The incidence of internal carotid artery occlusion in people with symptomatic (cerebral ischemia or retinal ischemia) carotid stenosis is about 15%, and most patients with internal carotid artery occlusion have no significant symptoms, and those with symptoms tend to present with multiple episodes of TIA. The risk of stroke in asymptomatic carotid stenosis is about 2-2.5%, and most patients have coexisting conditions such as coronary artery disease and hypertension, and the risk of surgical complications is equal to or exceeds the risk of disease in the natural state, therefore, patients with asymptomatic internal carotid artery occlusion should be followed up regularly by a specialist. The risk of surgical treatment is much lower than the risk of natural disease progression, and there is evidence that surgical treatment is more effective than pharmacological treatment. Therefore, patients with symptomatic internal carotid artery occlusion should be treated aggressively with surgery. If a patient has an occlusion of the internal carotid artery with severe stenosis of the contralateral carotid artery, endarterectomy of the occluded side should be preferred because of its low impact on cerebral blood flow and low incidence of perioperative cerebral ischemia. The main possible causes of internal carotid artery occlusion are: 1) thrombosis at the site of severe stenosis leading to occlusion; 2) hemorrhage within the atherosclerotic plaque of the carotid artery may also cause internal carotid artery occlusion; 3) thrombosis may also be caused by internal carotid artery entrapment. Color Doppler ultrasound can accurately identify secondary thrombosis, intraplaque hemorrhage and internal carotid artery entrapment by observing the morphology of carotid atherosclerotic plaque and the echo of the lumen filling. In this group of patients, there were 25 cases of atherosclerotic stenosis secondary to red thrombus, 10 cases of atherosclerotic plaque rupture with mechanized thrombus, and one case of internal carotid artery entrapment resulting in secondary thrombotic occlusion of the lumen. The pathological nature, extent, and length of the occluded segment of the internal carotid artery determined the effectiveness of surgical treatment. If the lesion is severe stenosis or bleeding within the plaque secondary to acute thrombosis, it is mostly a red thrombus, and the thrombus can be dissolved and self-passed by anticoagulation and antiplatelet therapy in a few patients. However, since it takes about 2 weeks for the cerebral blood supply to self-regulate into homeostasis, the restoration of blood flow after carotid endarterectomy in patients with cerebral infarction can cause amplification of the inflammatory response in brain tissue leading to increased ischemia or hemorrhage. Therefore, for patients with definite cerebral infarction after carotid artery occlusion, especially large cerebral infarction, it is recommended that surgery should be performed at least 1 month after the infarction . However, a randomized controlled clinical study found that patients with symptomatic severe carotid stenosis had the greatest benefit if surgery was performed within 2 weeks of the most recent ischemic event. Therefore, this principle was followed in patients with carotid artery occlusion without massive cerebral infarction, and the surgical outcome was satisfactory. In contrast, chronic internal carotid artery occlusive lesions have been formed for a long time, and the plaque and thrombus in the internal carotid artery occlusion have gradually become mechanized, fibrotic and calcified, making the internal carotid artery thinner and unable to completely remove the intima of the atherosclerotic plaque, thus reducing the success rate of surgery. Since the prognosis of patients after treatment of acute internal carotid artery occlusion and chronic internal carotid artery occlusion is different, when acute carotid artery occlusion is suspected, further ultrasound and MRA examinations should be performed to establish the diagnosis and then operate as soon as possible in order to achieve good treatment results. In the case of internal carotid artery occlusion, the blood flow may return from the collateral circulation of the skull base arterial ring to the distal end of the occluded internal carotid artery, therefore, the occluded internal carotid artery often appears as a narrowing of the initial segment of the internal carotid artery and gradually worsens until the lumen is completely occluded and the blood flow is completely blocked, and then the distal end gradually reveals the outflow tract. Therefore, for patients with long internal carotid artery lesions or patients with no or unsatisfactory regurgitant bleeding after endarterectomy, a 2F or 3F embolization catheter can be used to retrieve the embolus, which can expand the internal carotid artery in the intracranial segment while retrieving the embolus, thus increasing the regurgitant bleeding and improving the success rate of surgery. There are many branches of the internal carotid artery that can communicate with the external carotid artery through the meningeal artery and ophthalmic artery, which is one of the important reasons why some patients have complete occlusion of the internal carotid artery without cerebral infarction. Therefore, when it is impossible to surgically reopen the internal carotid artery, improving the blood flow of the external carotid artery can still achieve the purpose of preventing cerebral ischemia. In our group, four patients who failed to recanalize the internal carotid artery by surgical treatment and ligated it, their symptoms improved after external carotid arterioplasty. The surgical risk of occluded internal carotid endarterectomy is related to the extent of carotid involvement, the nature and location of the lesion and coexisting diseases such as hypertension, diabetes, chronic lung disease and congestive heart failure, and smoking. The main complications are perioperative stroke (both ipsilateral and/or contralateral to the occluded carotid artery), postoperative hypertension, cerebral reperfusion syndrome, intracranial hemorrhage, intracranial hypertension, and myocardial infarction. The intracranial blood flow will suddenly and dramatically increase after occluded carotid endarterectomy, and the preoperative capillaries, small arteries, and neurons may rupture and bleed or extravasate fluid when high-pressure blood flow passes through them due to ischemic injury. Because of the damage to the carotid sinus during carotid endarterectomy, the sinus arch reflex cannot be regulated normally, and acute hypertension will occur a few hours after CEA . Hypertension and increased cerebral blood flow can cause cerebral hemorrhage and cerebral edema after CEA. Therefore, in patients with carotid artery occlusion who have hypertension, strict monitoring and control of hypertension is extremely important to prevent complications such as cerebral perfusion syndrome and intracranial hemorrhage. Current trends in the treatment of carotid stenosis tend to be minimally invasive, and thus carotid stenting seems to have an extremely important place in the treatment of patients with severe stenosis. However, in patients with internal carotid artery occlusion, carotid stenting has limited ability to treat atherosclerotic occlusion of the lumen and old thrombotic lesions, despite the success stories reported, and CEA is an effective and safe method for the treatment of internal carotid artery occlusion.