Lipohyalinosis is an important concept in the independence of
lacunar stroke; however, its role has been overemphasized and has led to much
confusion in the understanding of
lacunar stroke. Classical lipohyalinosis has declined following the widespread availability of
antihypertensive therapy, and
lacunar stroke secondary to age-related hyaline
atherosclerosis is more commonly observed in clinical practice. Clinically diagnosed
lacunar stroke is associated with several etiopathogenetic contributors. Excluding cardiogenic
embolism,
lacunar stroke can be categorized based on the detection of an
atheroma.
Atheroma imaging is possible in recent years, and
strokes that are not associated with an
atheroma are shown to present with deep white matter hyperintensity on MRI. Additionally, risk gene analysis has confirmed a group of risk genes associated with the extracellular matrix in
lacunar stroke with white matter hyperintensity on MRI. These findings suggest the role of a variety of etiopathogenetic mechanisms underlying
lacunar stroke and that
lacunar stroke with deep white matter hyperintensity on MRI may be attributable to unique pathogenetic contributors. This group is known to be strongly associated with genetic contributors. Hopefully,
lacunar stroke will be diagnosed from this perspective with the development of interventional strategies tailored to the pathogenesis of this condition.