A Comparison of Location of Acute Symptomatic vs. ‘Silent’ Small Vessel Lesions

Abstract

BackgroundAcute 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.AimTo test if lesion location could be one reason why some small vessel disease lesions present with acute stroke, whereas others accumulate covertly.MethodsWe 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.ResultsIn 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/mm3), centrum semiovale (probability density = 0·15/mm3), medial lentiform nucleus/lateral thalamus (probability density = 0·09/mm3), and pons (probability density = 0·02/mm3). Most lacunes were in the lentiform nucleus (probability density = 0·01–0·04/mm3) or external capsule (probability density = 0·05/mm3). 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).ConclusionsLesions 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.

Interhemispheric characterization of small vessel disease imaging markers after subcortical infarct

“…There was no significant right‐left difference in RSSI volumes (Wilcoxon signed rank p  = .16), with spatial prevalence already reported in Valdes Hernandez, Maconick, et al. (2015). RSSI was distributed slightly more widely on the left (Figure 2).…”

“…RSSI was found almost exclusively in the posterior limb of the internal capsule and neighboring white and deep grey matter areas: posterior putamen, globus pallidus, and anterior thalamus; coincident with the region assumed to be crossed by the sensory and motor pathways as published previously (Valdes Hernandez, Maconick, et al., 2015). We also found a balance between the number of patients who had the RSSI in the left and right hemisphere, in agreement with another study (Mead, Lewis, Wardlaw, Dennis, & Warlow, 2000).…”

Blood pressure gradients in cerebral arteries: a clue to pathogenesis of cerebral small vessel disease

“…Wardlaw's group 43 reported that lacunar infarctions in the vascular centrencephalon were more likely to be symptomatic than small subcortical WMI over the convexity; it is possible that in SPRINT, lower blood diastolic pressures may have prevented hypertensive strokes, while an increase in subcortical WMI may have gone undetected. However, if WMI over the convexity and periventricular WMI are due to other forms of small vessel disease, then different approaches will be needed to prevent them.…”

Update on cerebral small vessel disease: a dynamic whole-brain disease

“…One explanation is the locations of lesions. A study using probability mapping shows that lesions presenting with stroke were predominantly located in or near the primary motor and sensory tracts, whereas silent lesions were mostly in the basal ganglia and centrum semiovale away from these main tracts 77. Another explanation could be the levels of vessels where the vascular pathologies happened.…”