What is the pathophysiology of trigeminal neuralgia (TN)?

Updated: Jul 11, 2019
  • Author: Manish K Singh, MD; Chief Editor: Robert A Egan, MD  more...
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Answer

Because the exact pathophysiology remains controversial, the etiology of trigeminal neuralgia (TN) may be central, peripheral, or both. The trigeminal nerve (cranial nerve V) can cause pain, because its major function is sensory. Usually, no structural lesion is present (85%), although many investigators agree that vascular compression, typically venous or arterial loops at the trigeminal nerve entry into the pons, is critical to the pathogenesis of the idiopathic variety. This compression results in focal trigeminal nerve demyelination. The etiology is labeled idiopathic by default and is then categorized as classic trigeminal neuralgia.

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).


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