4.6 Article

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

Journal

INTERNATIONAL JOURNAL OF STROKE
Volume 10, Issue 7, Pages 1044-1050

Publisher

SAGE PUBLICATIONS LTD
DOI: 10.1111/ijs.12558

Keywords

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

Funding

  1. Wellcome Trust [WT088134/Z/09/A, 063668, 075611]
  2. Row Fogo Charitable Trust
  3. Scottish Funding Council - Scottish Imaging Network: A Platform for Scientific Excellence collaboration
  4. China Scholarship Council/UoE
  5. Age-UK Disconnected Mind Study
  6. Medical Research Council
  7. UoE
  8. Binks Trust (The Edinburgh Stroke Study)
  9. Chief Scientist Office of the Scottish Executive [217 NTU R37933]
  10. Mild Stroke Study
  11. Brain Research Imaging Centre Edinburgh
  12. MRC [G1001245, G0701120] Funding Source: UKRI
  13. Medical Research Council [G0701120, MR/K026992/1, G1001245] Funding Source: researchfish

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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 exter-nal 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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