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In This Issue of JAMA Neurology
December 2017

Highlights

JAMA Neurol. 2017;74(12):1389. doi:10.1001/jamaneurol.2016.4029

Research

Although continuous electroencephalography use is increasing, there is not a validated way to determine the risk of seizure when ictal abnormalities are not found. Struck and coauthors used a prospective multicenter database of 5427 continuous EEG sessions from 4772 participants (median age, 61 years) to create a risk score to predict seizure occurrence in critically ill patients. The model, termed 2HELPS2B, has 6 variables to calculate the risk score: brief (ictal) rhythmic discharges (2 points); presence of lateralized periodic discharges, lateralized rhythmic delta activity, or bilateral independent periodic discharges (1 point); prior seizure (1 point); sporadic epileptiform discharges (1 point); frequency greater than 2.0 Hz of periodic/rhythmic pattern (1 point); and presence of “plus” features (1 point). The 2HELPS2B score combined with knowledge of the patient’s seizure history may help physicians assess seizure risk. Editorial perspective is provided by Czeisler and Claassen.

Editorial

Continuing Medical Education

Previous studies have shown that the immune system plays a role in amyotrophic lateral sclerosis (ALS), but these studies have not tracked immune cell changes over the course of ALS disease progression. Murdock and coauthors analyzed changes in the peripheral immune system in a longitudinal cohort study of 119 patients with ALS (mean [SD] age, 61.4 [11.5] years) and 35 controls (mean [SD] age, 63.5 [9.9] years) in an ALS clinic. They found changes in immune cell populations were correlated with changes in disease; increases in neutrophil numbers and decreases in CD4 T-cell numbers were correlated with rapid ALS progression. In addition, they report a rapid increase in the number of natural killer cells and a transient expansion of a nonmonocyte myeloid population. These data show that specific immune cell types are linked to ALS progression, and immunity may play a role in ALS.

Subjective cognitive decline (SCD) is considered a potential risk factor for progression to Alzheimer disease dementia, but the biological correlates of SCD are not clear. In this imaging substudy of the Harvard Aging Brain Study, Buckley and coauthors investigated the cross-sectional association of SCD with tau deposition in brain regions of interest associated with Alzheimer disease in 133 clinically healthy adults (mean [SD] age, 76 [6.9] years). Flortaucipir F 18 positron emission tomography scans were obtained and memory and cognition questionnaires administered. Greater abnormal tau burden in the entorhinal cortical region was most strongly associated with SCD. Editorial perspective is provided by Ossenkoppele and Jagust.

Editorial

Although Alzheimer disease biomarkers have been identified, they do not directly correlate with conversion from mild cognitive impairment to Alzheimer disease. van Maurik and coauthors constructed biomarker-based prognostic models (a cerebrospinal fluid model, a magnetic resonance imaging model, and a combined model) that enable prediction of future Alzheimer disease or any type of dementia in patients with mild cognitive impairment using the Alzheimer’s Biomarkers in Daily Practice project, a longitudinal cohort of 525 patients (mean [SD] age, 67.3 [8.4] years) with mild cognitive impairment from a tertiary referral center. The models also include patient characteristics (sex, age, and Mini-Mental State Examination score). Any value can be entered for the variables in these models, resulting in personalized probabilities with CIs. The models could aid clinicians interpret biomarker values and provide individually tailored prognostic information.

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