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In This Issue of JAMA Neurology
March 2015

Highlights

JAMA Neurol. 2015;72(3):251. doi:10.1001/jamaneurol.2014.2836
Research

Lim and colleagues indicate that the risk of early recurrent stroke after transient ischemic attack (TIA) may be modifiable by optimal treatment. They determine the rate of early recurrent stroke after TIA and its neuroimaging predictors. They find that a total of 500 patients (mean age, 64 years; male, 291 [58.2%]; median ABCD2 score, 4) completed 90-day follow-up with guideline-based management: antiplatelets (457 [91.4%]), anticoagulants (74 [14.8%]), and statins (345 [69.0%]). Recurrent stroke occurred in 25 patients (5.0%) and was associated with cerebral microbleeds.

Fleisher et al characterize and compare age-associated changes in brain imaging and fluid biomarkers in PSEN1 E280A mutation carriers and noncarriers. They found that, compared with noncarriers, cognitively unimpaired mutation carriers had significantly lower precuneus cerebral metabolic rates for glucose, smaller hippocampal volume, lower cerebrospinal fluid (CSF) Aβ1-42, higher CSF total tau and phosphorylated tau181, and higher plasma Aβ1-42 measurements. This cross-sectional study provides additional information about the course of different Alzheimer disease (AD) biomarkers in the preclinical and clinical stages of autosomal dominant AD.

Clinical Review & Education

Wechsler summarizes the current status of teleneurology. He reports that outcomes after intravenous tissue plasminogen activator treatment via telemedicine (telestroke) are similar to those achieved with in-person evaluations. Teleneurology provides neurological expertise to rural areas with limited availability of neurologists and improves care for patients with difficulty traveling owing to neurological disease.

Continuing Medical Education

Corps and coauthors searched articles in PubMed published between 1960 and August 1, 2014, using the following keywords: traumatic brain injury, sterile injury, inflammation, astrocytes, microglia, monocytes, macrophages, neutrophils, T cells, reactive oxygen species, alarmins, danger-associated molecular patterns, purinergic receptors, neuroprotection, and clinical trials. They report that traumatic brain injury is a diverse group of sterile injuries induced by primary and secondary mechanisms that give rise to cell death, inflammation, and neurologic dysfunction in patients of all demographics. The mechanisms that drive traumatic brain injury lesion development, as well as those that promote repair, are exceedingly complex and often superimposed.

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