What causes lacunar stroke?

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Abstract
Several factors have hampered the study of lacunar stroke. Firstly, few patients die from lacunar stroke; if they do, death may occur long after the stroke, making autopsy material scant and difficult to interpret, and the small cerebral vessels require meticulous dissection. Studies of risk factors and causation have predominantly used a clinical diagnosis of stroke type, probably resulting in some misclassification. Although lacunar infarcts are associated with specific neurological syndromes, and most patients with a clinical lacunar syndrome have a small deep subcortical infarct on brain imaging (if visible), 10–20% actually have a recent small cortical infarct in a location that explains their stroke presentation.7 Similarly, 10–20% of patients with a clinical mild cortical stroke actually have a recent relevant lacunar infarct on imaging.7 Epidemiologically, these patients behave more like the lesion type on imaging than the clinical syndrome of the lesion they actually have.7 Many studies have used an inappropriate control group; age matched normal controls can only indicate whether or not a particular risk factor is associated with stroke, whereas identification of associations specific to lacunar stroke requires a control group with a different type of ischaemic stroke. Finally, some classifications, such as the Trial of Org 10172 in Acute Stroke Treatment (TOAST) method8 actually use risk factors (such as embolic sources or hypertension) to determine the stroke type, thus potentially biasing studies of differences in risk factors. Hence, inadvertent misdiagnosis of lacunar as cortical stroke, and vice versa, the paucity of pathological material, and bias in some clinical classification systems may have confounded previous pathology, prognosis, and risk factor studies.

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