Trigeminal neuralgia as a consequence of circulatory disorders in the infratemporal and pterygopalatine fossae.
An extensive review of the well documented experimental and clinical findings related to trigeminal neuralgia shows, that it is possible to set up an unifying theory for trigeminal neuralgia, which would explain most clinical features of the disease and also would be congruent with several other theories that have previously been presented. Thus, trigeminal neuralgia is proposed to be the result of a combination of predisposing anatomical variations, impaired arterial and venous circulation, and morphological changes in the infratemporal fossa and cavum Meckeli. The process is initiated by disturbances of dental occlusion and mandibular function, resulting in muscular hypertrophy, which finally leads to increased perineural pressure and hypoxia in the nervous tissue. Through a series of related events this results in massive afferent discharges in the trigeminal nerve, which are strong enough to break through an inhibitory gating mechanism in the nucleus caudalis, and which are experienced by the patient as a pain attack. But the tissue hypoxia, which partly has elicited the pain, will finally also be the critically delimiting factor for further signal transmission, thereby stopping the pain attack.
D006801:Humans; D006984:Hypertrophy; D000860:Hypoxia / Q000150:complications; D008410:Masticatory Muscles / Q000098:blood supply* / Q000473:pathology; D009408:Nerve Compression Syndromes / Q000209:etiology; D009474:Neurons / Q000502:physiology; D011626:Pterygoid Muscles / Q000098:blood supply*; D012039:Regional Blood Flow; D009435:Synaptic Transmission; D013703:Temporal Muscle / Q000098:blood supply*; D014276:Trigeminal Nerve / Q000098:blood supply*; D014277:Trigeminal Neuralgia / Q000209:etiology*