We will also explore the clinical impact of SVDs not associated with a clear-cut symptomatology on the development of disabling conditions such as stroke and dementia.Īcute Ischemic Expression of SVD: Lacunar StrokesĬerebral SVD results in approximately one-fourth of all acute ischemic strokes, mainly in the form of lacunar infarction. In this special focus on clinical consequences of SVDs, we aim to provide a comprehensive overview of the main clinical manifestations of SVD. Hence, stroke specialists may face challenging clinical situations in balancing hemorrhagic and ischemic risk, especially when antithrombotic medication may be needed. The neuropathological substrates of SVDs lead to both ischemic and hemorrhagic consequences. 8 Population-based studies suggest that they are associated with subtle neurological symptoms, and their presence confer an increased risk of stroke and cognitive impairment. Finally, imaging markers of cerebral SVD, not associated with a clear-cut symptomatology, are among the most common incidental findings on MRI. Differently, an insidious clinical course may be associated with progressive cognitive decline, development of mood disorders, and motor problems related to small vessel pathologies. Diseases that affect small arteries and arterioles may present abruptly and dramatically like in intracerebral hemorrhage (ICH) and lacunar stroke. 7Ĭerebral SVDs can manifest with a widespread and heterogeneous range of clinical manifestations that often lead to functional disability in the late stages of the disease. 6 The second most common form of sporadic SVD is CAA, a pathological process characterized by the progressive accumulation of ß-amyloid protein in the wall of small cortical and leptomeningeal arterioles and arteries. Arteriolosclerosis has a predilection for the deep lenticulostriate arteries that are vulnerable to poorly controlled and long-standing hypertension or diabetes mellitus.

The former describes a group of small vessel pathological processes. Two main forms of sporadic SVD have been described: arteriolosclerosis and cerebral amyloid angiopathy (CAA). 4 Thus, the term SVD is also used to describe a range of neuroimaging and pathological features of parenchymal damage that can either be associated to clinical symptoms or clinically silent. 1, 3 Although recent investigational work has suggested that it may be possible to visualize pathologies in these small arteries with 7 Tesla magnetic resonance imaging (MRI), standard neuroimaging used in clinical practice does not yet allow the direct visualization of these vessels. 1–3 Small vessel pathological processes that involve small veins and venules have not only been less frequently reported (such as venous collagenosis) but also less frequently be the object of pathology studies that mostly focus on arterial disease. From a neuropathological perspective, SVD encompasses a group of pathologies that affect the perforating arteries, arterioles, capillaries that are located in the brain parenchyma or in the leptomeningeal vessels. The term SVD is used with various meanings according to the context (ie, clinical, research, neuropathology, and neuroimaging aspects). Nevertheless, SVDs play a crucial role in a large variety of conditions such as aging, stroke, cognitive impairment, and other age-related disabilities (motor and gait impairment, mood disorders, and urinary symptoms). Furthermore, although some fields of vascular neurology have been revolutionized with reperfusion therapies, stroke specialists have little to offer for diseases that affect small cerebral vessels. Until recent years, cerebral small vessel disease (SVD) has drawn little attention mostly because small cerebral arteries were difficult to observe in imaging and in vivo studies. See related articles, p 9, p 12, p 21, p 29, p 38 Customer Service and Ordering Information.Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).

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