“…The pathogenesis of “classical TN (cTN)” is frequently attributed to hyperexcitability of trigeminal ganglion neurons ( Burchiel, 1980a , 1980b ; Burchiel and Baumann, 2004 ; Devor et al., 2002 ) secondary to morphological compression of the trigeminal nerve root entry root by the cerebral vasculature (i.e., neurovascular compression [NVC]) ( Headache Classification Committee of the International Headache Society (IHS), 2013 ; Cruccu et al., 2016 ; Gardner and Miklos, 1959 ; Hilton et al., 1994 ; Rappaport et al., 1997 ). However, asymptomatic NVC has been noted in ∼13%–85% of asymptomatic subjects ( Haines et al., 1980 ; Hamlyn, 1997a , 1997b ; Jani et al., 2019 ). Other cases of TN are related to trigeminal nerve infection (e.g., herpes zoster), trauma, demyelination (as in multiple sclerosis), or compression from a space-occupying lesion in the cerebello-pontine angle and are termed “secondary TN.” However, a significant number of TN cases lack a demonstrable cause (“idiopathic TN [iTN]”) ( Hughes et al, 2019 ; Maarbjerg et al., 2017 ), including some cases with bilateral symptoms ( Brisman, 1987 ; Pollack et al., 1988 ).…”