We recently showed that inflammation causes arrhythmogenic properties in cardiac voltage gated sodium channels (Nav). Here, we hypothesize that inflammation, via Nav, is a common trigger for other pathologies including neurological disorders. Based on our previous work, we further postulated that cannabidiol (CBD), the primary non-psychoactive constituent of Cannabis sativa, may protect against inflammation-induced neuropathy through its direct effects on neurological Nav1.6. To test these ideas, we used whole-cell patch clamp of human embryonic kidney (HEK 293) cells transiently transfected with SCN8A cDNA encoding neurological Nav1.6 α-subunit and incubated the cells under control conditions or in a cocktail of inflammatory mediators for 24 hours. Incubation in inflammatory mediators right-shifted the voltage dependence of both activation and steady-state fast inactivation, and increased late sodium current. Perfusion of CBD (IC50; 5 µM) during recording rescued all the gating changes in Nav1.6 provoked by incubation with inflammatory mediators. These findings suggest that inflammation, by affecting Nav, is a potential pathogenic trigger for neurological pathologies. Moreover, CBD, through its direct effects on Nav, could potentially mitigate the dysfunction induced by inflammation.