The onset of cerebral small vessel disease is generally insidious and not easily recognized, and the current prevention and treatment relies only on clinical experience with unsatisfactory results. Therefore, early detection of cerebral small vessel disease and early intervention are imperative. Cerebral small vessel disease is a syndrome of clinical, cognitive, imaging and pathological manifestations resulting from various lesions of small intracranial vessels. The intracranial small vessels are the foundation necessary to maintain brain metabolism, cellular activity, and complex white matter network structure. For the past 15 years, cerebral small vessel disease has been considered a serious disease. However, because its onset is insidious and not easily recognized, its clinical manifestations are diverse and include sudden stroke symptoms, easily overlooked neurological signs and symptoms, conscious cognitive impairment, progressive cognitive decline, dementia, depression, and disability. Small vessel disease accounts for approximately 20% of strokes and can increase the risk of stroke by a factor of 1. It is also responsible for approximately 45% of dementia and has a significant cost to society. Since the cause of this disease is still unknown, prevention and treatment relying solely on clinical experience are unsatisfactory and even risky. Therefore, early detection of cerebral small vessel disease and early intervention are imperative. Imaging 1. lacunar infarcts: Most lacunar infarcts have a round, ovoid or tubular imaging morphology and are <20 mm in diameter. fisher found that tubular lesions are mostly found in the basal ganglia and internal capsule, and also about 5% of tubular lesions are from small hemorrhagic foci deep in the brain. Moreover, whether the lesion is located in the internal capsule determines whether the patient presents with clinical signs and symptoms, but is not related to the size of the lesion. The luminal space is a small cavity containing a small amount of cerebrospinal fluid in the basal ganglia or white matter, usually 3-15 mm in diameter. although lesions >15 mm in diameter are sometimes considered luminal, the larger the lesion, the greater the likelihood that its pathogenesis is different from that of cerebral small vessel disease. Many luminal lesions may present with no clinical signs or symptoms at all, but simply show pathological changes. The proportion of acute lacunar infarct foci that evolve into luminal spaces confirmed by diffusion-weighted imaging (DWI) is 28-94%, depending on the definition of the luminal space and other uncertainties, including follow-up time. However, not all patients evolve into lacunae, and DWI may show complete disappearance of larger acute lacunar infarct foci, or only white matter high signal changes without lacunae remain. 3. Cerebral white matter lesions: Cerebral white matter lesions are round in shape, with hypointense shadowing on CT, high signal on T2WI and FLAIR imaging, and low signal on T1WI between normal brain tissue and cerebrospinal fluid. These lesions are found in the periventricular area, deep white matter of the bilateral cerebral hemispheres, basal ganglia, pons, and occasionally in the cerebellum and other parts of the white matter of the brainstem. Compared with other stroke subtypes, acute lacunar infarcts with white matter high signal are more common and widely distributed, and are associated with lacunar and perivascular gap enlargement, cerebral microhemorrhage, and cerebral atrophy lesions. 4. Perivascular gap enlargement: MRI shows signal changes in the perivascular gap similar to those in the cerebrospinal fluid, which are round in vertical views and linear in parallel views, thus round in the basal ganglia and linear in the white matter of the lateral frontal and subcortical temporoparietal lobes. Although physiological peripheral gap enlargement can be present at any age, an excessive number is abnormal. The enlargement of the perivascular gap increases with the increase in the number of white matter hypersignals and symptomatic lacunar infarct foci, suggesting a correlation between the perivascular gap and other cerebral small vessel disease. Perivascular gap changes are also common in patients with mild cerebral atrophy, and although perivascular gap may be another manifestation of cerebral atrophy, it is never a simple result of cerebral atrophy. 5. Cerebral microhemorrhage: It appears on T2WI-gradient echo sequence (GRE) or magnetic susceptibility weighted imaging (SWI) as a uniform, ovoid, small focal hyposignal or signal deficit of 2-5 mm in diameter, with no edema in the surrounding brain tissue. However, attention should be paid to exclude signal loss caused by perivascular gaps, pallid bulb calcification, distal middle cerebral artery, and branched flow null shadow, atherosclerotic plaque or acute embolism in the fashion of definitive diagnosis. 6, brain atrophy: MRI shows deepening of the cerebral sulcus, narrowing of the gyrus and enlargement of the ventricles in a restricted and diffuse, symmetric or asymmetric distribution, which can be seen in a variety of diseases. Studies have shown that brain atrophy is correlated with the severity of cerebral small vessel lesions, including whole brain, corpus callosum, midbrain and hippocampal atrophy, and local cortical thinning of the brain is associated with subcortical infarction. Therefore, the study of brain atrophy should include the study of the degree of cerebrovascular damage; on the contrary, the measurement of brain atrophy volume is of great value when evaluating the degree of cerebrovascular damage. Cerebral atrophy may reflect or partially reflect the severity of cerebrovascular lesions. Pathogenesis: In recent years, some progress has been made in the study of cerebral small vessel disease. However, controversial studies on its pathogenesis have to some extent hindered the progress of its clinical diagnosis and treatment.Bailev et al. suggested that lacunar spaces are caused by occlusion of small intracranial penetrating arteries; Schmidt et al. observed that cerebral white matter lesions are due to long-term chronic hypoperfusion and suggested that there is an overlap in the pathogenesis of cerebral white matter lesions and lacunar spaces.Wardlaw et al. showed that Braun and Schreiber suggested that cerebral microhemorrhage is a key link in the progression of cerebral microangiopathy. In conclusion, the specific pathogenesis of cerebral microangiopathy is still inconclusive, and further studies are needed to confirm it, which will be one of the focuses of future research on cerebral microangiopathy. Clinical manifestations: 1. Ischemic stroke: The clinical manifestations of acute lacunar infarction are pure motor light hemiparesis (PMH), pure sensory stroke (PSS), sensorimotor stroke, ataxic light hemiparesis (AH), and dysarthria-hand clumsiness syndrome (DCHS). Compared with larger cortical infarcts, patients with lacunar infarcts have milder signs and symptoms and good short-term outcomes; however, they have a higher incidence and increased risk of cognitive impairment, depression, and neurological dysfunction. Cognitive dysfunction: Cerebral small vessel disease cognitive dysfunction has the following characteristics compared with vascular cognitive impairment (VCI) caused by other lesions: (1) high incidence, accounting for about 50% of vascular cognitive impairment. (2) Clinical symptoms and imaging manifestations are highly homogeneous. (3) Cognitive dysfunction progresses slowly with the progression of cerebral small vessel disease. Cognitive dysfunction due to cerebral small vessel disease is mainly characterized by decreased attention and executive ability, decreased effective attention, slowed information processing, decreased verbal fluency and delayed recall; its behavioral symptoms are dominated by apathy, emotional instability, depression and decreased ability to perform activities of daily living. jokinen et al. performed MRI examinations and neuropsychological tests on 387 patients with cerebral small vessel disease and followed up At 3 years, regression analysis of whole-brain cognitive function and specific cognitive domains showed that after controlling for numerous factors such as age, baseline cognitive function, lacunar infarct and white matter lesion load, and white matter lesion progression, new-onset lacunar infarcts were associated with a decline in mild cognitive function, particularly significantly diminished executive ability, motor function, and processing speed, while not significantly associated with memory and whole-brain function; ignoring the Ignoring the effects of lacunar infarction, the rate of progression of white matter lesions in the brain remained somewhat associated with decreased executive ability. Subclinical lacunar infarcts have a significant additive effect, increasing the incidence of dementia, clinical stroke, fall episodes, and morbidity and mortality. There is no doubt that patients with cerebral white matter lesions have physical, cognitive function and psychological impairment. Many white matter lesions are associated with cognitive dysfunction, gait abnormalities, falls, mood disturbances, and urinary and bowel disorders, with cognitive dysfunction manifesting itself primarily as a decrease in minor executive ability, reaction, and processing speed. Cross-sectional studies have confirmed the association of cerebral white matter lesions with depression, particularly frontal white matter lesions located around the ventricles, with gait instability, and a higher risk of fall episodes with more severe disease. It is worth highlighting that in a Meta-analysis containing 46 longitudinal clinical studies, cerebral white matter lesions put at significantly increased risk of stroke and dementia and higher morbidity and mortality, indicating its potential clinical significance as an important marker of geriatric disease. Treatment principles: 1. Treatment of stroke: The treatment of ischemic stroke caused by cerebral small vessel disease should follow the general principles of intravenous thrombolysis and antiplatelet drugs, following the requirements of domestic and international guidelines. It has been reported in the literature that cerebral white matter lesions, cerebral microhemorrhage, and multiple lacunar infarcts are associated with bleeding after thrombolytic therapy, but are not contraindications to thrombolytic therapy. At present, there is no reliable clinical evidence for secondary prevention of cerebral small vessel disease, but clinical use of antihypertensive and lipid-regulating therapy is mainly used. The Perindopril Prevention of Recurrent Stroke Study (PROGRESS) and the Regression of Cerebral Artery Stenosis Study (ROCAS) have shown that angiotensin-converting enzyme inhibitors (ACEI) or statins are associated with slow progression of cerebral white matter lesions on MRI, and that increased use of these agents may be beneficial, pending evidence from larger sample size clinical trials. The results of the Prevention of Stroke Recurrence by Aggressive Cholesterol Lowering (SPARCL) study showed that atorvastatin did not significantly alter cerebrovascular reactivity in patients with symptomatic lacunar infarction, thus questioning the effectiveness of lipid-modifying therapy. Results from two clinical studies looking at the efficacy of drugs in Japanese patients with cerebral small vessel disease suffering from type 2 diabetes showed a relatively low incidence of subclinical lacunar infarction in patients taking antiplatelet agents, but further confirmation of their clinical effectiveness in large clinical trials is awaited. The effectiveness of carotid endarterectomy (CEA) as a secondary preventive measure for lacunar infarction is not well understood. 2. Treatment of cognitive dysfunction: At present, the effectiveness of excitatory amino acid blockers, cholinesterase inhibitors and calcium antagonists and other related drugs for the treatment of cognitive function and impairment caused by cerebral small vessel disease is still controversial and awaits further confirmation in clinical trials. To date, no convincing evidence has been obtained for slowing the progression of cerebral white matter lesions by lifestyle changes or pharmacological treatment. The clinical significance of cerebral microhemorrhages is a hot topic of research today, and there is substantial evidence that cerebral microhemorrhages are associated with symptomatic hemorrhage; there is an additive effect between the load of cerebral microhemorrhages and cognitive dysfunction, especially in patients with a history of prior stroke. Other cognitive functions, including processing speed, were not associated. It is unclear whether cerebral microhemorrhages should be used as a therapeutic target or simply as a marker of cerebral microvascular disease. Prospects: The reliability and validity of different neuropsychological test scales to screen for cognitive dysfunction vary, and splitting and recounting according to function may reveal that certain neuropsychological test scores correlate with imaging performance or are linearly related to imaging performance when multiple regressions are performed to disaggregate clinical information. The future research direction of cerebrovascular disease researchers should adopt large sample and multicenter prospective studies to comprehensively grasp the risk factors of cerebrovascular disease cognitive dysfunction, as well as disease occurrence, progression and regression, and strive to find sensitive and effective neuropsychological test scales, combined with imaging and other auxiliary examination, blood and cerebrospinal fluid biological markers, genetic testing and other techniques to improve the early diagnosis rate of cerebrovascular disease In order to reduce the pain and family burden of patients with cerebrovascular disease, we have developed reasonable prevention strategies and treatment plans. From the perspective of imaging, we combine the neuropsychological test scale to systematically evaluate patients, further explore the correlation between imaging and cognitive dysfunction in cerebral small vessel disease, and finally realize the cognitive dysfunction of patients based on imaging performance, so as to eliminate the cumbersome neuropsychological evaluation process and apply it to clinical practice more conveniently and intuitively, so that more patients with cerebral small vessel disease can receive formal treatment at an early stage, and provide relief to patients and the nation. This will enable more patients with small cerebral vascular disease to receive formal treatment at an early stage and reduce the pain for patients and the burden for the country.