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<title>Neurology current issue</title>
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<prism:eIssn>1526-632X</prism:eIssn>
<prism:coverDisplayDate>Nov 24 2009 12:00:00:000AM</prism:coverDisplayDate>
<prism:publicationName>Neurology</prism:publicationName>
<prism:issn>0028-3878</prism:issn>
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<title>Neurology</title>
<url>http://www.neurology.org/icons/banner/title.gif</url>
<link>http://www.neurology.org</link>
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<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/e99?rss=1">
<title><![CDATA[Education Research: Cognitive performance is preserved in sleep-deprived neurology residents]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/e99?rss=1</link>
<description><![CDATA[
<p><b>Objective:</b> To test the hypotheses that sleep deprivation in neurology residents is associated with performance deficits and that vigilance and cognitive performance is more compromised after overnight on-call duty compared to night shift.</p>
<p><b>Methods:</b> Thirty-eight neurology residents of a university teaching hospital participated in a prospective single-blind comparison study. Residents were recruited according to their working schedule and divided into 3 groups: 24 hours overnight on-call duty, night shift, and regular day shift (controls). All participants underwent serial measurements of sleepiness and cognitive performance in the morning directly after or before their shift. Pupillary sleepiness test and Paced Auditory Serial Addition Test were applied. Perceived sleepiness was assessed by a questionnaire.</p>
<p><b>Results:</b> Sleepiness was increased in residents after night shift and overnight call compared to controls while the type of night duty was not associated with the extent of sleepiness. Sleep-deprived residents did not show any performance deficits on the Paced Auditory Serial Addition Test. Cognitive performance was not associated with sleepiness measures.</p>
<p><b>Conclusions:</b> Night shift and overnight call duty have a similar impact on alertness in neurology residents. Sleep-deprived neurology residents may be able to overcome sleep loss&ndash;related performance difficulties for short periods.</p>
]]></description>
<dc:creator><![CDATA[Reimann, M., Manz, R., Prieur, S., Reichmann, H., Ziemssen, T.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:52 PST</dc:date>
<dc:subject><![CDATA[Medical care, Executive function, Attention, Patient safety, Professional conduct and ethics]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34a93</dc:identifier>
<dc:title><![CDATA[Education Research: Cognitive performance is preserved in sleep-deprived neurology residents]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>e103</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>e99</prism:startingPage>
<prism:section>RESIDENT AND FELLOW SECTION</prism:section>
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<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/e104?rss=1">
<title><![CDATA[Sleep and neurology training]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/e104?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Klein, E.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:52 PST</dc:date>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c79062</dc:identifier>
<dc:title><![CDATA[Sleep and neurology training]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>e105</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>e104</prism:startingPage>
<prism:section>PATIENT PAGES</prism:section>
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<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1717?rss=1">
<title><![CDATA[This week in Neurology(R): Highlights of the November 24 issue]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1717?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c6573a</dc:identifier>
<dc:title><![CDATA[This week in Neurology(R): Highlights of the November 24 issue]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1717</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1717</prism:startingPage>
<prism:section>THIS WEEK IN NEUROLOGY</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1718?rss=1">
<title><![CDATA[Exploring white matter microstructure: New insights from diffusion tensor imaging]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1718?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Filley, C. M.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[Alzheimer's disease, MCI (mild cognitive impairment)]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c2936b</dc:identifier>
<dc:title><![CDATA[Exploring white matter microstructure: New insights from diffusion tensor imaging]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1719</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1718</prism:startingPage>
<prism:section>EDITORIALS</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1720?rss=1">
<title><![CDATA[Epilepsy and aggression: Proceed with caution]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1720?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Fessler, A. J., Treiman, D. M.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[EEG; see Epilepsy/Seizures, Epilepsy monitoring, Epilepsy semiology, SPECT in epilepsy, Complex partial seizures]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c467af</dc:identifier>
<dc:title><![CDATA[Epilepsy and aggression: Proceed with caution]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1721</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1720</prism:startingPage>
<prism:section>EDITORIALS</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1722?rss=1">
<title><![CDATA[Regional pattern of white matter microstructural changes in normal aging, MCI, and AD]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1722?rss=1</link>
<description><![CDATA[
<p><b>Objective:</b> To cross-sectionally compare the regional white matter fractional anisotropy (FA) of cognitively normal (CN) older individuals and patients with mild cognitive impairment (MCI) and Alzheimer disease (AD), separately focusing on the normal-appearing white matter (NAWM) and white matter hyperintensities (WMH), and to test the independent effects of presumed degenerative and vascular process on FA differences.</p>
<p><b>Methods:</b> Forty-seven patients with AD, 73 patients with MCI, and 95 CN subjects received diffusion tensor imaging and vascular risk evaluation. To properly control normal regional variability of FA, we divided cerebral white matter into 4 strata as measured from a series of young healthy individuals (H1 = highest; H2 = intermediate high; H3 = intermediate low; H4 = lowest anisotropy stratum).</p>
<p><b>Results:</b> For overall cerebral white matter, patients with AD had significantly lower FA than CN individuals or patients with MCI in the regions with higher baseline anisotropy (H1, H2, and H3), corresponding to long corticocortical association fibers, but not in H4, which mostly includes heterogeneously oriented fibers. Vascular risk showed significant independent effects on FA in all strata except H1, which corresponds to the genu and splenium of the corpus callosum. Similar results were found within NAWM. FA in WMH was significantly lower than NAWM across all strata but was not associated with diagnosis or vascular risk.</p>
<p><b>Conclusions:</b> Both vascular and Alzheimer disease degenerative process contribute to microstructural injury of cerebral white matter across the spectrum of cognitive ability and have different region-specific injury patterns.</p>
]]></description>
<dc:creator><![CDATA[Lee, D. Y., Fletcher, E., Martinez, O., Ortega, M., Zozulya, N., Kim, J., Tran, J., Buonocore, M., Carmichael, O., DeCarli, C.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[Alzheimer's disease, MCI (mild cognitive impairment)]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c33afb</dc:identifier>
<dc:title><![CDATA[Regional pattern of white matter microstructural changes in normal aging, MCI, and AD]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1728</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1722</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1729?rss=1">
<title><![CDATA[Characteristics of hormone therapy, cognitive function, and dementia: The prospective 3C Study]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1729?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> To examine the association between hormone therapy (HT) and cognitive performance or dementia, focusing on the duration and type of treatment used, as well as the timing of initiation of HT in relation to the menopause.</p>
<p><b>Methods:</b> Women 65 years and older were recruited in France as part of the Three City Study. At baseline and 2- and 4-year follow-up, women were administered a short cognitive test battery and a clinical diagnosis of dementia was made. Detailed information was also gathered relating to current and past HT use. Analysis was adjusted for a number of sociodemographic, behavioral, physical, and mental health variables, as well as <I>APOE</I> 4.</p>
<p><b>Results:</b> Among 3,130 naturally postmenopausal women, current HT users performed significantly better than never users on verbal fluency, working memory, and psychomotor speed. These associations varied according to the type of treatment and a longer duration of HT appeared to be more beneficial. However, initiation of HT close to the menopause was not associated with better cognition. HT did not significantly reduce dementia risk over 4 years but current treatment diminished the negative effect associated with <I>APOE</I> 4.</p>
<p><b>Conclusions:</b> Current hormone therapy (HT) was associated with better performance in certain cognitive domains but these associations are dependent on the duration and type of treatment used. We found no evidence that HT needs to be initiated close to the menopause to have a beneficial effect on cognitive function in later life. Current HT may decrease the risk of dementia associated with the <I>APOE</I> 4 allele.</p>
]]></description>
<dc:creator><![CDATA[Ryan, J., Carriere, I., Scali, J., Dartigues, J. F., Tzourio, C., Poncet, M., Ritchie, K., Ancelin, M. L.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[All Cognitive Disorders/Dementia, Alzheimer's disease, Cognitive aging, All epidemiology]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34b0c</dc:identifier>
<dc:title><![CDATA[Characteristics of hormone therapy, cognitive function, and dementia: The prospective 3C Study]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1737</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1729</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1738?rss=1">
<title><![CDATA[Validity of the MoCA and MMSE in the detection of MCI and dementia in Parkinson disease]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1738?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Due to the high prevalence of mild cognitive impairment (MCI) and dementia in Parkinson disease (PD), routine cognitive screening is important for the optimal management of patients with PD. The Montreal Cognitive Assessment (MoCA) is more sensitive than the commonly used Mini-Mental State Examination (MMSE) in detecting MCI and dementia in patients without PD, but its validity in PD has not been established.</p>
<p><b>Methods:</b> A representative sample of 132 patients with PD at 2 movement disorders centers was administered the MoCA, MMSE, and a neuropsychological battery with operationalized criteria for deficits. MCI and PD dementia (PDD) criteria were applied by an investigator blinded to the MoCA and MMSE results. The discriminant validity of the MoCA and MMSE as screening and diagnostic instruments was ascertained.</p>
<p><b>Results:</b> Approximately one third of the sample met diagnostic criteria for a cognitive disorder (12.9% PDD and 17.4% MCI). Mean (SD) MoCA and MMSE scores were 25.0 (3.8) and 28.1 (2.0). The overall discriminant validity for detection of any cognitive disorder was similar for the MoCA and the MMSE (receiver operating characteristic area under the curve [95% confidence interval]): MoCA (0.79 [0.72, 0.87]) and MMSE (0.76 [0.67, 0.85]), but as a screening instrument the MoCA (optimal cutoff point = 26/27, 64% correctly diagnosed, lack of ceiling effect) was superior to the MMSE (optimal cutoff point = 29/30, 54% correctly diagnosed, presence of ceiling effect).</p>
<p><b>Conclusions:</b> The Montreal Cognitive Assessment, but not the Mini-Mental State Examination, has adequate psychometric properties as a screening instrument for the detection of mild cognitive impairment or dementia in Parkinson disease. However, a positive screen using either instrument requires additional assessment due to suboptimal specificity at the recommended screening cutoff point.</p>
]]></description>
<dc:creator><![CDATA[Hoops, S., Nazem, S., Siderowf, A. D., Duda, J. E., Xie, S. X., Stern, M. B., Weintraub, D.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[Parkinson's disease/Parkinsonism, Parkinson's disease with dementia, MCI (mild cognitive impairment)]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34b47</dc:identifier>
<dc:title><![CDATA[Validity of the MoCA and MMSE in the detection of MCI and dementia in Parkinson disease]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1745</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1738</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1746?rss=1">
<title><![CDATA[Subthalamic nucleus stimulation in Parkinson disease induces apathy: A PET study]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1746?rss=1</link>
<description><![CDATA[
<p><b>Objective:</b> Apathy may be induced by subthalamic nucleus deep brain stimulation (STN-DBS) in Parkinson disease (PD). We therefore wished to test the hypothesis that apathy induced by STN-DBS correlates with changes in glucose metabolism, using <sup>18</sup>FDG-PET.</p>
<p><b>Methods:</b> Twelve patients with PD were assessed 3 months before (M&ndash;3) and 3 months after (M+3) STN-DBS with <sup>18</sup>FDG-PET and the Apathy Evaluation Scale.</p>
<p><b>Results:</b> Apathy had significantly worsened at M+3 after STN-DBS. Positive correlations were observed between this variation in apathy scores and changes in glucose metabolism, especially in the right frontal middle gyrus (Brodmann area [BA] 10) and right inferior frontal gyrus (BA 46 and BA 47). Negative correlations between the two were observed in the right posterior cingulate gyrus (BA 31) and left medial frontal lobe (BA 9).</p>
<p><b>Conclusion:</b> These preliminary results confirm the role of the subthalamic nucleus in associative and limbic circuitry in humans and suggest that it is a key basal ganglia structure in motivation circuitry.</p>
]]></description>
<dc:creator><![CDATA[Le Jeune, F., Drapier, D., Bourguignon, A., Peron, J., Mesbah, H., Drapier, S., Sauleau, P., Haegelen, C., Travers, D., Garin, E., Malbert, C. H., Millet, B., Verin, M.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[PET, Parkinson's disease/Parkinsonism, All Neuropsychology/Behavior]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34b34</dc:identifier>
<dc:title><![CDATA[Subthalamic nucleus stimulation in Parkinson disease induces apathy: A PET study]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1751</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1746</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1752?rss=1">
<title><![CDATA[Medical records documentation of constipation preceding Parkinson disease: A case-control study]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1752?rss=1</link>
<description><![CDATA[
<p><b>Objective:</b> Parkinson disease (PD) may affect the autonomic nervous system and may cause constipation; however, few studies have explored constipation preceding the motor onset of PD. We investigated constipation preceding PD using a case-control study design in a population-based sample.</p>
<p><b>Methods:</b> Using the medical records-linkage system of the Rochester Epidemiology Project, we identified 196 subjects who developed PD in Olmsted County, MN, from 1976 through 1995. Each incident case was matched by age (&plusmn;1 year) and sex to a general population control. We reviewed the complete medical records of cases and controls in the medical records-linkage system to ascertain the occurrence of constipation preceding the onset of PD (or index year).</p>
<p><b>Results:</b> Constipation preceding PD or the index year was more common in cases than in controls (odds ratio [OR] 2.48; 95% confidence interval [CI] 1.49 to 4.11; <I>p</I> = 0.0005). This association remained significant after adjusting for smoking and coffee consumption (ever vs never), and after excluding constipation possibly induced by drugs. In addition, the association remained significant in analyses restricted to constipation documented 20 or more years before the onset of motor symptoms of PD. Although the association was stronger in women than in men and in patients with PD with rest tremor compared with patients with PD without rest tremor, these differences were not significant.</p>
<p><b>Conclusions:</b> Our findings suggest that constipation occurring as early as 20 or more years before the onset of motor symptoms is associated with an increased risk of Parkinson disease.</p>
]]></description>
<dc:creator><![CDATA[Savica, R., Carlin, J. M., Grossardt, B. R., Bower, J. H., Ahlskog, J. E., Maraganore, D. M., Bharucha, A. E., Rocca, W. A.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[Gastrointestinal, Parkinson's disease/Parkinsonism, Case control studies, Risk factors in epidemiology]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34af5</dc:identifier>
<dc:title><![CDATA[Medical records documentation of constipation preceding Parkinson disease: A case-control study]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1758</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1752</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1759?rss=1">
<title><![CDATA[The Microbleed Anatomical Rating Scale (MARS): Reliability of a tool to map brain microbleeds]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1759?rss=1</link>
<description><![CDATA[
<p><b>Objective:</b> Brain microbleeds on gradient-recalled echo (GRE) T2*-weighted MRI may be a useful biomarker for bleeding-prone small vessel diseases, with potential relevance for diagnosis, prognosis (especially for antithrombotic-related bleeding risk), and understanding mechanisms of symptoms, including cognitive impairment. To address these questions, it is necessary to reliably measure their presence and distribution in the brain. We designed and systematically validated the Microbleed Anatomical Rating Scale (MARS). We measured intrarater and interrater agreement for presence, number, and anatomical distribution of microbleeds using MARS across different MRI sequences and levels of observer experience.</p>
<p><b>Methods:</b> We studied a population of 301 unselected consecutive patients admitted to our stroke unit using 2 GRE T2*-weighted MRI sequences (echo time [TE] 40 and 26 ms). Two independent raters with different MRI rating expertise identified, counted, and anatomically categorized microbleeds.</p>
<p><b>Results:</b> At TE = 40 ms, agreement for microbleed presence in any brain location was good to very good (intrarater  = 0.85 [95% confidence interval (CI) 0.77&ndash;0.93]; interrater  = 0.68 [95% CI 0.58&ndash;0.78]). Good to very good agreement was reached for the presence of microbleeds in each anatomical region and in individual cerebral lobes. Intrarater and interrater reliability for the number of microbleeds was excellent (intraclass correlation coefficient [ICC] = 0.98 [95% CI 0.97&ndash;0.99] and ICC = 0.93 [0.91&ndash;0.94]). Very good interrater reliability was obtained at TE = 26 ms ( = 0.87 [95% CI 0.61&ndash;1]) for definite microbleeds in any location.</p>
<p><b>Conclusion:</b> The Microbleed Anatomical Rating Scale has good intrarater and interrater reliability for the presence of definite microbleeds in all brain locations when applied to different MRI sequences and levels of observer experience.</p>
]]></description>
<dc:creator><![CDATA[Gregoire, S. M., Chaudhary, U. J., Brown, M. M., Yousry, T. A., Kallis, C., Jager, H. R., Werring, D. J.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[MRI, All Cerebrovascular disease/Stroke, Intracerebral hemorrhage]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34a7d</dc:identifier>
<dc:title><![CDATA[The Microbleed Anatomical Rating Scale (MARS): Reliability of a tool to map brain microbleeds]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1766</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1759</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1767?rss=1">
<title><![CDATA[A novel stroke locus identified in a northern Sweden pedigree: Linkage to chromosome 9q31-33]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1767?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> The population of northern Sweden is characterized by reduced genetic diversity and a high incidence of stroke. We sought to reduce genetic variation further, using genealogic analysis in a set of nuclear families affected by stroke, and we subsequently performed a genome-wide scan to identify novel stroke susceptibility loci.</p>
<p><b>Methods:</b> Through genealogy, 7 nuclear families with a common ancestor, connected over 8 generations, were identified. A genome-wide scan using 449 microsatellite markers was performed with subsequent haplotype analyses.</p>
<p><b>Results:</b> A maximum allele-sharing lod score of 4.81 on chromosome 9q31-q33 was detected. Haplotype analysis identified a common 2.2-megabase interval in the chromosomal region in 4 of the nuclear families, where an overrepresentation of intracerebral hemorrhage was observed.</p>
<p><b>Conclusions:</b> We have identified a novel susceptibility locus for stroke. Haplotype analysis suggests that a shared genetic factor is of particular importance for intracerebral hemorrhage.</p>
]]></description>
<dc:creator><![CDATA[Janunger, T., Nilsson-Ardnor, S., Wiklund, P. -G., Lindgren, P., Escher, S. A., Lackovic, K., Nilsson, A. K., Stegmayr, B., Asplund, K., Holmberg, D.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[All Cerebrovascular disease/Stroke, Intracerebral hemorrhage, Genetic linkage]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34b1d</dc:identifier>
<dc:title><![CDATA[A novel stroke locus identified in a northern Sweden pedigree: Linkage to chromosome 9q31-33]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1773</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1767</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1774?rss=1">
<title><![CDATA[Physical activity and risk of ischemic stroke in the Northern Manhattan Study]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1774?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> It is controversial whether physical activity is protective against first stroke among older persons. We sought to examine whether physical activity, as measured by intensity of exercise and energy expended, is protective against ischemic stroke.</p>
<p><b>Methods:</b> The Northern Manhattan Study is a prospective cohort study in older, urban-dwelling, multiethnic, stroke-free individuals. Baseline measures of leisure-time physical activity were collected via in-person questionnaires. Cox proportional hazards models were constructed to examine whether energy expended and intensity of physical activity were associated with the risk of incident ischemic stroke.</p>
<p><b>Results:</b> Physical inactivity was present in 40.5% of the cohort. Over a median follow-up of 9.1 years, there were 238 incident ischemic strokes. Moderate- to heavy-intensity physical activity was associated with a lower risk of ischemic stroke (adjusted hazard ratio [HR] 0.65, 95% confidence interval [0.44&ndash;0.98]). Engaging in any physical activity vs none (adjusted HR 1.16, 95% CI 0.88&ndash;1.51) and energy expended in kcal/wk (adjusted HR per 500-unit increase 1.01, 95% CI 0.99&ndash;1.03) were not associated with ischemic stroke risk. There was an interaction of sex with intensity of physical activity (<I>p</I> = 0.04), such that moderate to heavy activity was protective against ischemic stroke in men (adjusted HR 0.37, 95% CI 0.18&ndash;0.78), but not in women (adjusted HR 0.92, 95% CI 0.57&ndash;1.50).</p>
<p><b>Conclusions:</b> Moderate- to heavy-intensity physical activity, but not energy expended, is protective against risk of ischemic stroke independent of other stroke risk factors in men in our cohort. Engaging in moderate to heavy physical activities may be an important component of primary prevention strategies aimed at reducing stroke risk.</p>
]]></description>
<dc:creator><![CDATA[Willey, J. Z., Moon, Y. P., Paik, M. C., Boden-Albala, B., Sacco, R. L., Elkind, M.S.V.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[Stroke prevention, All Cerebrovascular disease/Stroke, Incidence studies, Risk factors in epidemiology]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34b58</dc:identifier>
<dc:title><![CDATA[Physical activity and risk of ischemic stroke in the Northern Manhattan Study]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1779</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1774</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1780?rss=1">
<title><![CDATA[Coccidioidal meningitis and brain abscesses: Analysis of 71 cases at a referral center]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1780?rss=1</link>
<description><![CDATA[
<p><b>Objective:</b> <I>Coccidioides</I> species are the most common etiologic agents of chronic meningitis in regions endemic for coccidioidomycosis. Occasionally, even short-term travel to endemic regions results in the acquisition of meningeal disease, so awareness of this complication of coccidioidomycosis is important even in nonendemic areas. The prognosis depends on the early recognition and treatment of the disease, so it is important to be familiar with the varied clinical manifestations, risk factors associated with meningeal involvement, diagnostic challenges, and therapeutic modalities.</p>
<p><b>Methods:</b> We performed a retrospective analysis of 71 cases with coccidioidomycosis involving the CNS seen from 1996 to 2007 at a referral medical center in southern Arizona.</p>
<p><b>Results:</b> The only presenting symptom found in the majority of patients was headache. Those who were immunocompromised (most commonly HIV/AIDS and chronic steroid therapy) were at increased risk, but diabetics were not at increased risk. There was a preponderance of males (2:1) and people of Hispanic, African, and Asian (especially Pacific Isles) background. CSF anticoccidioidal antibody and culture were frequently negative on presentation, but in these cases, the serum antibody test was usually positive. Imaging studies were helpful in two thirds of cases, most commonly demonstrating basilar meningitis or hydrocephalus, which frequently required ventriculoperitoneal shunting. Most were treated with fluconazole, and prognosis was good for most of those who remained on treatment.</p>
<p><b>Conclusions:</b> Coccidioidal meningitis remains a diagnostic challenge, but the diagnosis can usually be made successfully when coccidioidal serum and CSF antibodies and cultures are combined with appropriate imaging studies.</p>
]]></description>
<dc:creator><![CDATA[Drake, K. W., Adam, R. D.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[Hydrocephalus, Abscess, Meningitis, Fungal infections, Risk factors in epidemiology]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34b69</dc:identifier>
<dc:title><![CDATA[Coccidioidal meningitis and brain abscesses: Analysis of 71 cases at a referral center]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1786</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1780</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1787?rss=1">
<title><![CDATA[Dysphagia in spinal muscular atrophy type II: More than a bulbar problem?]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1787?rss=1</link>
<description><![CDATA[
<p><b>Objective:</b> In patients with spinal muscular atrophy (SMA) type II, feeding problems and dysphagia are common, but the underlying mechanisms of these problems are not well defined. This case control study was designed to determine the underlying mechanisms of dysphagia in SMA type II.</p>
<p><b>Methods:</b> Six children with SMA type II and 6 healthy matched controls between 6.4 and 13.4 years of age were investigated during swallowing liquid and solid food in 2 different postures using surface EMG (sEMG) of the submental muscle group (SMG) and a video fluoroscopic swallow study (VFSS).</p>
<p><b>Results:</b> The VFSS showed postswallow residue of solid food in the vallecula and above the upper esophageal sphincter (UES), which can be responsible for indirect aspiration. Better results in swallowing were achieved in a more forward head position. These findings were supported by the sEMG measurements of the SMG during swallowing.</p>
<p><b>Conclusions:</b> Dysphagia in spinal muscular atrophy type II is due to a neurologic dysfunction (lower motor neuron problems from the cranial nerves in the brainstem) influencing the muscle force and efficiency of movement of the tongue and the submental muscle group in combination with a biomechanical component (compensatory head posture). The results suggest an integrated treatment with an adapted posture during meals and the advice of drinking water after meals to prevent aspiration pneumonias.</p>
]]></description>
<dc:creator><![CDATA[van den Engel-Hoek, L., Erasmus, C. E., van Bruggen, H. W., de Swart, B.J.M., Sie, L. T.L., Steenks, M. H., de Groot, I. J.M.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[Nutritional, Anterior nerve cell disease, All Rehabilitation, EMG]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34aa6</dc:identifier>
<dc:title><![CDATA[Dysphagia in spinal muscular atrophy type II: More than a bulbar problem?]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1791</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1787</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1792?rss=1">
<title><![CDATA[IDH1 mutations in low-grade astrocytomas predict survival but not response to temozolomide]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1792?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Mutations in isocitrate dehydrogenase 1 and 2 (<I>IDH1</I> and <I>IDH2</I>) have been implicated in tumorigenesis of gliomas. Patients with high-grade astrocytomas with <I>IDH1</I> or <I>IDH2</I> mutations were reported to have a better survival, but it is unknown if this improved survival also holds for low-grade astrocytoma and whether these mutations predict outcome to specific treatment.</p>
<p><b>Methods:</b> We retrospectively investigated the correlation of <I>IDH1</I> and <I>IDH2</I> mutations with overall survival and response to temozolomide in a cohort of patients with dedifferentiated low-grade astrocytomas treated with temozolomide at the time of progression after radiotherapy.</p>
<p><b>Results:</b> <I>IDH1</I> mutations were present in 86% of the 49 progressive astrocytomas. No mutations in <I>IDH2</I> were found. Presence of <I>IDH1</I> mutations were early events and significantly improved overall survival (median survival 48 vs 98 months), but did not affect outcome of temozolomide treatment.</p>
<p><b>Conclusion:</b> These results indicate that <I>IDH1</I> mutations identify a subgroup of gliomas with an improved survival, but are unrelated to the temozolomide response.</p>
]]></description>
<dc:creator><![CDATA[Dubbink, H. J., Taal, W., van Marion, R., Kros, J. M., van Heuvel, I., Bromberg, J. E., Zonnenberg, B. A., Zonnenberg, C.B.L., Postma, T. J., Gijtenbeek, J. M.M., Boogerd, W., Groenendijk, F. H., Smitt, P. A.E. S., Dinjens, W. N.M., van den Bent, M. J.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[Primary brain tumor, Chemotherapy-tumor, Gene expression studies]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34ace</dc:identifier>
<dc:title><![CDATA[IDH1 mutations in low-grade astrocytomas predict survival but not response to temozolomide]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1795</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1792</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1796?rss=1">
<title><![CDATA[Primary headache disorders in the Republic of Georgia: Prevalence and risk factors]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1796?rss=1</link>
<description><![CDATA[
<p><b>Objective:</b> To estimate the 1-year prevalences of migraine and tension-type headache (TTH), and identify their principal risk factors, in the general population of the Republic of Georgia.</p>
<p><b>Methods:</b> In a community-based door-to-door survey, 4 medical residents interviewed all biologically unrelated adult members (&ge;16 years) of 500 adjacent households in Tbilisi, the capital city, and 300 in rural Kakheti in eastern Georgia, using a previously validated questionnaire based on International Headache Society diagnostic criteria.</p>
<p><b>Results:</b> The target population included 1,145 respondents, 690 (60%) women, mean age 45.4 &plusmn; 12.0 years. The 1-year prevalences were as follows: migraine 6.5% (95% confidence interval 5.0&ndash;7.9), probable migraine 9.2% (7.5&ndash;10.8), all migraine 15.6% (13.5%&ndash;17.7%), TTH 10.0% (8.2&ndash;11.7), probable TTH 27.3% (24.8&ndash;29.9), all TTH 37.3% (34.5%&ndash;40.1%). Female gender and low socioeconomic status were risk factors for migraine but not for TTH. Headache on &ge;15 days/month was reported by 87 respondents, a prevalence of 7.6% (6.1&ndash;9.1). Female gender, low socioeconomic status, and frequent use (&ge;10 days/month) of acute headache drugs were risk factors. The likely prevalence of medication overuse headache was 0.9% (0.3&ndash;1.4), of chronic migraine 1.4% (0.7&ndash;2.1), and of chronic TTH 3.3% (2.3&ndash;4.4), but caution is needed in interpreting these estimates.</p>
<p><b>Conclusions:</b> While the prevalences of migraine and tension-type headache are comparable with those in Europe and the United States, a remarkably high percentage of the population of Georgia have headache on &ge;15 days/month. This study demonstrates the importance of socioeconomic factors in a developing country and unmasks the unmet needs of people with headache disorders.</p>
]]></description>
<dc:creator><![CDATA[Katsarava, Z., Dzagnidze, A., Kukava, M., Mirvelashvili, E., Djibuti, M., Janelidze, M., Jensen, R., Stovner, L. J., Steiner, T. J., On behalf of Lifting The Burden: The Global Campaign to Reduce the Burden of Headache Worldwide and the Russian Linguistic Subcommittee of the International Headache Society]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[All Headache, Migraine, Quality of life, Risk factors in epidemiology]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34abb</dc:identifier>
<dc:title><![CDATA[Primary headache disorders in the Republic of Georgia: Prevalence and risk factors]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1803</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1796</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1804?rss=1">
<title><![CDATA[DIRECTED AGGRESSIVE BEHAVIOR IN FRONTAL LOBE EPILEPSY: A VIDEO-EEG AND ICTAL SPECT CASE STUDY]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1804?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Shih, J. J., LeslieMazwi, T., Falcao, G., Van Gerpen, J.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[EEG; see Epilepsy/Seizures, Epilepsy monitoring, Epilepsy semiology, SPECT in epilepsy, Complex partial seizures]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c2933f</dc:identifier>
<dc:title><![CDATA[DIRECTED AGGRESSIVE BEHAVIOR IN FRONTAL LOBE EPILEPSY: A VIDEO-EEG AND ICTAL SPECT CASE STUDY]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1806</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1804</prism:startingPage>
<prism:section>CLINICAL/SCIENTIFIC NOTES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1806?rss=1">
<title><![CDATA[ENDPLATE DESTRUCTION DUE TO MATERNAL ANTIBODIES IN ARTHROGRYPOSIS MULTIPLEX CONGENITA]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1806?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Reimann, J., Jacobson, L., Vincent, A., Kornblum, C.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[Autoimmune diseases, All Neuromuscular Disease, Myasthenia, Developmental disorders]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34a65</dc:identifier>
<dc:title><![CDATA[ENDPLATE DESTRUCTION DUE TO MATERNAL ANTIBODIES IN ARTHROGRYPOSIS MULTIPLEX CONGENITA]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1808</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1806</prism:startingPage>
<prism:section>CLINICAL/SCIENTIFIC NOTES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1808?rss=1">
<title><![CDATA[TREATMENT OF VNS-INDUCED LARYNGOSPASM WITH BOTULINUM TOXIN]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1808?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kumar, S., Sharafkhaneh, A., Edmonds, J., Schultz, R., Hopkins, B.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:subject><![CDATA[All Clinical Neurology, Sleep apnea, All clinical neurophysiology, Vagus nerve stimulation, All Epilepsy/Seizures]]></dc:subject>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c34ae3</dc:identifier>
<dc:title><![CDATA[TREATMENT OF VNS-INDUCED LARYNGOSPASM WITH BOTULINUM TOXIN]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1810</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1808</prism:startingPage>
<prism:section>CLINICAL/SCIENTIFIC NOTES</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1811?rss=1">
<title><![CDATA[ACGME, TEST THYSELF!]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1811?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Dodick, D. W., Capobianco, D., Kash, K., Clough, J., Nash, D., Leas, B., Bance, L., Feske, S.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181bd696a</dc:identifier>
<dc:title><![CDATA[ACGME, TEST THYSELF!]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1811</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1811</prism:startingPage>
<prism:section>CORRESPONDENCE</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1812?rss=1">
<title><![CDATA["NOT MULTIPLE SCLEROSIS" AND THE CHANGING FACE OF HTLV-1: A CASE REPORT OF DOWNBEAT NYSTAGMUS]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1812?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Daroff, R. B., Dell'Osso, L. F., Frohman FAAN, E.M., Beeravolu, L.R., Frohman BA, T.C., Remington RN, BSN, MSCN, G.M., Lee, S., Levin, M.C.]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c134db</dc:identifier>
<dc:title><![CDATA["NOT MULTIPLE SCLEROSIS" AND THE CHANGING FACE OF HTLV-1: A CASE REPORT OF DOWNBEAT NYSTAGMUS]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1813</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1812</prism:startingPage>
<prism:section>CORRESPONDENCE</prism:section>
</item>

<item rdf:about="http://www.neurology.org/cgi/content/short/73/21/1813?rss=1">
<title><![CDATA["Not multiple sclerosis" and the changing face of HTLV-1: A case report of downbeat nystagmus]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1813?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181c5bd78</dc:identifier>
<dc:title><![CDATA["Not multiple sclerosis" and the changing face of HTLV-1: A case report of downbeat nystagmus]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1813</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1813</prism:startingPage>
<prism:section>CORRECTIONS</prism:section>
</item>

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<title><![CDATA[Calendar]]></title>
<link>http://www.neurology.org/cgi/content/short/73/21/1814?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Mon, 23 Nov 2009 13:01:51 PST</dc:date>
<dc:identifier>info:doi/10.1212/WNL.0b013e3181bd1c65</dc:identifier>
<dc:title><![CDATA[Calendar]]></dc:title>
<dc:publisher>American Academy of Neurology</dc:publisher>
<prism:number>21</prism:number>
<prism:volume>73</prism:volume>
<prism:endingPage>1814</prism:endingPage>
<prism:publicationDate>2009-11-24</prism:publicationDate>
<prism:startingPage>1814</prism:startingPage>
<prism:section>DEPARTMENTS</prism:section>
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