The voltage-gated sodium channel NaV1.7 is expressed in nociceptive and sympathetic neurons, where it aids in action potential creation and regulation. The mutations in this gene that have received study all alter the channel's ability to inactivate. Sodium channel inactivation is vital for the proper cessation of action potentials. The decreased inactivation caused by these mutations, then, is expected to cause prolonged action potentials and repetitive firing. Such altered firing will cause increased pain sensation and increased sympathetic nervous system activity, producing the phenotype observed in patients with PEPD.
Paroxysmal extreme pain disorder
Nociplastic pain
Functional somatic syndrome
Psychogenic pain
Mass psychogenic illness
Syndrome of subjective doubles
Cephalalgiaphobia
Postorgasmic illness syndrome