5939 articles - 08.09.10
1: Neurology. 2010 Sep 7;75(10):924-932.
Granerod J, Tam CC, Crowcroft NS, Davies NW, Borchert M, Thomas SL.
Health Protection Agency Centre for Infections, Virus Reference Department, 61 Colindale Avenue, London NW9 5EQ, UK Julia.granerod@hpa.org.uk.
BACKGROUND: The threat of emerging infections and recognition of novel immune-mediated forms of encephalitis has raised the profile of this condition in recent years. Incidence is poorly defined and most cases have an unknown cause. There is currently much interest in identification of new microbial agents of encephalitis, but no work has investigated systematically reasons for lack of pathogen identification in studies. METHODS: We systematically reviewed published literature on incidence and etiology of encephalitis in non-outbreak settings and explored possible explanations for the large number of cases of unknown etiology. RESULTS: Annual incidence ranged from 0.07 to 12.6 cases per 100,000 population with an evident decrease over time (p = 0.01). The proportion of cases with unknown etiology was high across studies (>50% in 26 of 41 studies), with strong evidence of heterogeneity in study findings (p < 0.001). Our meta-regression identified study period, setting, and subsyndrome to be the main contributors to between-study variation, rather than methodologic factors such as study design, case definitions, sample types, and testing strategies. CONCLUSIONS: Our findings support the hypothesis that new and emerging infectious agents, or new forms of immune-mediated encephalitis, may be responsible for cases currently of unknown cause and encourage the ongoing global effort to identify these. Our review highlights research areas that might lead to a better understanding of the causes of encephalitis and ultimately reduce the morbidity and mortality associated with this devastating condition.
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PMID: 20820004 [PubMed - as supplied by publisher]2: Brain. 2010 Sep 3; [Epub ahead of print]
Kasper BS, Taylor DC, Janz D, Kasper EM, Maier M, Williams MR, Crow TJ.
1 Epilepsy Centre, Department of Neurology, University of Erlangen, 91054 Erlangen, Germany.
Professor J.A.N. Corsellis, whose life and work is recalled here, gained great insight into the meaning of morphological cerebral aberrations found in neuropsychiatric disease through exact neuropathological investigations of tissue specimens obtained from patients with distinct syndromes. He was a leading authority in the field. We have searched and compiled resources relating to J.A.N. Corsellis' life and work, including personal memories from colleagues and data from scientific publications. J.A.N. Corsellis made seminal contributions to the understanding of neuropsychiatric disease; his works substantially added to the understanding of the dementias, schizophrenia and the psychoses, and morphological sequelae of boxing. In seizure disorders, his name is linked to the first description of focal cortical dysplasia and limbic encephalitis, the pathology of status epilepticus and Ammon's horn sclerosis, and the systematic investigation of epilepsy surgery specimens in general. Both his life and work are closely linked to Runwell Hospital, Wickford, Essex and the Maudsley Hospital. During his professional life he established a large brain bank, now known as the Corsellis Collection. J.A.N. Corsellis had significant impact on neuroscience; many of his observations were groundbreaking and are still valid.
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PMID: 20817923 [PubMed - as supplied by publisher]3: Stroke. 2010 Sep 2; [Epub ahead of print]
Wolf SL, Thompson PA, Winstein CJ, Miller JP, Blanton SR, Nichols-Larsen DS, Morris DM, Uswatte G, Taub E, Light KE, Sawaki L.
From the Department of Rehabilitation Medicine, Departments of Medicine and Cell Biology, Emory University School of Medicine, Atlanta, Ga; Methodology and Data Analysis Center, Sanford Research/University of South Dakota, Vermillion, SD; Division of Biostatistics, Washington University School of Medicine, St. Louis, Mo; Division of Biokinesiology and Physical Therapy at the School of Dentistry, University of Southern California, Los Angeles, Calif; School of Allied Medical Professions, The Ohio State University, Columbus, Ohio; Department of Physical Therapy, Department of Psychology, University of Alabama at Birmingham, Birmingham, Ala; Department of Physical Therapy, University of Florida, Gainesville, Fla; Department of Physical Medicine and Rehabilitation, University of Kentucky, Lexington, Ky.
BACKGROUND AND PURPOSE: Although constraint-induced movement therapy (CIMT) has been shown to improve upper extremity function in stroke survivors at both early and late stages after stroke, the comparison between participants within the same cohort but receiving the intervention at different time points has not been undertaken. Therefore, the purpose of this study was to compare functional improvements between stroke participants randomized to receive this intervention within 3 to 9 months (early group) to participants randomized on recruitment to receive the identical intervention 15 to 21 months after stroke (delayed group). METHODS: Two weeks of CIMT was delivered to participants immediately after randomization (early group) or 1 year later (delayed group). Evaluators blinded to group designation administered primary (Wolf Motor Function Test, Motor Activity Log) and secondary (Stroke Impact Scale) outcome measures among the 106 early participants and 86 delayed participants before delivery of CIMT, 2 weeks thereafter, and 4, 8, and 12 months later. RESULTS: Although both groups showed significant improvements from pretreatment to 12 months after treatment, the earlier CIMT group showed greater improvement than the delayed CIMT group in Wolf Motor Function Test Performance Time and the Motor Activity Log (P<0.0001), as well as in Stroke Impact Scale Hand and Activities domains (P<0.0009 and 0.0214, respectively). Early and delayed group comparison of scores on these measures 24 months after enrollment showed no statistically significant differences between groups. CONCLUSIONS: CIMT can be delivered to eligible patients 3 to 9 months or 15 to 21 months after stroke. Both patient groups achieved approximately the same level of significant arm motor function 24 months after enrollment. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT00057018.">Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20814005&dopt=ExternalLink
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PMID: 20814005 [PubMed - as supplied by publisher]4: Stroke. 2010 Sep 2; [Epub ahead of print]
Khatri P, Kleindorfer DO, Yeatts SD, Saver JL, Levine SR, Lyden PD, Moomaw CJ, Palesch YY, Jauch EC, Broderick JP.
From the University of Cincinnati.
BACKGROUND AND PURPOSE: The pivotal National Institute of Neurological Disorders and Stroke recombinant tissue plasminogen activator trials excluded patients with ischemic stroke with specific minor presentations or rapidly improving symptoms. The recombinant tissue plasminogen activator product label notes that its use for minor neurological deficit or rapidly improving stroke symptoms has not been evaluated. As a result, patients with low National Institutes of Health Stroke Scale scores are not commonly treated in clinical practice. We sought to further characterize the patients with minor stroke who were included in the National Institute of Neurological Disorders and Stroke trials. METHODS: Minor strokes were defined as National Institutes of Health Stroke Scale score </=5 at baseline for this retrospective analysis, because this subgroup is most commonly excluded from treatment in clinical practice and trials. Clinical stroke syndromes were defined based on prespecified National Institutes of Health Stroke Scale item score clusters. Clinical outcomes were reviewed generally and within these cluster subgroups. RESULTS: Only 58 cases had National Institutes of Health Stroke Scale scores of 0 to 5 in the National Institute of Neurological Disorders and Stroke trials (42 recombinant tissue plasminogen activator and 16 placebo), and 2971 patients were excluded from the trials due to "rapidly improving" or "minor symptoms" as the primary reason. No patients were enrolled with isolated motor symptoms, isolated facial droop, isolated ataxia, dysarthria, isolated sensory symptoms, or with only symptoms/signs not captured by the National Institutes of Health Stroke Scale score (ie, National Institutes of Health Stroke Scale=0). There were </=3 patients with each of the other isolated deficits enrolled in the trial. CONCLUSIONS: The National Institute of Neurological Disorders and Stroke trials excluded a substantial number of strokes with minor presentations, those that were included were small in number, and conclusions about outcomes based on specific syndromes cannot be drawn. Further prospective, systematic study of this subgroup is needed.
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PMID: 20814000 [PubMed - as supplied by publisher]5: Lancet Neurol. 2010 Aug 26; [Epub ahead of print]
Kirschner J, Schessl J, Schara U, Reitter B, Stettner GM, Hobbiebrunken E, Wilichowski E, Bernert G, Weiss S, Stehling F, Wiegand G, Muller-Felber W, Thiele S, Grieben U, von der Hagen M, Lutschg J, Schmoor C, Ihorst G, Korinthenberg R.
Division of Neuropaediatrics and Muscle Disorders, University Medical Centre, Freiburg, Germany.
BACKGROUND: Duchenne muscular dystrophy is a rare X-linked progressive disease characterised by loss of ambulation at about age 10 years, with death in early adulthood due to respiratory and cardiac insufficiency. Steroids are effective at slowing the progression of muscle weakness; however, their use is limited by side-effects, prompting the search for alternatives. We assessed the effect of ciclosporin A as monotherapy and in combination with intermittent prednisone for the treatment of ambulant patients with this disorder. METHODS: Our study was a parallel-group, placebo-controlled, double-blind, multicentre trial at trial sites of the German muscular dystrophy network, MD-NET, over 36 months. Ambulant patients with Duchenne muscular dystrophy who were aged 5 years or older were randomly assigned to receive either ciclosporin A (3.5-4.0 mg/kg per day) or matching placebo. Allocation was done centrally with computer-generated random numbers. Patients and investigators were masked to the allocated treatment. After 3 months of treatment, both groups were also given intermittent prednisone for a further 12 months (0.75 mg/kg, alternating 10 days on with 10 days off). All patients who received at least one dose of study drug or placebo were included in the primary analysis. The primary outcome measure was manual muscle strength measured on the Medical Research Council (MRC) scale. This trial is registered with the German clinical trial register DRKS, number DRKS00000445. FINDINGS: 77 patients were randomly assigned to the ciclosporin A group and 76 to the placebo group; 73 patients on ciclosporin A and 73 on placebo received at least one dose and were available for efficacy analyses. 3 months of treatment with ciclosporin A alone did not show any significant improvement in primary outcome measures (mean change in the proportion of a possible total MRC score [%MRC] was -2.6 [SD 6.0] for patients on ciclosporin A and -0.8 [4.9] for patients on placebo; adjusted group difference estimate -0.88, 97.5% CI -2.6 to 0.9; p=0.26). The combination of ciclosporin A with intermittent steroids was not better than intermittent steroids alone over 12 months (mean change in %MRC was 0.7 [7.1] for patients on ciclosporin A and -0.3 [7.9] for patients on placebo; adjusted group difference estimate -0.85, -3.6 to 1.9; p=0.48). Numbers of adverse events (75 in patients on ciclosporin A and 74 on placebo) and serious adverse events (four with ciclosporin A and four with placebo) did not differ significantly between groups. INTERPRETATION: Ciclosporin A alone or in combination with intermittent prednisone does not improve muscle strength or functional abilities in ambulant boys with Duchenne muscular dystrophy, but is safe and well tolerated. FUNDING: German Federal Ministry of Education and Research, Action Benni and co eV, Novartis Pharma AG, and Deutsche Gesellschaft fur Muskelkranke eV. Copyright (c) 2010 Elsevier Ltd. All rights reserved.
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PMID: 20801085 [PubMed - as supplied by publisher]6: Stroke. 2010 Aug 26; [Epub ahead of print]
Taylor A, Castle A, Merino JG, Hsia A, Kidwell CS, Warach S.
From Section on Stroke Diagnostics and Therapeutics, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland; Department of Neurology, Georgetown University Hospital, Washington, DC; Suburban Hospital Stroke Program, Bethesda, Maryland; Washington Hospital Center Stroke Center, Washington, DC.
BACKGROUND AND PURPOSE: Clinical trial planning and site selection require an accurate estimate of the number of eligible patients at each site. In this study, we developed a tool to calculate the proportion of patients who would meet a specific trial's age, baseline severity, and time to treatment inclusion criteria. METHODS: From a sample of 1322 consecutive patients with acute ischemic cerebrovascular syndromes, we developed regression curves relating the proportion of patients within each range of the 3 variables. We used half the patients to develop the model and the other half to validate it by comparing predicted vs actual proportions who met the criteria for 4 current stroke trials. RESULTS: The predicted proportion of patients meeting inclusion criteria ranged from 6% to 28% among the different trials. The proportion of trial-eligible patients predicted from the first half of the data were within 0.4% to 1.4% of the actual proportion of eligible patients. This proportion increased logarithmically with National Institutes of Health Stroke Scale score and time from onset; lowering the baseline limits of the National Institutes of Health Stroke Scale score and extending the treatment window would have the greatest impact on the proportion of patients eligible for a stroke trial. CONCLUSIONS: This model helps estimate the proportion of stroke patients eligible for a study based on different upper and lower limits for age, stroke severity, and time to treatment, and it may be a useful tool in clinical trial planning.
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PMID: 20798375 [PubMed - as supplied by publisher]7: BMC Neurol. 2010 Aug 23;10(1):72 [Epub ahead of print]
Hosseini AA, Sobhani-Rad D, Ghandehari K, Benamer HT.
ABSTRACT: BACKGROUND: Cerebrovascular disease is the second commonest cause of death, and over a third of stroke deaths occur in developing countries. To fulfil the current gap on data, this systematic review is focused on the frequency of stroke, risk factors, stroke types and mortality in Iran. METHODS: Thirteen relevant articles were identified by keyword searching of PubMed, Iranmedex, Iranian University index Libraries and the official national data on burden of diseases. RESULTS: The publication dates ranged from 1990 to 2008. The annual stroke incidence of various ages ranged from 23 to 103 per 100,000 population. This is comparable to the figures from Arab Countries, higher than sub-Saharan Africa, but lower than developed countries, India, the Caribbean, Latin America, and China. Similarly to other countries, ischaemic stroke was the commonest subtype. Likewise, the most common related risk factor is hypertension in adults, but cardiac causes in young stroke. The 28-day case fatality rate is reported at 19-31%. CONCLUSIONS: Data on the epidemiology of stroke, its pattern and risk factors from Iran is scarce, but the available data highlights relatively low incidence of stroke. This may reflect a similarity towards the neighbouring nations, and a contrast with the West.
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PMID: 20731823 [PubMed - as supplied by publisher]8: Pain. 2010 Aug 18; [Epub ahead of print]
Glombiewski JA, Sawyer AT, Gutermann J, Koenig K, Rief W, Hofmann SG.
Department of Psychology, Boston University, Boston, MA, USA; University of Marburg, Department of Clinical Psychology and Psychotherapy, Marburg, Germany.
The aims of the present analysis were to investigate the short- and long-term efficacies and treatment moderators of psychological interventions for fibromyalgia. A literature search using PubMed, PsychINFO, the Cochrane Library, and manual searches identified 23 eligible studies including 30 psychological treatment conditions and 1396 patients. Meta-analytic integration resulted in a significant but small effect size for short-term pain reduction (Hedges's g=0.37, 95% confidence interval (CI): 0.27-0.48) and a small-to-medium effect size for long-term pain reduction over an average follow-up phase of 7.4months (Hedges's g=0.47, 95% CI: 0.3-0.65) for any psychological intervention. Psychological treatments also proved effective in reducing sleep problems (Hedges's g=0.46, 95% CI: 0.28-0.64), depression (Hedges's g=0.33, 95% CI: 0.20-0.45), functional status (Hedges's g=0.42, 95% CI: 0.25-0.58), and catastrophizing (Hedges's g=0.33, 95% CI: 0.17-0.49). These effects remained stable at follow-up. Moderator analyses revealed cognitive-behavioral treatment to be significantly better than other psychological treatments in short-term pain reduction (Hedges's g=0.60, 95% CI: 0.46-0.76). Higher treatment dose was associated with better outcome. Publication-bias analyses demonstrated that the effect sizes were robust. The results suggest that the effects of psychological treatments for fibromyalgia are relatively small but robust and comparable to those reported for other pain and drug treatments used for this disorder. Cognitive-behavioral therapy was associated with the greatest effect sizes. Copyright (c) 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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PMID: 20727679 [PubMed - as supplied by publisher]9: Stroke. 2010 Aug 19; [Epub ahead of print]
Pickett CA, Jackson JL, Hemann BA, Atwood JE.
From Keller Army Hospital, U.S. Military Academy, West Point, NY; Department of Cardiology, Walter Reed Army Medical Center, Washington, DC; and the Division of General Medicine, Zablocki VA Medical Center, Milwaukee, Wisc.
BACKGROUND AND PURPOSE: Current guidelines recommend against routine auscultation of carotid arteries, believing that carotid bruits are poor predictors of either underlying carotid stenosis or stroke risk in asymptomatic patients. We investigated whether the presence of a carotid bruit is associated with increased risk for transient ischemic attack, stroke, or death by stroke (stroke death). METHODS: We searched Medline (1966 to December 2009) and EMBASE (1974 to December 2009) with the terms "carotid" and "bruit." Bibliographies of all retrieved articles were also searched. Articles were included if they prospectively reported the incidence of transient ischemic attack, stroke, or stroke death in asymptomatic adults. Two authors independently reviewed and extracted data. RESULTS: We included 28 prospective cohort articles that followed a total of 17 913 patients for 67 708 patient-years. Among studies that directly compared patients with and without bruits, the rate ratio for transient ischemic attack was 4.00 (95% CI, 1.8 to 9.0, P<0.0005, n=5 studies), stroke was 2.5 (95% CI, 1.8 to 3.5, P<0.0005, n=6 studies), and stroke death was 2.7 (95% CI, 1.33 to 5.53, P=0.002, n=3 studies). Among the larger pool of studies that provided data on rates, transient ischemic attack rates were 2.6 per 100 patient-years (95% CI, 2.0 to 3.2, P<0.0005, n=24 studies) for those with bruits compared with 0.9 per 100 patient-years (95% CI, 0.2 to 1.6, P=0.02, n=5 studies) for those without carotid bruits. Stroke rates were 1.6 per 100 patient-years (95% CI, 1.3 to 1.9, P<0.0005, n=26 studies) for those with bruits compared with 1.3 per 100 patient-years (95% CI, 0.8 to 1.7, P<0.0005, n=6) without carotid bruits, and death rates were 0.32 (95% CI, 0.20 to 0.44, P<0.005, n=13 studies) for those with bruits compared with 0.35 (95% CI, 0.00 to 0.81, P=0.17, n=3 studies) for those without carotid bruits. CONCLUSIONS: The presence of a carotid bruit may increase the risk of cerebrovascular disease.
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PMID: 20724720 [PubMed - as supplied by publisher]10: Lancet Neurol. 2010 Sep;9(9):921-32.
Petzold A, de Boer JF, Schippling S, Vermersch P, Kardon R, Green A, Calabresi PA, Polman C.
UCL Institute of Neurology/National Hospital for Neurology and Neurosurgery, Department of Neuroimmunology, Queen Square, London, UK. a.petzold@ion.ucl.ac.uk
Optical coherence tomography (OCT) is a new method that could aid analysis of neurodegeneration in multiple sclerosis (MS) by capturing thinning of the retinal nerve fibre layer (RNFL). Meta-analyses of data for time domain OCT show RNFL thinning of 20.38 microm (95% CI 17.91-22.86, n=2063, p<0.0001) after optic neuritis in MS, and of 7.08 microm (5.52-8.65, n=3154, p<0.0001) in MS without optic neuritis. The estimated RNFL thinning in patients with MS is greater than the extent expected in normal ageing, probably because of retrograde trans-synaptic degeneration and progressive loss of retinal ganglion cells, in addition to the more pronounced thinning caused by optic neuritis if present. RNFL thickness correlates with visual and neurological functioning as well as with paraclinical data. Developments that could improve understanding of the relation between structure and function in MS pathophysiology include spectral or Fourier domain OCT technology, polarisation-sensitive OCT, fluorescence labelling, structural assessment of action-potential propagation, and segmentation algorithms allowing quantitative assessment of retinal layers. Copyright 2010 Elsevier Ltd. All rights reserved.
Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't
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PMID: 20723847 [PubMed - in process]11: BMC Neurol. 2010 Aug 19;10(1):70 [Epub ahead of print]
van Nimwegen M, Speelman AD, Smulders K, Overeem S, Borm GF, Backx FJ, Bloem BR, Munneke M, Study Group OB.
ABSTRACT: BACKGROUND: Many patients with Parkinson's disease (PD) lead a sedentary lifestyle. Promotion of physical activities may beneficially affect the clinical presentation of PD, and perhaps even modify the course of PD. However, because of physical and cognitive impairments, patients with PD require specific support to increase their level of physical activity. METHODS: We developed the ParkFit Program: a PD-specific and multifaceted behavioral program to promote physical activity. The emphasis is on creating a behavioral change, using a combination of accepted behavioral motivation techniques. In addition, we designed a multicentre randomized clinical trial to investigate whether this ParkFit Program increases physical activity levels over two years in sedentary PD patients. We intended to include 700 sedentary patients. Primary endpoint is the time spent on physical activities per week, which will be measured every six months using an interview-based 7-day recall. RESULTS: In total 3453 PD patients were invited to participate. Ultimately, 586 patient - with a mean (SD) age of 64.1 (7.6) years and disease duration of 5.3 (4.5) years - entered the study. Study participants were younger, had a shorter disease duration and were less sedentary compared with eligible PD patients not willing to participate. DISCUSSION: The ParkFit trial is expected to yield important new evidence about behavioral interventions to promote physical activity in sedentary patients with PD. The results of the trial are expected in 2012. Trial registration: clinicaltrials.gov (nr NCT00748488).
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PMID: 20723221 [PubMed - as supplied by publisher]12: Pain. 2010 Aug 10; [Epub ahead of print]
Cifuentes M, Webster B, Genevay S, Pransky G.
Liberty Mutual Research Institute for Safety, University of Massachusetts Lowell, USA.
Despite utilization concerns, little information is available on opioid prescribing for acute, disabling low back pain (LBP) and how opioid features (purity, strength, and length of action) and dose change over time. This information is important in targeting guideline implementation efforts and identifying risks for inappropriate prescribing. Using 2002-2003 United States' workers compensation claims, a cohort of 2868 cases with a new episode of work-related LBP and at least one opioid prescription was followed for 2years. Opioid prescriptions (timing, dose, and formulation), demographics, and medical data were captured. A longitudinal model of change was used to evaluate factors associated with dosing changes. Opioid prescribing typically began early in the course of care (median=8days, Inter-Quartile Range (IQR)=3, 43days) and was often prolonged (median=46days, IQR=14, 329). At the end of the observation period, 7.1% of non-surgical cases and 30.6% of surgical cases were still receiving opioids. The number of days between the initial LBP report and the first opioid prescription had the greatest association with subsequent dose escalation. Dose escalation was greater with pure formulations, and was not related to clinical severity or surgery. In contrast to previous and current guideline recommendations, opioid prescribing for acute LBP was often prolonged, and longer for surgical cases. These results reinforce recommendations to limit opioid duration, and suggest that consideration of opioid features, purity as an important one, can be part of a strategy to prevent escalating dosages. Copyright (c) 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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PMID: 20705393 [PubMed - as supplied by publisher]13: Neurology. 2010 Aug 10;75(6):508-12.
Tan EK, Kwok HK, Tan LC, Zhao WT, Prakash KM, Au WL, Pavanni R, Ng YY, Satake W, Zhao Y, Toda T, Liu JJ.
Department of Neurology, Singapore General Hospital, Singapore. gnrtek@sgh.com.sg
OBJECTIVE: A genome-wide association study (GWAS) in the Japanese population identified 2 new Parkinson disease (PD) susceptibility loci on 1q32 (PARK16) (OMIM 613164) and BST1. We analyzed single nucleotide polymorphism (SNPs) located at the GWAS-linked loci (PARK16, PARK8, PARK1, and BST1) in a Chinese population and also conducted a meta-analysis in Asians by pooling 2 independent replication studies from Japan. METHODS: We conducted an analysis of 13 SNPs associated with PD GWAS-linked loci in 2 case-control cohorts comprised of 1,349 ethnic Chinese subjects. RESULTS: PARK16, PARK8, and PARK1 loci but not BST1 were found to be associated with PD. PARK16 SNPs were associated with a decreased risk while PARK1 and PARK8 SNPs were associated with an increased risk of PD. A pooled analysis of our Chinese cohorts and 2 Japanese replication cohorts involving 1,366 subjects with PD and 16,669 controls revealed robust association with these 3 loci and also BST1. There was a trend toward a stronger protective effect of SNPs at the PARK16 locus in sporadic PD compared to familial cases and in older compared to younger subjects. CONCLUSIONS: Our study reaffirms the role of GWAS-linked loci in PD in Asian subjects and the strength of association is similar between Chinese and Japanese subjects. Efforts to elucidate the associated gene within PARK16 locus are warranted.
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PMID: 20697102 [PubMed - in process]14: Arch Neurol. 2010 Aug;67(8):949-56.
De Meyer G, Shapiro F, Vanderstichele H, Vanmechelen E, Engelborghs S, De Deyn PP, Coart E, Hansson O, Minthon L, Zetterberg H, Blennow K, Shaw L, Trojanowski JQ; Alzheimer's Disease Neuroimaging Initiative.
Innogenetics, Industriepark Zwijnaarde 7, Box 4, B-9052 Gent, Belgium.
OBJECTIVE: To identify biomarker patterns typical for Alzheimer disease (AD) in an independent, unsupervised way, without using information on the clinical diagnosis. DESIGN: Mixture modeling approach. SETTING: Alzheimer's Disease Neuroimaging Initiative database. Patients or Other PARTICIPANTS: Cognitively normal persons, patients with AD, and individuals with mild cognitive impairment. MAIN OUTCOME MEASURES: Cerebrospinal fluid-derived beta-amyloid protein 1-42, total tau protein, and phosphorylated tau(181P) protein concentrations were used as biomarkers on a clinically well-characterized data set. The outcome of the qualification analysis was validated on 2 additional data sets, 1 of which was autopsy confirmed. RESULTS: Using the US Alzheimer's Disease Neuroimaging Initiative data set, a cerebrospinal fluid beta-amyloid protein 1-42/phosphorylated tau(181P) biomarker mixture model identified 1 feature linked to AD, while the other matched the "healthy" status. The AD signature was found in 90%, 72%, and 36% of patients in the AD, mild cognitive impairment, and cognitively normal groups, respectively. The cognitively normal group with the AD signature was enriched in apolipoprotein E epsilon4 allele carriers. Results were validated on 2 other data sets. In 1 study consisting of 68 autopsy-confirmed AD cases, 64 of 68 patients (94% sensitivity) were correctly classified with the AD feature. In another data set with patients (n = 57) with mild cognitive impairment followed up for 5 years, the model showed a sensitivity of 100% in patients progressing to AD. CONCLUSIONS: The mixture modeling approach, totally independent of clinical AD diagnosis, correctly classified patients with AD. The unexpected presence of the AD signature in more than one-third of cognitively normal subjects suggests that AD pathology is active and detectable earlier than has heretofore been envisioned.
Publication Types: Research Support, Non-U.S. Gov't
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PMID: 20697045 [PubMed - indexed for MEDLINE]15: Arch Neurol. 2010 Aug;67(8):941-7.
Lynch DR, Perlman SL, Meier T.
Division of Neurology, Children's Hospital of Philadelphia, 502 Abramson Bldg, Philadelphia, PA 19104-4318, USA. lynch@pharm.med.upenn.edu
OBJECTIVE: To assess the efficacy of idebenone on neurological function in patients with Friedreich ataxia. DESIGN: Randomized, double-blind, placebo-controlled intervention trial. SETTING: Children's Hospital of Philadelphia and the University of California at Los Angeles. PARTICIPANTS: Seventy ambulatory pediatric patients (age, 8-18 years) with a baseline International Cooperative Ataxia Rating Scale (ICARS) score of 10 to 54. INTERVENTIONS: Participants were randomized into 1 of 3 treatment arms: 450 or 900 mg of idebenone per day (in those with a body weight < or = or >45 kg, respectively; n = 22); 1350 or 2250 mg of idebenone per day (n = 24); or placebo (n = 24). MAIN OUTCOME MEASURES: Mean change from baseline to week 24 in ICARS score was the primary efficacy variable. Mean change in Friedreich Ataxia Rating Scale (FARS) score, performance measures, and activities of daily living were the secondary efficacy variables. RESULTS: Patients who received idebenone improved by 2.5 points on mean ICARS score compared with baseline, while patients in the placebo group improved by 1.3 points. Patients who took idebenone also improved by 1.6 points on the FARS, while patients taking placebo declined by 0.6 points. For both end points, the difference between the idebenone and placebo groups was not statistically different. CONCLUSIONS: Idebenone did not significantly alter neurological function in Friedreich ataxia during the 6-month study. Larger studies of longer duration may be needed to assess the therapeutic potential of drug candidates on neurological function in Friedreich ataxia. Trial Registration clinicaltrials.gov Identifier: NCT00537680.
Publication Types: Clinical Trial, Phase III Randomized Controlled Trial Research Support, N.I.H., Extramural
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20697044&dopt=ExternalLink
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PMID: 20697044 [PubMed - indexed for MEDLINE]16: Arch Neurol. 2010 Aug;67(8):931-40.
Neligan A, Shorvon SD.
Box 5, Department of Clinical and Experimental Epilepsy, UCL Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom.
We conducted a systematic review of all studies of status epilepticus (SE) with more than 30 patients published between January 1, 1990, and December 31, 2008, to determine the frequencies of the common underlying causes and the extent to which the underlying causes affect the prognosis of an episode of SE. The frequencies of underlying causes vary among studies and show marked geographic differences, but in most studies, the most common underlying causes were cerebrovascular disease and low antiepileptic drug levels. A relatively good prognosis of SE is found when the underlying cause is associated with low antiepileptic drug levels or alcohol abuse, and a relatively poor outcome occurs when the underlying cause is cerebrovascular disease, particularly in the case of SE due to acute cerebral anoxia, but in most conditions, the reported prognosis is variable. Also, when SE occurs in the context of an acute cerebral insult, such as cerebral infection or cerebrovascular disease, the prognosis of the acute cerebral event is worsened.
Publication Types: Research Support, Non-U.S. Gov't Review
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20697043&dopt=ExternalLink
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PMID: 20697043 [PubMed - indexed for MEDLINE]17: Arch Neurol. 2010 Sep 3; [Epub ahead of print]
Jun G, Naj AC, Beecham GW, Wang LS, Buros J, Gallins PJ, Buxbaum JD, Ertekin-Taner N, Fallin MD, Friedland R, Inzelberg R, Kramer P, Rogaeva E, St George-Hyslop P, Arnold SE, Baldwin CT, Barber R, Beach T, Bigio EH, Bird TD, Boxer A, Burke JR, Cairns N, Carroll SL, Chui HC, Clark DG, Cotman CW, Cummings JL, Decarli C, Diaz-Arrastia R, Dick M, Dickson DW, Ellis WG, Fallon KB, Farlow MR, Ferris S, Frosch MP, Galasko DR, Gearing M, Geschwind DH, Ghetti B, Gilman S, Giordani B, Glass J, Graff-Radford NR, Green RC, Growdon JH, Hamilton RL, Harrell LE, Head E, Honig LS, Hulette CM, Hyman BT, Jicha GA, Jin LW, Johnson N, Karlawish J, Karydas A, Kaye JA, Kim R, Koo EH, Kowall NW, Lah JJ, Levey AI, Lieberman A, Lopez OL, Mack WJ, Markesbery W, Marson DC, Martiniuk F, Masliah E, McKee AC, Mesulam M, Miller JW, Miller BL, Miller CA, Parisi JE, Perl DP, Peskind E, Petersen RC, Poon W, Quinn JF, Raskind M, Reisberg B, Ringman JM, Roberson ED, Rosenberg RN, Sano M, Schneider JA, Schneider LS, Seeley W, Shelanski ML, Smith CD, Spina S, Stern RA, Tanzi RE, Trojanowski JQ, Troncoso JC, Van Deerlin VM, Vinters HV, Vonsattel JP, Weintraub S, Welsh-Bohmer KA, Woltjer RL, Younkin SG, Cantwell LB, Dombroski BA, Saykin AJ, Reiman EM, Bennett DA, Morris JC, Lunetta KL, Martin ER, Montine TJ, Goate AM, Blacker D, Tsuang DW, Beekly D, Cupples LA, Hakonarson H, Kukull W, Foroud TM, Haines J, Mayeux R, Farrer LA, Pericak-Vance MA, Schellenberg GD; Alzheimer's Disease Genetics Consortium; Arnold SE, Baldwin CT, Barber R, Beach T, Bigio EH, Bird TD, Boxer A, Burke JR, Cairns N, Carroll SL, Chui HC, Clark DG, Cotman CW, Cummings JL, Decarli C, Diaz-Arrastia R, Dick M, Dickson DW, Ellis WG, Fallon KB, Farlow MR, Ferris S, Frosch MP, Galasko DR, Gearing M, Geschwind DH, Ghetti B, Gilman S, Giordani B, Glass J, Graff-Radford NR, Green RC, Growdon JH, Hamilton RL, Harrell LE, Head E, Honig LS, Hulette CM, Hyman BT, Jicha GA, Jin LW, Johnson N, Karlawish J, Karydas A, Kaye JA, Kim R, Koo EH, Kowall NW, Lah JJ, Levey AI, Lieberman A, Lopez OL, Mack WJ, Markesbery W, Marson DC, Martiniuk F, Masliah E, McKee AC, Mesulam M, Miller JW, Miller BL, Miller CA, Parisi JE, Perl DP, Peskind E, Petersen RC, Poon W, Quinn JF, Raskind M, Reisberg B, Ringman JM, Roberson ED, Rosenberg RN, Sano M, Schneider JA, Schneider LS, Seeley W, Shelanski ML, Smith CD, Spina S, Stern RA, Tanzi RE, Trojanowski JQ, Troncoso JC, Van Deerlin VM, Vinters HV, Vonsattel JP, Weintraub S, Welsh-Bohmer KA, Woltjer RL, Younkin SG.
Ophthalmology (Dr Jun), Biostatistics (Drs Jun, Lunetta, and Cupples), Neurology (Dr Farrer), and Genetics and Genomics and Epidemiology (Dr Farrer), Boston University, Boston, and Department of Psychiatry and Epidemiology (Dr Blacker), Massachusetts General Hospital, Charlestown; The John P. Hussman Institute for Human Genomics (Drs Naj, Beecham, and Pericak-Vance and Mr Gallins) and Dr John T. Macdonald Foundation Department of Human Genetics (Drs Beecham, Martin, and Pericak-Vance), University of Miami, Miami, and Departments of Neuroscience and Neurology, Mayo Clinic Jacksonville, Jacksonville (Dr Ertekin-Taner), Florida; Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine (Drs Wang, Dombroski, and Schellenberg and Ms Cantwell), and Center for Applied Genomics, Children's Hospital of Philadelphia (Dr Hakonarson), Philadelphia; Departments of Psychiatry, Neuroscience, and Genetics and Genomic Sciences, Mount Sinai School of Medicine (Dr Buxbaum), and Sergievsky Center and Taub Institute (Dr Mayeux), Columbia University, New York, New York; Department of Epidemiology, Johns Hopkins University, Baltimore, Maryland (Dr Fallin); Department of Neurology, University of Louisville, Louisville, Kentucky (Dr Friedland); Sheba Medical Center, Departments of Neurology and Medicine, Tel Aviv University, Israel (Dr Inzelberg); Departments of Neurology and Molecular and Medical Genetics, Oregon Health and Science University, Portland (Dr Kramer); Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto, Toronto, Ontario, Canada (Drs Rogaeva and St. George-Hyslop); Cambridge Institute for Medical Research, Department of Clinical Neurosciences, University of Cambridge, Cambridge, England (Dr St. George-Hyslop); Departments of Radiology and Imaging Sciences (Dr Saykin) and Medical and Molecular Genetics (Drs Saykin and Foroud), Indiana University, Indianapolis; Arizona Alzheimer's Consortium and Banner Alzheimer's Institute and Neurogenomics Division, Translational Genomics Research Institute and Department of Psychiatry, University of Arizona, Phoenix (Dr Reiman); Rush Alzheimer's Disease Center and Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois (Dr Bennett); Departments of Neurology (Dr Morris), Pathology and Immunology (Dr Morris), and Psychiatry (Dr Goate), Washington University, St Louis, Missouri; Departments of Pathology (Dr Montine) and Psychiatry and Behavioral Sciences (Dr Tsuang), National Alzheimer's Coordinating Center (Mr Beekly and Dr Kukull), and Department of Epidemiology, University of Washington (Dr Kukull), Seattle; and Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee (Dr Haines).
OBJECTIVES: To determine whether genotypes at CLU, PICALM, and CR1 confer risk for Alzheimer disease (AD) and whether risk for AD associated with these genes is influenced by apolipoprotein E (APOE) genotypes. DESIGN: Association study of AD and CLU, PICALM, CR1, and APOE genotypes. SETTING: Academic research institutions in the United States, Canada, and Israel. PARTICIPANTS: Seven thousand seventy cases with AD, 3055 with autopsies, and 8169 elderly cognitively normal controls, 1092 with autopsies, from 12 different studies, including white, African American, Israeli-Arab, and Caribbean Hispanic individuals. RESULTS: Unadjusted, CLU (odds ratio [OR], 0.91; 95% confidence interval [CI], 0.85-0.96 for single-nucleotide polymorphism [SNP] rs11136000), CR1 (OR, 1.14; 95% CI, 1.07-1.22; SNP rs3818361), and PICALM (OR, 0.89; 95% CI, 0.84-0.94, SNP rs3851179) were associated with AD in white individuals. None were significantly associated with AD in the other ethnic groups. APOE epsilon4 was significantly associated with AD (ORs, 1.80-9.05) in all but 1 small white cohort and in the Arab cohort. Adjusting for age, sex, and the presence of at least 1 APOE epsilon4 allele greatly reduced evidence for association with PICALM but not CR1 or CLU. Models with the main SNP effect, presence or absence of APOE epsilon4, and an interaction term showed significant interaction between presence or absence of APOE epsilon4 and PICALM. CONCLUSIONS: We confirm in a completely independent data set that CR1, CLU, and PICALM are AD susceptibility loci in European ancestry populations. Genotypes at PICALM confer risk predominantly in APOE epsilon4-positive subjects. Thus, APOE and PICALM synergistically interact.
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20697030&dopt=ExternalLink
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PMID: 20697030 [PubMed - as supplied by publisher]18: Ann Neurol. 2010 Aug;68(2):126-35.
Perkes I, Baguley IJ, Nott MT, Menon DK.
Westmead Hospital, Australia.
Severe excessive autonomic overactivity occurs in a subgroup of people surviving acquired brain injury, the majority of whom show paroxysmal sympathetic and motor overactivity. Delayed recognition of paroxysmal sympathetic hyperactivity (PSH) after brain injury may increase morbidity and long-term disability. Despite its significant clinical impact, the scientific literature on this syndrome is confusing; there is no consensus on nomenclature, etiological information for diagnoses preceding the condition is poorly understood, and the evidence base underpinning our knowledge of the pathophysiology and management strategies is largely anecdotal. This systematic literature review identified 2 separate categories of paroxysmal autonomic overactivity, 1 characterized by relatively pure sympathetic overactivity and another group of disorders with mixed parasympathetic/sympathetic features. The PSH group comprised 349 reported cases, with 79.4% resulting from traumatic brain injury (TBI), 9.7% from hypoxia, and 5.4% from cerebrovascular accident. Although TBI is the dominant causative etiology, there was some suggestion that the true incidence of the condition is highest following cerebral hypoxia. In total, 31 different terms were identified for the condition. Although the most common term in the literature was dysautonomia, the consistency of sympathetic clinical features suggests that a more specific term should be used. The findings of this review suggest that PSH be adopted as a more clinically relevant and appropriate term. The review highlights major problems regarding conceptual definitions, diagnostic criteria, and nomenclature. Consensus on these issues is recommended as an essential basis for further research in the area.
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20695005&dopt=ExternalLink
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PMID: 20695005 [PubMed - in process]19: Pain. 2010 Aug 5; [Epub ahead of print]
Niesters M, Dahan A, Kest B, Zacny J, Stijnen T, Aarts L, Sarton E.
Department of Anesthesiology, Leiden University Medical Center, 2300 RC Leiden, The Netherlands.
Although a contribution of sex in opioid efficacy has garnered much attention, the confirmation and direction of any such difference remain elusive. We performed a systematic review of the available literature on sex differences in mu and mixed mu/kappa opioid effect on acute and experimental pain. Fifty unique studies (including three unpublished studies) were included in the analyses. Across the 25 clinical studies on mu-opioids there was no significant sex-analgesia association. Restricting the analysis to patient-controlled analgesia (PCA) studies (irrespective of the opioid) yielded greater analgesia in women (n=15, effect size 0.22, 95% c.i. 0.02-0.42, P=0.028). Further restricting the analysis to PCA morphine studies yielded an even greater effect in women (n=11, effect size=0.36, 95% c.i. 0.17-0.56, P=0.003). Meta-regression indicated that the longer the duration of PCA, the difference in effect between the sexes further increased. Across experimental pain studies on mu-opioids women had greater antinociception from opioids (n=11, effect size=0.35; 95% c.i. 0.01-0.69, P=0.047), which was predominantly due to 6 morphine studies. Female patients had greater mu/kappa opioid analgesia (n=7, effect size 0.84; 95% c.i. 0.25-1.43, P=0.005), but no sex-analgesia association was present in experimental studies (n=7). Sex differences exist in morphine-induced analgesia in both experimental pain studies and clinical PCA studies, with greater morphine efficacy in women. The data on non-morphine mu and mixed mu/kappa-opioids are less convincing and require further study. Copyright (c) 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20692097&dopt=ExternalLink
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PMID: 20692097 [PubMed - as supplied by publisher]20: Lancet Neurol. 2010 Sep;9(9):875-84. Epub 2010 Aug 4.
Katsuno M, Banno H, Suzuki K, Takeuchi Y, Kawashima M, Yabe I, Sasaki H, Aoki M, Morita M, Nakano I, Kanai K, Ito S, Ishikawa K, Mizusawa H, Yamamoto T, Tsuji S, Hasegawa K, Shimohata T, Nishizawa M, Miyajima H, Kanda F, Watanabe Y, Nakashima K, Tsujino A, Yamashita T, Uchino M, Fujimoto Y, Tanaka F, Sobue G; Japan SBMA Interventional Trial for TAP-144-SR (JASMITT) study group.
Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
BACKGROUND: Spinal and bulbar muscular atrophy is a hereditary motor neuron disease caused by the expansion of a polyglutamine tract in the androgen receptor. At present there are no treatments for spinal and bulbar muscular atrophy, although leuprorelin suppressed the accumulation of pathogenic androgen receptors in a phase 2 trial. We aimed to assess the efficacy and safety of leuprorelin for spinal and bulbar muscular atrophy. METHODS: The Japan SBMA Interventional Trial for TAP-144-SR (JASMITT) was a 48-week, randomised, double-blind, placebo-controlled trial done at 14 hospitals between August, 2006, and March, 2008. Patients with spinal and bulbar muscular atrophy were randomly assigned (1:1) by minimisation to subcutaneous 11.25 mg leuprorelin or identical placebo every 12 weeks. Patients and investigators were masked to treatment allocation. The primary endpoint was pharyngeal barium residue, which indicates incomplete bolus clearance, measured at week 48 by videofluorography. All patients who were randomly assigned and who were assessed with videofluorography at least once were included in the analyses. This study is registered with the JMACCT clinical trials registry, number JMA-IIA00009, and the UMIN clinical trials registry, number UMIN000000465. FINDINGS: 204 patients were randomly assigned and 199 started treatment: 100 with leuprorelin and 99 with placebo. At week 48, the pharyngeal barium residue after initial swallowing had changed by -5.1% (SD 21.0) in the leuprorelin group and by 0.2% (18.2) in the placebo group (difference between groups -5.3%; 95% CI -10.8 to 0.3; p=0.063). The mean difference in pharyngeal barium residue after piecemeal deglutition at week 48 was -3.2% (-6.4 to 0.0; p=0.049), but there was no significant difference between the groups after covariate adjustment for the baseline data (-4.1 to 1.6; p=0.392). In a predefined subgroup analysis, leuprorelin treatment was associated with a greater reduction in barium residue after initial swallowing than was placebo in patients with a disease duration less than 10 years (difference between groups -9.8, -17.1 to -2.5; p=0.009). There were no significant differences in the number of drug-related adverse events between groups (57 of 100 in the leuprorelin group and 54 of 99 in the placebo group; p=0.727). INTERPRETATION: 48 weeks of treatment with leuprorelin did not show significant effects on swallowing function in patients with spinal and bulbar muscular atrophy, although it was well tolerated. Disease duration might influence the efficacy of leuprorelin and thus further clinical trials with sensitive outcome measures should be done in subpopulations of patients. FUNDING: Large Scale Clinical Trial Network Project, Japan and Takeda Pharmaceuticals. Copyright 2010 Elsevier Ltd. All rights reserved.
Publication Types: Research Support, Non-U.S. Gov't
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PMID: 20691641 [PubMed - in process]