The increasing prevalence of multifocal cerebral microhemorrhages (CMHs, also known as "cerebral microbleeds") is a significant, newly recognized problem in the aging population of the Western world. CMHs are associated with rupture of small intracerebral vessels and are thought to progressively impair neuronal function, potentially contributing to cognitive decline, geriatric psychiatric syndromes, and gait disorders. Clinical studies show that aging and hypertension significantly increase prevalence of CMHs. CMHs are also now recognized by the National Institutes of Health as a major factor in Alzheimer's disease pathology. Moreover, the presence of CMHs is an independent risk factor for subsequent larger intracerebral hemorrhages. In this article, we review the epidemiology, detection, risk factors, clinical significance, and pathogenesis of CMHs. The potential age-related cellular mechanisms underlying the development of CMHs are discussed, with a focus on the structural determinants of microvascular fragility, age-related alterations in cerebrovascular adaptation to hypertension, the role of oxidative stress and matrix metalloproteinase activation, and the deleterious effects of arterial stiffening, increased pulse pressure, and impaired myogenic autoregulatory protection on the brain microvasculature. Finally, we examine potential treatments for the prevention of CMHs based on the proposed model of aging- and hypertension-dependent activation of the reactive oxygen species-matrix metalloproteinases axis, and we discuss critical questions to be addressed by future studies.

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Chronic venous insufficiency (CVI) results from venous hypertension secondary to superficial or deep venous valvular reflux. Treatment modalities are aimed at reducing venous valvular reflux, thereby inhibiting the ensuing pathologic inflammatory process. Compression therapy using pumps, bandaging, and/or graded compression stockings is the mainstay of treatment for CVI. Compression therapy has been shown to be effective in reducing venous hypertension retarding the development of inflammation and pathologic skin changes. Pharmacologic agents such as diuretics and topical steroid creams reduce swelling and pain short term but offer no long-term treatment advantage. Herbal supplements may reduce the inflammatory response to venous hypertension, but are not licensed by the US Food and Drug Administration, and vary in their efficacy, quality, and safety. However, several randomized controlled trials using the herbal horse chestnut seed extract containing aescin have shown short-term improvement in signs and symptoms of CVI. Endovascular and surgical techniques aimed at treatment of primary and secondary venous valvular reflux have been shown to improve venous hemodynamics promoting healing of venous ulcers and improving quality of life. The newer endovascular treatments of varicose veins using laser, radiofrequency ablation, and chemical foam sclerotherapy show some promise.