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September 2019 - July 1959

Decade

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Issue

March 2011, Vol 68, No. 3, Pages 285-399

Editorial

On Curves, Bends, Blisters, and Strokes

Abstract Full Text
Arch Neurol. 2011;68(3):292-293. doi:10.1001/archneurol.2011.24
Original Contribution

Vitamin D, Pregnancy, Breastfeeding, and Postpartum Multiple Sclerosis Relapses

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Arch Neurol. 2011;68(3):310-313. doi:10.1001/archneurol.2010.291
ObjectiveTo determine whether low levels of 25-hydroxyvitamin D (25[OH]D) contribute to the increased risk of postpartum multiple sclerosis (MS) relapses.DesignProspective cohort study.SettingOutpatients identified through membership records of Kaiser Permanente Northern California or Stanford University outpatient neurology clinics.PatientsTwenty-eight pregnant women with MS.InterventionsWe prospectively followed up patients through the postpartum year and assessed exposures and symptoms through structured interviews. Total serum 25(OH)D levels were measured using the DiaSorin Liaison Assay during the third trimester and 2, 4, and 6 months after giving birth. The data were analyzed using longitudinal multivariable methods.Main Outcome MeasuresLevels of 25(OH)D and relapse rate.ResultsFourteen (50%) women breastfed exclusively, and 12 women (43%) relapsed within 6 months after giving birth. During pregnancy, the average 25(OH)D levels were 25.4 ng/mL (range, 13.7-42.6) and were affected only by season (P = .009). In contrast, in the postpartum period, 25(OH)D levels were significantly affected by breastfeeding and relapse status. Levels of 25(OH)D remained low in the exclusive breastfeeding group, yet rose significantly in the nonexclusive breastfeeding group regardless of season (P = .007, unadjusted; P = .02, adjusted for season). By 4 and 6 months after childbirth, 25(OH)D levels were, on average, 5 ng/mL lower in the women who breastfed exclusively compared with the nonbreastfeeding group (P = .001).ConclusionsPregnancy and exclusive breastfeeding are strongly associated with low 25(OH)D levels in women with MS. However, these lower vitamin D levels were not associated with an increased risk of postpartum MS relapses. These data suggest that low vitamin D in isolation is not an important risk factor for postpartum MS relapses.

High Prevalence of Hypovitaminosis D Status in Patients With Early Parkinson Disease

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Arch Neurol. 2011;68(3):314-319. doi:10.1001/archneurol.2011.30

Identification of Novel Loci for Alzheimer Disease and Replication of CLU, PICALM, and BIN1 in Caribbean Hispanic Individuals

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Arch Neurol. 2011;68(3):320-328. doi:10.1001/archneurol.2010.292
ObjectivesTo identify novel loci for late-onset Alzheimer disease (LOAD) in Caribbean Hispanic individuals and to replicate the findings in a publicly available data set from the National Institute on Aging Late-Onset Alzheimer's Disease Family Study.DesignNested case-control genome-wide association study.SettingThe Washington Heights–Inwood Columbia Aging Project and the Estudio Familiar de Influencia Genetica de Alzheimer study.ParticipantsFive hundred forty-nine affected and 544 unaffected individuals of Caribbean Hispanic ancestry.InterventionThe Illumina HumanHap 650Y chip for genotyping.Main Outcome MeasureClinical diagnosis or pathologically confirmed diagnosis of LOAD.ResultsThe strongest support for allelic association was for rs9945493 on 18q23 (P = 1.7 × 10−7), but 22 additional single-nucleotide polymorphisms (SNPs) had a P value less than 9 × 10−6 under 3 different analyses: unadjusted and stratified by the presence or absence of the APOEε4 allele. Of these SNPs, 5 SNPs (rs4669573 and rs10197851 on 2p25.1; rs11711889 on 3q25.2; rs1117750 on 7p21.1; and rs7908652 on 10q23.1) were associated with LOAD in an independent cohort from the National Institute on Aging Late-Onset Alzheimer's Disease Family Study. We also replicated genetic associations for CLU, PICALM, and BIN1.ConclusionsOur genome-wide search of Caribbean Hispanic individuals identified several novel genetic variants associated with LOAD and replicated these associations in a white cohort. We also replicated associations in CLU, PICALM, and BIN1 in the Caribbean Hispanic cohort.

Temporoparietal Hypometabolism in Frontotemporal Lobar Degeneration and Associated Imaging Diagnostic Errors

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Arch Neurol. 2011;68(3):329-337. doi:10.1001/archneurol.2010.295
ObjectiveTo evaluate the cause of diagnostic errors in the visual interpretation of positron emission tomographic scans with fludeoxyglucose F 18 (FDG-PET) in patients with frontotemporal lobar degeneration (FTLD) and patients with Alzheimer disease (AD).DesignTwelve trained raters unaware of clinical and autopsy information independently reviewed FDG-PET scans and provided their diagnostic impression and confidence of either FTLD or AD. Six of these raters also recorded whether metabolism appeared normal or abnormal in 5 predefined brain regions in each hemisphere—frontal cortex, anterior cingulate cortex, anterior temporal cortex, temporoparietal cortex, and posterior cingulate cortex. Results were compared with neuropathological diagnoses.SettingAcademic medical centers.PatientsForty-five patients with pathologically confirmed FTLD (n = 14) or AD (n = 31).ResultsRaters had a high degree of diagnostic accuracy in the interpretation of FDG-PET scans; however, raters consistently found some scans more difficult to interpret than others. Unanimity of diagnosis among the raters was more frequent in patients with AD (27 of 31 patients [87%]) than in patients with FTLD (7 of 14 patients [50%]) (P = .02). Disagreements in interpretation of scans in patients with FTLD largely occurred when there was temporoparietal hypometabolism, which was present in 7 of the 14 FTLD scans and 6 of the 7 scans lacking unanimity. Hypometabolism of anterior cingulate and anterior temporal regions had higher specificities and positive likelihood ratios for FTLD than temporoparietal hypometabolism had for AD.ConclusionsTemporoparietal hypometabolism in FTLD is common and may cause inaccurate interpretation of FDG-PET scans. An interpretation paradigm that focuses on the absence of hypometabolism in regions typically affected in AD before considering FTLD is likely to misclassify a significant portion of FTLD scans. Anterior cingulate and/or anterior temporal hypometabolism indicates a high likelihood of FTLD, even when temporoparietal hypometabolism is present. Ultimately, the accurate interpretation of FDG-PET scans in patients with dementia cannot rest on the presence or absence of a single region of hypometabolism but rather must take into account the relative hypometabolism of all brain regions.

Eccentric Narrowing and Enhancement of Symptomatic Middle Cerebral Artery Stenoses in Patients With Recent Ischemic Stroke

Abstract Full Text
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Arch Neurol. 2011;68(3):338-342. doi:10.1001/archneurol.2011.20

The Structured Interview & Scoring Tool–Massachusetts Alzheimer's Disease Research Center (SIST-M): Development, Reliability, and Cross-Sectional Validation of a Brief Structured Clinical Dementia Rating Interview

Abstract Full Text
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Arch Neurol. 2011;68(3):343-350. doi:10.1001/archneurol.2010.375

Cognitive Decline in Prodromal Alzheimer Disease and Mild Cognitive Impairment

Abstract Full Text
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Arch Neurol. 2011;68(3):351-356. doi:10.1001/archneurol.2011.31

Dementia Risk in Parkinson Disease: Disentangling the Role of MAPT Haplotypes

Abstract Full Text
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Arch Neurol. 2011;68(3):359-364. doi:10.1001/archneurol.2011.17
Images in Neurology

Delayed Sudden Coma Due to Artery of Percheron Infarction

Abstract Full Text
Arch Neurol. 2011;68(3):386-387. doi:10.1001/archneurol.2010.377

Multifocal Extracranial Meningioma Metastases

Abstract Full Text
Arch Neurol. 2011;68(3):388-389. doi:10.1001/archneurol.2011.28

Oculogyric Crisis in a Midbrain Lesion

Abstract Full Text
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Arch Neurol. 2011;68(3):390-391. doi:10.1001/archneurol.2011.27
Research Letter

No Effect on SOD1 Splicing by TARDP or FUS Mutations

Abstract Full Text
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Arch Neurol. 2011;68(3):395-399. doi:10.1001/archneurol.2011.1
Observation

Arterial Tortuosity Syndrome With Multiple Intracranial Aneurysms: A Case Report

Abstract Full Text
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Arch Neurol. 2011;68(3):369-371. doi:10.1001/archneurol.2011.29

Long-term Treatment With Rituximab of Autoimmune Autonomic Ganglionopathy in a Patient With Lymphoma

Abstract Full Text
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Arch Neurol. 2011;68(3):372-375. doi:10.1001/archneurol.2010.289
ObjectiveTo report on the response to therapy in a patient with autoimmune autonomic ganglionopathy with a high titer of an autoantibody directed against the α-3 subunit of the nicotinic acetylcholine receptor (nAChR) of the autonomic ganglia.DesignCase report.SettingUniversity-based referral center for autonomic dysfunction.PatientPatient with prior indolent B-cell lymphoma who presented with symptomatic orthostatic hypotension and autonomic failure and was found to have a high titer of nAChR antibody.InterventionPlasma exchange and rituximab therapy (both initial 4-week therapy and maintenance therapy).Main Outcome MeasuresAutonomic ganglionic antibody titer; the autonomic assessments were the presence of orthostatic hypotension, the concentration of plasma norepinephrine, and quantitative sweat testing.ResultsTreatment with rituximab followed by plasma exchange significantly decreased the nAChR antibody titers for a short time, and then the titers increased. The titers suppressed to almost undetectable levels once regular maintenance therapy with rituximab was initiated. Reduction in nAChR antibody titer resulted in a decrease in orthostatic hypotension, an increased concentration of upright plasma norepinephrine, improvement in some sweat function, and improvement in symptoms.ConclusionsLong-term rituximab therapy suppressed autoantibody production to undetectable levels over the course of 2 years and resulted in sustained clinical improvement in this patient with debilitating autoimmune autonomic ganglionopathy. More data are needed before rituximab therapy can be recommended as routine therapy for this disorder.

Sporadic Corticobasal Syndrome With Progranulin Mutation Presenting as Progressive Apraxic Agraphia

Abstract Full Text
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Arch Neurol. 2011;68(3):376-380. doi:10.1001/archneurol.2011.26

Cingulate Gyrus Epilepsy: Clinical and Behavioral Aspects, With Surgical Outcomes

Abstract Full Text
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Arch Neurol. 2011;68(3):381-385. doi:10.1001/archneurol.2011.21
Book Reviews

Parkinson’s Disease Treatment Guide for Physicians

Abstract Full Text
Arch Neurol. 2011;68(3):393-394. doi:10.1001/archneurol.2011.14

The Parkinson's Disease Treatment Book: Partnering With Your Doctor to Get the Most From Your Medications

Abstract Full Text
Arch Neurol. 2011;68(3):393-394. doi:10.1001/archneurol.2011.19
This Month in Archives of Neurology

This Month in Archives of Neurology

Abstract Full Text
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Arch Neurol. 2011;68(3):290-291. doi:10.1001/archneurol.2011.12
Article
Neurological Review

The Emerging Role of Epigenetics in Stroke: III. Neural Stem Cell Biology and Regenerative Medicine

Abstract Full Text
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Arch Neurol. 2011;68(3):294-302. doi:10.1001/archneurol.2011.6

Error in Acknowledgments in: No Association Between Genetic Polymorphism at Codon 129 of the Prion Protein Gene and Primary Progressive Multiple Sclerosis

Abstract Full Text
Arch Neurol. 2011;68(3):302. doi:10.1001/archneurol.2011.37

Advances in Translational Research in Neuro-oncology

Abstract Full Text
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Arch Neurol. 2011;68(3):303-308. doi:10.1001/archneurol.2010.293

During the last decade, we have witnessed several key advances in the field of neuro-oncology. First, there were conceptual advances in the molecular and cell biology of malignant gliomas including the discovery in 2004 of brain tumor stem cells. Second, the Cancer Genome Atlas project has been extremely useful in the discovery of new molecular markers, including mutations in the IDH1 gene, and has led to a new classification of gliomas based on the differentiation status and mesenchymal transformation. In addition, use of the 1p/19q marker and O6-methylguanine-DNA methyltransferase methylation status have been identified as guides for patient selection for therapies and represent the first steps toward personalized medicine for treating gliomas. Finally, progress has been made in treatment strategies including the establishment of temozolomide as the criterion standard for treating gliomas, the adoption of bevacizumab in the clinical setting, and developments in experimental biological therapies including cancer vaccines and oncolytic adenoviruses.

From the Archives

Smoking in Midlife and Dementia in Old Age: Risk Across the Life Course

Abstract Full Text
Arch Neurol. 2011;68(3):365-368. doi:10.1001/archneurol.2011.25

Error in Byline in: Reversible Extralimbic Paraneoplastic Encephalopathies With Large Abnormalities on Magnetic Resonance Images

Abstract Full Text
Arch Neurol. 2011;68(3):371. doi:10.1001/archneurol.2011.35
Correspondence

Thrombolysis-Associated Symptomatic Intracerebral Hemorrhage—Reply

Abstract Full Text
Arch Neurol. 2011;68(3):395-399. doi:10.1001/archneurol.2011.10

Primum non nocere

Abstract Full Text
Arch Neurol. 2011;68(3):395-399. doi:10.1001/archneurol.2011.15

Acute Neuromuscular Respiratory Failure

Abstract Full Text
Arch Neurol. 2011;68(3):395-399. doi:10.1001/archneurol.2011.15a

Acute Neuromuscular Respiratory Failure—Reply

Abstract Full Text
Arch Neurol. 2011;68(3):395-399. doi:10.1001/archneurol.2011.16

Laryngospasm and “Sudden Unexpected Death Related to Medullary Brain Lesions”

Abstract Full Text
Arch Neurol. 2011;68(3):395-399. doi:10.1001/archneurol.2011.18

Primum non nocere—Reply

Abstract Full Text
Arch Neurol. 2011;68(3):395-399. doi:10.1001/archneurol.2011.22

Thrombolysis-Associated Symptomatic Intracerebral Hemorrhage

Abstract Full Text
Arch Neurol. 2011;68(3):395-399. doi:10.1001/archneurol.2011.9
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