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Premotor Parkinson's disease: Clinical features, detection, and prospects for treatment

Identifieur interne : 000E96 ( Main/Corpus ); précédent : 000E95; suivant : 000E97

Premotor Parkinson's disease: Clinical features, detection, and prospects for treatment

Auteurs : Andrew Siderowf ; Matthew B. Stern

Source :

RBID : ISTEX:5341BF0D9691240B11E22FE2E30386C28C0EE4A4

Abstract

The period immediately before the onset of motor symptoms of Parkinson's disease (PD) often has a recognizable phenotype with features including autonomic dysfunction and impaired olfaction. Subclinical dopaminergic cell loss can also be detected at this time using molecular imaging techniques. A greater recognition of the features of premotor PD and improvements in screening technologies have opened the possibility of predictive testing for PD. In addition to molecular imaging of the dopamine system, screening tests that can potentially be used to identify the physiological abnormalities in premotor PD include olfactory testing, imaging of the sympathetic innervation of the heart, transcranial ultrasound, and genetic testing for mutations known to cause hereditary PD. All of these technologies have trade‐offs as screening tests for accuracy, availability, and costs. Using these tests in combination may produce a more favorable combination of reasonable cost and accuracy than using any single test alone. Ultimately, the value of screening for PD depends on development of neuroprotective treatments for PD that would create an imperative for early identification and treatment. Ann Neurol 2008;64 (suppl):S139–S147

Url:
DOI: 10.1002/ana.21462

Links to Exploration step

ISTEX:5341BF0D9691240B11E22FE2E30386C28C0EE4A4

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<abstract lang="en">The period immediately before the onset of motor symptoms of Parkinson's disease (PD) often has a recognizable phenotype with features including autonomic dysfunction and impaired olfaction. Subclinical dopaminergic cell loss can also be detected at this time using molecular imaging techniques. A greater recognition of the features of premotor PD and improvements in screening technologies have opened the possibility of predictive testing for PD. In addition to molecular imaging of the dopamine system, screening tests that can potentially be used to identify the physiological abnormalities in premotor PD include olfactory testing, imaging of the sympathetic innervation of the heart, transcranial ultrasound, and genetic testing for mutations known to cause hereditary PD. All of these technologies have trade‐offs as screening tests for accuracy, availability, and costs. Using these tests in combination may produce a more favorable combination of reasonable cost and accuracy than using any single test alone. Ultimately, the value of screening for PD depends on development of neuroprotective treatments for PD that would create an imperative for early identification and treatment. Ann Neurol 2008;64 (suppl):S139–S147</abstract>
<note type="content">*Potential conflicts of interest: This article is part of a supplement sponsored by Boehringer Ingelheim (BI). A.S. has received consulting fees and speaking honoraria from BI. A.S. has also received honoraria from Teva and Merck Serano. M.S. has received speaking and consulting honoraria from BI. M.S. has held consulting relationships with Teva, NuPathe, Vernalis, and Novartis.</note>
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<title>Annals of Neurology</title>
<subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle>
</titleInfo>
<titleInfo type="abbreviated">
<title>Ann Neurol.</title>
</titleInfo>
<genre type="Journal">journal</genre>
<subject>
<genre>article category</genre>
<topic>Future Issues</topic>
</subject>
<identifier type="ISSN">0364-5134</identifier>
<identifier type="eISSN">1531-8249</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8249</identifier>
<identifier type="PublisherID">ANA</identifier>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>64</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>S2</number>
</detail>
<detail type="supplement">
<caption>Suppl. no.</caption>
<number>2</number>
</detail>
<extent unit="pages">
<start>S139</start>
<end>S147</end>
<total>9</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">5341BF0D9691240B11E22FE2E30386C28C0EE4A4</identifier>
<identifier type="DOI">10.1002/ana.21462</identifier>
<identifier type="ArticleID">ANA21462</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 American Neurological Association</accessCondition>
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<recordContentSource>WILEY</recordContentSource>
<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
</recordInfo>
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