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- W2062864603 endingPage "138" @default.
- W2062864603 startingPage "127" @default.
- W2062864603 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." @default.
- W2062864603 created "2016-06-24" @default.
- W2062864603 creator A5029228633 @default.
- W2062864603 creator A5089751343 @default.
- W2062864603 date "1994-02-01" @default.
- W2062864603 modified "2023-09-23" @default.
- W2062864603 title "Trigeminal neuralgia: The role of self-sustaining discharge in the trigeminal ganglion" @default.
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- W2062864603 doi "https://doi.org/10.1016/0304-3959(94)90086-8" @default.
- W2062864603 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8008402" @default.
- W2062864603 hasPublicationYear "1994" @default.
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