Trigeminal neuralgia (TIC) is described as "a painful, unilateral affliction of the face, characterized by brief electric-shock-like (lancinating) pain limited to the distribution of one or more divisions of the trigeminal nerve. Pain is commonly evoked by trivial stimuli, including washing, shaving, smoking, talking and brushing the teeth, but may also occur spontaneously. The pain is abrupt in onset and termination may remit for varying periods." Symptomatic trigeminal neuralgia is described as "pain indistinguishable from trigeminal neuralgia, caused by a demonstrable structural lesion." This lesion is usually a tumor, such as an acoustic neuroma, or may be due to demyelination, as seen in multiple sclerosis. If there is tissue or nerve injury, there may be an ensuing continuous trigeminal neuralgia, which is usually referred to as traumatic trigeminal neuralgia or trigeminal deafferentation (TD).
TIC is usually unilateral and only occurs bilaterally in four percent of subjects. There is no genetic link to the disorder. The average age at onset is between the sixth and seventh decades, with women slightly more affected than men in a 3:2 ratio. The bright stimulating pain perceived is short-lived, lasting seconds to minutes. If not questioned carefully the patient may report the pain lasts all day, as there is often a dull pain associated with TIC or the sharp volleys come and go continuously. The author believes the persistent aching pain may be secondary to a reflex muscle splinting and can be controlled with stretching exercise and a vapocoolant spray. TIC pain can be triggered usually by a mechanical maneuver of the trigeminal sensory system. The area from which the pain is activated has been described as a trigger zone. Characteristically, trigger zones occur around the supraorbital, infraorbital foramina, the inner canthus of the eye, lateral to the ala and over the mental foramen. Trigger zones are also common intraoral. Pain is not elicited from the trigger zone if deep pressure is used or during a latency period between paroxysms. The second and third divisions of the trigeminal nerve are most commonly affected, and less than five percent of cases involve the first division. Often there is a reflex spasm of the face on the affected side, hence the term "tic douloureux," which has been used synonymously with TIC.
It is postulated that TIC may be due to a focal demyelination of the trigeminal nerve at any point along its course. In between 60 to 88% of cases, exploration of the posterior cranial fossa reveals vascular compression of the trigeminal nerve root as it exits the pons. This has been postulated to set up a centrally mediated disinhibition of pain modulation and/or peripheral repetitive ectopic action potentials. Once there is sensitization there may be increased afferent fiber activity and enhanced tactile stimulation, resulting in trigeminal nucleus interneuron discharge and trigeminothalamic neuron producing pain. Tumors may be the cause in up to six percent of cases. These include acoustic neurinomas, cholesteatomas, meningiomas, osteomas and angiomas. Aneurysms and adhesions have also been implicated. Although the pain may be typical of TIC, usually there are additional symptoms or cranial deficits present. When patients are in the 20- to 40-year age range and present with trigeminal neuralgia, multiple sclerosis should be ruled out. It is suggested that all patients with trigeminal neuralgia obtain a brain MRI or CT scan, with particular attention paid to the posterior cranial fossa.
TIC treatment may be divided into pharmacological and surgical. Table 1 outlines the drugs that may be used in TIC therapy.
The surgical treatments for TIC are summarized in Table 2.
