Non-invasive Evaluation of Cerebrovascular Reactivity in Spontaneous Intracerebral Hemorrhage

Spontaneous intracerebral hemorrhage (ICH) remains a significant cause of morbidity and mortality around the globe. The most common etiology of nontraumatic spontaneous ICH is hypertensive arteriopathy (HA), while cerebral amyloid angiopathy (CAA) is the most prevalent cause of spontaneous lobar ICH in the elderly. Both HA and CAA belong to the family of cerebral small vessel disease (cSVD). cSVD involves pathological processes that affect the arteries, arterioles, capillaries, and veins on the surface and beneath the brain. The resultant changes of cSVD in the brain vasculatures can be detected with neuroimaging, includes cerebral microbleeds, white matter hyperintensities, lacunes, dilated perivascular spaces, and brain atrophy. Investigators of this study have probe into various imaging markers in patients with cSVD. Investigators found that the lacune and cerebral microbleeds location was related to distinct underlying etiology of cSVD. Further, investigators utilized amyloid PET study to directly quantified the cerebral amyloid burden, and demonstrated the correlation between amyloid deposition and deep/superficial microbleeds ratio. The association between cerebellum microbleeds, which is a novel marker for cSVD, and the underlying pathology in patient with spontaneous ICH has been investigated. Investigators also summarized and published the current research of different cSVD imaging markers and its implication on patient care. Cerebrovascular reactivity (CVR) represents the phenomenon that cerebral vessels dilate or constrict in response to stimuli, which provides insights into the vascular reserve information. The vascular reserve parameter is complementary to steady-state vascular index, such as cerebral perfusion or other neuroimaging markers. Measurement of CVR using advanced MR techniques is an emerging technique with multiple potential clinical utilities, and impaired autoregulation may contribute to the pathogenesis of cSVD. Recently, diminished CVR