Described are mutant Nav1.7 sodium channel alpha-subunits and nucleic acid sequences encoding such mutants. Further described are methods for characterizing a nucleic acid sequence that encodes a Nav1 sodium channel alpha-subunit, methods for determining a Nav1.7 haplotype, methods for determining a subject's predisposition to a neurologic disorder associated with a sodium channel mutation, and methods of identifying a compound that modulates mutant Nav1.7 sodium channels. Other materials, compositions, articles, devices, and methods relating to mutant Nav1.7 sodium channels are also described herein.