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        <title>Editor's picks</title>
        <link>http://www.biomedcentral.com/bmcneurol/</link>
        <description>The editor's pick of recent articles published by BMC Neurology</description>
        <dc:date>2012-05-06T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2377/12/25" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2377/12/21" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2377/12/20" />
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        <title>Incidence of and risk factors for Motor Neurone
Disease in UK women: a prospective study
</title>
        <description>Background:
Motor neuron disease (MND) is a severe neurodegenerative disease with largely unknown etiology.  Most epidemiological studies are hampered by small sample sizes and/or the retrospective collection of information on behavioural and lifestyle factors.
Methods:
1.3 million women from the UK Million Women Study, aged 56 years on average at recruitment, were followed up for incident and/or fatal MND using NHS hospital admission and mortality data. Adjusted relative risks were calculated using Cox regression models.FindingsDuring follow-up for an average of 9.2 years, 752 women had a new diagnosis of MND.  Age-specific rates increased with age, from 1.9 (95% CI 1.3 - 2.7) to 12.5 (95% CI 10.2 - 15.3) per 100,000 women aged 50-54 to 70-74, respectively, giving a cumulative risk of diagnosis with the disease of 1. 74 per 1000 women between the ages of 50 and 75 years.  There was no significant variation in risk of MND with region of residence, socio-economic status, education, height, alcohol use, parity, use of oral contraceptives or hormone replacement therapy.  Ever-smokers had about a 20% greater risk than never smokers (RR 1.19 95% CI 1.02 to 1.38, p=0.03). There was a statistically significant reduction in risk of MND with increasing body mass index (pfor trend=0.009): obese women (body mass index, 30 kg/m2 or more) had a 20% lower risk than women of normal body mass index (20 to &lt;25 Kg/m2)(RR 0.78 95% CI 0.65-0.94; p=0.03). This effect persisted after exclusion of the first three years of follow-up.Interpretation.  MND incidence in UK women rises rapidly with age, and an estimated 1 in 575 women are likely to be affected between the ages of 50 and 75 years. Smoking slightly increases the risk of MND, and adiposity in middle age is associated with a lower risk of the disease.</description>
        <link>http://www.biomedcentral.com/1471-2377/12/25</link>
                <dc:creator>Pat Doyle</dc:creator>
                <dc:creator>Anna Brown</dc:creator>
                <dc:creator>Valerie Beral</dc:creator>
                <dc:creator>Gillian Reeves</dc:creator>
                <dc:creator>Jane Green</dc:creator>
                <dc:source>BMC Neurology 2012, 12:25</dc:source>
        <dc:date>2012-05-06T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-2377-12-25</dc:identifier>
                            <dc:title>Risk factors for MND</dc:title>
                            <dc:description>Female smokers in the UK have a modest increased risk of developing motor neurone disease (MND) whilst adiposity in middle age is associated with a decreased risk, however there appears to be no association with factors such as education level.</dc:description>
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                <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>25</prism:startingPage>
        <prism:publicationDate>2012-05-06T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1471-2377/12/21">
        <title>Valid and reliable instruments for arm-hand assessment at ICF activity level in persons with hemiplegia: a systematic review</title>
        <description>Background:
Loss of arm-hand performance due to a hemiparesis as a result of stroke or cerebral palsy (CP), leads to large problems in daily life of these patients. Assessment of arm-hand performance is important in both clinical practice and research. To gain more insight in e.g. effectiveness of common therapies for different patient populations with similar clinical characteristics, consensus regarding the choice and use of outcome measures is paramount. To guide this choice, an overview of available instruments is necessary. The aim of this systematic review is to identify, evaluate and categorize instruments, reported to be valid and reliable, assessing arm-hand performance at the ICF activity level in patients with stroke or cerebral palsy.
Methods:
A systematic literature search was performed to identify articles containing instruments assessing arm-hand skilled performance in patients with stroke or cerebral palsy. Instruments were identified and divided into the categories capacity, perceived performance and actual performance. A second search was performed to obtain information on their content and psychometrics.
Results:
Regarding capacity, perceived performance and actual performance, 18, 9 and 3 instruments were included respectively. Only 3 of all included instruments were used and tested in both patient populations. The content of the instruments differed widely regarding the ICF levels measured, assessment of the amount of use versus the quality of use, the inclusion of unimanual and/or bimanual tasks and the inclusion of basic and/or extended tasks.
Conclusions:
Although many instruments assess capacity and perceived performance, a dearth exists of instruments assessing actual performance. In addition, instruments appropriate for more than one patient population are sparse. For actual performance, new instruments have to be developed, with specific focus on the usability in different patient populations and the assessment of quality of use as well as amount of use. Also, consensus about the choice and use of instruments within and across populations is needed.</description>
        <link>http://www.biomedcentral.com/1471-2377/12/21</link>
                <dc:creator>Ryanne JM Lemmens</dc:creator>
                <dc:creator>Annick AA Timmermans</dc:creator>
                <dc:creator>Yvonne JM Janssen-Potten</dc:creator>
                <dc:creator>Rob JEM Smeets</dc:creator>
                <dc:creator>Henk AM Seelen</dc:creator>
                <dc:source>BMC Neurology 2012, 12:21</dc:source>
        <dc:date>2012-04-12T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-2377-12-21</dc:identifier>
                            <dc:title>Lack of instruments to assess arm-hand performance</dc:title>
                            <dc:description>Patients with a loss of arm-hand performance, due to a hemiparesis as a result of stroke or cerebral palsy, lack instruments appropriate for use in more than patient population and that are able to assess actual arm-hand performance.</dc:description>
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                <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>21</prism:startingPage>
        <prism:publicationDate>2012-04-12T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
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        <item rdf:about="http://www.biomedcentral.com/1471-2377/12/20">
        <title>Dexmedetomidine is neuroprotective in an &lt;it&gt;in vitro &lt;/it&gt;model for traumatic brain injury</title>
        <description>Background:
The &#945;2-adrenoreceptor agonist dexmedetomidine is known to provide neuroprotection under ischemic conditions. In this study we investigated whether dexmedetomidine has a protective effect in an in vitro model for traumatic brain injury.
Methods:
Organotypic hippocampal slice cultures were subjected to a focal mechanical trauma and then exposed to varying concentrations of dexmedetomidine. After 72 h cell injury was assessed using propidium iodide. In addition, the effects of delayed dexmedetomidine application, of hypothermia and canonical signalling pathway inhibitors were examined.
Results:
Dexmedetomidine showed a protective effect on traumatically injured hippocampal cells with a maximum effect at a dosage of 1 &#956;M. This effect was partially reversed by the simultaneous administration of the ERK inhibitor PD98059.
Conclusion:
In this TBI model dexmedetomidine had a significant neuroprotective effect. Our results indicate that activation of ERK might be involved in mediating this effect.</description>
        <link>http://www.biomedcentral.com/1471-2377/12/20</link>
                <dc:creator>Marc Schoeler</dc:creator>
                <dc:creator>Philip D Loetscher</dc:creator>
                <dc:creator>Rolf Rossaint</dc:creator>
                <dc:creator>Astrid V Fahlenkamp</dc:creator>
                <dc:creator>Georg Eberhardt</dc:creator>
                <dc:creator>Steffen Rex</dc:creator>
                <dc:creator>Joachim Weis</dc:creator>
                <dc:creator>Mark Coburn</dc:creator>
                <dc:source>BMC Neurology 2012, 12:20</dc:source>
        <dc:date>2012-04-11T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-2377-12-20</dc:identifier>
                            <dc:title>Dexmedetomidine neuroprotective in injured brains</dc:title>
                            <dc:description>The &amp;#945;2-adrenoreceptor agonist dexmedetomidine shows a protective effect on traumatically injured mouse hippocampal cells which is partially reversed by administration of an extracellular signal-regulated protein kinase (ERK) inhibitor suggesting that ERK activation helps mediate this effect</dc:description>
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                <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>20</prism:startingPage>
        <prism:publicationDate>2012-04-11T00:00:00Z</prism:publicationDate>
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