Trigeminal neuralgia pathophysiology

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The pain of trigeminal neuralgia is often falsely attributed to a pathology of dental origin. Rarely do patients come to the surgeon without having had removed many, and not infrequently all, teeth on the affected side or both sides.[1] Extractions do not help for the pain is originating in the trigeminal nerve and not in an individual nerve of a tooth. Because of this difficulty, many patients may go untreated for long periods of time before a correct diagnosis is made. The trigeminal nerve is the fifth cranial nerve, a mixed cranial nerve responsible for sensory data such as tactition (pressure), thermoception (temperature), and nociception (pain) originating from the face above the jawline; it is also responsible for the motor function of the muscles of mastication, the muscles involved in chewing but not facial expression. Presence of refractory periods after a triggered episode, trains of painful sensations after a single stimulus, and latency from the time of stimulation to the onset of pain shows the role of central pain mechanisms involved in the pathogenesis of the pain of trigeminal neuralgia.[2] Several theories exist to explain the possible causes of this pain syndrome. The leading explanation is that a blood vessel is likely to be compressing the trigeminal nerve near its connection with the pons. The superior cerebellar artery is the most-cited culprit. Such a compression can injure the nerve's protective myelin sheath and cause erratic and hyperactive functioning of the nerve. This can lead to pain attacks at the slightest stimulation of any area served by the nerve as well as hinder the nerve's ability to shut off the pain signals after the stimulation ends. This type of injury also may be caused by an aneurysm (an outpouching of a blood vessel); by a tumor; by an arachnoid cyst in the cerebellopontine angle,[3] or by a traumatic event such as a car accident or even a tongue piercing. Two to four percent of patients with TN, usually younger, have evidence of multiple sclerosis, which may damage either the trigeminal nerve or other related parts of the brain. When there is no structural cause, the syndrome is called idiopathic. Postherpetic neuralgia, which occurs after shingles, may cause similar symptoms if the trigeminal nerve is affected.

Evidence for a role of central pain mechanisms includes the presence of refractory periods after a triggered episode, trains of painful sensations after a single stimulus, and latency from the time of stimulation to the onset of pain 


  1. Dandy, Sir Walter (1987). The Brain. The Classics of Neurology and Neurosurgery (Special edition ed.). Birmingham: Gryphon editions. p. 179.
  2. Fromm GH, Terrence CF, Maroon JC (November 1984). "Trigeminal neuralgia. Current concepts regarding etiology and pathogenesis". Arch. Neurol. 41 (11): 1204–7. PMID 6487105.
  3. Babu R, Murali R. "Arachnoid cyst of the cerebellopontine angle manifesting as contralateral trigeminal neuralgia: case report", Neurosurgery 1991 Jun;28(6):886-7. (PMID 2067614)

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