Peripheral pathogenesis Lesions anywhere from the trigeminal nerve terminals to the brainstem nuclei can cause the disease. Cushing (1920) found that mechanical compression of the tumor during surgery could cause trigeminal neuralgia. Jennetta (1966) suggested that more than 90% of the entrance to the trigeminal nerve’s pons had heterogeneous tortuous vessels compressing the posterior trigeminal roots, resulting in localized demyelination of the nerve roots. Gardner suggested that a short circuit is created between adjacent fibers in the demyelinated area, through which minor tactile stimuli can be transmitted to the center, and impulses from the center are converted into afferent impulses by this “short circuit”, which superimpose and reach above-threshold intensity to produce symptoms. The symptoms are produced by the superposition of these impulses. There are many similarities between trigeminal neuralgia and focal epilepsy. There are some phenomena that cannot be explained by the peripheral pathogenic theory, such as the autopsy finding of nerve-vascular contact in many normal subjects and the absence of vascular compression in some patients with trigeminal neuralgia. Sensory seizures Trigeminal neuralgia may be a form of sensory seizure. This is supported by the fact that trigeminal neuralgia seizures have a trigger point, are sudden, short in duration, and effective with antiepileptic drugs. This theory does not explain the fact that the majority of cases are unilateral, that the pain is confined to one or two branches for a long time without progression, and that brainstem lesions do not produce trigeminal neuralgia.