An hypothesis on the mechanism of pain attacks in trigeminal neuralgia is presented. It is based on the analysis of clinical characteristics and pathology of a series of 278 cases submitted to different methods of treatment, and on physiological data of the literature. The hypothesis is that trigeminal neuralgia is a sort of sensory reflex epilepsy. The posterior root, damaged and distorted by a vessel or compressed by other lesions shows demyelination, micro-neuromas, and so on. At the site of this chronic damage ectopic impulses and afterdischarges are generated; the gasserian ganglion cells too give rise to spontaneous impulse generation. Owing to this chronic anomalous afferent barrage, an epileptic subliminal focus is "kindled" in the trigeminal nucleus. The pain paroxysms develop when this subliminal activity is driven in prolonged seizure discharges by peripheral (trigger zone stimulation) or other (not perceived) afferences. Clinical characteristics of the attacks (triggering by innocuous stimulations; persistence of pain after stimulus stops; diffusion of pain outside the stimulated division; refractory period after each paroxysm; increase in frequency of the attacks up to an epileptic-like status; sensibility to carbamazepine and phenytoin) and recurrence following diverse procedures are discussed on the basis of experimental research in reflex epilepsy and "kindling". If this hypothesis is true, the treatment of choice of trigeminal neuralgia should be a direct approach to the posterior fossa in order to relieve neurovascular compression which, in more than 75% of the cases, is the causative factor of the disease.