Paroxysmal extreme pain disorder: a molecular lesion of peripheral neurons

Sodium Channels in Normal and Pathological Pain

(2010) Sulayman D. Dib-Hajj et al.   Annual Review of Neuroscience

Mutations at opposite Ends of the DIII/S4-S5 Linker of Sodium Channel NaV1.7 Produce Distinct Pain Disorders

(2010) Xiaoyang Cheng et al.   Molecular Pain

A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia

(2009) Tanya Z. Fischer et al.   ANNALS OF NEUROLOGY

Mexiletine-responsive erythromelalgia due to a new Nav1.7 mutation showing use-dependent current fall-off

(2009) Jin-Sung Choi et al.   EXPERIMENTAL NEUROLOGY

NaV1.7 Gain-of-Function Mutations as a Continuum: A1632E Displays Physiological Changes Associated with Erythromelalgia and Paroxysmal Extreme Pain Disorder Mutations and Produces Symptoms of Both Disorders

(2008) M. Estacion et al.   JOURNAL OF NEUROSCIENCE

Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation

(2008) Brian W. Jarecki et al.   JOURNAL OF PHYSIOLOGY-LONDON

Paroxysmal Extreme Pain Disorder M1627K Mutation in Human Nav1.7 Renders DRG Neurons Hyperexcitable

(2008) Sulayman D Dib-Hajj et al.   Molecular Pain