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<b>Stroke: Patients on statins have better outcome of intracerebral hemorrhage</b>
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<b>Altered motion perception in autism</b>
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<p>Nature Reviews Neurology 5, 353 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.87">doi:10.1038/nrneurol.2009.87</a>
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<b>Parkinson disease: New genetic risk factor for sporadic PD</b>
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<p>Nature Reviews Neurology 5, 354 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.79">doi:10.1038/nrneurol.2009.79</a>
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<dc:title>Parkinson disease: New genetic risk factor for sporadic PD</dc:title>
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<b>Parkinson disease: Intrajejunal duodopa improves nonmotor symptoms</b>
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<p>Nature Reviews Neurology 5, 354 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.84">doi:10.1038/nrneurol.2009.84</a>
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<p>Author: Lisa Richards</p>
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<dc:title>Parkinson disease: Intrajejunal duodopa improves nonmotor symptoms</dc:title>
<dc:creator>Lisa Richards</dc:creator>
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<title>Milestone: Neurology's growth factor: 100 years of Rita Levi-Montalcini</title>
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<description>On Wednesday 22 April 2009, Rita Levi-Montalcini, Nobel Prize laureate and discoverer of the first neural growth factor, turned 100 years old. Her scientific work drastically changed basic neuroscience and could have important implications for the treatment of neurological disorders.</description>
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<p>
<b>Milestone: Neurology's growth factor: 100 years of Rita Levi-Montalcini</b>
</p>
<p>Nature Reviews Neurology 5, 355 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.91">doi:10.1038/nrneurol.2009.91</a>
</p>
<p>Author: Jeroen J. G. Geurts</p>
<p>On Wednesday 22 April 2009, Rita Levi-Montalcini, Nobel Prize laureate and discoverer of the first neural growth factor, turned 100 years old. Her scientific work drastically changed basic neuroscience and could have important implications for the treatment of neurological disorders.</p>
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<dc:title>Milestone: Neurology's growth factor: 100 years of Rita Levi-Montalcini</dc:title>
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<title>Epilepsy: Is localization-related epilepsy a progressive disorder? Maybe...</title>
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<description>The issue of whether progressive brain injury occurs in pharmacoresistant epilepsy remains important and controversial. A combined longitudinal and cross-sectional MRI study, in which an automated method was used to measure cortical thickness, has demonstrated accelerated brain atrophy in patients with chronic epilepsy.</description>
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<p>
<b>Epilepsy: Is localization-related epilepsy a progressive disorder? Maybe...</b>
</p>
<p>Nature Reviews Neurology 5, 356 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.82">doi:10.1038/nrneurol.2009.82</a>
</p>
<p>Authors: Ruben Kuzniecky, Thomas Thesen &amp; Orrin Devinsky</p>
<p>The issue of whether progressive brain injury occurs in pharmacoresistant epilepsy remains important and controversial. A combined longitudinal and cross-sectional MRI study, in which an automated method was used to measure cortical thickness, has demonstrated accelerated brain atrophy in patients with chronic epilepsy.</p>
]]></content:encoded>
<dc:title>Epilepsy: Is localization-related epilepsy a progressive disorder? Maybe...</dc:title>
<dc:creator>Ruben Kuzniecky</dc:creator>
<dc:creator>Thomas Thesen</dc:creator>
<dc:creator>Orrin Devinsky</dc:creator>
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<title>Dementia: What is behavioral variant frontotemporal dementia?</title>
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<description>In an era of etiology-specific therapies, defining the criteria for behavioral variant frontotemporal dementia is essential. How do we determine whether bad manners, laziness, or unsolicited friendliness represents the earliest presentation of this condition? Diagnostic criteria are being actively evaluated to help establish a foundation for diagnostic decisions regarding this and other neurodegenerative diseases.</description>
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<p>
<b>Dementia: What is behavioral variant frontotemporal dementia?</b>
</p>
<p>Nature Reviews Neurology 5, 358 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.81">doi:10.1038/nrneurol.2009.81</a>
</p>
<p>Author: Murray Grossman</p>
<p>In an era of etiology-specific therapies, defining the criteria for behavioral variant frontotemporal dementia is essential. How do we determine whether bad manners, laziness, or unsolicited friendliness represents the earliest presentation of this condition? Diagnostic criteria are being actively evaluated to help establish a foundation for diagnostic decisions regarding this and other neurodegenerative diseases.</p>
]]></content:encoded>
<dc:title>Dementia: What is behavioral variant frontotemporal dementia?</dc:title>
<dc:creator>Murray Grossman</dc:creator>
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<dc:source>Nature Reviews Neurology 5, 358 (2009)</dc:source>
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<title>Pain: Clinical pain assessment: from bedside to better treatment</title>
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<description>Successfully treating chronic pain is challenging, as patients respond heterogeneously to analgesic treatments. Such variation in response can be attributed to differing underlying pain-generating mechanisms. A novel clinical bedside test that identifies distinct pain phenotypes might help deliver more-effective mechanism-based treatment strategies.</description>
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<p>
<b>Pain: Clinical pain assessment: from bedside to better treatment</b>
</p>
<p>Nature Reviews Neurology 5, 359 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.93">doi:10.1038/nrneurol.2009.93</a>
</p>
<p>Authors: Gunnar Wasner &amp; Ralf Baron</p>
<p>Successfully treating chronic pain is challenging, as patients respond heterogeneously to analgesic treatments. Such variation in response can be attributed to differing underlying pain-generating mechanisms. A novel clinical bedside test that identifies distinct pain phenotypes might help deliver more-effective mechanism-based treatment strategies.</p>
]]></content:encoded>
<dc:title>Pain: Clinical pain assessment: from bedside to better treatment</dc:title>
<dc:creator>Gunnar Wasner</dc:creator>
<dc:creator>Ralf Baron</dc:creator>
<dc:identifier>doi:10.1038/nrneurol.2009.93</dc:identifier>
<dc:source>Nature Reviews Neurology 5, 359 (2009)</dc:source>
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<prism:doi>10.1038/nrneurol.2009.93</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrneurol.2009.93</prism:url>
<prism:volume>5</prism:volume>
<prism:number>7</prism:number>
<prism:section>News and Views</prism:section>
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<title>Alzheimer disease: Hippocampal volume loss and Alzheimer disease progression</title>
<link>http://dx.doi.org/10.1038/nrneurol.2009.94</link>
<description>The progression of Alzheimer disease might be monitored by measuring the rate of hippocampal volume loss by means of MRI. Research suggests that a reduction in hippocampal volume can be detected over a period as short as 6 months, and that such volume loss is associated with cognitive decline and other indicators of Alzheimer disease neuropathology.</description>
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<p>
<b>Alzheimer disease: Hippocampal volume loss and Alzheimer disease progression</b>
</p>
<p>Nature Reviews Neurology 5, 361 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.94">doi:10.1038/nrneurol.2009.94</a>
</p>
<p>Authors: Wiesje M. van der Flier &amp; Philip Scheltens</p>
<p>The progression of Alzheimer disease might be monitored by measuring the rate of hippocampal volume loss by means of MRI. Research suggests that a reduction in hippocampal volume can be detected over a period as short as 6 months, and that such volume loss is associated with cognitive decline and other indicators of Alzheimer disease neuropathology.</p>
]]></content:encoded>
<dc:title>Alzheimer disease: Hippocampal volume loss and Alzheimer disease progression</dc:title>
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<dc:creator>Philip Scheltens</dc:creator>
<dc:identifier>doi:10.1038/nrneurol.2009.94</dc:identifier>
<dc:source>Nature Reviews Neurology 5, 361 (2009)</dc:source>
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<title>Management of new-onset epilepsy in the elderly</title>
<link>http://dx.doi.org/10.1038/nrneurol.2009.74</link>
<description>The incidence of new-onset epilepsy is high among elderly patients. Seizures can present differently to and with more subtle semiology than those in younger adults. This difference in presentation frequently poses a diagnostic challenge. Elderly patients also often have comorbidities, are usually on multiple medications </description>
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<p>
<b>Management of new-onset epilepsy in the elderly</b>
</p>
<p>Nature Reviews Neurology 5, 363 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.74">doi:10.1038/nrneurol.2009.74</a>
</p>
<p>Authors: Amir M. Arain &amp; Bassel W. Abou-Khalil</p>
<p>The incidence of new-onset epilepsy is high among elderly patients. Seizures can present differently to and with more subtle semiology than those in younger adults. This difference in presentation frequently poses a diagnostic challenge. Elderly patients also often have comorbidities, are usually on multiple medications </p>
]]></content:encoded>
<dc:title>Management of new-onset epilepsy in the elderly</dc:title>
<dc:creator>Amir M. Arain</dc:creator>
<dc:creator>Bassel W. Abou-Khalil</dc:creator>
<dc:identifier>doi:10.1038/nrneurol.2009.74</dc:identifier>
<dc:source>Nature Reviews Neurology 5, 363 (2009)</dc:source>
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<title>Critical illness polyneuropathy and myopathy in the intensive care unit</title>
<link>http://dx.doi.org/10.1038/nrneurol.2009.75</link>
<description>Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are major complications that occur in severely ill patients who require intensive care treatment. CIP and CIM affect the limb and respiratory muscles, and, as a consequence, they characteristically complicate weaning from the ventilator, increase the </description>
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<p>
<b>Critical illness polyneuropathy and myopathy in the intensive care unit</b>
</p>
<p>Nature Reviews Neurology 5, 372 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.75">doi:10.1038/nrneurol.2009.75</a>
</p>
<p>Authors: Wolfgang Zink, Rainer Kollmar &amp; Stefan Schwab</p>
<p>Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are major complications that occur in severely ill patients who require intensive care treatment. CIP and CIM affect the limb and respiratory muscles, and, as a consequence, they characteristically complicate weaning from the ventilator, increase the </p>
]]></content:encoded>
<dc:title>Critical illness polyneuropathy and myopathy in the intensive care unit</dc:title>
<dc:creator>Wolfgang Zink</dc:creator>
<dc:creator>Rainer Kollmar</dc:creator>
<dc:creator>Stefan Schwab</dc:creator>
<dc:identifier>doi:10.1038/nrneurol.2009.75</dc:identifier>
<dc:source>Nature Reviews Neurology 5, 372 (2009)</dc:source>
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<title>Epileptogenesis in the immature brain: emerging mechanisms</title>
<link>http://dx.doi.org/10.1038/nrneurol.2009.80</link>
<description>Epileptogenesis is defined as the process of developing epilepsy&#8212;a disorder characterized by recurrent seizures&#8212;following an initial insult. Seizure incidence during the human lifespan is at its highest in infancy and childhood. Animal models of epilepsy and human tissue studies suggest that epileptogenesis involves a cascade </description>
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<p>
<b>Epileptogenesis in the immature brain: emerging mechanisms</b>
</p>
<p>Nature Reviews Neurology 5, 380 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.80">doi:10.1038/nrneurol.2009.80</a>
</p>
<p>Authors: Sanjay N. Rakhade &amp; Frances E. Jensen</p>
<p>Epileptogenesis is defined as the process of developing epilepsy&#8212;a disorder characterized by recurrent seizures&#8212;following an initial insult. Seizure incidence during the human lifespan is at its highest in infancy and childhood. Animal models of epilepsy and human tissue studies suggest that epileptogenesis involves a cascade </p>
]]></content:encoded>
<dc:title>Epileptogenesis in the immature brain: emerging mechanisms</dc:title>
<dc:creator>Sanjay N. Rakhade</dc:creator>
<dc:creator>Frances E. Jensen</dc:creator>
<dc:identifier>doi:10.1038/nrneurol.2009.80</dc:identifier>
<dc:source>Nature Reviews Neurology 5, 380 (2009)</dc:source>
<prism:publicationName>Nature Reviews Neurology</prism:publicationName>
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<title>Lumbar spinal stenosis: syndrome, diagnostics and treatment</title>
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<description>Lumbar spinal stenosis (LSS) comprises narrowing of the spinal canal with subsequent neural compression, and is frequently associated with symptoms of neurogenic claudication. To establish a diagnosis of LSS, clinical history, physical examination results and radiological changes all need to be considered. Patients who exhibit </description>
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<p>
<b>Lumbar spinal stenosis: syndrome, diagnostics and treatment</b>
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<p>Nature Reviews Neurology 5, 392 (2009). <a href="http://dx.doi.org/10.1038/nrneurol.2009.90">doi:10.1038/nrneurol.2009.90</a>
</p>
<p>Authors: Eberhard Siebert, Harald Pr&#252;ss, Randolf Klingebiel, Vieri Failli, Karl M. Einh&#228;upl &amp; Jan M. Schwab</p>
<p>Lumbar spinal stenosis (LSS) comprises narrowing of the spinal canal with subsequent neural compression, and is frequently associated with symptoms of neurogenic claudication. To establish a diagnosis of LSS, clinical history, physical examination results and radiological changes all need to be considered. Patients who exhibit </p>
]]></content:encoded>
<dc:title>Lumbar spinal stenosis: syndrome, diagnostics and treatment</dc:title>
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<dc:creator>Harald Pr&#252;ss</dc:creator>
<dc:creator>Randolf Klingebiel</dc:creator>
<dc:creator>Vieri Failli</dc:creator>
<dc:creator>Karl M. Einh&#228;upl</dc:creator>
<dc:creator>Jan M. Schwab</dc:creator>
<dc:identifier>doi:10.1038/nrneurol.2009.90</dc:identifier>
<dc:source>Nature Reviews Neurology 5, 392 (2009)</dc:source>
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