In clinical practice, trigeminal neuralgia is usually divided into two types: primary (idiopathic) and secondary (symptomatic). Secondary trigeminal neuralgia refers to the type in which there is a clear organic lesion of the trigeminal nerve itself or its surrounding structures, and the neurological examination is usually positive. The more common clinical causes are mainly tumors of the pontocerebellar horn and arachnoiditis of the skull base; in addition, certain tumors of the middle cranial fossa, metastases of the skull base, medullary cavitation, vascular disease, cranial bone lesions, trigeminal radiculitis and certain metabolic toxic diseases can also cause painful attacks, but they are rare. Because secondary trigeminal neuralgia generally has a clear cause, the treatment is generally more effective when the cause is addressed. Primary trigeminal neuralgia mainly refers to those with unclear etiology, which do not show neurological signs and cannot find any organic or functional lesions related to the onset of the pain. This area is thought to be the intersection of the central and peripheral myelin sheaths, without Schwann’s cells, and is particularly sensitive to pulsatile and transverse compressions that can easily produce microvascular compressions. As the brain shifts downward with age, the vasculature comes into contact with the REZ of the trigeminal nerve, creating microvascular compression. Arteriosclerotic arterial lengthening may in turn increase the degree of compression. Based on this theory, we carried out microvascular decompression to move the blood vessels compressing the nerve away from the REZ zone to treat TN, and the pain could be relieved or even disappeared after the surgery. Recent studies have also shown that more than 95% of the causes of primary trigeminal neuralgia are due to vascular compression; currently, most domestic scholars also believe that vascular compression is the main cause of primary trigeminal neuralgia. Some scholars have studied the relationship between the site of vascular compression and the distribution of trigger point location. The sensory endings of the trigeminal nerve produce nerve impulses after stimulation, and the impulses are transmitted to the sensory center via nerve fibers to form sensation, so the trigeminal nerve fibers are the structural basis for the formation of TN nociception. In terms of the distribution of vascular compression sites and trigger point locations, an exact correspondence between the two still exists. It was found in the study9 that, taking the trigeminal nerve root into the brainstem area as an example, the trigger point was mostly located within the mandibular nerve distribution area when the vessel compressed the upper part of the nerve root; the trigger point was mostly located within the ophthalmic meridian or maxillary nerve distribution area when the vessel compressed the lower part of the nerve root; and the trigger point was located within the maxillary nerve distribution area when the vessel compressed the medial or lateral part of the nerve root. Therefore, vascular compression may have affected the impulse afferents of the sensory roots of the trigeminal nerve, thus causing facial pain and trigger point attacks within the distribution area of the corresponding nerve fibers.