“Bilateral lateral paraventricular demyelinating changes” is one of the diagnostic conclusions that we often see on cranial CT or MRI report cards. Often patients or friends with such a report card, anxious to ask: “demyelination” is a disease, how to cure? To give you an answer to this question. First, demyelination “demyelination changes” is actually a pathological phenomenon, in the image should be accurately referred to as “cerebral white matter laxity (Leukoaraiosis, LA)”, refers to the bilateral lateral paraventricular and half-ovoid center of the brain diffuse white matter of the mottled or patchy changes. It is a diffuse, speckled or patchy change in the white matter of the bilateral paraventricles and centers of the semiovals. It is hypointense on CT and hyperintense on MRI-T2 and FLAIR. The pathology that corresponds to this imaging change is accompanied by loss of myelin sheaths of white matter fibers, which is why it is also called “demyelinating change”. Therefore, “leukoencephalopathy” or “demyelinating changes” is only an imaging description, not a diagnosis of a disease, and can be found in the normal population, but only when accompanied by clinical symptoms can it be called “leukoencephalopathy”. The term “cerebral leukoaraiosis” is used only when accompanied by clinical symptoms. It occurs in approximately 10% of the middle-aged and older population (50-75 years) and in approximately 49.7% of the elderly population (>70 years). Most of them can be clinically asymptomatic, 7% with ischemic stroke and 30-40% with cognitive impairment. As the degree of LA increases, the proportion of stroke and dementia increases. Clinical symptoms The main clinical manifestations of leukoaraiosis are: dementia, lower limb movement disorder, ischemic stroke, defecation disorder. Common diseases are: 1. Binswanger disease. That is, subcortical atherosclerotic encephalopathy, manifested by cognitive impairment (dementia), walking difficulties and falls, urinary incontinence, etc., with a high incidence of stroke, most of which are TIAs or minor strokes. Imaging can see multiple lacunar cerebral infarct foci in the basal ganglia region and semiovoid center. Cerebral amyloid angiopathy, manifested by recurrent lobar hemorrhage, progressive cognitive impairment and ischemic stroke. Lobar hemorrhage can be seen in the image, especially in the occipital lobe, occipito-parietal region or frontal cortex and subcortical white matter. CADASIL: Autosomal dominant cerebral arteriopathy with subcortical infarcts and white matter encephalopathy, characterized by a family history of recurrent ischemic strokes, dementia, gait disorders, and urinary incontinence in the middle age, and early onset of migraine with aura. Imaging can see characteristic temporal pole cerebral white matter sparing changes. If there is poisoning, systemic metabolic diseases and other primary diseases, the primary disease should be actively treated. 2.Actively control risk factors: stabilize blood pressure and blood sugar, quit smoking and drinking, and reduce homocysteine level. 3.Prevention: Unlike general secondary prevention, patients with LA have a greater risk of bleeding than those without LA, and caution should be exercised when applying anticoagulant and antiplatelet drugs. Improvement of cognitive function: according to the degree of damage, cholinesterase inhibitors or NMDA receptor antagonists can be chosen, and drugs to improve brain metabolism such as Idebenone and Anethole Piracetam can be given. 5.Dilating small blood vessels: Because the main pathophysiological changes of LA are small arterial atherosclerosis, small blood vessel dilating drugs such as nimodipine and nicergoline can be given.