Stroke in young people is defined as stroke patients with an age of onset between 15 and 45 years. In recent years, with the development of social and economic development, there is a tendency for stroke to occur at a younger age. As young people are the pillars of families and society, the increase of stroke in young people will bring great loss and burden to the society and families, so the prevention and treatment of stroke in young people is especially important. Studies by many experts have shown that the causes of stroke in young people aged 15-35 years are mostly arterial entrapment, cardiogenic embolism, non-atherosclerotic vascular disease and hypercoagulable states, whereas the traditional atherosclerotic risk factors are the main causes in adults aged 35 years and older. The common cause of intracranial and extracranial arterial stenosis is atherosclerosis, followed by non-atherosclerotic vascular lesions such as aortitis, carotid artery entrapment and myofibrillar dysplasia. Early-onset atherosclerosis is generally seen in people over 40 years old. Most scholars believe that early-onset atherosclerosis is the main cause of stroke in young people, especially in those over 30 years of age. Although the causes of early-onset atherosclerosis are different from those of stroke in young adults and stroke in middle-aged and older adults, the most common cause of ischemic stroke in young adults is also atherosclerosis, followed by vasculitis and cardiac disorders. Studies have shown that early atherosclerotic lesions in some young people’s arteries are associated with an increasing number of young people with dyslipidemia, hypertension, diabetes, obesity, smoking, stressful jobs, and a high-calorie diet. Among ischemic stroke patients aged 18 to 45 years, 20.5% of small vessel occlusion stroke cases, 7.2% of large atherosclerosis cases, 17.8% of patients with cardiac thrombosis, the other 22.3% with a definite etiology and 23.5% with unknown etiology, indicating that other definite etiology and unknown etiology groups are the most common ischemic strokes in young people. 2. Carotid artery entrapment (CAD) CAD is a condition in which blood enters the vessel wall through the damaged carotid artery intima and forms an intramural hematoma between the vessel walls and forms a thromboembolism or narrow lumen at the locally damaged intima affecting the hemodynamics thus leading to ischemic stroke. Arterial entrapment is the underlying mechanism in approximately 2.5% of all stroke patients and is the second leading cause of stroke in patients younger than 45 years of age, accounting for 20% of stroke patients younger than 45 years of age. Approximately 70% of CAD onset is between 35 and 50 years of age. The annual incidence of spontaneous carotid artery entrapment is 2.5 to 3/100,000, while the annual incidence of spontaneous vertebral artery dissection is 1 to 1.5/100,000. However, in Japan, such a lesion is frequently reported to occur in the intracranial vertebral artery. Traumatic dissection occurs in approximately 1% of all patients with blunt injury mechanisms and is often not recognized at first. However, detailed epidemiological data on the disease are still lacking in China. DSA is the most reliable method to diagnose CAD. DSA manifestations are divided into direct and indirect signs based on the morphology of the lumen and the presence or absence of contrast filling within the entrapment. Individual studies were found to report a strong association of CAD with the following risk factors: aortic root diameter >34 mm, migraine, change in relative diameter during the cardiac cycle of the common carotid artery and small trauma in neck thrust therapy (>11.8%), while homocysteine and recent infection were weakly associated with CAD. Arterial entrapment may form ischemic stroke through thrombus formation at the site of injury or due to hemodynamic deficits due to severe stenosis or occlusion, and the available evidence strongly supports embolization as the most common cause. Healing of arterial entrapment occurs within 3 to 6 months, with 90% of stenoses resolving and 50% of occlusions recanalizing. 3, fibromuscular dysplasia (FMD) Fibromuscular dysplasia (FMD), formerly known as myofibrillar tissue hyperplasia, is a non-atherosclerotic, non-inflammatory arterial disease that most commonly involves the renal arteries and the internal carotid and vertebral arteries; FMD of the internal carotid and vertebral arteries is rare and occurs more often in children and young adults, and in women It is more common in women aged 30 to 50 years than in men; the site mostly occurs at the level of the second cervical vertebrae in the extracranial part; 80% of patients with FMD have angiographic multiple stenoses. The incidence of symptomatic renal artery FMD is about 4 per 1,000, while the incidence of carotid artery FMD may be half that of renal artery. Head and neck myofibrillar dysplasia is complicated by headache due to entrapment, Horner syndrome or stroke, or is associated with an intracranial aneurysm that may have a risk of subarachnoid hemorrhage or intracranial hemorrhage.The etiology of FMD is not well understood, but mechanisms such as genetic predisposition, sex hormones, and arterial wall ischemia have been proposed to be involved.The pathology of FMD is characterized by smooth muscle hyperplasia or thinning, destruction of elastic fibers, and proliferation of fibrous tissue. Computed tomography or magnetic resonance angiography or digital subtraction angiography show characteristic “bead-like” changes with high bilateral stenosis. FMD without complications can cause nonspecific symptoms such as headache and vertigo, but when it results in arterial entrapment or aneurysm, it can lead to cerebral infarction or subarachnoid hemorrhage. 4, Multiple aortitis (Takayasuarteritis, TA) TA is also known as primary or non-specific aortitis, aortic arch syndrome, pulselessness, Takayasu arteritis (TA), non-specific arteritis. Its development is associated with autoimmune, endocrine and genetic factors. The disease is mostly seen in Asia and Latin America. TA is a chronic progressive inflammatory disease of the aorta and its main branches caused by autoimmune reactions, and is a total arteritis with predominantly intimal and intimal lesions. The clinical manifestations of TA are non-specific and clinically TA is divided into 3 stages, namely, pre-pulseless, vasculitis and fibrosis stages; angiography is the gold standard for TA diagnosis. The lesions have thickened walls, narrowed or occluded lumens, and symptoms of insufficient blood supply to the corresponding organs and tissues. When it leads to cranial vascular occlusion or severe stenosis, the clinical manifestation can be TIA, cerebral infarction, luminal or watershed infarction. diffuse circumferential thickening of the wall of the common carotid artery characteristic of TA reflects the inflammatory changes of the intima and mesentery, which is an important sign for the diagnosis of TA and can occur before the lumen abnormality, and high-frequency ultrasound can clearly show such changes as diffuse thickening of the intima and mesentery of the artery and lumen thickening toward The lumen is thickened centripetally. Among the affected vessels, stenosis was the most common lesion, present in 93% of patients, followed by obstruction (57%), dilatation (16%), and aneurysm (7%). Most patients (81%) had one or more disease recurrences, and 94% were in long-term remission with a 5-year survival rate of 94%. Common systemic manifestations during disease flares were fever (69%), arthralgia (25%), weight loss (19%) and vascular symptoms, arm claudication (100%), headache (69%), dizziness (56%) and hypertension (37%). All patients had multiple arterial murmurs and 88% had diminished or absent left brachial arteries; erythrocyte sedimentation rate and C-reactive protein levels were elevated in 63% and 80% of patients, respectively; arteriography showed multiple stenoses or occlusions of multiple arteries, with stenosis of the left subclavian artery being the most common lesion (88%). According to the site of the vascular lesion, it can be clinically classified into: type I: cephalobrachial type, mainly involving the aortic arch and its branches; type II: thoracoabdominal aortic type, mainly involving the descending aorta as well as the abdominal aorta; type III: extensive type, with the above two clinical features; and type IV: pulmonary artery type. 5.PatentForamenOvale (PFO) The presence of right-to-left shunt (RLS) can lead to paradoxical cerebral embolism, which is an important cause of ischemic stroke, especially in young adults. In contrast, RLS of patent foramen ovale (PFO) and pulmonary arteriovenous fistula are among the most important causes. The gold standard for detecting RLS is contrast-enhanced transesophageal echocardiography. More than 40% of acute ischemic strokes in young adults are cryptogenic, meaning that the etiology cannot be determined, and in this group of patients there is an increased incidence of atrial septal tumors and more than half of them have patent foramen ovale. In the younger population with ischemic stroke due to cardiac embolism, atrial septal abnormalities play an important role, and the association between atrial fibrillation and other major causes of cardiac embolism appears to be mild compared to older stroke patients. Atherosclerosis-mediated mechanisms may be involved in the mechanism of cerebrovascular events in patients with unexplained ischemic stroke/transient ischemic attack without PFO, whereas a non-atherosclerotic mechanism may mediate cerebrovascular events in patients with PFO present. The available evidence does not demonstrate that the presence of a PFO increases the relative risk of recurrent ischemic events in patients with unexplained ischemic stroke or TIA, so oval foramen closure cannot be recommended in these patients until the results of a new clinical trial are reported. 6. Infectious/non-infectious cerebral arteritis Various infectious/non-infectious cerebral arteritis is also a common cause of cerebral infarction in young people. For example, infectious cerebral arteritis due to syphilis, tuberculous meningitis, septic meningitis, leptospirosis, coccidioidomycosis, and various non-infectious cerebral arteritis such as periarteritis nodosa, SLE cerebral arteritis, granulomatous cerebral arteritis, rheumatic cerebral arteritis, scleroderma complicating cerebral arteritis and non-specific cerebral arteritis can lead to cerebral infarction, especially in young patients with unknown etiology. Especially in young ischemic stroke patients, it is important to be aware of the possibility that these rare causes of infarction exist.