N vascular trapping syndrome is mainly of youth onset. The exact etiology of N vascular entrapment syndrome is unknown, but anatomical variations between the muscles and blood vessels of the N fossa of the lower extremities underlie the pathogenesis. Since the N artery can be located on the deep surface of the N muscle, the persistence of the deep N artery can lead to N artery entrapment syndrome from an embryological basis. In contrast, excessive migration of the medial head of the gastrocnemius along the femur to the cephalad can also cause lesions, and the N artery can be found located medial to or across the medial head of the gastrocnemius. Most commonly, the N artery enters the N fossa after encircling the medial head medially and then laterally, traveling on the deep surface of the medial head between the medial head and the medial femoral condyle. other muscles, muscle bundles, and fibrous fascicles of the N fossa can also be involved in this complex alteration, sometimes even involving tissues such as veins and nerves. Some reports in the literature indicate that veins are involved in 7, 6% of cases in N vascular entrapment syndrome. Another functional N artery entrapment syndrome may be related to vascular compression caused by hypertrophy of the gastrocnemius, N muscle, metatarsal muscle or semimembranosus muscle, often in athletes. Clinical manifestations: 1. Intermittent claudication The manner in which claudication appears is not entirely consistent. Initially, mostly in fast walking or running and jumping, there is numbness, weakness and spasmodic pain in the lower leg, and the symptoms disappear after being forced to stop walking. However, there are no symptoms during brisk walking. This may be related to the pressure on the gastrocnemius muscle during contraction. In contrast, a minority of patients have no symptoms during brisk walking and have intermittent claudication only during slow walking. These patients do not show ischemia in the resting situation. Once the artery is blocked, ischemic intermittent claudication and other ischemic manifestations occur. 2, limb ischemia According to statistics, about 1/3 of patients have an acute onset, but the duration of the disease in most patients can last for months or years, or longer. After the arterial blockage, the affected limbs show typical ischemic manifestations such as chilliness, pale skin and muscle atrophy. Since the main cause of the disease is arterial compression, it is important to relieve the compression during treatment. Endovascular lumpectomy alone cannot be done.