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January 2017 - July 1959

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February 14, 2011, Vol 68, No. 2, Pages 153-271

Editorial

Of Horse Races, Trials, Meta-analyses, and Carotid Artery Stenosis

Abstract Full Text
Arch Neurol. 2011;68(2):157-159. doi:10.1001/archneurol.2010.268
Original Contribution

Carotid Artery Stenting vs Carotid EndarterectomyMeta-analysis and Diversity-Adjusted Trial Sequential Analysis of Randomized Trials

Abstract Full Text
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Arch Neurol. 2011;68(2):172-184. doi:10.1001/archneurol.2010.262
BackgroundThe role of carotid artery stenting (CAS) when compared with carotid endarterectomy (CEA) is controversial, with recent trials showing an increased risk of harm with CAS.ObjectiveTo evaluate the periprocedural and intermediate to long-term benefits and harms of CAS compared with CEA.Data Sources and Study SelectionPubMed, EMBASE, and Cochrane Central Register of Controlled Trials searches for randomized clinical trials until June 2010 of CAS compared with CEA for carotid artery disease. Periprocedural (≤30-day) outcomes (death, myocardial infarction [MI], or stroke; death or any stroke; any stroke; and MI) and intermediate to long-term outcomes (outcomes as in the Stenting and Angioplasty With Protection in Patients at High Risk for Endarterectomy [SAPPHIRE] trial: composite of periprocedural death, MI, or stroke plus ipsilateral stroke or death thereafter; periprocedural death or stroke plus ipsilateral stroke thereafter; death or any stroke; and any stroke) were evaluated.Data ExtractionTwo of us independently extracted data in duplicate. Baseline characteristics, inclusion and exclusion criteria, use of an embolic protection device, US vs non-US study, and the earlier-mentioned outcomes of interest were extracted from each trial.Data SynthesisWe identified 13 randomized clinical trials randomizing 7477 participants. Carotid artery stenting was associated with an increased risk of periprocedural outcomes of death, MI, or stroke (odds ratio = 1.31; 95% confidence interval, 1.08-1.59), 65% and 67% increases in death or stroke and any stroke, respectively, but with 55% and 85% reductions in the risk of MI and cranial nerve injury, respectively, when compared with CEA. The trial sequential monitoring boundary was crossed by the cumulative z curve, suggesting firm evidence for at least a 20% relative risk increase of periprocedural death or stroke and any stroke and at least a 15% reduction in MI with CAS compared with CEA. Similarly, CAS was associated with 19%, 38%, 24%, and 48% increases in the intermediate to long-term outcomes of SAPPHIRE-like outcome, periprocedural death or stroke and ipsilateral stroke thereafter, death or any stroke, and any stroke, respectively. The trial sequential monitoring boundary was crossed by the cumulative z curve, suggesting firm evidence for at least a 20% relative risk increase of any stroke.ConclusionsIn this largest and most comprehensive meta-analysis to date using outcomes that are standard in contemporary studies, CAS was associated with an increased risk of both periprocedural and intermediate to long-term outcomes, but with a reduction in periprocedural MI and cranial nerve injury. Strategies are urgently needed to identify patients who are best served by CAS vs CEA.

Immune Reconstitution Inflammatory Syndrome in Patients With Multiple Sclerosis Following Cessation of Natalizumab Therapy

Abstract Full Text
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Arch Neurol. 2011;68(2):186-191. doi:10.1001/archneurol.2010.257
ObjectiveTo assess clinical consequences of temporary natalizumab dosage suspension.DesignProspective cohort study.SettingMultiple sclerosis (MS) center at an academic medical center in the United States.PatientsThirty-two patients with MS who had received at least 12 consecutive natalizumab infusions.Main Outcomes MeasuresRecurrent MS disease activity, defined as a clinically documented exacerbation with objective findings and/or the development of 1 or more new gadolinium-enhancing lesions on magnetic resonance imaging.ResultsThirty-eight percent of patients with relapsing-remitting and secondary progressive MS experienced relapses during therapy interruption or shortly after restarting natalizumab therapy (9 of 24 and 3 of 8, respectively), but relapses were severe with unusually widespread evidence of inflammatory activity on magnetic resonance imaging in several patients with secondary progressive MS with greater inflammatory disease activity prior to starting natalizumab therapy. Imaging and cerebrospinal fluid findings in these cases were suggestive of an immune reconstitution inflammatory syndrome. Overall, relapses occurred more often in younger patients with fewer natalizumab infusions prior to therapy interruption. The number of gadolinium-enhancing lesions at the time of relapse after therapy interruption was modestly correlated with the number of gadolinium-enhancing lesions prior to starting natalizumab therapy (r = 0.51; P = .45). Prior disease control resumed after reinstitution of natalizumab therapy in all patients.ConclusionsIn this cohort of patients with MS who had disease refractive to multiple therapeutics before starting natalizumab treatment, magnetic resonance imaging and clinical disease activity returned, often aggressively, following discontinuation of natalizumab therapy. These findings suggest we should consider strategies to minimize the risk of immune reconstitution inflammatory syndrome after natalizumab discontinuation.

Mass Spectrometric–Based Proteomic Analysis of Amyloid Neuropathy Type in Nerve Tissue

Abstract Full Text
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Arch Neurol. 2011;68(2):195-199. doi:10.1001/archneurol.2010.261
ObjectiveTo determine the specific type of amyloid from nerve biopsies using laser microdissection (LMD) and mass spectrometric (MS)–based proteomic analysis.Design, Setting, and PatientsTwenty-one nerve biopsy specimens (17 sural, 3 sciatic, and 1 root amyloidoma) infiltrated by amyloid were studied. Immunohistochemical subtyping was unable to determine the specific amyloid type for these 21 cases, but the clinical diagnosis was made based on additional testing. Clinical diagnosis was made through evaluation of serum monoclonal proteins, biopsy of bone marrow for acquired monoclonal immunoglobulin light chain amyloidosis, and kindred evaluations with DNA sequencing of transthyretin (TTR) and gelsolin (GSN) genes. Our study included 8 cases of acquired monoclonal immunoglobulin light chain amyloidosis, 11 cases of transthyretin amyloidosis (3 with the Val30Met mutation, 2 with the Val32Ala mutation, 2 with the Thr60Ala mutation, 1 with the Ala109Ser mutation, 1 with the Phe64Leu mutation, 1 with the Ala97Ser mutation, and 1 not sequenced), and 2 cases of gelsolin amyloidosis (1 with the Asp187Asn mutation and 1 not sequenced). One patient with transthyretin amyloidosis and 1 patient with gelsolin amyloidosis with no specific mutation identified were diagnosed based on genetic confirmation in their first-degree relative. Congophilic proteins in the tissues of these 21 cases underwent LMD, were digested into tryptic peptides, and were analyzed using liquid chromatography electrospray tandem MS. Identified proteins were reviewed using bioinformatics tools with interpreters blinded to clinical information.Main Outcome MeasureSpecific amyloid type was ascertained by LMD tandem MS and compared with clinical diagnosis.ResultsSpecific types of amyloid were accurately detected by LMD/MS in all cases (8 cases of acquired monoclonal immunoglobulin light chain amyloidosis, 2 cases of gelsolin amyloidosis, and 11 cases of transthyretin amyloidosis). Incidental serum monoclonal proteins did not interfere with detection of transthyretin amyloidosis in 2 patients. Additionally, specific TTR mutations were identified in 10 cases by LMD/MS. Serum amyloid P-component and apolipoprotein E proteins were commonly found among all cases.ConclusionsProteomic analysis of nerve tissue using LMD/MS distinguishes specific types of amyloid independent of clinical information. This new proteomic approach will enhance both diagnostic and research efforts in amyloidosis and other neurologic diseases.

Skin Denervation and Its Clinical Significance in Late-Stage Chronic Kidney Disease

Abstract Full Text
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Arch Neurol. 2011;68(2):200-206. doi:10.1001/archneurol.2010.372

Smoking and Risk of Amyotrophic Lateral SclerosisA Pooled Analysis of 5 Prospective Cohorts

Abstract Full Text
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Arch Neurol. 2011;68(2):207-213. doi:10.1001/archneurol.2010.367

Hearing Loss and Incident Dementia

Abstract Full Text
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Arch Neurol. 2011;68(2):214-220. doi:10.1001/archneurol.2010.362

Excessive Daytime Sleepiness in Multiple System Atrophy (SLEEMSA Study)

Abstract Full Text
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Arch Neurol. 2011;68(2):223-230. doi:10.1001/archneurol.2010.359

In Vivo Fibrillar β-Amyloid Detected Using [11C]PiB Positron Emission Tomography and Neuropathologic Assessment in Older Adults

Abstract Full Text
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Arch Neurol. 2011;68(2):232-240. doi:10.1001/archneurol.2010.357
Images in Neurology

Anterior Opercular Syndrome Caused by Acute, Simultaneous, Isolated Bilateral Infarcts

Abstract Full Text
Arch Neurol. 2011;68(2):254-255. doi:10.1001/archneurol.2010.369

Carotid Cavernous Fistula Imitating Brainstem Glioma

Abstract Full Text
Arch Neurol. 2011;68(2):256-257. doi:10.1001/archneurol.2010.366

Hyoid Bone Compression–Induced Repetitive Occlusion and Recanalization of the Internal Carotid Artery in a Patient With Ipsilateral Brain and Retinal Ischemia

Abstract Full Text
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Arch Neurol. 2011;68(2):258-259. doi:10.1001/archneurol.2010.371
Research Letters

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

Abstract Full Text
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Arch Neurol. 2011;68(2):264-271. doi:10.1001/archneurol.2010.354

Validation of Plasma Branched Chain Amino Acids as Biomarkers in Huntington Disease

Abstract Full Text
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Arch Neurol. 2011;68(2):264-271. doi:10.1001/archneurol.2010.358
Observation

Default Mode Network Disruption Secondary to a Lesion in the Anterior Thalamus

Abstract Full Text
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Arch Neurol. 2011;68(2):242-247. doi:10.1001/archneurol.2010.259
ObjectiveTo describe the neuroanatomical correlations of an isolated lesion in the anterior thalamus using functional imaging in a 40-year-old man with multiple sclerosis.DesignCase report with 10 cognitively normal controls.SettingMayo Clinic, Rochester, Minnesota.PatientA 40-year-old man with a 2-week course of acute-onset amnesia, abulia, poor concentration, hypersomnolence, and reclusiveness.InterventionFunctional magnetic resonance imaging.ResultsMagnetic resonance imaging demonstrated a large gadolinium-enhancing plaque in the left anterior thalamus and other demyelinating plaques in the subcortical and periventricular white matter, consistent with the diagnosis of multiple sclerosis. His symptoms persisted at the 7-month follow-up. The patient's resting state functional magnetic resonance image demonstrated an asymmetric disruption of the posterior cingulate portion of the default mode network ipsilateral to the left thalamic lesion.ConclusionsA large multiple sclerosis plaque in the deep gray matter altered the resting state functional connectivity in a patient presenting with pure cognitive dysfunction. Such altered connectivity may underlie cognitive symptoms in neurologic disease. In addition, this case provides lesional evidence of default mode network circuitry involving the pathways of the circuit of Papez.

Preserved Musical Semantic Memory in Semantic Dementia

Abstract Full Text
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Arch Neurol. 2011;68(2):248-250. doi:10.1001/archneurol.2010.364

Metabolic Imaging Correlate of Truncal Onset Seizures

Abstract Full Text
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Arch Neurol. 2011;68(2):251-253. doi:10.1001/archneurol.2010.370
Book Reviews

Doctor Olaf van Schuler’s Brain

Abstract Full Text
Arch Neurol. 2011;68(2):260-263. doi:10.1001/archneurol.2010.368

Atlas of Polysomnography, 2nd ed

Abstract Full Text
Arch Neurol. 2011;68(2):260-263. doi:10.1001/archneurol.2011.8
This Month in Archives of Neurology

This Month in Archives of Neurology

Abstract Full Text
Arch Neurol. 2011;68(2):155-156. doi:10.1001/archneurol.2010.363
Article
Neurological Review

Deep Brain Stimulation for Parkinson DiseaseAn Expert Consensus and Review of Key Issues

Abstract Full Text
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Arch Neurol. 2011;68(2):165-165. doi:10.1001/archneurol.2010.260
ObjectiveTo provide recommendations to patients, physicians, and other health care providers on several issues involving deep brain stimulation (DBS) for Parkinson disease (PD).Data Sources and Study SelectionAn international consortium of experts organized, reviewed the literature, and attended the workshop. Topics were introduced at the workshop, followed by group discussion.Data Extraction and SynthesisA draft of a consensus statement was presented and further edited after plenary debate. The final statements were agreed on by all members.Conclusions(1) Patients with PD without significant active cognitive or psychiatric problems who have medically intractable motor fluctuations, intractable tremor, or intolerance of medication adverse effects are good candidates for DBS. (2) Deep brain stimulation surgery is best performed by an experienced neurosurgeon with expertise in stereotactic neurosurgery who is working as part of a interprofessional team. (3) Surgical complication rates are extremely variable, with infection being the most commonly reported complication of DBS. (4) Deep brain stimulation programming is best accomplished by a highly trained clinician and can take 3 to 6 months to obtain optimal results. (5) Deep brain stimulation improves levodopa-responsive symptoms, dyskinesia, and tremor; benefits seem to be long-lasting in many motor domains. (6) Subthalamic nuclei DBS may be complicated by increased depression, apathy, impulsivity, worsened verbal fluency, and executive dysfunction in a subset of patients. (7) Both globus pallidus pars interna and subthalamic nuclei DBS have been shown to be effective in addressing the motor symptoms of PD. (8) Ablative therapy is still an effective alternative and should be considered in a select group of appropriate patients.
Correspondence

Different Phenotypes Among Lesch-Nyhan Variants: Clinical Reality or Limitation of Ascertainment?

Abstract Full Text
Arch Neurol. 2011;68(2):264-271. doi:10.1001/archneurol.2010.360

Different Phenotypes Among Lesch-Nyhan Variants: Clinical Reality or Limitation of Ascertainment?—Reply

Abstract Full Text
Arch Neurol. 2011;68(2):264-271. doi:10.1001/archneurol.2010.361

Vascular Risk Scores for Dementia: Age Matters

Abstract Full Text
Arch Neurol. 2011;68(2):264-271. doi:10.1001/archneurol.2011.2

Improving Risk Scores for Dementia

Abstract Full Text
Arch Neurol. 2011;68(2):264-271. doi:10.1001/archneurol.2011.3

Accuracy of Summary Risk Score for Prediction of Alzheimer Disease: Better Than Demographics Alone?

Abstract Full Text
Arch Neurol. 2011;68(2):264-271. doi:10.1001/archneurol.2011.4

Accuracy of Summary Risk Score for Prediction of Alzheimer Disease: Better Than Demographics Alone?—Reply

Abstract Full Text
Arch Neurol. 2011;68(2):264-271. doi:10.1001/archneurol.2011.5
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