[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.197.65.227. Please contact the publisher to request reinstatement.
Sign In
Individual Sign In
Create an Account
Institutional Sign In
OpenAthens Shibboleth
[Skip to Content Landing]
Citations 0
This Month in Archives of Neurology
Oct 2011

This Month in Archives of Neurology

Arch Neurol. 2011;68(10):1234-1235. doi:10.1001/archneurol.2011.226

Shepardson et alArticle examine the complex preclinical and clinical literature on cholesterol level and Alzheimer disease. Statin use as a potential therapeutic agent in patients with Alzheimer disease is the focus of this first segment of a 2-part review.

In this secondary analysis of the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL), which tested the effect of treatment with atorvastatin in reducing stroke in subjects with a recent stroke or transient ischemic attack, Callahan and colleaguesArticle explore the effects of treatment in subjects with type 2 diabetes mellitus or metabolic syndrome (MetS). The SPARCL subjects with type 2 diabetes were at higher risk of recurrent stroke and cardiovascular events. This exploratory analysis found no difference in the effect of statin treatment in reducing these events in subjects with or without type 2 diabetes or MetS.

In his lecture, Louis R. CaplanArticle describes both the positive and negative aspects of personalized medicine vs evidence-based medicine in evaluating and treating patients.

Lo and colleaguesArticle aim to delineate the trajectories of Aβ42 level in cerebrospinal fluid (CSF), fludeoxyglucose F18 (FDG) uptake using positron emission tomography, and hippocampal volume using magnetic resonance imaging and their relative associations with cognitive change at different stages in aging and Alzheimer disease (AD). They report that trajectories of Aβ42 level in CSF, FDG uptake, and hippocampal volume vary across different cognitive stages. The longitudinal patterns support a hypothetical sequence of AD pathology in which amyloid deposition is an early event before hypometabolism or hippocampal atrophy, suggesting that biomarker prediction for cognitive change is stage dependent. Editorial perspective is provided by Roger N. Rosenberg, MDArticle.

Farez and CorrealeArticle indicate that, for patients with multiple sclerosis traveling to endemic yellow fever areas, vaccination should be recommended on the basis of carefully weighing the risk of exacerbation against the likelihood of exposure to the yellow fever virus.

Holmes et alArticle determine the frequency of malformations among infants born to women who had taken lamotrigine or carbamazepine as part of polytherapy during the first trimester of pregnancy. They indicate that the risk of malformations among infants exposed to lamotrigine and carbamazepine as polytherapy was higher than the corresponding monotherapies only when the polytherapy includes valproate. These findings suggest that counseling for fetal risks from antiepileptic drug polytherapy should be based on the specific drugs included.

Prevalence of major malformations in antiepileptic drug (AED) polytherapies with and without valproic acid (VPA). Results shown are from the North American AED Pregnancy Registry and 2 previously published studies, the UK Epilepsy Pregnancy Register6 and the International Lamotrigine Pregnancy Registry.7 CBZ indicates carbamazepine; and LTG, lamotrigine.

Prevalence of major malformations in antiepileptic drug (AED) polytherapies with and without valproic acid (VPA). Results shown are from the North American AED Pregnancy Registry and 2 previously published studies, the UK Epilepsy Pregnancy Register6 and the International Lamotrigine Pregnancy Registry.7 CBZ indicates carbamazepine; and LTG, lamotrigine.

McKeon and colleaguesArticle investigate the full extent of Purkinje cell cytoplasmic autoantibody type 1 autoimmunity (classically associated with paraneoplastic cerebellar degeneration) from clinical, immunohistochemical, and neuropathological perspectives. They show that Purkinje cell cytoplasmic autoantibody type 1 autoimmunity most commonly affects the cerebellum, but the spectrum of neurological symptoms and presentations is broad. Neurological outcomes are usually poor, even when cancer remission is achieved.

Moon et alArticle assess the prevalence, risk covariates, and implication of medial arterial calcification (MAC) in a controlled study of healthy subjects and patients with diabetes mellitus (DM). Medial arterial calcification of legs was approximately 4 times as prevalent in population-representative ambulatory persons with DM as in healthy subjects. Advancing age, male sex, DM, and retinopathy were the significant risk covariates for MAC of legs. Medial arterial calcification of legs, although significantly associated with distal, length-dependent sensorimotor polyneuropathy (DSPN), was not a useful surrogate marker of DSPN. Also, MAC was not shown to be a risk covariate for late worsening of DSPN, although other lines of evidence suggest that peripheral arterial disease may worsen DSPN.

Klein and colleaguesArticle study a newly identified mitofusin 2 (MFN2) mutation, Leu146Phe (a mitochondrial membrane protein mediating mitochondrial fusion and function), and the associated phenotypes in a large kindred. They find that this novel MFN2 mutation Leu146Phe causes Charcot-Marie-Tooth type 2A2.

Naeije et alArticle test the hypothesis that treatment with cefepime hydrochloride leads to higher incidence of periodic epileptiform discharges compared to treatment with other β-lactams. Their study shows a prevalence of electroencephalographic test results with continuous epileptiform discharges in 14 of 1120 patients receiving cefepime (1.25%) but of only 3 of 1572 patients receiving meropenem (0.19%).

Simone and colleaguesArticle study N -acetylaspartate (NAA) in serum samples as a possible biomarker of amyotrophic lateral sclerosis (ALS). High serum NAA level was found in patients with ALS, which may relate to greater excretion of NAA into the blood circulation following increased release of this metabolite from damaged neurons. The correlation between serum NAA level and disease progression rate suggests that it may be a useful biomarker of ALS.

Xiong et alArticle assess whether family history (FH) of Alzheimer disease (AD) alone influences AD biomarker abnormalities. They report that, independent of APOE4, FH is associated with age-related change of several cerebrospinal fluid, Pittsburgh compound B, and diffusion tensor imaging biomarkers in cognitively normal middle- to older-age individuals, suggesting that non- APOE susceptibility genes for AD influence AD biomarkers.

×