Moyamoya disease (MMD) is a group of occlusive diseases characterized by progressive stenosis or occlusion of the end of the internal carotid arteries and their large branches bilaterally, and the formation of an abnormal neovascular network at the base of the skull. The name “smog” comes from the fact that cerebral angiograms show a fuzzy mesh-like shadow at the base of the brain due to abnormal capillary proliferation, like a puff of smoke from a cigarette, hence the name. The clinical manifestations of smoker’s disease are mainly divided into two categories: hemorrhage and ischemia, with a bimodal distribution of the age of onset between 5 and 40 years old, and ischemia as the main clinical manifestation in children, while ischemia and hemorrhage manifestations are basically the same in adult patients. The essence of the disease is occlusion of the arterial trunk at the base of the brain with compensatory vascular proliferation. The onset of smoker’s disease is more common in children and adolescents, and often begins as a stroke, which can manifest as cerebral thrombosis or as cerebral hemorrhage and subarachnoid hemorrhage. Patients may present with varying degrees of hemiparesis or sequential paralysis on the right and left sides, which may be accompanied by aphasia, choking on water, dysphagia, mental retardation, dementia, seizures, headaches, and transient ischemic attacks. Infarcts or hemorrhagic changes are usually seen on CT scans of the head. Infarcts are often multiple, with frontal, temporal, parietal, occipital, basal ganglia regions, and thalamus being the most common, and frontal lobe atrophy may be combined in half of the patients. Hemorrhages can be lobar, basal ganglia, or subarachnoid hemorrhages, and those caused by hypertension are mostly located in the basal ganglia. Patients with cerebral hemorrhage may also be found to have infarct foci and/or brain atrophy. Cerebral angiography may reveal stenosis or opacification of the beginning of the internal carotid artery, the beginning of the anterior and middle cerebral arteries, and a large number of small vascular clusters in the basal ganglia, such as smoke exhaled from smoking. In addition, a compensatory branch of the collateral circulation can be formed in the brain. With the prolongation of the disease, the number of compensatory anastomotic branches gradually decreases or shrinks. Clinical manifestations of smoky disease 1, TIA type: the most common, about 70% of all idiopathic smoky disease. It is characterized by recurrent transient paralysis or weakness, mostly hemiparesis, or alternating right and left hemiparesis or double hemiparesis. There is complete recovery of motor function after an attack. The course of the disease is mostly benign, with a tendency to spontaneous remission or complete cessation of attacks. Very few cases are associated with hemiplegic attacks, headache or migraine. Rarely, there is transient sensory impairment, involuntary movement or mental retardation. 2. Infarct type: acute stroke resulting in permanent type of paralysis, aphasia, visual impairment and mental retardation. 3.Epileptic type: frequent seizures, partial seizures or seizure continuity with EEG epileptiform discharges. 4.Hemorrhagic type: subarachnoid hemorrhage or brain parenchymal hemorrhage, seen in older children and adult cases. Diagnostic examination of smoker’s disease 1. Medical history: Ask whether there is meningitis, leptospirosis, cranial infection, history of trauma or radiotherapy; whether there is limb paralysis, aphasia, epilepsy, severe headache, fainting and impaired consciousness. Pay attention to the onset and duration of the disease. 2. Physical examination: presence of fundus edema, limb paralysis, aphasia and meningeal irritation signs. 3.Laboratory examination: serum and cerebrospinal fluid for syphilis, leptospirosis immunoreactivity, blood sedimentation, which can help to understand the etiology. 4.Lumbar puncture: bloody cerebrospinal fluid is seen in those with secondary subarachnoid hemorrhage. 5.Cerebral angiography: narrowing of the upper siphon of the internal carotid artery and the beginning of the anterior and middle cerebral arteries, smoky abnormal vascular network at the base of the brain and extensive formation of collateral circulation are seen. It should be differentiated from cerebral atherosclerotic cerebral infarction and arteriovenous malformation. 6.CT scan: In secondary cerebral infarction, hypodense areas consistent with vascular distribution can be seen. In cases of subarachnoid hemorrhage, increased density or hematoma formation can be seen.