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Introduction: The primary aim of this paper is to improve the clinical interpretation of white matter hyperintensities (WMHs) and provide an overarching summary of methodological approaches, allowing researchers to design future studies targeting current knowledge gaps. Methods: A meta‐analysis and systematic review was performed investigating associations between baseline WMHs and longitudinal cognitive outcomes in cognitively normal populations, and populations with mild cognitive impairment (MCI), Alzheimer's disease (AD), and stroke. Results: Baseline WMHs increase the risk of cognitive impairment and dementia across diagnostic categories and most consistently in MCI and post‐stroke populations. Apolipoprotein E (APOE) genotype and domain‐specific cognitive changes relating to strategic anatomical locations, such as frontal WMH and executive decline, represent important considerations. Meta‐analysis reliability was assessed using multiple methods of estimation, and results suggest that heterogeneity in study design and reporting remains a significant barrier. Discussion: Recommendations and future directions for study of WMHs are provided to improve cross‐study comparison and translation of research into consistent clinical interpretation. [ABSTRACT FROM AUTHOR]

A study was conducted to evaluate the effect of blinded peer review on the association between abstract characteristics and likelihood of abstract acceptance at a national research meeting. The study provided evidence of bias in the open review of abstracts, favoring authors from the United States, English-speaking countries outside the U.S. and prestigious academic institutions.

Patients enrolled in the Extracranial/Intracranial Bypass Study (EC/IC Bypass Study) were examined to determine if site differences in intracranial and extracranial arterial lesions among racial groups could be explained by differences in risk factors. In all there were 1,367 subjects. Among blacks, high blood pressure or diabetes was more common, and they were more likely to be smokers. Whites had higher average systolic blood pressure and levels of hemoglobin (a pigmented protein-iron compound in the blood that carries oxygen to the cells, and carbon dioxide away). Asians (Chinese and Japanese) had the lowest prevalence of vascular risk factors. The study attempted to determine whether risk factors and race have independent effects on the location of cerebrovascular lesions (i.e. those involved in the vascular system that supplies blood to the brain) among different ethnic groups. It is unclear whether race and risk factors play separate roles or whether their roles are interdependent. The authors list three categories of risk factors: information on demographics, life style, and medical history; results of the physical examination at the first visit; and baseline laboratory test results. The location of cerebrovascular lesions, the prevalence of abnormal sounds in the neck artery, ischemic heart disease (diminished blood flow to the heart), and intermittent weakness and cramps in the legs due to poor circulation, were all seen to differ by race in this study. Frequencies of middle cerebral artery lesions decrease, and the frequency of internal carotid artery lesions increase from Asians to blacks to whites. There were no differences by sex and age, but statistically significant differences in types of risk factors were found. Both whites and blacks had higher cholesterol values than Asians. In general, the number of risk factors was lower in Asians than in the other two groups. The results indicate that large differences may exist between groups of patients of different races with symptoms of cerebral ischemia, and between groups of patients with a different site of lesion, according to the distribution of the conventional risk factors. (Consumer Summary produced by Reliance Medical Information, Inc.)

Sudden unexpected death accounts for one quarter of mortality in the United States, approximately 450,000 people each year. The autopsy findings typically involve atherosclerosis without any obvious evidence of myocardial infarction (heart attack) or coronary thrombosis; there is no clear-cut cause of death. Only 12 percent of victims of sudden unexpected death have a history of cardiac problems. Considerable evidence, though much of it circumstantial, implicates the brain as the cause of death in these people. There is considerable evidence that the electrocardiographic abnormalities that are found may follow cerebral events such as hemorrhage or stroke. Arrhythmias, irregularities of the heart beat, may also be seen during epileptic seizures, emotional incidents, and migraine headaches. It is suspected that in many cases the induced arrhythmias are sufficient to cause what is later called sudden unexpected death. The cause of the cardiac abnormalities that may result from cerebral incidents is not known, but it is believed that the disinhibition of the hypothalamus or other autonomic center is involved. This view is supported by the observation of increased levels of norepinephrine in many cases of brain hemorrhage or infarction. The authors believe that the insula, part of the cerebral cortex with many connections to the hypothalamus and the limbic system, may be involved. It is hypothesized that damage to the insula results in inappropriate signals to many centers of the autonomic nervous system. The heart is forced to operate in the presence of abnormal and perhaps conflicting signals. The result is arrhythmia, and in the more severe cases, subsequent death. (Consumer Summary produced by Reliance Medical Information, Inc.)

Subcortical ischemic strokes are among the leading causes of cognitive impairment. Selective atrophy of remote brain regions connected to the infarct is thought to contribute to deterioration of cognitive functions. The mechanisms underlying this secondary degenerative process are incompletely understood, but are thought to include inflammation. We induce ischemia by unilateral injection of endothelin-I into the rat dorsomedial thalamic nucleus, which has defined reciprocal connections to the frontal cortex. We use a comprehensive test battery to probe for changes in behaviour, including executive functions. After a four-week recovery period, brain sections are stained with markers for degeneration, microglia, astrocytes and myelin. Degenerative processes are localized within the stroke core and along the full thalamocortical projection, which does not translate into measurable behavioural deficits. Significant microglia recruitment, astrogliosis or myelin loss along the axonal projection or within the frontal cortex cannot be detected. These findings indicate that critical effects of stroke-induced axonal degeneration may only be measurable beyond a threshold of stroke severity and/or follow a different time course. Further investigations are needed to clarify the impact of inflammation accompanying axonal degeneration on delayed remote atrophy after stroke. [ABSTRACT FROM AUTHOR]