Trigeminal neuralgia is a recurrent pain strictly limited to one or more branches of the trigeminal nerve, characterized by a brief unilateral electric shock-like pain with sudden onset and discontinuation of pain. The pain often arises spontaneously and can also be triggered by washing, shaving, smoking, talking, brushing teeth, etc. According to the second edition of the International Headache Society’s Classification and Diagnostic Criteria for Head and Facial Pain, trigeminal neuralgia that can be clearly caused by tumor compression, inflammatory invasion, multiple sclerosis, etc. is called symptomatic trigeminal neuralgia; the original so-called primary trigeminal neuralgia is now found to be mostly caused by vascular compression, so it is now called classical trigeminal neuralgia. 1. Advances in trigeminal neuralgia research Physicians must be able to identify trigeminal neuralgia or classical trigeminal neuralgia because this most severe pain syndrome can be largely controlled by drugs or surgery. Trigeminal neuralgia has long been recognized by the medical community. Trigeminal neuralgia is documented to have been described in stone carvings at Willows Cathedral in the 16th century. 1672 saw the first documentation of trigeminal neuralgia. 1756 saw Andre’s first use of the term to describe trigeminal neuralgia. 1773 saw a vivid description of this pain syndrome. In the early days, the application of pharmacological treatment for trigeminal neuralgia did not produce an effect. The first effective treatment was probably the inhalation of trichloroethylene in 1920. 2. Epidemiology of trigeminal neuralgia Trigeminal neuralgia is an age-related disease that is infrequent in younger people, with peak incidence in the 50s to 70s. Although early literature suggested a strong female predominance among patients with trigeminal neuralgia, current data suggest that only 60% of patients are female. It is not known whether there is a racial factor in the occurrence of trigeminal neuralgia. The etiology of trigeminal neuralgia has not been adequately explained in terms of the etiology and pathophysiology of trigeminal neuralgia, but Dandy Jannetta and other neurosurgeons have found that the majority of patients with trigeminal neuralgia have mechanical compression, which often occurs where the trigeminal nerve leaves the pontine brain and crosses the subarachnoid space toward the foramen of Meckel. The most common finding is compression of the trigeminal nerve by an artery, usually the superior cerebellar artery, but occasionally the posterior inferior cerebellar artery, the vertebral artery, and the inferior anterior cerebellar artery. Some patients have been found to have veins crossing or even crossing the trigeminal nerve, and a few cases of trigeminal nerve compression by arteriovenous malformations or tumors have been reported. At the root of the trigeminal nerve, the extent of vascular invasion is associated with facial pain. When observing pain caused by the 2nd and 3rd branches of the trigeminal nerve, the anastomotic end and anterior part of the nerve are often found to be compressed by the superior cerebellar artery; if 1st branch pain is present, cross-compression is most often found caudal or posterior to the trigeminal nerve root, often caused by compression of the inferior anterior cerebellar artery. In a small percentage of patients, trigeminal neuralgia is the underlying lesion of multiple sclerosis. Autopsy reveals the presence of demyelinating plaques in the posterior trigeminal roots in a small percentage of patients. However, plaques are often found in the trigeminal nerve pathway again. It is currently considered unlikely that trigeminal root plaques are necessary and sufficient to cause trigeminal neuralgia, and patients with multiple sclerosis also have cross-compression of the trigeminal nerve roots. Another theory has been described in the dental literature. rantner et al. and Shaber et al. hypothesized that trigeminal neuralgia is due to an abscess focus or bone destruction that irritates the trigeminal again nerve in the maxilla or mandible, but this theory is not widely accepted, even among dentists. Similar lesions can be seen in the jaws of patients without a history of pain or soreness, and treatment of them does not provide rapid, uniform relief. Some patients with trigeminal neuralgia do not show such lesions. Although some disagree that abscesses and other pathologic processes can trigger the disease, this view persists in the dental literature. 4. Pathophysiology of trigeminal neuralgia How demyelinating plaques, jaw infections, arterial and tumor compression of the trigeminal nerve can cause trigeminal neuralgia is not known. There are two theories to explain trigeminal neuralgia, namely “central theory” and “peripheral theory”. The former is based on the mechanism that trigeminal neuralgia resembles epileptic seizures and emphasizes the effect of overactive ethibromoacetamide on neurotransmitter impulses. The use of an epileptogenic agent injected into the trigeminal nerve induces ethibromoacetamide hyperactivity in cats and monkeys and produces a pain syndrome. The role of dorsal root reflexes and synapses in the trigeminal system has been described. The “peripheral theory” concept focuses on the fact that alterations in the myelin sheath and axons of the trigeminal nerve can cause the altered peripheral nerve to be sensitive to chemical and mechanical stimuli and can link the pain syndrome to a perceived extrinsic cause. Other theories based on pseudosynaptic connections, reflex loops, and altered central connections caused by afferent nerve blocks have been proposed. 5. Symptoms and signs of trigeminal neuralgia Although the classification of cephalofacial pain syndrome is not clear, it is possible to distinguish trigeminal neuralgia from other types of pain. Trigeminal neuralgia has the following features: discharge-like pain; any kind of attack is unilateral, sudden and abrupt, with no pain between attacks; pain is stimulated by non-injurious stimuli, often occurs in different areas of the face, with little or no sensory loss in the onset area, and pain is limited to the trigeminal nerve range; atypical pain can also occur, but the more unusual features the patient exhibits, the fewer drugs or surgical methods may be beneficial for treatment. surgical approach may be less favorable. About 3% of patients have a history of bilateral throbbing pain, and it is rare to have bilateral throbbing pain in a single episode, which usually alternates bilaterally over several years. Damage to the trigeminal nerve by surgical or anesthetic means can cause changes in trigeminal nerve and restorative symptoms, so it is necessary to identify the symptoms before performing this procedure. Nerve damage can cause a pain with a burning component that is usually not present in patients without nerve damage. If a significant sensory deficit is present, it is required to look for pathological structures such as tumors or infections that are damaging the trigeminal nerve.