The trigeminal nerve is like a wire with insulation, and from the brainstem emanates the motor nerve, which is in charge of chewing, in parallel with the sensory nerve from the face. As people age, the blood vessels gradually begin to harden and become curved. This curved blood vessel may then approach the trigeminal nerve and press on it. This prolonged compression causes the insulation of the trigeminal nerve to fall off and the nerve fibers inside to “short circuit”. When washing, brushing, talking and eating, the “current” in the trigeminal nerve is particularly active and “short-circuiting” is unavoidable, and this is when facial pain attacks are frequent. The effect of carbamazepine can inhibit the “short circuit” inside the nerve, and in the early stage, there are few “short circuits”, so the effect is not bad. However, as the disease progresses, the number of “short circuits” increases, and carbamazepine cannot completely control the occurrence of “short circuits”, and increasing the dose cannot completely relieve the pain.