Naci and Owen test whether selective auditory attention can be used to detect conscious awareness and communicate with behaviorally nonresponsive patients.
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Wang and colleagues perform a cross-sectional cohort study to assess the relationship between default mode network integrity and cerebrospinal fluid biomarkers of Alzheimer disease pathology. Resting-state functional connectivity magnetic resonance imaging measures were obtained in 207 cognitively normal older individuals.
Day and coauthors correlate baseline resting-state measures within the salience network and changes in behavior with functional magnetic resonance imaging data and longitudinal clinical measures in patients with frontotemporal dementia.
Muehlschlegel et al identify predictors that can distinguish reversible cerebral vasoconstriction syndrome with subarachnoid hemorrhage (SAH) from aneurysmal SAH and cryptogenic “angiogram-negative” SAH at the time of clinical presentation.
Continuing Medical Education
Ghani and colleagues test the hypothesis that the late-onset Alzheimer disease (AD) in a Caribbean Hispanic population might be explained in part by the homozygosity of unknown loci that could harbor recessive AD risk haplotypes or pathologic mutations.
In a combined genome-wide association (GWA) analysis, Moskvina and coauthors assess the genetic overlap between Parkinson disease (PD) and Alzheimer disease (AD) by testing for the presence of potentially pleiotropic loci in 2 recent GWA studies of PD and AD.
Kang and colleagues evaluate the baseline characteristics and relationship to clinical features of cerebrospinal fluid biomarkers (β-amyloid 1-42 [Aβ1-42], total tau [T-tau], tau phosphorylated at threonine 181 [P-tau181], and α-synuclein) in drug-naive patients with early Parkinson disease (PD) and demographically matched healthy controls enrolled in the Parkinson’s Progression Markers Initiative study.
Gaspard and colleagues describe an electroencephalography pattern, lateralized rhythmic delta activity, encountered in critically ill subjects and determine its clinical significance in this setting.
Noreau and coauthors evaluate the prevalence of SYNE1 mutations in individuals with mild pure cerebellar ataxia and cerebellar atrophy by sequencing the gene in a cohort of 19 French-Canadians and 21 individuals from other ethnic backgrounds.
Brück and colleagues relate safety issues of newer disease-modifying treatments for relapsing-remitting multiple sclerosis to their molecular targets, mechanism of action, chemical structure, and metabolism and describe how identification of adverse events observed with established drugs within the same class provides clues regarding safety and toxic effects of newer multiple sclerosis therapeutics.
Rasmussen and Eliasmith review recent work that seeks to expand mechanistic functional modeling to encompass the whole brain.
Highlights. JAMA Neurol. 2013;70(10):1209-1211. doi:10.1001/jamaneurol.2013.2887