The prevention and treatment of cerebrovascular disease includes various aspects such as standardized examination, health education, life guidance, disease management and standardized treatment. At present, many hospitals will screen high-risk groups over 50 years old with stroke risk factors such as hypertension, diabetes, coronary heart disease, hyperlipidemia and smoking, establish health management files and guide patients to prevent and treat stroke. Patients have an understanding of their health status and medical knowledge related to stroke prevention and treatment through standardized examination. However, due to misconceptions, many patients are too optimistic or too pessimistic in the face of some examination reports and do not have a comprehensive understanding of their condition, leading to delays or negative emotions affecting their lives. Myth 1: Cerebral white matter degeneration is Alzheimer’s disease 56-year-old Ms. Li went through a series of examinations, and the results were “no obvious abnormalities”. The only thing that was written on the report sheet of the CT scan of the head was “white matter degeneration of the brain”. She was told that this might be a precursor of Alzheimer’s disease, which scared Ms. Li, and since then she was distracted every day and fell into a deep fear, and even felt that she had really aged a lot at once, always forgetting the east and the west, and her memory was obviously not as good as before. The white matter of the brain is mainly composed of nerve fibers and glial cells, and the diffuse hypointense lesions in the white matter of the brain on CT and the diffuse high signal on T2-weighted images on MRI can be called “white matter degeneration”. In the literature, there are different names for these imaging manifestations, such as cerebral white matter lesions, white matter hypersignal, and cerebral white matter sparing. The white matter of the brain itself is ischemic and vulnerable. The white matter of the adult brain accounts for approximately 50% of the whole brain volume, and the tissue metabolic rate is only slightly lower than that of the gray matter, which can be damaged by mild ischemia. Age and hypertension are currently considered to be the main risk factors, with increased T2 high signal in the white matter of the brain with increasing age. Large white matter T2 hyperintensities impair motor, cognitive, and psychological performance and are associated with stroke, dementia, and death. It is important to note that T2 hyper-signal in the white matter of the brain can be detected at a very early stage of disease onset and may be too sensitive to changes in the white matter, and increased water in the white matter does not necessarily indicate loss of function. Preclinical cerebral white matter T2 hyper-signal appears to be benign and progresses slowly, correlating poorly with cognitive impairment, with functional decline entering an accelerated phase only when damage accumulates to a certain level and functional reserves are depleted.” With the progressive increase in the frequency of application of modern neuroimaging techniques, white matter damage is seen clinically in many diseases of the central nervous system. Numerous studies have shown that a significant amount of white matter damage is also found in the normal elderly. Ischemic damage to the white matter can be exacerbated when cerebral ischemia or hypoperfusion occurs. Myth 2: Carotid plaques are all high-risk 60-year-old Ms. Bai’s carotid ultrasound indicated “intimal thickening of the internal carotid artery with multiple plaques”, and looking at the report sheet with several large and small plaques, Ms. Bai was worried about both oversized and dislodged plaques, fearing that she would be paralyzed in bed one day. The whole family was in a fog of worry. Carotid plaque is a mass-like structure formed by multiple risk factors that cause damage to the wall of carotid artery and deposition of cholesterol in the blood vessels. The formation of plaque is a complex and lengthy process, much like the accumulation of grease and grime in a sewer pipe, which over time can lead to a clogged pipe. The danger of carotid plaque lies mainly in the instability of the plaque, that is, the plaque that is not strong and easy to fall off in the vessel wall. Once the plaque is dislodged, it becomes an embolus in the blood flow and reaches the brain with the blood flow to block the distal cerebral arteries, leading to the occurrence of blood clots. In fact, not all plaques lead to cerebral thrombosis, and plaques can occur in any part of the blood vessels. Carotid artery plaque mostly occurs in the bifurcation of the carotid artery, followed by the beginning of the carotid artery and the common carotid artery. They are divided into the following types according to the internal echogenicity: hypoechoic – mainly composed of thrombus, hemorrhage or cholesterol; isoechoic – mainly composed of fibrous tissue; strong echogenicity – mainly composed of calcification. According to the morphology, they are further divided into flat plaques and irregular plaques. Generally speaking, plaques with strong echogenicity and flat shape are more stable. When you find a plaque that is described as “hypoechoic or unevenly echogenic” by carotid ultrasound, it is more likely to fall off and cause a stroke. Don’t panic if you have plaque. With strict control of lipids, unstable plaques can be calcified and turned into stable plaques. It is recommended that those who have already had a stroke should have their carotid ultrasound reviewed regularly to track the size and stability of the plaque. It is also advisable to screen the carotid ultrasound during regular health check-ups to detect carotid plaque as early as possible, so that the size and nature of the plaque can be observed and the neurologist can be consulted in time to adjust the medication to control the development of the disease. Myth 3: People with normal blood lipids do not need to take lipid-lowering drugs. 72-year-old Mr. Ren visited the doctor for “dizziness and dullness for 2 months, and biochemical examination found that total cholesterol and LDL-C were higher than normal. The doctor prescribed him lipid-lowering drugs for this condition. After taking the medication regularly for six months, Mr. Ren found that all the indicators related to lipids were below the normal range at his follow-up appointment, but the doctor still told him not to stop taking the lipid-lowering medication, so he had this question: Why did the doctor continue to let me take the lipid-lowering medication even though my blood lipids were already below the normal range? In addition, he heard his relatives and friends say, “You can’t take lipid-lowering drugs for a long time, they can do more harm than good to your body.” After thinking about it, Mr. Ren decided to stop the lipid-lowering drugs on his own. This is a big misunderstanding. In the clinic, people often ask, “My blood lipids are normal, so I don’t need to take medication. First of all, your normal blood lipids are lowered after taking medication, while cholesterol and triglycerides are continuously metabolized and may rise again if not controlled by medication. Therefore, we require that if the lipid control is at the target value, the medication must be continued for a long time, but the dose of medication can be reduced according to the extent of lipid reduction, muscle enzyme spectrum and liver function, and the medication can be adjusted dynamically. As for when and how to reduce the lipid-lowering drugs, it is best to go to a regular hospital to have a look, and never stop the drugs privately. Secondly, a lipid test result in the normal range does not mean that treatment is not necessary, because the requirements for lipid indicators vary from person to person. For example, the normal value of LDL cholesterol on the lab test is between 2.08-3.12mmol/l, but if the patient has plaque, LDL cholesterol should be lowered to below 2.59mmol/l; if the patient has narrowed blood vessels, unstable plaque or with metabolic syndrome, the lipid needs to be more strictly controlled, and LDL cholesterol needs to be lowered to 2.01mmol/l or lower.” It is well known that the determinants of cardiovascular events depend on the stability of atherosclerotic plaques, and statin lipid-lowering drugs can not only lower lipids, but also stabilize and reverse plaques, exerting cardiovascular protective effects beyond the lipid-lowering effect of the drug. After strict lipid-lowering treatment, the prognosis of patients can be significantly improved and the occurrence of cardiovascular and cerebrovascular events can be reduced.