A comparison of location of acute symptomatic vs. 'silent' small vessel lesions

急性症状性小血管病变与“无症状”小血管病变位置的比较

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Abstract

BACKGROUND: Acute lacunar ischaemic stroke, white matter hyperintensities, and lacunes are all features of cerebral small vessel disease. It is unclear why some small vessel disease lesions present with acute stroke symptoms, whereas others typically do not. AIM: To test if lesion location could be one reason why some small vessel disease lesions present with acute stroke, whereas others accumulate covertly. METHODS: We identified prospectively patients who presented with acute lacunar stroke symptoms with a recent small subcortical infarct confirmed on magnetic resonance diffusion imaging. We compared the distribution of the acute infarcts with that of white matter hyperintensity and lacunes using computational image mapping methods. RESULTS: In 188 patients, mean age 67 ± standard deviation 12 years, the lesions that presented with acute lacunar ischaemic stroke were located in or near the main motor and sensory tracts in (descending order): posterior limb of the internal capsule (probability density 0·2/mm(3)), centrum semiovale (probability density = 0·15/mm(3)), medial lentiform nucleus/lateral thalamus (probability density = 0·09/mm(3)), and pons (probability density = 0·02/mm(3)). Most lacunes were in the lentiform nucleus (probability density = 0·01-0·04/mm(3) ) or external capsule (probability density = 0·05/mm(3)). Most white matter hyperintensities were in centrum semiovale (except for the area affected by the acute symptomatic infarcts), external capsules, basal ganglia, and brainstem, with little overlap with the acute symptomatic infarcts (analysis of variance, P < 0·01). CONCLUSIONS: Lesions that present with acute lacunar ischaemic stroke symptoms may be more likely noticed by the patient through affecting the main motor and sensory tracts, whereas white matter hyperintensity and asymptomatic lacunes mainly affect other areas. Brain location could at least partly explain the symptomatic vs. covert development of small vessel disease.

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