• Harry Z Rappaport and Marshall Devor.
• Department of Neurosurgery, Beilinson Hospital, Tel Aviv University Medical School, Petah Tikva 49100 Israel Department of Cell and Animal Biology, Life Sciences Institute, Hebrew University of Jerusalem, Jerusalem 91904 Israel.
• Pain. 1994 Feb 1; 56 (2): 127138127-138.

AbstractIdiosyncrasies 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.

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