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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.strokejournal.org/?rss=yes"><title>Journal of Stroke &amp; Cerebrovascular Diseases</title><description>Journal of Stroke &amp; Cerebrovascular Diseases RSS feed: Current Issue.    
 The Journal of Stroke &amp; Cerebrovascular Diseases  publishes original papers on basic and clinical science related to the 
fields of stroke and cerebrovascular diseases. The Journal also features review articles, controversies, methods and technical notes, 
selected case reports and other original articles of special nature. Its editorial mission is to focus on prevention and repair of cerebrovascular 
disease. Clinical papers emphasize medical and surgical aspects of stroke, clinical trials and design, epidemiology, stroke care delivery 
systems and outcomes, imaging sciences and rehabilitation of stroke. The Journal will be of special interest to specialists involved 
in caring for patients with cerebrovascular disease, including neurologists, neurosurgeons and cardiologists.   </description><link>http://www.strokejournal.org/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 National Stroke Association. Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:issn>1052-3057</prism:issn><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:publicationDate>February 2012</prism:publicationDate><prism:copyright> © 2012 National Stroke Association. Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001254/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001266/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS105230571000128X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001291/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001308/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS105230571000131X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001321/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001345/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001278/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001333/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001370/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001382/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305710001394/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305711003387/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305711003399/abstract?rss=yes"/><rdf:li rdf:resource="http://www.strokejournal.org/article/PIIS1052305711003405/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001254/abstract?rss=yes"><title>Detection of Atrial Fibrillation With Concurrent Holter Monitoring and Continuous Cardiac Telemetry Following Ischemic Stroke and Transient Ischemic Attack</title><link>http://www.strokejournal.org/article/PIIS1052305710001254/abstract?rss=yes</link><description>Atrial fibrillation (AF) is a major risk factor for recurrent ischemic stroke. We aimed to compare the detection rate of AF using continuous cardiac telemetry (CCT) versus Holter monitoring in hospitalized patients with ischemic stroke or transient ischemic attack (TIA). Between June 2007 and December 2008, 133 patients were admitted to an academic institution for ischemic stroke or TIA and underwent concurrent inpatient CCT and Holter monitoring. Rates of AF detection by CCT and Holter monitoring were compared using the McNemar paired proportion test. Among the 133 patients, 8 (6.0%) were diagnosed with new-onset AF. On average, Holter monitoring was performed for 29.8 hours, and CCT was performed for 73.6 hours. The overall rate of AF detection was higher for Holter monitoring compared with CCT (6.0%; 95% confidence interval [CI], 2.9-11.6 vs 0; 95% CI, 0-3.4; P = .008). Holter detection of AF was even higher in specific subgroups (those with an embolic infarct pattern, those age &gt;65 years, and those with coronary artery disease). Holter monitoring detected AF in 6% of hospitalized ischemic stroke and TIA patients, with higher proportions in high-risk subgroups. Compared with CCT, Holter monitoring is significantly more likely to detect arrhythmias.</description><dc:title>Detection of Atrial Fibrillation With Concurrent Holter Monitoring and Continuous Cardiac Telemetry Following Ischemic Stroke and Transient Ischemic Attack</dc:title><dc:creator>Marc A. Lazzaro, Kousik Krishnan, Shyam Prabhakaran</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.05.006</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-07-26</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-07-26</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>89</prism:startingPage><prism:endingPage>93</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001266/abstract?rss=yes"><title>Computed Tomography Perfusion Imaging in Spectacular Shrinking Deficit</title><link>http://www.strokejournal.org/article/PIIS1052305710001266/abstract?rss=yes</link><description>Spectacular shrinking deficit (SSD) is characterized by abrupt onset of a major hemispheric stroke syndrome, followed by dramatic and rapid improvement. We retrospectively identified patients with SSD diagnosed at our institution between December 1, 2007, and June 30, 2009. We reviewed computed tomography perfusion (CTP) imaging to determine perfusion defect as a measure of initial ischemic penumbra, and magnetic resonance imaging diffusion-weighted imaging (DWI) to determine the final infarct core. Among the 472 consecutive ischemic stroke patients, 126 (27%) presented with major hemispheric ischemic stroke syndrome, defined as National Institutes of Health Stroke Scale score (NIHSS) ≥8 in the territory of the middle cerebral artery (MCA) or internal carotid artery (ICA). Out of these patients, we identified 8 SSD patients with available CTP data. In these 8 patients, the mean time to dramatic recovery was 3.4 hours (range, 0.75-7 hours), and the mean time from onset to CTP was 12.7 hours (range, 3-30 hours). All 8 patients had perfusion abnormalities in portions of the MCA territory (partial MCA territory in 5 patients and complete MCA territory in 3 patients). The mean time from onset to MRI DWI was 15.5 hours (range, 7.9-34 hours). Restricted diffusion was present in all patients in the corresponding MCA distribution. Vascular imaging revealed MCA occlusion in 2 patients. Cervical vascular imaging revealed carotid occlusion in 2 patients and high-grade carotid stenosis in 2 patients. The stroke mechanisms were cardioembolism in 2 patients, large artery in 4 patients, and unknown in 2 patients. Four patients had repeat CTP imaging available that demonstrated eventual resolution of the perfusion defect. SSD is associated with a “shrinking” clinical syndrome and a “shrinking” perfusion pattern on CTP that lags behind clinical recovery. CTP imaging corroborates that a larger territory is at risk in SSD and contributes to better understanding of SSD.</description><dc:title>Computed Tomography Perfusion Imaging in Spectacular Shrinking Deficit</dc:title><dc:creator>Vivien H. Lee, Sayona John, Yousef Mohammad, Shyam Prabhakaran</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.05.007</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-08-12</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-08-12</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>94</prism:startingPage><prism:endingPage>101</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS105230571000128X/abstract?rss=yes"><title>Effects of Edaravone, a Free Radical Scavenger, on Serum Levels of Inflammatory Biomarkers in Acute Brain Infarction</title><link>http://www.strokejournal.org/article/PIIS105230571000128X/abstract?rss=yes</link><description>The potent free radical scavenger edavarone is widely used in Japan to treat acute ischemic stroke within 24 hours after onset. Recent experimental studies have shown that edavarone alleviates blood-brain barrier disruption in conjunction with suppression of the inflammatory reaction in acute brain ischemia. We investigated the effects of edaravone on circulating inflammatory biomarkers in patients with ischemic stroke. Patients with acute ischemic stroke admitted 12-36 hours after onset of symptoms were prospectively enrolled. Intravenous edaravone at 60 mg/day for 14 days was administered to patients admitted 12-24 hours after symptom onset (edaravone group; n = 29). Patients admitted 24-36 hours after onset served as controls (control group; n = 34). Venous blood samples were obtained on admission and at 48 hours, 7 days, and 14 days after symptom onset. Serum concentrations of high-sensitivity C-reactive protein, interleukin (IL)-6, IL-10, IL-18, tumor necrosis factor α, matrix metalloproteinase (MMP)-2, and MMP-9 were measured. General linear models were used to compare changes in concentrations of these biomarkers over time between the groups. In the control group, the mean MMP-9 concentration increased gradually from 3.857 ± 1.880 ng/mL to 4.538 ± 1.966 ng/mL over the 14-day period (P = .027, one-way repeated-measures analysis of variance [ANOVA]), but the edavarone group demonstrated no such increase (P = .564). A significant group–time interaction was demonstrated only for MMP-9 (P = .029, two-way repeated-measures ANOVA), and no significant differences in other biomarkers were seen between groups. Our data indicate that edaravone suppresses serum MMP-9 level in patients with acute ischemic stroke. Further studies with a larger sample size are needed to explore the relationship between circulating MMP-9 level and the protective effect of edaravone.</description><dc:title>Effects of Edaravone, a Free Radical Scavenger, on Serum Levels of Inflammatory Biomarkers in Acute Brain Infarction</dc:title><dc:creator>Kenji Isahaya, Koji Yamada, Masato Yamatoku, Kenzo Sakurai, Satoshi Takaishi, Bunta Kato, Toshikazu Hirayama, Yasuhiro Hasegawa</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.05.009</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2011-01-10</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2011-01-10</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>102</prism:startingPage><prism:endingPage>107</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001291/abstract?rss=yes"><title>Significance of Magnetic Resonance Angiography–Diffusion Weighted Imaging Mismatch in Hyperacute Cerebral Infarction</title><link>http://www.strokejournal.org/article/PIIS1052305710001291/abstract?rss=yes</link><description>Therapeutic results with respect to lesion size were analyzed and compared in patients with hyperacute cerebral infarction with and without major artery lesions on magnetic resonance angiography (MRA) and in those who did and did not receive intravenous (IV) tissue plasminogen activator (t-PA). Of the patients with cerebral infarction who visited the hospital within 3 hours of onset between April 2007 and September 2009, 127 patients with cerebral infarction in the anterior circulation region in whom head magnetic resonance imaging (diffusion-weighted imaging [DWI]) or MRA was performed (81 men and 46 women; mean age, 71 ± 11 years) were enrolled. Major artery lesions (+) were defined as internal carotid artery occlusion and middle cerebral artery (M1/M2 segment) occlusion and ≥50% stenosis. Based on the presence or absence of major artery lesions and the size of DWI lesions, the subjects were divided into 3 groups: MRA-DWI mismatch (+) group [major artery lesion (+) and DWI-ASPECTS ≥6], MRA-DWI mismatch (−) group [major artery lesion (+) and DWI-ASPECTS &lt;6], and major artery lesion (-) group. IV t-PA was given to 21 of the 64 patients in the MRA-DWI mismatch (+) group, to 1 of the 24 patients in the MRA-DWI mismatch (-) group, and to 9 of the 39 patients in the major artery lesion (-) group. In the MRA-DWI mismatch (+) group (n = 64), the median National Institutes of Health Stroke Scale (NIHSS) score on admission was higher in t-PA–treated patients than in t-PA–untreated patients (15 vs 11). The modified Rankin scale (mRS) score at day 90 after onset was more favorable in t-PA–treated patients (0-2 in 10 patients [48%] and 3-6 in 11 patients [52%]) than in t-PA–untreated patients (0-2 in 12 patients [28%] and 3-6 in 31 patients [72%]). After adjusting for admission NIHSS score, there was a significant difference in outcome (mRS score) between t-PA–treated patients (0-2 in 10 patients [48%] and 3-6 in 11 patients [52%]) and t-PA–untreated patients (0-2 in 3 patients [9%] and 3-6 in 29 patients [91%]) (P = .002). In the MRA-DWI mismatch (-) group (n = 24), mRS scores at day 90 after onset were poor in both t-PA–treated (3-6 in 1 patient [100%]) and t-PA–untreated patients (0-2 in 1 patient [4%] and 3-6 in 22 patients [96%]). In the major artery lesion (-) group (n = 39), mRS scores at day 90 after onset were favorable in both t-PA–treated (0-2 in 9 patients [100%]) and t-PA–untreated patients (0-2 in 28 patients [93%] and 3-6 in 2 patients [7%]). When comparing major artery lesions in the MRA-DWI mismatch (+) group, outcomes were more favorable in patients with M1/M2 segment lesions who received t-PA than in those who did not receive t-PA. In the MRA-DWI mismatch (+) group, the prognosis was significantly better for t-PA–treated patients than for t-PA–untreated patients, suggesting that IV t-PA is indicated in patients with MRA-DWI mismatch.</description><dc:title>Significance of Magnetic Resonance Angiography–Diffusion Weighted Imaging Mismatch in Hyperacute Cerebral Infarction</dc:title><dc:creator>Ichiro Deguchi, Hidetaka Takeda, Daisuke Furuya, Tomohisa Dembo, Harumitsu Nagoya, Yuji Kato, Yasuo Ito, Takuya Fukuoka, Hajime Maruyama, Norio Tanahashi</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.03.019</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-09-20</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-09-20</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>108</prism:startingPage><prism:endingPage>113</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001308/abstract?rss=yes"><title>Predictors of Percutaneous Endoscopic Gastrostomy Tube Placement in Patients With Severe Dysphagia From an Acute-Subacute Hemispheric Infarction</title><link>http://www.strokejournal.org/article/PIIS1052305710001308/abstract?rss=yes</link><description>This study investigated the influence of age, National Institutes of Health Stroke Scale (NIHSS) score, time from stroke onset, infarct location and volume in predicting placement of a percutaneous endoscopic gastrostomy (PEG) tube in patients with severe dysphagia from an acute-subacute hemispheric infarction. We performed a retrospective analysis of a hospital-based patient cohort to analyze the effect of the aforementioned variables on the decision of whether or not to place a PEG tube. Consecutive patients were identified using International Classification of Diseases, Ninth Revision (ICD-9) codes for acute ischemic stroke, Current Procedural Terminology (CPT)-4 codes for a formal swallowing evaluation by a speech pathologist, and procedure codes for PEG placement over a 5-year period from existing medical records at our institution. Only patients with severe dysphagia were enrolled. A total of 77 patients met inclusion criteria; 20 of them underwent PEG placement. The relationship between age (dichotomized; &lt; and ≥75 years), time from stroke onset (days), NIHSS score, acute infarct lesion volume (dichotomized; &lt; and ≥100 cc), and infarct location (ie, insula, anterior insula, periventricular white matter, inferior frontal gyrus, motor cortex, or bilateral hemispheres) with PEG tube placement were analyzed using logistic regression analysis. In univariate analysis, NIHSS score (P = .005), lesion volume (P = .022), and presence of bihemispheric infarction (P = .005) were found to be the main predictors of interest. After multivariate adjustment, only NIHSS score (odds ratio [OR], 1.15; 90% confidence interval [CI], 1.02-1.29; P = .04) and presence of bihemispheric infarcts (OR, 4.67; 90% CI, 1.58-13.75; P = .018) remained significant. Our data indicates that baseline NIHSS score and the presence of bihemispheric infarcts predict PEG placement during hospitalization from an acute-subacute hemispheric infarction in patients with severe dysphagia. These results require further validation in future studies.</description><dc:title>Predictors of Percutaneous Endoscopic Gastrostomy Tube Placement in Patients With Severe Dysphagia From an Acute-Subacute Hemispheric Infarction</dc:title><dc:creator>Sandeep Kumar, Susan Langmore, Richard P. Goddeau, Adel Alhazzani, Magdy Selim, Louis R. Caplan, Lin Zhu, Adnan Safdar, Cynthia Wagner, Colleen Frayne, David E. Searls, Gottfried Schlaug</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.05.010</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-09-20</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-09-20</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>114</prism:startingPage><prism:endingPage>120</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS105230571000131X/abstract?rss=yes"><title>Accuracy of the New ICD-9-CM Code for “Drip-and-Ship” Thrombolytic Treatment in Patients With Ischemic Stroke</title><link>http://www.strokejournal.org/article/PIIS105230571000131X/abstract?rss=yes</link><description>A new International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) diagnosis code, V45.88, was approved by the Centers for Medicare and Medicaid Services (CMS) on October 1, 2008. This code identifies patients in whom intravenous (IV) recombinant tissue plasminogen activator (rt-PA) is initiated in one hospital's emergency department, followed by transfer within 24 hours to a comprehensive stroke center, a paradigm commonly referred to as “drip-and-ship.” This study assessed the use and accuracy of the new V45.88 code for identifying ischemic stroke patients who meet the criteria for drip-and-ship at 2 advanced certified primary stroke centers. Consecutive patients over a 12-month period were identified by primary ICD-9-CM diagnosis codes related to ischemic stroke. The accuracy of V45.88 code utilization using administrative data provided by Health Information Management Services was assessed through a comparison with data collected in prospective stroke registries maintained at each hospital by a trained abstractor. Out of a total of 428 patients discharged from both hospitals with a diagnosis of ischemic stroke, 37 patients were given ICD-9-CM code V45.88. The internally validated data from the prospective stroke database demonstrated that a total of 40 patients met the criteria for drip-and-ship. A concurrent comparison found that 92% (sensitivity) of the patients treated with drip-and-ship were coded with V45.88. None of the non-drip-and-ship stroke cases received the V45.88 code (100% specificity). The new ICD-9-CM code for drip-and-ship appears to have high specificity and sensitivity, allowing effective data collection by the CMS.</description><dc:title>Accuracy of the New ICD-9-CM Code for “Drip-and-Ship” Thrombolytic Treatment in Patients With Ischemic Stroke</dc:title><dc:creator>Silvina B. Tonarelli, Michael Tibbs, Gabriela Vazquez, Kamakshi Lakshminarayan, Gustavo J. Rodriguez, Adnan I. Qureshi</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.05.011</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-09-20</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-09-20</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>121</prism:startingPage><prism:endingPage>123</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001321/abstract?rss=yes"><title>Subtle Problems in Activities of Daily Living after a Transient Ischemic Attack or an Apparently Fully Recovered Non-disabling Stroke</title><link>http://www.strokejournal.org/article/PIIS1052305710001321/abstract?rss=yes</link><description>Little is known about the effects on the performance of activities of daily living (ADL) and quality of life (QoL) of transient ischemic attack (TIA) or a nondisabling stroke (NDS) with a full recovery in 72 hours. The present study evaluated ADL performance and QoL, as well as symptoms of anxiety and depression, in patients at 1 and 6 months after a TIA or an NDS. Consecutive hospitalized TIA/NDS patients not requiring rehabilitation were assessed at 1 and 6 months after discharge from a hospital or emergency department. ADL performance was evaluated using the Assessment of Motor and Process Skills (AMPS), QoL was assessed with the Short Form 36 (SF-36), and depression and anxiety symptoms were assessed with the Hospital Anxiety and Depression Scale (HADS). A total of 45 patients completed the follow-up. At 1 month after TIA/NDS, all patients were independent in ADL performance but had AMPS and SF-36 scores below the norm. In addition, 12 patients (27%) had anxiety symptoms, and 9 patients (20%) had symptoms of depression. Although initially considered fully recovered, 23 patients (51%) required rehabilitation after the first follow-up. After 6 months, their AMPS, SF-36, and HADS scores were lower than those of the patients who did not require rehabilitation after the first screening. Half of the patients with a TIA or an NDS who were initially considered fully recovered exhibited ADL limitations, decreased QoL, and symptoms of anxiety or depression after 6 months.</description><dc:title>Subtle Problems in Activities of Daily Living after a Transient Ischemic Attack or an Apparently Fully Recovered Non-disabling Stroke</dc:title><dc:creator>Marieke E. Verbraak, Agnes F. Hoeksma, Robert Lindeboom, Vincent I.H. Kwa</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.05.012</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-11-09</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-11-09</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>124</prism:startingPage><prism:endingPage>130</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001345/abstract?rss=yes"><title>Low Patient Enrollment Sites in Multicenter Randomized Clinical Trials of Cerebrovascular Diseases: Associated Factors and Impact on Trial Outcomes</title><link>http://www.strokejournal.org/article/PIIS1052305710001345/abstract?rss=yes</link><description>Wide variability in patient enrollment among participating sites is a common phenomenon in multicenter trials. We examined stroke trial–related factors associated with the proportion of sites with low patient enrollment and the effect of these low-enrollment sites on trial outcome. We identified efficacy clinical trials enrolling patients with cerebrovascular diseases between 1980 and 2008 using an electronic database. The trials included in our analyses were multicenter randomized controlled trials (RCTs) comparing efficacy endpoints between two or more treatment groups and having &gt;5 sites. Sites enrolling &lt;10 patients or &lt;2% of total trial patients were defined as low- enrollment sites. Trials were classified into tertiles based on the proportion of low-enrollment sites. Factors associated with trials that could be ascertained through a systematic review of published data were identified and examined. The association between low enrollment and a conclusive trial designation (defined by the ability to reject the primary null hypothesis either at or before target enrollment or demonstrate equivalence/noninferiority with adequate statistical power, depending on the initial design) was assessed using a multivariate logistic regression model. We identified 51 trials that met the inclusion criteria and provided information regarding patients enrolled per center. A total of 3059 participating centers enrolled a total of 53,742 trial participants; 78% of the participating sites enrolled &lt;2% of trial participants. Trials enrolling acute stroke patients (within 24 hours of symptom onset) or those evaluating endovascular/surgical intervention had a higher proportion of low-enrollment sites (&lt;10 patients per site). Studies with a higher proportion of low-enrollment sites were more likely to target acute stroke patients and less likely to randomize ≥1000 patients, use general efficacy endpoints, and stratify by site. There was no association between the studies with a higher proportion of low-enrollment sites and designation as a conclusive trial. A better understanding of factors associated with low-enrollment sites in clinical trials and the impact on a trial's ability to demonstrate conclusive outcomes may lead to strategies to make trial enrollments more efficient and cost-effective.</description><dc:title>Low Patient Enrollment Sites in Multicenter Randomized Clinical Trials of Cerebrovascular Diseases: Associated Factors and Impact on Trial Outcomes</dc:title><dc:creator>Adnan I. Qureshi, Nauman Tariq, Gabriela Vazquez, Jill Novitzke, M. Fareed K. Suri, Kamakshi Lakshminarayan, Stephen J. Haines</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.05.014</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-08-19</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-08-19</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>131</prism:startingPage><prism:endingPage>142</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001278/abstract?rss=yes"><title>An Unusual Case of Elderly-Onset Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL) With Multiple Cerebrovascular Risk Factors</title><link>http://www.strokejournal.org/article/PIIS1052305710001278/abstract?rss=yes</link><description>Here we report a female patient with elderly-onset cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). At age 71, she developed gait disturbance, followed by memory disturbance 1 year later. She had been treated for hypertension and diabetes mellitus for 19 years. There apparently was low penetrance of disease. Magnetic resonance imaging (MRI) findings showed typical features of CADASIL, and the R607C mutation was detected in exon 11 in NOTCH3. This case strongly indicates that CADASIL should be considered when typical findings are observed on MRI even in cases of elderly onset with multiple cerebrovascular risk factors.</description><dc:title>An Unusual Case of Elderly-Onset Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL) With Multiple Cerebrovascular Risk Factors</dc:title><dc:creator>Mitsunori Watanabe, Yoshiki Adachi, Mandy Jackson, Yukiko Yamamoto-Watanabe, Yasuhito Wakasaya, Ikumi Shirahama, Ayumi Takamura, Etsuro Matsubara, Takeshi Kawarabayashi, Mikio Shoji</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.05.008</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-09-20</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-09-20</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>143</prism:startingPage><prism:endingPage>145</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001333/abstract?rss=yes"><title>Isolated Hypersomnia Due to Bilateral Thalamic Infarcts</title><link>http://www.strokejournal.org/article/PIIS1052305710001333/abstract?rss=yes</link><description>We describe a unique patient who developed hypersomnia as the sole presenting symptom of bilateral thalamic infarcts.</description><dc:title>Isolated Hypersomnia Due to Bilateral Thalamic Infarcts</dc:title><dc:creator>Munish Kumar Goyal, Gyanendra Kumar, Pradeep Kumar Sahota</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.05.013</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-09-20</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-09-20</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>146</prism:startingPage><prism:endingPage>147</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001370/abstract?rss=yes"><title>Middle Cerebral Artery Infarct following Multiple Bee Stings</title><link>http://www.strokejournal.org/article/PIIS1052305710001370/abstract?rss=yes</link><description>Neurologic events following bee stings are very rare. We report a 59-year-old man who became drowsy with slurred speech following multiple bee stings. In the hospital, he was found to have left-sided hemplegia, seventh cranial nerve palsy, and left conjugate gaze palsy. Further investigation revealed dyslipidemia, impaired glucose tolerance, and a middle cerebral artery territory infarct. His limb weakness and speech improved before his discharge from the hospital.</description><dc:title>Middle Cerebral Artery Infarct following Multiple Bee Stings</dc:title><dc:creator>Stalin Viswanathan, Vivekanandan Muthu, Ajai P. Singh, Rajarajan Rajendran, Robin George</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.06.003</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-08-12</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-08-12</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>148</prism:startingPage><prism:endingPage>150</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001382/abstract?rss=yes"><title>Delayed Catastrophic Intracerebral Hemorrhage Preceded by Progressive Recovery after Carotid Stenting for Acute Ischemic Stroke</title><link>http://www.strokejournal.org/article/PIIS1052305710001382/abstract?rss=yes</link><description>Background: Hemorrhagic transformation (HT) is a feared complication of reperfusion therapy for treatment of acute ischemic stroke. Generally, HT occurs within 24-36 hours after thrombolysis.Summary of Case: We present a case of a fatal symptomatic HT of an infarction that occurred 7 days after acute ischemic stroke which was preceded by a remarkable recovery following a combination of acute revascularization therapies.Conclusion: Fatal symptomatic HT is a rare potential complication that can occur after several days of treatment of acute ischemic stroke.</description><dc:title>Delayed Catastrophic Intracerebral Hemorrhage Preceded by Progressive Recovery after Carotid Stenting for Acute Ischemic Stroke</dc:title><dc:creator>Jason S. Day, Harold P. Adams</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.06.004</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-10-15</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-10-15</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>151</prism:startingPage><prism:endingPage>154</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305710001394/abstract?rss=yes"><title>Economy Class Stroke Syndrome after a Long Drive</title><link>http://www.strokejournal.org/article/PIIS1052305710001394/abstract?rss=yes</link><description>Economy class stroke syndrome is a cardiovascular complication associated with long periods of travel, only a few cases have been reported after long drives, however. The patient, a 62-year-old professional driver, had driven a truck for 2 days with minimal rest. While driving, he noted left foot paresis and numbness, along with geographical disorientation. Magnetic resonance imaging of the brain revealed multiple cerebral embolisms in the bilateral cerebral hemisphere. The only complications representing a stroke risk in this patient were a patent foramen ovale and an anterior septal aneurysm, as detected by transesophageal echocardiography. The patient was diagnosed with paradoxical cerebral embolism following his long drive. This case report examines the paradoxical cerebral emboli documented in a patient following a long period of driving.</description><dc:title>Economy Class Stroke Syndrome after a Long Drive</dc:title><dc:creator>Ryota Tanaka, Tadaaki Kawanabe, Yoshiya Yamauchi, Hideki Shimura, Yasutaka Tanaka, Nobukazu Miyamoto, Yuji Ueno, Takao Urabe, Nobutaka Hattori, Shigeki Tanaka</dc:creator><dc:identifier>10.1016/j.jstrokecerebrovasdis.2010.06.005</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2010-07-26</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2010-07-26</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>155</prism:startingPage><prism:endingPage>157</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305711003387/abstract?rss=yes"><title>Masthead</title><link>http://www.strokejournal.org/article/PIIS1052305711003387/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1052-3057(11)00338-7</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A1</prism:startingPage><prism:endingPage>A1</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305711003399/abstract?rss=yes"><title>Editorial Board</title><link>http://www.strokejournal.org/article/PIIS1052305711003399/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1052-3057(11)00339-9</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A2</prism:startingPage><prism:endingPage>A2</prism:endingPage></item><item rdf:about="http://www.strokejournal.org/article/PIIS1052305711003405/abstract?rss=yes"><title>Contents</title><link>http://www.strokejournal.org/article/PIIS1052305711003405/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1052-3057(11)00340-5</dc:identifier><dc:source>Journal of Stroke &amp; Cerebrovascular Diseases 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Stroke &amp; Cerebrovascular Diseases</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1052-3057(11)X0009-5</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A3</prism:startingPage><prism:endingPage>A4</prism:endingPage></item></rdf:RDF>
