It is a well-known reality that genetic variants can alter the pain perception
of an individual in correlation with painless and painful voltage-gated Nachannelopathies
for the better understanding of molecular transmission and detection
events to noxious stimuli. Mutations in Nav 1.7 gene coding for the Na-ion channel can
cause severe syndromes of distinctive pain such as small-fiber neuropathy, inherited
erythromelalgia, and paroxysmal pain disorder. Whereas the inactivation of SCN9A
mutations that encodes Nav 1.7, as a consequence, leads to insensitivity to pain
congenitally. The TRPA1 heterozygous mutations code for Nav1.9 (SCN11A) and
Nav1.8 (SCN10A) can cause insensitivity to pain while other variants are responsible
for the potential-cation channel of the transient-receptor which can cause episodes of
familial pain syndromes. Moreover, recently found few other novel genetic
polymorphisms essentially identify the severity and complexity of the pain phenotypes.
Various pain models for a better understanding of the sensory disorders and heritable
disorders of pain are in the developmental phase. Therefore, devising new therapeutic
approaches, genome-guided therapy, and understanding the structure of receptors for
novel drug development and delivery in correlation with Na-ion channel is imminent.
Keywords: Erythromelalgia, Gene Therapy, Heritable Disorder, Neuropathy,
Paroxysmal Pain Disorder, Polymorphisms, Sensory Disorders.
