Trigeminal neuralgia at the present stage: Pathophysiology, classification, diagnosis and treatment (literature review)

The incidence of trigeminal neuralgia (TN) is 4–5 cases per 100,000 population per year, and the prevalence is about 20–50 cases per 100,000 population. According to the modern classification, the following types of TN are distinguished: classical, symptomatic and idiopathic. The cause of classical TN is a neurovascular conflict, of symptomatic TN – neoplasms in the petroclival area, vascular anomalies, multiple sclerosis, etc. In the absence of a reliable etiological factor, TN is considered idiopathic. TN pathogenesis remains one of the most challenging topics in neuroscience. Today, there are many theories and hypotheses regarding the peripheral and central mechanisms of trigeminal neuralgia. The most popular theory is the neurovascular conflict that occurs between the trigeminal nerve and the cerebral vessels, but this theory is not the only one. It is known that even after microvascular decompression, patients may continue to experience facial pain. Therefore, other pathogenetic mechanisms are discussed: short circuit theory, multineuronal mechanism, allergic and immune hypothesis, gate theory, bioresonance hypothesis, trigeminal convergence projection theory, “ignition” hypothesis and ion channel pathology. TN is a clinical diagnosis, and its establishing requires certain criteria proposed by the International Headache Society. Using instrumental research methods, namely magnetic resonance imaging of the brain, is necessary for the differential diagnosis of classical and symptomatic TN, and imaging results should always be interpreted in combination with clinical data to make correct decisions on further treatment tactics.