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    <title>AMA Publishing Group: Autoimmune Diseases Topic Collection</title>
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    <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
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      <title>Imaging Cortical Damage and Dysfunction in Multiple Sclerosis Imaging Cortical Damage and Dysfunction in MS </title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1659732</link>
      <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
      <author>Filippi M, Rocca MA, Horsfield MA, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;In line with pathological investigations, in vivo magnetic resonance imaging has consistently shown both focal and diffuse damage in the cerebral cortex of patients with multiple sclerosis. Cortical injury tends to progress over time and is only partially related to white matter abnormalities. This review summarizes the main findings from studies using both conventional and modern quantitative magnetic resonance–based techniques for the assessment of cortical damage and dysfunction in patients with multiple sclerosis.&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">556</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">564</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamaneurol.2013.1954</prism:doi>
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      <title>The Gender Gap in Multiple Sclerosis Intersection of Science and Society  The Gender Gap in Multiple Sclerosis </title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1659733</link>
      <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
      <author>Dunn SE, Steinman L. </author>
      <description>&lt;span class="paragraphSection"&gt;More than 3 times more women than men have multiple sclerosis (MS). Over the past 50 years, this ratio has been steadily increasing. The burdens to those who battle this disease, as well as the costs for society in dealing with MS, are substantial, and deciphering this 50-year-old trend in female preponderance in this disease is critical. In attempting to understand this growing imbalance, a number of intriguing discoveries have been made. These discoveries illuminate the pathogenesis of MS, with applications and benefits for both men and women. These breakthroughs potentially allow for the repurposing of certain approved drugs for potential use as treatments of MS.&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">634</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">635</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamaneurol.2013.55</prism:doi>
      <guid>http://pubs.jamanetwork.com/article.aspx?articleID=1659733</guid>
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    <item>
      <title>Microcystic Inner Nuclear Layer Abnormalities and Neuromyelitis Optica Microcystic Inner Nuclear Layer and NMO </title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1671736</link>
      <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
      <author>Gelfand JM, Cree BA, Nolan R, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;&lt;div class="boxTitle"&gt;Importance&lt;/div&gt;Microcystic abnormalities involving the inner nuclear layer of the retina occurs in a subset of patients with multiple sclerosis, most commonly in eyes previously affected by symptomatic optic neuritis. Acute optic neuritis is a cardinal manifestation of neuromyelitis optica (NMO). To our knowledge, microcystic inner nuclear layer abnormalities have not been investigated in NMO.&lt;div class="boxTitle"&gt;Objective&lt;/div&gt;To establish whether microcystic inner nuclear layer abnormalities occur in NMO.&lt;div class="boxTitle"&gt;Design&lt;/div&gt;Observational, retrospective study.&lt;div class="boxTitle"&gt;Setting&lt;/div&gt;University of California at San Francisco Multiple Sclerosis Center (academic specialty clinic).&lt;div class="boxTitle"&gt;Patients&lt;/div&gt;Twenty-five consecutive patients with NMO based on 2006 diagnostic criteria or with NMO spectrum disease (defined by seropositivity for anti–aquaporin 4 IgG in the context of a single episode of transverse myelitis or optic neuritis).&lt;div class="boxTitle"&gt;Exposure&lt;/div&gt;Spectral-domain optical coherence tomography.&lt;div class="boxTitle"&gt;Main Outcomes and Measures&lt;/div&gt;Identification of microcystic inner nuclear layer pathology on spectral-domain optical coherence tomography. Multivariable linear regression was used to examine associations between microcystic changes and measures of retinal structure and function. The hypothesis was generated prior to the data being reviewed and analyzed.&lt;div class="boxTitle"&gt;Results&lt;/div&gt;Microcystic changes were identified in 5 of 25 patients with NMO (20%) and 7 of 48 total eyes, including 7 of 29 eyes (24%) previously affected by optic neuritis. Microcystic changes occurred exclusively in eyes with a history of acute symptomatic optic neuritis (100% of eyes with microcystic changes had experienced prior optic neuritis compared with 71% of NMO eyes without microcystic abnormalities). There were no significant differences between patients with NMO with and without microcystic changes in terms of age, sex, and aquaporin 4–IgG antibody status. The mean age in this cohort was 44 years (range, 13-81 years); 84% were women; 80% were aquaporin 4–IgG seropositive; and the median Expanded Disability Status Scale score was 4.0 (interquartile range, 3.0-6.5).&lt;div class="boxTitle"&gt;Conclusions and Relevance&lt;/div&gt;Microcystic inner nuclear layer pathology occurs in a proportion of patients with NMO in eyes previously affected by acute optic neuritis. Additional research is needed to understand the cause of this retinal pathology and determine whether it contributes to persistent visual disability in patients with NMO following optic neuritis.&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">629</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">633</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamaneurol.2013.1832</prism:doi>
      <guid>http://pubs.jamanetwork.com/article.aspx?articleID=1671736</guid>
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    <item>
      <title>Interferon Beta and Long-term Disability in Multiple Sclerosis</title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1685327</link>
      <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
      <author>Shirani A, Zhao Y, Karim M, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;Greenberg et al highlighted our recent paper, which reported a “lack of evidence for a strong association between interferon beta treatment and disability progression.” This should not be interpreted as “interferon use does not prevent disability in patients with multiple sclerosis.” Nor does it seem appropriate to conclude that “the relapses prevented by interferon have been shown to lead to disability accumulation” by citing 2 short-term randomized clinical trials. It has become apparent that short-term effects may not translate into long-term benefits. This is consistent with the observation that the association between relapses and disability progression diminishes over time.&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">651</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">653</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamaneurol.2013.2197</prism:doi>
      <guid>http://pubs.jamanetwork.com/article.aspx?articleID=1685327</guid>
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    <item>
      <title>Interferon Beta and Long-term Disability in Multiple Sclerosis—Reply</title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1685328</link>
      <pubDate>Wed, 01 May 2013 00:00:00 GMT</pubDate>
      <author>Greenberg BM, Frohman E. </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">651</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">653</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamaneurol.2013.1</prism:doi>
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