart type="family">Silveira‐Moriyama</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Susanne A</namePart>
<namePart type="family">Schneider</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Georg</namePart>
<namePart type="family">Kägi</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Francisco J</namePart>
<namePart type="family">Palomar</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Unidad de Trastornos del Movimiento, Servicio de Neurología, Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, CIBERNED, Seville, Spain</affiliation>
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</name>
<name type="personal"><namePart type="given">Penelope</namePart>
<namePart type="family">Talelli</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">John</namePart>
<namePart type="family">Dickson</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Institute of Nuclear Medicine, UCL, London, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">Andrew J.</namePart>
<namePart type="family">Lees</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Niall</namePart>
<namePart type="family">Quinn</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">Pablo</namePart>
<namePart type="family">Mir</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Unidad de Trastornos del Movimiento, Servicio de Neurología, Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, CIBERNED, Seville, Spain</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">John C.</namePart>
<namePart type="family">Rothwell</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Kailash P.</namePart>
<namePart type="family">Bhatia</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation>
<description>Correspondence: Sobell Department, Institute of Neurology, UCL, Queen Square, London WC1N 3BG, United Kingdom</description>
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<dateIssued encoding="w3cdtf">2010-04-15</dateIssued>
<dateCaptured encoding="w3cdtf">2009-10-19</dateCaptured>
<dateValid encoding="w3cdtf">2009-12-18</dateValid>
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<abstract lang="en">Approximately 10% of patients diagnosed clinically with early Parkinson's disease (PD) have normal dopaminergic functional imaging (Scans Without Evidence of Dopaminergic Deficit [SWEDDs]). An important subgroup of SWEDDs are those with asymmetric rest tremor resembling parkinsonian tremor. Clinical and pathophysiological features which could help to distinguish SWEDDs from PD have not been explored. We therefore studied clinical details including non‐motor symptoms in 25 tremulous SWEDDs patients in comparison to 25 tremor‐dominant PD patients. Blinded video rating was used to compare examination findings. Electrophysiological tremor parameters and also response to a cortical plasticity protocol using paired associative stimulation (PAS) was studied in 9 patients with SWEDDs, 9 with tremor‐dominant PD (with abnormal dopamine transporter single photon emission computed tomography findings), 8 with segmental dystonia, and 8 with essential tremor (ET). Despite clinical overlap, lack of true bradykinesia, presence of dystonia, and head tremor favored a diagnosis of SWEDDs, whereas re‐emergent tremor, true fatiguing or decrement, good response to dopaminergic drugs, and presence of non‐motor symptoms favored PD. A single tremor parameter could not differentiate between groups, but the combination of re‐emergent tremor and highest tremor amplitude at rest was characteristic of PD tremor. SWEDDs and segmental dystonia patients exhibited an abnormal exaggerated response to the PAS protocol, in contrast to a subnormal response in PD and a normal response in ET. We conclude that despite clinical overlap, there are features that can help to distinguish between PD and SWEDDs which may be useful in clinical practice. The underlying pathophysiology of SWEDDs differs from PD but has similarities with primary dystonia. © 2010 Movement Disorder Society</abstract>
<note type="content">*Potential conflict of interest: nothing to report.</note>
<note type="funding">Austrian Science Fund (FWF) - No. J 2764; </note>
<note type="funding">Action Medical Research</note>
<note type="funding">National Institutes of Health Research (NIHR)</note>
<note type="funding">Ministerio de Educación y Ciencia de España - No. SAF2007–60700; </note>
<note type="funding">Consejería de Innovación, Ciencia y Empresa de la Junta de Andalucía - No. CVI‐02526; </note>
<note type="funding">Consejería de Salud de la Junta de Andalucía - No. PI‐0377/2007; </note>
<note type="funding">Sociedad Andaluza de Neurología</note>
<note type="funding">Brain Research Trust UK</note>
<note type="funding">Swiss Parkinson's Disease Association</note>
<note type="funding">Sir Halley Stewart Trust</note>
<subject lang="en"><genre>Keywords</genre>
<topic>SWEDDs</topic>
<topic>123I FP‐CIT SPECT</topic>
<topic>benign tremulous Parkinson's disease</topic>
<topic>dystonic tremor</topic>
<topic>accelerometry</topic>
<topic>paired associative stimulation</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
</titleInfo>
<titleInfo type="abbreviated"><title>Mov. Disord.</title>
</titleInfo>
<note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supplemental Information. - Supplemental Information. - Video. - </note>
<subject><genre>article category</genre>
<topic>Research Article</topic>
</subject>
<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part><date>2010</date>
<detail type="volume"><caption>vol.</caption>
<number>25</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>5</number>
</detail>
<extent unit="pages"><start>560</start>
<end>569</end>
<total>10</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">7D1AF556E57AD115978369268BD9F1FE2DE8B0C3</identifier>
<identifier type="DOI">10.1002/mds.23019</identifier>
<identifier type="ArticleID">MDS23019</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition>
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