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    <title>AMA Publishing Group: Movement Disorders Topic Collection</title>
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    <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
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      <title>Lessons for Parkinson Disease From the  Parkin  Genotype Lessons for PD From the  Parkin  Genotype </title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1659730</link>
      <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
      <author>Ahlskog J. </author>
      <description>&lt;span class="paragraphSection"&gt;Monogenetic forms of parkinsonism now include 16 established loci in the “ PARK ” nomenclature. In this issue of JAMA Neurology, Doherty and colleagues describe details of the most common autosomal recessive parkinsonism, PARK2, which is associated with parkin gene mutations. In the most comprehensive description of PARK2, these investigators detail the clinical phenotype of 5 patients, who were observed for decades, plus their neuropathology. Notably, the pathology was a non–Lewy body pathology. Although parkin is uncommon in Parkinson disease (PD) clinics, this report should be of interest to general neurologists once it is put into a broader context.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">70</prism:volume>
      <prism:number xmlns:prism="prism">5</prism:number>
      <prism:startingPage xmlns:prism="prism">551</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">552</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamaneurol.2013.104</prism:doi>
      <guid>http://pubs.jamanetwork.com/article.aspx?articleID=1659730</guid>
    </item>
    <item>
      <title>Prognosis of Mild Cognitive Impairment in Early Parkinson Disease The Norwegian ParkWest Study  Cognitive Impairment in Early Parkinson Disease </title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1671737</link>
      <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
      <author>Pedersen K, Larsen J, Tysnes O, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;&lt;div class="boxTitle"&gt;Importance&lt;/div&gt;Mild cognitive impairment (MCI) is common in Parkinson disease (PD), but the prognostic value of MCI in early PD is unknown.&lt;div class="boxTitle"&gt;Objective&lt;/div&gt;To examine the course of MCI and its progression to dementia in an incident PD cohort.&lt;div class="boxTitle"&gt;Design&lt;/div&gt;Prospective longitudinal cohort study.&lt;div class="boxTitle"&gt;Setting&lt;/div&gt;The Norwegian ParkWest study, an ongoing population-based study of the incidence, neurobiology, and prognosis of PD in western and southern Norway.&lt;div class="boxTitle"&gt;Participants&lt;/div&gt;A population-based cohort of 182 patients with incident PD monitored for 3 years.&lt;div class="boxTitle"&gt;Main Outcomes and Measures&lt;/div&gt;Serial neuropsychological tests of attention, executive function, verbal memory, and visuospatial skills were administered at baseline, 1 year, and 3 years. Patients were classified as having MCI and received a diagnosis of dementia according to published consensus criteria.&lt;div class="boxTitle"&gt;Results&lt;/div&gt;Significantly more patients with MCI than without MCI at baseline (10 of 37 [27.0%] vs 1 of 145 [0.7%]; relative risk, 39.2 [95% CI, 5.2-296.5]; P &lt; .001) progressed to dementia during follow-up. Of those with MCI at baseline, 8 of 37 (21.6%) had MCI that reverted to normal cognition during follow-up. Mild cognitive impairment at the 1-year visit was associated with a similar progression rate to dementia (10 of 36 patients [27.8%]) and reversion rate to normal cognition (7 of 36 [19.4%]). However, among the 22 patients with persistent MCI at baseline and the 1-year visit, 10 (45.5%) developed dementia and only 2 (9.1%) had MCI that reverted to normal cognition by the end of study.&lt;div class="boxTitle"&gt;Conclusions and Relevance&lt;/div&gt;Mild cognitive impairment at PD diagnosis predicts a highly increased risk for early dementia. Repeated neuropsychological testing increases the prognostic accuracy of MCI with respect to early dementia development in PD.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">70</prism:volume>
      <prism:number xmlns:prism="prism">5</prism:number>
      <prism:startingPage xmlns:prism="prism">580</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">586</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamaneurol.2013.2110</prism:doi>
      <guid>http://pubs.jamanetwork.com/article.aspx?articleID=1671737</guid>
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    <item>
      <title>A Mild Form of Adult-Onset Opsoclonus-Myoclonus Syndrome Associated With Antiglutamate Receptor Antibodies</title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1685332</link>
      <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
      <author>Kambe T, Takahashi Y, Furukawa Y. </author>
      <description>&lt;span class="paragraphSection"&gt;We read with interest the article by Klaas and colleagues on adult-onset opsoclonus-myoclonus syndrome (OMS). The authors reported the clinical characteristics of 21 patients at the Mayo Clinic and 116 patients in the literature, and they found 2 patients with adult-onset OMS associated with anti– N-methyl-D-aspartate receptor antibodies in their literature review. Initial symptoms of these 2 patients were behavioral and/or mood changes, and they developed severe encephalopathy.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">70</prism:volume>
      <prism:number xmlns:prism="prism">5</prism:number>
      <prism:startingPage xmlns:prism="prism">654</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">655</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamaneurol.2013.59</prism:doi>
      <guid>http://pubs.jamanetwork.com/article.aspx?articleID=1685332</guid>
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    <item>
      <title>A Mild Form of Adult-Onset Opsoclonus-Myoclonus Syndrome Associated With Antiglutamate Receptor Antibodies—Reply</title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1685333</link>
      <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
      <author> McKeon A, Pittock S. </author>
      <description>&lt;span class="paragraphSection"&gt;In reply&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">70</prism:volume>
      <prism:number xmlns:prism="prism">5</prism:number>
      <prism:startingPage xmlns:prism="prism">654</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">655</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamaneurol.2013.107</prism:doi>
      <guid>http://pubs.jamanetwork.com/article.aspx?articleID=1685333</guid>
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