Trigeminal neuralgia: The role of self-sustaining discharge in the trigeminal ganglion

Z. Harry Rappaport, Marshall Devor*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

Abstract

Idiosyncrasies of trigeminal neuralgia provide both clues and constraints on candidate hypotheses concerning the underlying neural mechanism. After reviewing the key clinical aspects of the disease, we propose here a novel hypothesis based on recent findings from experimental nerve-injury preparations. The hypothesis states that trigger stimuli set off bursts of activity in a small cluster of trigeminal ganglion (TRG) neurons that have been rendered hyperexcitable as a result of TRG or trigeminal root damage. Activity then spreads from this "TRG ignition focus" to encompass more widespread portions of the ganglion. After a brief period of autonomous firing (seconds to minutes), activity is quenched and a refractory period is initiated by an intrinsic suppressive (hyperpolarizing) process engaged as a result of the rapid firing. The primary abnormality resides in the TRG and trigeminal root, rather than in the skin or the CNS. Because of this, sensation is essentially normal between periods of ectopic paroxysmal TRG discharge.

Original languageEnglish
Pages (from-to)127-138
Number of pages12
JournalPain
Volume56
Issue number2
DOIs
StatePublished - Feb 1994

Funding

FundersFunder number
Hebrew UniversityC enter for Researcho n Pain
German-Israeli Foundation for Scientific Research and Development

    Keywords

    • Ectopic discharge
    • Microvascular compression
    • Nerve injury
    • Pain
    • Tic doloreux
    • Trigeminal neuralgia

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