Trigeminal neuralgia (TN), also known as tic douloureux, is a distinctive facial pain syndrome that may become recurrent and chronic. It is characterized by unilateral pain following the sensory distribution of cranial nerve V (typically radiating to the maxillary or mandibular area in 35% of affected patients) and is often accompanied by a brief facial spasm or tic.
Although a questionable family clustering exists, trigeminal neuralgia (TN) is most likely multifactorial.
Most cases of trigeminal neuralgia are idiopathic, but compression of the trigeminal roots by tumors or vascular anomalies may cause similar pain, as discussed in Pathophysiology. In one study, 64% of the compressing vessels were identified as an artery, most commonly the superior cerebellar (81%). [6] Venous compression was identified in 36% of cases. [6]
Neuropathic pain is the cardinal sign of injury to the small unmyelinated and thinly myelinated primary afferent fibers that subserve nociception. The pain mechanisms themselves are altered. Microanatomic small and large fiber damage in the nerve, essentially demyelination, [4] commonly observed at its root entry zone (REZ), leads to ephaptic transmission, in which action potentials jump from one fiber to another.[5] A lack of inhibitory inputs from large myelinated nerve fibers plays a role. Additionally, a reentry mechanism causes an amplification of sensory inputs. A clinical correlate, for instance, is the potential for vibration to trigger an attack. However, features also suggest an additional central mechanism (eg, delay between stimulation and pain, refractory period).
No geographic tendency or racial differences have been found for trigeminal neuralgia. However, females are affected up to twice as often as males (range, 3:2 to 2:1). In addition, in 90% of patients, the disease begins after age 40 years, with a typical onset of 60-70 years (middle and later life). Patients who present with the disease when aged 20-40 years are more likely to suffer from a demyelinating lesion in the pons secondary to multiple sclerosis; younger patients also tend to have symptomatic or secondary trigeminal neuralgia .
Patients may find immediate and satisfying relief with one medication, typically carbamazepine. However, because this disorder may remit spontaneously after 6-12 months, patients may elect to discontinue their medication in the first year following the diagnosis. Most must restart medication in the future. Furthermore, over the years, they may require a second or third drug to control breakthrough episodes and finally may need surgical intervention. (Medscape)