The classical explanation for CTN is the so-called neuro-vascular contact between the root entry zone of the tri-

geminal nerve and, in particular, the superior cerebellar artery.107 In support of this explanation are biopsies from

TN patients showing axonal swelling and demyelination. As a consequence of the loss of myelin, ephaptic activity and high-frequency discharges of touch-transmitting axons to nociceptive axons can lead to the paroxysms of pain. The fact that not all patients with CTN have a demonstrable neurovascular conflict and that patients who do appear to have a neurovascular conflict do not have CTN has led to some doubts about this as the universal explanation for TN.

Devor et al.108 have promoted the "ignition hypothesis'' based on an up-regulation of ion channels in response to an injury of the trigeminal nerve. Another possibility to be discussed is the involvement of the secondary neurons in the trigeminal sensory nuclear complex and that central sensitization may be part of the pathophysiological mechanisms.102

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