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December 2020 - July 1959

Decade

Year

Issue

June 2011, Vol 68, No. 6, Pages 701-830

Editorial

Another Good Reason to Consider Surgical Treatment for Epilepsy More Often and Sooner

Abstract Full Text
Arch Neurol. 2011;68(6):707-708. doi:10.1001/archneurol.2011.113
Original Contribution

Population-Based Analysis of Morbidity and Mortality Following Surgery for Intractable Temporal Lobe Epilepsy in the United States

Abstract Full Text
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Arch Neurol. 2011;68(6):725-729. doi:10.1001/archneurol.2011.7
ObjectiveTo assess the morbidity of temporal lobe epilepsy (TLE) surgery on a nationwide level in order to address reservations regarding the morbidity of anterior temporal lobectomy (ATL) for TLE despite class I evidence demonstrating the superiority of ATL over continued medical therapy.DesignRetrospective cohort study.SettingThe Nationwide Inpatient Sample from 1988 to 2003 was used for analysis.PatientsOnly patients who were admitted for ATL for TLE (International Classification of Diseases, Ninth Revision, Clinical Modification codes 345.41 and 345.51; primary procedure code, 01.53) were included.Main Outcome MeasuresMorbidity and mortality. Analysis was adjusted for several variables including patient age, race, sex, admission type, primary payer for care, income in zip code of residence, and hospital volume of care.ResultsMultivariate analyses revealed that the overall morbidity (postoperative morbidity and/or adverse discharge disposition) following ATL for TLE was 10.8%, with no mortality. Private insurance decreased postoperative morbidity (odds ratio [OR] = 0.52; 95% confidence interval [CI] = 0.28-0.98; P = .04) and adverse discharge disposition (OR = 0.31; 95% CI = 0.12-0.81; P = .02). Increased patient age increased postoperative morbidity (OR = 1.04; 95% CI = 1.01-1.07; P = .03) and adverse discharge disposition (OR = 1.08; 95% CI = 1.02-1.13; P = .004). Neither sex, income, race, nor hospital volume was predictive of postoperative morbidity. The degree of medical comorbidity directly correlated with the incidence of postoperative morbidity.ConclusionsMorbidity following ATL for TLE is low throughout the United States regardless of sex, race, insurance status, or income. Younger age and private insurance status are independently predictive of reduced postoperative morbidity. In patients with low medical comorbidity, ATL for TLE is safe, with low morbidity and no mortality.

Sleep Manifestations of Voltage-Gated Potassium Channel Complex Autoimmunity

Abstract Full Text
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Arch Neurol. 2011;68(6):733-738. doi:10.1001/archneurol.2011.106

Association of Long ATXN2 CAG Repeat Sizes With Increased Risk of Amyotrophic Lateral Sclerosis

Abstract Full Text
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Arch Neurol. 2011;68(6):739-742. doi:10.1001/archneurol.2011.111

Diet Intervention and Cerebrospinal Fluid Biomarkers in Amnestic Mild Cognitive Impairment

Abstract Full Text
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Arch Neurol. 2011;68(6):743-752. doi:10.1001/archneurol.2011.125
Original Contributions

Clinical Correlates of White Matter Tract Degeneration in Progressive Supranuclear Palsy

Abstract Full Text
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Arch Neurol. 2011;68(6):753-760. doi:10.1001/archneurol.2011.107

Clinical Correlates of White Matter Tract Degeneration in Progressive Supranuclear Palsy

Abstract Full Text
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Arch Neurol. 2011;68(6):753-760. doi:10.1001/archneurol.2011.107

Outcomes of Mild Cognitive Impairment by Definition: A Population Study

Abstract Full Text
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Arch Neurol. 2011;68(6):761-767. doi:10.1001/archneurol.2011.101

Positron Emission Tomography of Brain β-Amyloid and Tau Levels in Adults With Down Syndrome

Abstract Full Text
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Arch Neurol. 2011;68(6):768-774. doi:10.1001/archneurol.2011.104

Reliability of Seizure Semiology in Patients With 2 Seizure Foci

Abstract Full Text
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Arch Neurol. 2011;68(6):775-778. doi:10.1001/archneurol.2011.97

Observational Study of Spinal Muscular Atrophy Type 2 and 3: Functional Outcomes Over 1 Year

Abstract Full Text
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Arch Neurol. 2011;68(6):779-786. doi:10.1001/archneurol.2010.373
ObjectiveTo characterize the short-term course of spinal muscular atrophy (SMA) in a genetically and clinically well-defined cohort of patients with SMA.DesignA comprehensive multicenter, longitudinal, observational study.SettingThe Pediatric Neuromuscular Clinical Research Network for SMA, a consortium of clinical investigators at 3 clinical sites.ParticipantsSixty-five participants with SMA types 2 and 3, aged 20 months to 45 years, were prospectively evaluated.InterventionWe collected demographic and medical history information and determined the SMN 2 copy number.Main Outcome MeasuresClinical outcomes included measures of motor function (Gross Motor Function Measure and expanded Hammersmith Functional Motor Scale), pulmonary function (forced vital capacity), and muscle strength (myometry). Participants were evaluated every 2 months for the initial 6 months and every 3 months for the subsequent 6 months. We evaluated change over 12 months for all clinical outcomes and examined potential correlates of change over time including age, sex, SMA type, ambulatory status, SMN2 copy number, medication use, and baseline function.ResultsThere were no significant changes over 12 months in motor function, pulmonary function, and muscle strength measures. There was evidence of motor function gain in ambulatory patients, especially in those children younger than 5 years. Scoliosis surgery during the observation period led to a subsequent decline in motor function.ConclusionsOur results confirm previous clinical reports suggesting that SMA types 2 and 3 represent chronic phenotypes that have relatively stable clinical courses. We did not detect any measurable clinical disease progression in SMA types 2 and 3 over 12 months, suggesting that clinical trials will have to be designed to measure improvement rather than stabilization of disease progression.

Inclusion Body Myopathy With Paget Disease of Bone and Frontotemporal Dementia Linked to VCP p.Arg155Cys in a Korean Family

Abstract Full Text
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Arch Neurol. 2011;68(6):787-796. doi:10.1001/archneurol.2010.376
BackgroundMissense mutations in the valosin-containing protein (VCP) gene on chromosome 9p13.3-p12 cause inclusion body myopathy with Paget disease of bone and frontotemporal dementia (hereafter referred to as IBMPFD; OMIM 167320).ObjectiveTo describe detailed clinical, electrophysiological, biochemical, and neuroimaging findings in IBMPFD linked to VCP p.Arg155Cys in a Korean family.DesignCase series. Clinical, electrophysiological, biochemical, and neuroimaging findings were obtained by direct evaluation and from previous medical records.SettingTertiary referral hospital.ParticipantsThree affected family members in a Korean family.ResultsThe clinical features of myopathy, Paget disease of bone, and semantic dementia (a clinical subtype of frontotemporal dementia) in our patients were similar to those of previously reported cases. However, the brain magnetic resonance imaging features in our patients, including asymmetric anterior and lateral temporal and inferior parietal atrophy with ventricular dilatation on the affected side, differed from those of previously published features in patients with IBMPFD and in patients with typical semantic dementia who show anterior temporal and frontal atrophy.ConclusionTo our knowledge, this report provides the first documented IBMPFD family in Asia and broadens the phenotypic spectrum of VCP mutation–associated frontotemporal dementia.
Images in Neurology

Vein of Galen Aneurysmal Malformation

Abstract Full Text
Arch Neurol. 2011;68(6):822-823. doi:10.1001/archneurol.2011.121

Prominent Forehead Scalp Arteries a Diagnostic Clue to Unruptured Anterior Cranial Fossa Dural Arteriovenous Fistula

Abstract Full Text
Arch Neurol. 2011;68(6):824-825. doi:10.1001/archneurol.2011.119

Magnetic Resonance Imaging Characteristics at Onset of Spontaneous Intracerebral Hemorrhage

Abstract Full Text
Arch Neurol. 2011;68(6):826-827. doi:10.1001/archneurol.2011.109

A Dramatic Case of Intraventricular Cysticercosis

Abstract Full Text
Arch Neurol. 2011;68(6):828-829. doi:10.1001/archneurol.2011.122
Observation

Functional Magnetic Resonance Imaging Evidence of Incomplete Maternal Imprinting in Myoclonus-Dystonia

Abstract Full Text
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Arch Neurol. 2011;68(6):802-805. doi:10.1001/archneurol.2011.23
BackgroundMyoclonus-dystonia is an autosomal dominantly inherited movement disorder, clinically characterized by myoclonic jerks and dystonic postures or movements. A previous functional magnetic resonance imaging study showed altered cortical activation patterns in clinically affected SGCE mutation carriers when compared with controls consistent with defective sensorimotor integration. Genetically, the disorder is characterized by the maternal imprinting mechanism; ie, patients who inherit the mutation from their fathers will develop symptoms. However, several clinically manifest patients with myoclonus-dystonia who inherited the mutation from their mother have been described.ObjectiveTo compare cerebral activation patterns of paternally inherited SGCE mutation carriers are with maternally inherited mutation carriers and a control group.DesignCase-control study using functional magnetic resonance imaging.ParticipantsEight paternally inherited SGCE mutation carriers, 8 asymptomatic or slightly affected (4 of 8) symptomatic maternally inherited mutation carriers, and 11 control subjects.InterventionsParticipants were studied using a 3-T functional magnetic resonance imaging scanner with a finger tapping task.ResultsWhen paternal and maternal gene mutation carriers were compared, hyperresponsiveness was seen in the contralateral secondary somatosensory cortex. When maternal mutation carriers and control subjects were compared, hyperresponsiveness of the ipsilateral cerebellum and supplementary motor area were found. Using a nonparametric analysis to study only the 4 clinically asymptomatic patients, no significant differences were found between groups. Contrast estimates were plotted for the known affected sensorimotor brain areas, showing intermediate activation in maternally inherited mutation carriers, even when this was performed for only the 4 clinically unaffected mutation carriers.ConclusionsThe results suggest biased gene expression based on parent of origin rather than a strictly dichotomous maternal imprinting mechanism, consistent with clinical observations.

Novel POLG Splice Site Mutation and Optic Atrophy

Abstract Full Text
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Arch Neurol. 2011;68(6):806-811. doi:10.1001/archneurol.2011.124

Mutation of SCARB2 in a Patient With Progressive Myoclonus Epilepsy and Demyelinating Peripheral Neuropathy

Abstract Full Text
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Arch Neurol. 2011;68(6):812-813. doi:10.1001/archneurol.2011.120

Neuropathy in a Human Without the PMP22 Gene

Abstract Full Text
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Arch Neurol. 2011;68(6):814-821. doi:10.1001/archneurol.2011.110
This Month in Archives of Neurology

This Month in Archives of Neurology

Abstract Full Text
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Arch Neurol. 2011;68(6):705-706. doi:10.1001/archneurol.2011.112
Neurological Review

Translational Research in Neurology and Neuroscience 2011: Movement Disorders

Abstract Full Text
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Arch Neurol. 2011;68(6):709-716. doi:10.1001/archneurol.2011.11

We provide an update on the state of translational research in movement disorders, using examples of Huntington disease, Parkinson disease, and dystonia. While substantial progress in our understanding of these disorders has been achieved, development of neuroprotective treatments remains an unrealized goal. Here we highlight some of the emerging research areas that show the most promise for translational research in Huntington disease, Parkinson disease, and dystonia. Aetiology and pathogenesis, biomarker directions, and causal treatment opportunities are discussed for each disease, followed by a brief discussion drawing attention to important translational initiatives.

Movement Disorders Emergencies Part 2: Hyperkinetic Disorders

Abstract Full Text
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Arch Neurol. 2011;68(6):719-724. doi:10.1001/archneurol.2011.117
Article
Commentary in Neurology

Stroke and Alzheimer Disease: Fellow Travelers or Partners in Crime?

Abstract Full Text
Arch Neurol. 2011;68(6):797-798. doi:10.1001/archneurol.2011.118
From JAMA

Plasma β-Amyloid Linked to Cognitive Decline

Abstract Full Text
Arch Neurol. 2011;68(6):799-801. doi:10.1001/archneurol.2011.114
Correspondence

Dissection or Hemorrhage Into Arteriosclerotic Plaque

Abstract Full Text
Arch Neurol. 2011;68(6):830. doi:10.1001/archneurol.2011.115

Dissection or Hemorrhage Into Arteriosclerotic Plaque—Reply

Abstract Full Text
Arch Neurol. 2011;68(6):830. doi:10.1001/archneurol.2011.116
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