For example, there is a kind of occipital nerve pain that is misdiagnosed as cervical spondylosis, which is found in the place next to the wind pool and a little bit above the ridge of the external occipital ridge. The occipital nerve is a posterior C2 nerve. The greater occipital nerve is the medial branch of the posterior branch of the C2 nerve, which innervates the posterior cranial spine, the hemithorax, and the orbit. The intraosseous segment runs between the cephalic semispinalis and the longest muscle of the head, and the occipital nerve runs superficially under the skin with the occipital artery and adjacent to the sympathetic nerve when it exits the spinal canal. The inflammation of the muscles and the contraction of the muscle spasms produce the symptoms of nerve compression that cause occipital neuralgia, or the stimulation of arterial spasms that cause dizziness and dizziness in the back of the head, neck infarction, the patient is afraid to turn his head, and his eyes are hazy as if he is sleepy, etc. Clinical syndrome. The anatomical causes of occipital neuralgia can be broadly summarized as follows: the rhomboid tendon of the head and the longest head muscle are attached to the external occipital ramus, the occipital nerve is superficial to the rhomboid tendon membrane, and the intramuscular segment penetrates between the head and the longest head muscle in the case of periapical inflammation, the muscle attached to the ramus becomes inflamed, and the occipital nerve is spasmodically contracted by the inflamed muscle at the superficial rhomboid tendon membrane, resulting in neurological compression symptoms. The beginning of the muscular segment of the nerve is surrounded by fiber intervals, and the intrafascial segment penetrates between the subtenon membrane of the trapezius muscle and the deep fascia to cause compression, and is most likely to be compressed by the spastic muscle or tendon membrane when it penetrates the bony fiber hole at the superior collar line. When the neck is moved, the nerve at the junction of the active and fixed areas is “twisted”, and the fixation of the nerve by the tendon membrane tissue at the superficial point of emergence can aggravate the “compression” of the nerve, and the patient is afraid to turn his head. Due to the long-term compression, it is inevitable to lead to impaired neurohumoral supply, imbalance, chronic aseptic inflammation, and then tissue proliferation and sclerosis adhesions, especially under the stimulation of fatigue, weather changes, wet and cold, etc., can intensify the degree of compression and adhesion of the vascular nerve, resulting in a variety of clinical symptoms and signs. Treatment: Relieving the compression in the stroke of occipital nerve is the key to treat occipital neuralgia. 1. Eliminate bruising and edema and relax the spastic muscles so as to reduce the symptoms: Fotarine or carbamazepine can be used for those with significant pain. Local Fasthone or oil essence massage massage Fengchi next to the thick ridge of the occipital bone bulge place, massage after feeling very relaxed, eyes immediately shine. 2, closed treatment, such as 1-2% Nufocaine 2ml plus Depo-Provera 1ml in the occipital thick ridge bone ridge closed, the symptoms can be relieved. 3, the movement of the occipital nerve medical gymnastics, through the relaxation of the neck in all directions of movement, active cervical spine area blood circulation, eliminate bruising edema, while stretching the neck ligaments, relax the spastic muscles, so as to reduce the symptoms; strengthen the neck muscles, enhance its ability to tolerate fatigue, improve the stability of the cervical spine, so as to consolidate the treatment effect and prevent recurrent attacks. Auxiliary do Ye’s chair exercise, may be very effective due to frequent cervical spine activities, can make the nerve in the joint muscle ligament and other travel turns or bone fiber hole, fiber canal within the long-term chronic stimulation, and produce chronic edema, fibrosis and Waller’s degeneration and other pathological changes, and through the change of axoplasmic flow caused by the end effector and central neuron pathological injury.