I. Diagnosis of PAES N artery entrapment syndrome (PAES) was previously underreported and easily misdiagnosed. In recent years, due to the improvement of its understanding and the development of imaging, the number of reports in the literature has increased. The disease is a syndrome in which the N artery is compressed by the femoral and gastrocnemius muscles due to congenital abnormalities in the relationship between the N artery and the gastrocnemius or N muscle, causing a series of local ischemic symptoms in the lower limbs. Sometimes the veins and nerves are also involved, causing corresponding symptoms, but the involvement of the N artery is the most common. Clinically, it is more common in young males and often develops after running or strenuous exercise, and is characterized by progressive worsening of intermittent claudication. It is sometimes bilateral, but often presents with symptoms on one side or sequentially. During the onset of pain, there may be pallor, coldness, and numbness in the lower legs and feet. In a few cases, there is bruising. The physical examination may show diminished dorsal and posterior tibial artery pulsations, dorsiflexion of the foot, disappearance of artery pulsations, sometimes bending the knee and dorsiflexion of the foot may induce symptoms, and pigeon gait, i.e. walking with the toes inward, may relieve symptoms, probably related to the degree of contraction of the medial head of the gastrocnemius muscle.The most important sign of PAES is the PST (Positional stress test). If the dorsalis pedis artery pulsation is weakened during plantarflexion or dorsiflexion, and the ankle-brachial index (ABI) decreases >0.2, the diagnosis of PAES is positive. ServelloH o first found that the dorsalis pedis artery pulsation was weakened when the affected foot was dorsiflexed in patients with PAES. However, the significance of the PST in the diagnosis of PAES is not as reliable as initially thought. Some of the PAESN arteries have progressed to occlusion, where the dorsalis pedis artery pulsation is absent in neutral position and the PST is negative. the false positive rate of PST is also high, especially in athletes with muscular lower limbs. Therefore, a negative PST on physical examination does not exclude PAES, but a positive result can be suspicious for PAES. in cases of N artery occlusion, a positive PST after reopening is suggestive for the diagnosis of PAES. Similarly, Doppler ultrasonography and arteriography have limited diagnostic significance for PAES, and arteriography after reopening of the N artery is useful for definitive diagnosis of PAES. the advent of multi-row spiral CT is a major advance in the diagnostics of vascular disease, and as a non-invasive examination, CT can demonstrate not only the patency of the vessel lumen, but also the structure of the vessel wall and the relationship between the vessel and surrounding tissues such as muscles, bones, and ligaments. In our group of 1l patients, the positive rate of spiral CT for the diagnosis of PAES was 100%. Because of the current limitations of spiral CT in resolving soft tissues, it is not yet possible to completely distinguish type II from type III PAES. spiral CT imaging features of PAES include (1) axial images showing abnormally developed medial head or muscle bundle of the gastrocnemius muscle, outward displacement of the muscle attachment point, or abnormally located N artery; (2) thickening of the N artery wall, luminal narrowing, pre- or post-stenosis dilatation, or occlusion; (3) Three-dimensional reconstruction shows occlusion of the coarctation artery and formation of collateral circulation; (4) Three-dimensional reconstruction shows abnormal spatial location relationship between muscle and N artery; (5) Excluding other diseases such as cystic change of the outer membrane of N artery and N artery aneurysm. In conclusion, spiral CT can be used for the diagnosis and staging of PAES, and is valid even for N artery occlusive lesions. There was no type IV PAES in this group of patients, and the value of spiral CT in diagnosing type IV lesions could not be judged yet. Another about part of the patients also have N vein trapping, which causes deep vein return obstruction in the lower leg, such as deep vein thrombosis and varicose veins. Ultrasound, CTA, MRA, DSA, etc. can assist in the diagnosis. However, it needs to be differentiated from other arterial occlusive diseases, such as atherosclerosis and Buerger’s disease. The treatment strategy of PAES is mainly based on surgical treatment, and the progressive worsening of symptoms is an indication for surgical treatment. The principle of surgery is to correct the abnormal anatomy, repair the compressed artery and restore the blood flow, while for the simple compression of N artery, only the medial head of gastrocnemius muscle or the abnormal fibrous band can be cut and N artery can be released, while for the damaged or occluded N artery, reconstruction is needed, and autologous saphenous vein graft is preferred. If the long segment of N artery occlusion needs to be diverted, a supine knee flexion position is preferable to a medial approach. If the endothelium of the N artery is not yet involved and the degree of luminal stenosis is <50%, simply cutting the abnormal medial head or bundle of the gastrocnemius muscle can achieve good therapeutic results¨.... In fact, most of the PAES patients have severe stenosis or occlusion of the N artery at the time of consultation. The methods of managing N artery occlusion include dissection for embolization, thrombolysis or bypass surgery. Arterial dissection and thrombectomy is a common method to manage N artery occlusion in PAES, but the recurrence rate is high if the diagnosis of PAES is not taken into account and thrombectomy alone is performed. The literature reports good patency rates for short-segment occlusive lesions of the N artery via posterior N fossa maneuvering for release of compression and patch shaping|. Our treatment experience shows that for patients with short segment occlusion of the N artery <5 cm in PAES, the medium-term patency rate is more satisfactory with N artery release and patching with autologous vein or artificial vessel; however, when the lesion develops to an advanced stage with severe intimal hyperplasia and almost occlusion of the lumen, patching should not be performed reluctantly, and instead, autologous vein should be carefully searched for and N artery interposition surgery should be performed, and artificial vessel can also be used if necessary. In patients with N artery occluded segment >5 cm, direct bypass surgery has a better patency rate than local N artery release and revascularization|. Our results also showed that direct autologous vein bypass of the femoral-N (infrapopliteal) artery in long segments of N artery occlusive lesions had satisfactory mid-term patency rates. Thrombolysis is one of the important methods to manage acute lower extremity ischemia, and catheter thrombolysis can be considered for patients with PAES within 2 weeks of onset. From the process of thrombolysis, it can be seen that catheter thrombolysis is effective in treating acute thrombosis in the N artery of PAES, and if the imaging shows no stenosis in the N artery lumen after thrombolysis, N artery release alone can be performed, while avoiding dissection of the N artery and reducing surgical trauma, and the long-term efficacy remains to be observed. The risk of recurrence is higher if thrombolysis alone opens the N artery without relieving the compression. The patients in this group had progressed to N artery occlusion at the time of presentation, and were treated with warfarin anticoagulation after thrombectomy, thrombolysis, and diversion. One of the patients had a recurrence of thrombosis 20 months after discontinuing warfarin anticoagulation on his own. In patients with PAES with N artery occlusion, the N artery intima is involved and the intimal surface is rough. If there is no contraindication to anticoagulation, postoperative anticoagulation with warfarin to maintain the coagulation time international standardized ratio of 2.0 to 3.0 helps to maintain the N artery patency. If the patient is combined with hyperhomocysteinemia and antiphospholipid antibody syndrome and eosinophilia, respectively, folic acid, hormones and anticoagulation are given. The combined hypercoagulable state may also be an important factor in accelerating the progression of PAES and should be screened and treated with care. Interventional treatment is generally not chosen because of unsatisfactory near- and long-term results of intracavitary intervention for PAES.