Trigeminal neuralgia is a common type of neuralgia that occurs in middle-aged and elderly people. The disease is usually clinically classified into two types: primary and secondary. In secondary cases, organic lesions, such as tumors, vascular malformations, aneurysms, etc., are found or detected in or around the trigeminal nerve pathway, and the corresponding neurological symptoms and signs are manifested as the lesion develops. In primary cases, trigeminal neuralgia is usually caused by pulsatile vascular compression of the sensory roots of the trigeminal nerve into the brainstem. The reason why trigeminal neuralgia is more common in middle-aged and elderly people is that the brainstem shifts downward with age, and atherosclerosis causes the blood vessels to shift or lengthen accordingly, which leads to contact with and compression of the trigeminal nerve into the brainstem segment, causing pseudo-synapses to form between the nerve fibers in this segment and short-circuiting, and tiny tactile stimuli can be transmitted to the center through the short-circuit, while the central efferent impulses can also be changed into afferent impulses through the short-circuit, and so on repeatedly. Some scholars believe that impulses are continuously uploaded to centers at all levels, so that the trigeminal spinal nucleus, thalamus and cortical sensory centers are all in a state of hyperexcitation, and due to the accumulation of constantly incoming stimuli below the pain threshold, the excitation of the trigeminal nerve centers can intermittently cause facial pain. The pain can also be induced by certain nonspecific stimuli attracted by the foci of hyperexcitation. Primary trigeminal neuralgia generally has a chronic course, mostly progressively aggravated, and is characterized by recurrent episodes of transient lightning-like or knife-like severe pain in the trigeminal nerve distribution area of one side of the face. Since the trigeminal nerve is located on the face, patients sometimes cannot distinguish the source of pain and easily mistake it for toothache or headache, resulting in delayed treatment. More than 1/3 of patients are particularly sensitive in a certain area of the affected face, and every slight touch can cause a painful attack, so this area is called “trigger point” or “trigger point”. The “trigger point” is mostly concentrated in the mouth and nose, there can be one or several, so the mechanical stimulation of the face, such as talking, eating, brushing teeth, washing face, wind blowing, etc. can trigger the pain, the patient’s life is extremely difficult and painful. In severe cases, the attack is often accompanied by reflex twitching of the facial muscles on the affected side, so the disease is also called “painful twitching”, and can be combined with facial flushing, lacrimation, runny nose and other autonomic symptoms. With the gradual aggravation of trigeminal neuralgia, the treatment is in a three-step process, i.e. medication → trigeminal nerve closure → surgery. The most widely used and effective medication is carbamazepine, usually 100mg twice a day, which can be increased when it is ineffective or poorly treated, but the daily dosage should not exceed 1.2g. If the side effects such as dizziness, drowsiness and gastrointestinal discomfort occur when taking the drug for a long time or in a few patients, the dosage should be reduced or stopped. In addition, sodium dentin and wild papaya tablets also have certain efficacy. The trigeminal nerve closure method includes alcohol closure of the trigeminal nerve and its surrounding branches and radiofrequency thermal coagulation of the trigeminal nerve. The principle is to block the nerve conduction to achieve pain relief through the chemical action of alcohol or the physical action of thermal coagulation on the trigeminal nerve fibers to cause necrosis. The closure method cannot cure trigeminal neuralgia, and it will still recur. Surgical treatment includes trigeminal nerve microvascular decompression, trigeminal nerve sensory root amputation and trigeminal nerve peripheral branch avulsion, among which trigeminal nerve microvascular decompression for “vascular compression” is a more ideal and effective surgical method than other treatment methods. Patients with trigeminal neuralgia diagnosed by regular hospitals, without systemic organic lesions such as serious cardiovascular diseases, can be considered for treatment by microvascular decompression. The procedure is performed under general anesthesia, and a minimally invasive “locking hole” craniotomy is performed under the occiput behind the affected ear to expose the trigeminal nerve into the brainstem segment under the microscope. If no “compression vessel” is found during surgery, the sensory roots of the trigeminal nerve into the brainstem can be cut from the posterior to the anterior for 2/3 or 3/4, that is, trigeminal sensory root amputation. After the operation, the trigeminal nerve is usually bedridden for 2-3 days, and the incision can be discharged after 7 days of stitching. According to domestic and international reports, the clinical efficiency of microvascular decompression for trigeminal neuralgia is 82%-96%, and the mortality and complication rates of the operation are extremely low. Postoperatively, patients may have transient headache, dizziness, nausea, vomiting, fever and other reactions, most of which can disappear within a week.