The patient in this report was admitted to the hospital with dizziness and paroxysmal limb movement disorder. He had been seen in three hospitals and four departments and was finally diagnosed with cerebral infarction due to an unclosed foramen ovale. Clinically, in young patients, recurrent cerebral infarction, myocardial infarction, migraine, and multi-site embolism should be considered for foramen ovale nonocclusion for targeted treatment to reduce repeated patient visits. Clinical data [History] The patient, female, 52 years old, was admitted to the hospital mainly because of “intermittent dizziness for 5 months and paroxysmal limb movement disorder for 1 month”. 5 months ago, the patient had sudden onset of dizziness, headache, nausea with weakness, and vomited stomach contents without coffee-colored material for 6-7 times without any obvious cause. He was treated with mannitol dehydration, aspirin and lipid-lowering therapy (details unknown) for 3 weeks, and then improved. 1 month ago, he suddenly developed right upper limb elbow and shoulder joint flexion in the anterior chest, unable to move freely, accompanied by speech inability, and after 20 minutes right upper limb could move freely, but still unable to speak. He was seen in an outside hospital, BP 160/80mmHg was measured, cranial MRI “left cerebral hemisphere cortical infarction”, routine blood tests, immunoglobulin, complement, RF, CRP, ANCA, thyroid function were not abnormal, ANA was weakly positive, SSA was positive, remaining ANA spectrum (-), cerebral angiography No abnormality was seen, considering not excluding hypoglycemic neurological reaction. He has mild memory loss and irritability. From time to time, he still has episodes of dizziness and headache. The patient used to climb mountains and self-monitored oxygen saturation of 96% using a portable oxygen saturation monitor before climbing, and it could drop to as low as 89% after climbing, and was admitted to the hospital for further diagnosis and treatment. (1) Cerebrovascular ultrasound showed no abnormalities in bilateral carotid, subclavian and vertebral arteries; TCD and EEG showed no abnormalities; (2) Deep vein ultrasound of both lower extremities showed no thrombosis; (3) Transthoracic echocardiography showed mild mitral and tricuspid valve incompetence and normal left ventricular ejection fraction; (4) Holter showed no atrial fibrillation; (5) Oxygen saturation was 94% in prone position and 96% in standing position. (6) TCD foam test was positive; (7) transesophageal echocardiography and right heart acoustic angiography: suggesting the presence of an unclosed foramen ovale with right-to-left shunt, no plaque in the scanned aorta, and no suspected coronary valve redundancy in the aortic valve. Diagnosis and analysis] The patient was a middle-aged female with a history of hypertension and recurrent cerebral infarction, and acute cerebrovascular disease was first considered. However, there was no evidence of cerebrovascular lesions, so she was repeatedly referred to three hospitals and three departments (neurology, endocrinology, and cardiology). The clinical manifestations, the previous and further ancillary examinations of this admission were analyzed as follows: the patient had an acute onset, multiple sites of cerebrovascular involvement, rapid improvement of clinical symptoms, no cerebrovascular abnormalities on ultrasound and cerebral angiography, consistent with cerebral embolism; positive TCD foaming test, suggesting the presence of intra- or extra-cardiac right-to-left shunt. Transesophageal echocardiography and right heart acoustic angiography suggested the presence of an unclosed foramen ovale with a right-to-left shunt (contrast was visible in the left atrium) [Final referral] The patient was finally diagnosed with paradoxical embolism caused by an unclosed foramen ovale. After full communication with the patient about his condition, occlusion of the unclosed foramen ovale was performed. The patient’s previously existing hypoxia in the horizontal position disappeared, and the exertional hypoxia symptoms also disappeared. Discussion】This case is a middle-aged female with recurrent cerebral infarction, with an acute onset, recurrent attacks, different attacks involving different parts of the brain, rapid improvement of clinical symptoms, and no evidence of organic cerebrovascularity, which is consistent with cerebral embolism, and the final causative agent is paradoxical embolism caused by unclosed foramen ovale. Cerebral embolism is one of the important manifestations of heart disease. The most common direct causes are atrial fibrillation; infective endocarditis; myocardial infarction or myocardial disease with appendage thrombus; and cardiac mucinous tumors. However, the paradoxical embolism caused by an embolus from the venous system through an unclosed foramen ovale is often overlooked. The foramen ovale is a physiologic channel during fetal life that allows umbilical venous blood to flow from the right atrium into the left atrium, maintaining fetal circulation. If the foramen ovale does not close after 3 years of age, it is called patent foramen ovale (PFO). The detection rate is 20-30% in the population. It was previously thought that there was no clear pathological significance of patent foramen ovale, but recent studies have shown that patent foramen ovale may be associated with certain clinical conditions, such as cerebral embolism due to paradoxical embolism. Paradoxical embolism refers to embolism of the body circulation caused by emboli originating from the venous system or the right heart through abnormal intracardiac (patent foramen ovale, atrial septal defect, etc.) or extracardiac pathways (pulmonary arteriovenous fistula, etc.). In general, the pressure in the left heart system is higher than that in the right heart system, and the patent foramen ovale does not cause a right-to-left shunt, but in some cases, such as cough, pulmonary embolism, or defecation, the increased pressure in the right heart can cause a right-to-left shunt through the patent foramen ovale and cause a paradoxical embolism. In addition to cerebral embolism, oval foramen insufficiency may also lead to myocardial infarction, peripheral artery embolism, decompression sickness, platypnea pulmonary edema, migraine, exercise-induced hypoxemia and upright hypoxemia (Platypnea-orthodeoxia syndrome), etc. Platypnea-orthodeoxia syndrome is a very rare clinical syndrome that refers to It is a very rare clinical syndrome in which the patient presents with dyspnea and hypoxemia in the upright position, which is relieved by lying down. It is mainly due to the presence of an underlying right-to-left shunt, such as an unclosed foramen ovale, and the upright position causes an increase in right-to-left shunt due to increased pressure in the right cardiac system, resulting in upright hypoxia, but the exact pathogenesis remains unclear. Diagnosis of patent foramen ovale can be made by TCD foaming test and echocardiographic (transthoracic and transesophageal) right heart sonography, which generally requires valsalva’s maneuver to determine the presence of a right-to-left shunt. We gave our patient antiplatelet and percutaneous foramen ovale nonocclusion occlusion. Ovular foramen nonocclusion is associated with upright hypoxia as well as exercise hypoxia. This patient’s exercise hypoxia disappeared after occlusion, but this patient had prone hypoxia, presumably related to the increased right atrial pressure in the patient after prone position, resulting in a right-to-left shunt through the unoccluded foramen ovale. The relationship between unoccluded foramen ovale and prone hypoxia has not been clearly reported in the literature. The absence of recurrent cerebral embolism during the post-treatment follow-up also confirmed the diagnosis. This patient started with cerebral embolism and had a tortuous consultation. In strokes of unknown cause one needs to be alert to the fact that unclosed foramen ovale, which we do not often think of, may also lead to paradoxical embolism. Percutaneous patent foramen ovale closure, illustrated with the blocker closing the foramen ovale.