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September 2019 - July 1959

Decade

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Issue

May 2011, Vol 68, No. 5, Pages 559-686

Editorial

Expedited Publication Initiative

Abstract Full Text
Arch Neurol. 2011;68(5):563. doi:10.1001/archneurol.2010.353

Statins After Intracerebral Hemorrhage: To Treat or Not to Treat

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Arch Neurol. 2011;68(5):565-566. doi:10.1001/archneurol.2010.349
Original Contribution

Statin Use Following Intracerebral Hemorrhage: A Decision Analysis

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Arch Neurol. 2011;68(5):573-579. doi:10.1001/archneurol.2010.356
ContextStatins are widely prescribed for primary and secondary prevention of ischemic cardiac and cerebrovascular disease. Although serious adverse effects are uncommon, results from a recent clinical trial suggested increased risk of intracerebral hemorrhage (ICH) associated with statin use. For patients with baseline elevated risk of ICH, it is not known whether this potential adverse effect offsets the cardiovascular and cerebrovascular benefits.ObjectiveTo address the following clinical question: Given a history of prior ICH, should statin therapy be avoided?DesignA Markov decision model was used to evaluate the risks and benefits of statin therapy in patients with prior ICH.Main Outcome MeasureLife expectancy, measured as quality-adjusted life-years. We investigated how statin use affects this outcome measure while varying a range of clinical parameters, including hemorrhage location (deep vs lobar), ischemic cardiac and cerebrovascular risks, and magnitude of ICH risk associated with statins.ResultsAvoiding statins was favored over a wide range of values for many clinical parameters, particularly in survivors of lobar ICH who are at highest risk of ICH recurrence. In survivors of lobar ICH without prior cardiovascular events, avoiding statins yielded a life expectancy gain of 2.2 quality-adjusted life-years compared with statin use. This net benefit persisted even at the lower 95% confidence interval of the relative risk of statin-associated ICH. In patients with lobar ICH who had prior cardiovascular events, the annual recurrence risk of myocardial infarction would have to exceed 90% to favor statin therapy. Avoiding statin therapy was also favored, although by a smaller margin, in both primary and secondary prevention settings for survivors of deep ICH.ConclusionsAvoiding statins should be considered for patients with a history of ICH, particularly those cases with a lobar location.

Association of TMEM106B Gene Polymorphism With Age at Onset in Granulin Mutation Carriers and Plasma Granulin Protein Levels

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Arch Neurol. 2011;68(5):581-586. doi:10.1001/archneurol.2010.350
ObjectiveTo test whether rs1990622 (TMEM106B) is associated with age at onset (AAO) in granulin (GRN) mutation carriers and with plasma GRN levels in mutation carriers and healthy, elderly individuals. Rs1990622 (TMEM106B) was identified as a risk factor for frontotemporal lobar degeneration with TAR DNA-binding protein inclusions (FTLD-TDP) in a recent genome-wide association.DesignRs1990622 was genotyped in GRN mutation carriers and tested for association with AAO using the Kaplan-Meier method and a Cox proportional hazards model.SettingAlzheimer's Disease Research Center.SubjectsWe analyzed 50 affected and unaffected GRN mutation carriers from 4 previously reported FTLD-TDP families (HDDD1, FD1, HDDD2, and the Karolinska family). The GRN plasma levels were also measured in 73 healthy, elderly individuals.Main Outcome MeasuresAge at onset and GRN plasma levels.ResultsThe risk allele of rs1990622 was associated with a mean decrease of the AAO of 13 years (P = 9.9 × 10−7) and with lower plasma GRN levels in both healthy older adults (P = 4 × 10−4) and GRN mutation carriers (P = .0027). Analysis of the HapMap database identified a nonsynonymous single-nucleotide polymorphism rs3173615 (T185S) in perfect linkage disequilibrium with rs1990622.ConclusionsThe association of rs1990622 with AAO explains, in part, the wide range in the AAO of disease among GRN mutation carriers. We hypothesize that rs1990622 or another variant in linkage disequilibrium could act in a manner similar to APOE in Alzheimer disease, increasing risk for disease in the general population and modifying AAO in mutation carriers. Our results also suggest that genetic variation in TMEM106B may influence risk for FTLD-TDP by modulating secreted levels of GRN.

Resequencing of 29 Candidate Genes in Patients With Familial and Sporadic Amyotrophic Lateral Sclerosis

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Arch Neurol. 2011;68(5):587-593. doi:10.1001/archneurol.2010.351
ObjectiveTo identify novel disease-causing genes for amyotrophic lateral sclerosis (ALS).Design, Setting, and PatientsWe carried out a systematic mutation screening of the entire coding regions of 29 candidate genes encoding critically important proteins for proper differentiation and development of corticospinal motor neurons in 190 patients with familial and sporadic ALS.Main Outcome MeasuresWe focused our analysis on coding variants and evaluated the distribution of nonsynonymous and synonymous variants in our cohort of patients with ALS.ResultsWe identified 40 novel nonsynonymous variants and showed a significant excess of unique nonsynonymous variants in our cohort of patients with ALS, which suggests the presence of ALS-predisposing mutations.ConclusionsUsing a multifaceted approach based on the functional prediction of missense variants, the conservation of the altered amino acid, and the cosegregation of the variants identified in familial cases, we identified several promising novel genes for ALS such as LUM and CRYM. We have also highlighted the analytical challenges of large-scale sequencing screens to detect disease-causing variants.

Large Proportion of Amyotrophic Lateral Sclerosis Cases in Sardinia Due to a Single Founder Mutation of the TARDBP Gene

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Arch Neurol. 2011;68(5):594-598. doi:10.1001/archneurol.2010.352
ObjectiveTo perform an extensive screening for mutations of amyotrophic lateral sclerosis (ALS)–related genes in a consecutive cohort of Sardinian patients, a genetic isolate phylogenically distinct from other European populations.DesignPopulation-based, prospective cohort study.PatientsA total of 135 Sardinian patients with ALS and 156 healthy control subjects of Sardinian origin who were age- and sex-matched to patients.InterventionPatients underwent mutational analysis for SOD1, FUS, and TARDBP.ResultsMutational screening of the entire cohort found that 39 patients (28.7%) carried the c.1144G>A (p.A382T) missense mutation of the TARDBP gene. Of these, 15 had familial ALS (belonging to 10 distinct pedigrees) and 24 had apparently sporadic ALS. None of the 156 age-, sex-, and ethnicity-matched controls carried the pathogenic variant. Genotype data obtained for 5 ALS cases carrying the p.A382T mutation found that they shared a 94–single-nucleotide polymorphism risk haplotype that spanned 663 Kb across the TARDBP locus on chromosome 1p36.22. Three patients with ALS who carry the p.A382T mutation developed extrapyramidal symptoms several years after their initial presentation with motor weakness.ConclusionsThe TARDBP p.A382T missense mutation accounts for approximately one-third of all ALS cases in this island population. These patients share a large risk haplotype across the TARDBP locus, indicating that they have a common ancestor.

Test-Retest Reliability of Memory Task Functional Magnetic Resonance Imaging in Alzheimer Disease Clinical Trials

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Arch Neurol. 2011;68(5):599-606. doi:10.1001/archneurol.2011.94

Telephone-Based Identification of Mild Cognitive Impairment and Dementia in a Multicultural Cohort

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Arch Neurol. 2011;68(5):607-614. doi:10.1001/archneurol.2011.88

Cerebral Folate Deficiency Syndromes in Childhood: Clinical, Analytical, and Etiologic Aspects

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Arch Neurol. 2011;68(5):615-621. doi:10.1001/archneurol.2011.80

The APOE Gene Locus in Frontotemporal Dementia and Primary Progressive Aphasia

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Arch Neurol. 2011;68(5):622-628. doi:10.1001/archneurol.2011.90

Mild Cognitive Impairment, Dementia, and Their Subtypes in Oldest Old Women

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Arch Neurol. 2011;68(5):631-636. doi:10.1001/archneurol.2011.82

SCA15 Due to Large ITPR1 Deletions in a Cohort of 333 White Families With Dominant Ataxia

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Arch Neurol. 2011;68(5):637-643. doi:10.1001/archneurol.2011.81

Longitudinal Patterns of β-Amyloid Deposition in Nondemented Older Adults

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Arch Neurol. 2011;68(5):644-649. doi:10.1001/archneurol.2011.77
Images in Neurology

Multiple Pulmonary Arteriovenous Malformations in Hereditary Hemorrhagic Telangiectasia Complicated by Embolic Strokes

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Arch Neurol. 2011;68(5):672. doi:10.1001/archneurol.2011.96

Hemidystonia in Uncontrolled Type 2 Diabetes Mellitus

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Arch Neurol. 2011;68(5):674. doi:10.1001/archneurol.2011.92

Fibrous Cap Enhancement in Symptomatic Atherosclerotic Basilar Artery Stenosis

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Arch Neurol. 2011;68(5):676. doi:10.1001/archneurol.2011.89

Magnetic Resonance Imaging–Based Intravenous Thrombolysis 6 Hours After Onset of Minor Cerebellar Stroke

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Arch Neurol. 2011;68(5):678. doi:10.1001/archneurol.2011.87
Research Letter

Critical Role of PINK1 in Regulating Parkin Protein Levels In Vivo

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Arch Neurol. 2011;68(5):684-686. doi:10.1001/archneurol.2011.95
Observation

Huntington Chorea Presenting With Motor Neuron Disease

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Arch Neurol. 2011;68(5):650-652. doi:10.1001/archneurol.2011.76

SCA3 Presenting as an Isolated Axonal Polyneuropathy

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Arch Neurol. 2011;68(5):653-655. doi:10.1001/archneurol.2011.86

Lobar Distribution of Cerebral Microbleeds: The Rotterdam Scan Study

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Arch Neurol. 2011;68(5):656-659. doi:10.1001/archneurol.2011.93

In-flight Seizures and Fatal Air Embolism: The Importance of a Chest Radiograph

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Arch Neurol. 2011;68(5):661-664. doi:10.1001/archneurol.2011.85

Novel SCN1A Mutation in a Proband With Malignant Migrating Partial Seizures of Infancy

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Arch Neurol. 2011;68(5):665-671. doi:10.1001/archneurol.2011.98
Book Reviews

Clinical Handbook of Insomnia, 2nd ed

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Arch Neurol. 2011;68(5):682-683. doi:10.1001/archneurol.2011.72

Nervous System

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Arch Neurol. 2011;68(5):683. doi:10.1001/archneurol.2011.73
Obituary

In Memoriam: Hillel S. Panitch, MD (1940-2010)

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Arch Neurol. 2011;68(5):681. doi:10.1001/archneurol.2011.83
This Month in Archives of Neurology

This Month in Archives of Neurology

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Arch Neurol. 2011;68(5):561-562. doi:10.1001/archneurol.2011.71
Neurological Review

Movement Disorders Emergencies Part 1: Hypokinetic Disorders

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Arch Neurol. 2011;68(5):567-572. doi:10.1001/archneurol.2011.84
Correspondence

Blood-Based Biomarkers in Alzheimer Disease

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Arch Neurol. 2011;68(5):685-686. doi:10.1001/archneurol.2011.78

Blood-Based Biomarkers in Alzheimer Disease—Reply

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Arch Neurol. 2011;68(5):685-686. doi:10.1001/archneurol.2011.79
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