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January 28, 2014; 82 (4) Editorial

Expanding the genetics of huntingtonism

Andrew Feigin, Kevin Talbot
First published December 20, 2013, DOI: https://doi.org/10.1212/WNL.0000000000000067
Andrew Feigin
From the Center for Neurosciences (A.F.), The Feinstein Institute for Medical Research, Manhasset, NY; and the Nuffield Department of Clinical Neurosciences (K.T.), University of Oxford, UK.
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Kevin Talbot
From the Center for Neurosciences (A.F.), The Feinstein Institute for Medical Research, Manhasset, NY; and the Nuffield Department of Clinical Neurosciences (K.T.), University of Oxford, UK.
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Expanding the genetics of huntingtonism
Andrew Feigin, Kevin Talbot
Neurology Jan 2014, 82 (4) 286-287; DOI: 10.1212/WNL.0000000000000067

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The lines defining many clinical syndromes have become blurred. A patient presenting with what appears to be Parkinson disease may in fact have one of several genetic mutations (e.g., LRRK2, parkin), an atypical parkinsonian syndrome (e.g., multisystem atrophy, progressive supranuclear palsy), sporadic idiopathic Parkinson disease, or a number of other conditions. Conversely, known genetic mutations may have classical presentations, but they may also present with widely varying signs and symptoms.

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  • Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the editorial.

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  • © 2014 American Academy of Neurology
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