A quarter of all ischaemic strokes (a fifth of all strokes) are lacunar type.¹ Lacunar infarcts are small infarcts (2–20 mm in diameter) in the deep cerebral white matter, basal ganglia, or pons, presumed to result from the occlusion of a single small perforating artery supplying the subcortical areas of the brain.² Although a recognised stroke subtype for over 50 years, the cause of lacunar ischaemic stroke,² and whether it is different to cortical ischaemic stroke, remains under debate.^3,4 Furthermore, lacunar stroke is not benign; 30% of patients are left dependent,⁵ and scant long term data suggest that up to 25% of patients have a second stroke within 5 years.⁶ Therefore, the prevention and treatment of this common stroke subtype may be less than ideal.

PROBLEMS IN THE STUDY OF LACUNAR STROKE

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 …