Even in the absence of manifest stroke, AF is a risk factor for cognitive impairment and hippocampal atrophy. Therefore, cognition and measures of structural brain integrity should be considered in the evaluation of novel treatments for AF.

These data suggest that low-grade inflammation as assessed by high-sensitivity C-reactive protein is associated with cerebral microstructural disintegration that predominantly affects frontal pathways and corresponding executive function.

We propose diagnostic criteria for Susac syndrome that may help both experts and physicians not familiar with Susac syndrome to make a correct diagnosis and to prevent delayed treatment initiation.

Quantification of brain water uptake identifies stroke patients with symptom onset within 4.5 hours with high accuracy and may guide the decision to use thrombolysis in patients with unknown time of stroke onset. Ann Neurol 2016;80:924-934.

Abstract-While the relation between systolic blood pressure (SBP) and vascular events is linear down to the high-normal range, the relation between SBP and cognition is less clear. We cross-sectionally assessed the relation between SBP and cognition in a cohort extending from mid-to late-life. From a total of 2200 community-dwelling individuals we recruited 377 aged 44 to 82 years (median: 64 years, 171 male) in the SEARCH-Health study (Systematic evaluation and alteration of risk factors for cognitive health). Participants were studied with a comprehensive neuropsychological test battery that provided, based on principal component analysis, 5 composite scores for cognition (learning and memory, attention and executive function, spatial skills, working memory, and verbal skills). Key Words: hypertension Ⅲ cognition Ⅲ age Ⅲ risk factors E pidemiologic studies have shown that systolic blood pressure (SBP) is linearly associated with the risk of myocardial infarction and stroke. 1-3 Cardio-and cerebrovascular diseases are related to cognitive decline in large population and patient-based cohorts. 4 -11 Recent evidence further indicates that the summation of vascular brain lesions, white matter damage from small vessel disease, and typical Alzheimer pathology interact bidirectionally and jointly contribute to dementia, even when each type of lesion, on its own, would not be severe enough to cause dementia. 12,13 However, epidemiological reports suggest that the direct association between blood pressure and cognitive function, eg, without an intermediate clinical outcome such as stroke, is complex and may be life period-dependent. Long-term follow-up studies found that elevated SBP, occurring in midlife, increases the risk of developing clinical manifest dementia in old age. 14,15 Along the same line, time survival analyses demonstrate that use of antihypertensive medication is associated with a reduced incidence of dementia. 16 Clinical trials showed that antihypertensive treatment in nondemented elderly subjects with a resting systolic blood pressure of more than 160 mm Hg reduced the incidence of subsequent dementia. Thus after 4 years there were only half as many cases of dementia in the treatment as compared with the placebo group. [17][18][19] Conversely, other antihypertensive intervention studies did not reveal significant effects on cognition. 20 -22 However, problems were patients lost to follow-up, active medication given to placebo patients as their blood pressure exceeded per-set values, and insensitive cognitive testing. 23 Observational studies in late-life showed that also low blood pressure was associated with dementia. 24,25 In the Kungsholmen project participants with a SBP below 140 mm Hg were more often diagnosed as demented than those with SBP above 140 mm Hg. 26,27 The suggestion of a nonlinear J-or even U-shaped relation between cognitive function and SBP raises doubts as to how rigorously blood pressure should be lowered. The aim of our study was to determine the relation between cognitive ...

A compelling association has been observed between cardiovascular disease (CVD) and depression, suggesting individuals with depression to be at significantly higher risk for CVD and CVD-related mortality. Systemic immune activation, hypothalamic–pituitary–adrenal (HPA) axis hyperactivity, arterial stiffness and endothelial dysfunction have been frequently implicated in this relationship. Although a differential epidemiological association between CVD and depression subtypes is evident, it has not been determined if this indicates subtype specific biological mechanisms. A comprehensive systematic literature search was conducted using PubMed and PsycINFO databases yielding 147 articles for this review. A complex pattern of systemic immune activation, endothelial dysfunction and HPA axis hyperactivity is suggestive of the biological relationship between CVD and depression subtypes. The findings of this review suggest that diagnostic subtypes rather than a unifying model of depression should be considered when investigating the bidirectional biological relationship between CVD and depression. The suggested model of a subtype-specific biological relationship between depression and CVDs has implications for future research and possibly for diagnostic and therapeutic processes.

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Background and Purpose-Early decompressive surgery in patients with malignant middle cerebral artery (MCA) infarction improves outcome. Elevation of intracranial pressure depends on both the space occupying brain edema and the intracranial volume reserve (cerebrospinal fluid [CSF]