RESUMEN
Cerebral smal vessel disease (CSVD) can be divided into sporadic and hereditary CSVD. The exact pathogenesis of sporadic CSVD is unknow n. Genetic factors may also play an important role, except for environmental and vascular risk factors. As a complicated disease, sporadic CSVD has the characteristics of multigenetic susceptibility. Therefore, investigating the related genetic factors may contribute to understanding the pathogenesis of sporadic CSVD. This article review s the advances in research on the genetics of sporadic CSVD.
RESUMEN
Cerebral smal vessel disease (CSVD) refers to cerebral smal perforating arteries and arterioles (diameter 40 - 200 μm), capilaries, and venules caused syndromes of clinical, cognitive and pathological manifestations. Its imaging classification includes lacunar infarcts, white matter lesions, cerebral microbleed, and perivascular space enlargement, etc. The pathogenesis of CSVD is stil being explored, and imaging findings can not completely reflect the change process of its pathophysiology, especialy the early lesions. Therefore, the difficulties have increased for the prevention and treatment of CSVD. This article summarizes the progress in research on CSVD biomarkers in recent years in order to provide ideas for its etiology, pathogenesis, and clinical prevention and treatment.
RESUMEN
Cerebral smal vessel disease (CSVD) accounts for 25 to 30% of al strokes. It is a main cause of vascular cognitive impairment. Because of cerebral smal vessels can not easily be directly observed and studied in vivo and on imaging, so the term CSVD is generaly used to describe a syndrome of clinical, cognitive, neuroimaging, and neuropathological changes, and not focus on the pathological changes of the smal vessel wal itself that caused these syndromes. This article reviews the advances in research on CSVD, particularly its pathological changes of vessel wals.