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

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.

Keywords: acute lacunar infarct; lacunar stroke; lacunes; small vessel disease; stroke; white matter hyperintensities.

Figure 1

View in the axial, coronal, and sagittal planes to compare the distribution of recent small subcortical infarcts (left) and lacunes (middle) in stroke patients. The location of the corticospinal tracts as derived from tractography (right) is shown for comparison. Also, see Fig. S2.

Figure 2

WMH distribution of 188 stroke patients (left) and (for comparison) in 517 similarly aged subjects without stroke (right) in axial, coronal, and sagittal planes. Burden of WMH is less in stroke‐free subjects although the distribution is similar. See also Fig. S3.

Figure 3

Subtraction image to determine the difference in distribution of the recent small subcortical infarcts with respect to WMH (left) and lacunes (right) in stroke patients. Red–yellow indicates WMH (left hand image) or lacunes (right hand image); green–blue regions indicate the recent small subcortical infarcts that remain after subtraction from WMH and lacune maps (both sides). Images show a little overlap in location between the clinically symptomatic vs. covert lesions.