The exact etiology of trigeminal neuralgia is still unknown but considerable progress has been made in recent years to put forward a mechanism for this pain. Most researchers would agree that in the majority of patients with classic trigeminal neuralgia, the pain is generated due to compression of the trigeminal nerve in most instances by vascular structures but in a small proportion due to other causes. The compression is most likely to occur at the so-called root entry zone which is defined as the point at which the peripheral and central myelin of the Schwann cells and astrocytes meet. Compression of the nerve at this point results in plaques of demyelination. Nerve injury results in hyperexcitability of injured afferents which result in after-discharges large enough to result in a non-nociceptive signal being perceived as pain. This leads to wind-up and both peripheral and central sensitization.

This theory has been put forward by Devor et al. and is known as the ignition theory hypothesis [47]. It is supported by electron microscopy appearances of the trigeminal nerve taken from patients with trigeminal neuralgia [48] and they also showed evidence of remyelination which could result in the pain remissions that are so characteristic of this condition. However, not all patients are found to have compression of the trigeminal nerve and even if found, not all patients have 100% pain relief for the duration of their life. There are likely to be other factors involved, given the rarity of the disease, and there may be genetic causes.

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