Maximum carotid plaque thickness was associated with an increased risk of vascular outcomes, especially among Hispanics, in an analysis of 2,189 subjects in a population-based cohort, as reported in the April 1 Neurology. Carotid plaque was present in 58% of the participants. During the mean 6.9 years of follow-up, vascular events occurred among 319 subjects: 121 had ischemic strokes, 118 had myocardial infarctions, and 166 died of vascular causes. Although there was a 2.8-fold increased risk of combined vascular events among those with carotid plaque thickness greater than the prespecified cutoff of 1.9 mm compared with those with no carotid plaque, the association was only significant among Hispanics after full adjustment. “Approximately 44% of the low-risk individuals … had a 10-year vascular risk of 18.3% if having carotid plaque,” said the researchers. They concluded that maximum carotid plaque thickness may be a useful risk stratification tool and a surrogate end point in clinical trials.
Parenchymal volumetric loss dose-dependently correlated with severity of traumatic brain injury (TBI), according to the results of a study of 69 chronic-phase TBI patients reported in the March 4 Neurology. A minimum of one year after TBI, high-resolution structural MRI also detected a spatially extensive pattern of volume loss that covaried with TBI severity, “with particularly widespread effects in white matter volume and sulcal/subdural CSF.” Of the 38 brain regions imaged, the most reliable effects were observed in the frontal, temporal, and cingulate regions, stated the researchers. They noted that the pattern of volume loss was independent of contributions of focal and diffuse injury, as focal lesions were associated with greater frontal and temporal volume loss, but the loss remained marked when analyses were restricted to patients with diffuse injury.
Researchers have proposed a mechanism for the brain’s conversion to epilepsy following injury. As reported in the March 28 online Proceedings of the National Academy of Sciences, the researchers used a large-scale, biophysically realistic model of the epileptic rat dentate gyrus to reconnect the aberrant recurrent granule cell network. Although the investigators noted that network activity in the dentate gyrus was robust after a number of major changes, “the incorporation of a small number of highly interconnected granule cell hubs greatly increase[d] network activity, resulting in a hyperexcitable, potentially seizure-prone circuit.” They suggested that these neural hub cells may be a therapeutic target for epilepsy.
Impaired olfaction may predate clinical Parkinson’s disease in men by at least four years, reported researchers in the February Annals of Neurology. Olfaction was tested in 2,267 Parkinson’s disease– and dementia-free men ages 71 to 95 for up to eight years. Thirty-five men were diagnosed with Parkinson’s disease at an average age of 82.9. During the first four years of follow-up, age-adjusted incidence of Parkinson’s disease declined from the lowest to the highest quartiles of odor identification; the odds ratio for Parkinson’s disease in the lowest quartile compared with the two highest quartiles was 5.2. The researchers suggested that tests of olfaction may be a useful screening tool for risk of Parkinson’s disease in men.
—Jessica Dziedzic