基于虚气留滞理论探讨脑小血管病OA

Cerebral small vessel disease(CSVD)is a prevalent condition among the elderly population.This condition encompasses a spectrum of pathological states affecting the intraparenchymal penetrating arteries,arterioles,capillaries,venules,and leptomeningeal vessels.CSVD plays a significant role in the pathogenesis of stroke,dementia,and age-related cognitive decline.CSVD is progressing with age,and the prevalence of cerebrovascular risk factors such as hypertension and diabetes along with the aging of the global population is increasing.The incidence rate is more than 70%.The pathogenesis of the disease is highly complex,which may be related to cerebral hypoperfusion,chronic ischemia,impaired blood-brain barrier and abnormal vascular endothelial function,and genetic and inflammatory responses,CSVD is mainly defined by neuroimaging features,including white matter hyperintensities,lacunar infarction,enlarged perivascular spaces,cerebral microbleeds,and cerebral atrophy.Although CSVD prevalence is high and there may be a long treatment window,there is no mechanism-based therapy available.Through a systematic analysis of the literature on CSVD,combined with an exploration of its etiology and pathogenesis utilizing the"deficient-Qi(气)stagnation"theory proposed by Academician WANG Yongyan,it was ultimately elucidated that"deficient-Qi stagnation"constitutes the core pathogenesis mechanism of CSVD.Further systematic elucidation reveals its pathomechanistic characteristics:Cerebral small vessel disease manifests with deficient Qi as the root and stagnation as the branch.Root deficiency forms the pathological foundation for disease initiation,while branch excess constitutes the progressive condition for disease advancement.These two components interact through a dynamic,reciprocal causation that perpetuates a vicious cycle,thereby driving pathological progression.Under the pathological state of"deficient-Qi stagnation",the obstructed Qi-blood flow in the collateral vessels thereby induces ischemic pathological changes in the related viscera and tissues.Comprehending the dynamic evolution patterns of this pathomechanism provides novel directions for syndrome-differentiated clinical treatment.