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This Month in Archives of Neurology
Dec 2011

This Month in Archives of Neurology

Arch Neurol. 2011;68(12):1504-1505. doi:10.1001/archneurol.2011.1504

Filippi and colleaguesArticle discuss the application of new imaging modalities capable of measuring pathological processes related to the disease that have been neglected in the past (eg, iron deposition and perfusion abnormalities) and the advent of high- and ultrahigh-field magnets that have provided further insight into the pathobiological features of multiple sclerosis.

Marder and colleaguesArticle report that their study does not support the theory that chronic cerebral venous insufficiency exists in multiple sclerosis. Editorial perspective is provided by Michael A. Williams, MD, and Arun Venkatesan, MD, PhDArticle.

Jack et alArticle indicate a reduction in the cerebrospinal fluid (CSF) Aβ42 level denotes a pathophysiological process that significantly departs from normality (ie, becomes dynamic) early, whereas the CSF total tau level and the adjusted hippocampal volume are biomarkers of downstream pathophysiological processes.

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Box plots and superimposed data points showing the distribution of Alzheimer disease (AD) biomarkers by baseline diagnosis and visit. The horizontal line in each box indicates the median, whereas the top and bottom borders of the box mark the 75th and 25th percentiles, respectively. The whiskers above and below the box mark the largest and smallest data point that is within 1.5 times the interquartile range of the top and bottom of the box. A, For participants with both baseline and 12-month data, the cerebrospinal fluid (CSF) Aβ42 level did not change from baseline to 12 months in the cognitively normal (CN) group (P = .52), the mild cognitive impairment (MCI) group (P = .13), or the AD group (P = .51). B, The CSF total tau level is shown on the log scale. It increased from baseline to 12 months in CN participants (P = .002) but not in participants with MCI (P = .12) or AD (P = .36). The dotted horizontal line extending across all box plots represents the cut point denoting normal vs abnormal for each biomarker.

Qureshi and colleaguesArticle find that the adjusted rate of favorable outcomes is lower among patients with ischemic stroke with underlying arterial dissection following thrombolytic treatment compared with those without underlying dissections. However, the observed lower rates are not influenced by thrombolytic treatment.

Mateen et alArticle show that severe neurological sequelae occur frequently in adult extracorporeal membrane oxygenation (ECMO)–treated patients with otherwise reversible cardiopulmonary injury (conservative estimate, 50%) and include a range of potentially fatal neurological diagnoses that may be due to the precipitating event and/or ECMO treatment.

Castrioto and colleaguesArticle indicate that this class III study provides evidence that stimulation-induced motor improvement was overall sustained at 10 years, although part of the initial benefit wore off mainly because of progressive loss of benefit on axial signs over time.

Vaknin-Dembinsky et alArticle report that the incidence of central nervous system involvement in myasthenia gravis is higher than previously reported and is expressed predominantly as a pyramidal syndrome accompanied by optical tract involvement (frequently subclinical). These features bear some resemblance to neuromyelitis optica spectrum disease, supported also by the presence of anti-AQP4 antibodies in 7 of the 14 patients tested.

Weintraub and colleaguesArticle find that hippocampal atrophy is a biomarker of initial cognitive decline in Parkinson disease, including impaired memory encoding and storage, suggesting heterogeneity in the neural substrate of memory impairment.

Logue et alArticle suggest that some genes contribute to Alzheimer disease pathogenesis in both white and African American cohorts, although it is unclear whether the causal variants are the same. A larger African American sample will be needed to confirm novel gene associations, which may be population specific.

Bettencourt and colleaguesArticle provide findings that indicate that the polymorphism at the APOE gene plays a role as a genetic modifier of Machado-Joseph disease phenotype.