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PubMed 19593630


Referenced in Channelpedia wiki pages of: none

Automatically associated channels: Nav1.7



Title: Developments in autonomic research: a review of the latest literature.

Authors: Vaughan G Macefield

Journal, date & volume: Clin. Auton. Res., 2009 Aug , 19, 193-6

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/19593630


Abstract
Small-diameter afferents do not just subserve pain and temperature sensibilities, important for protection of the body though they are: there is a system of low-threshold unmyelinated afferents that respond to light stroking (C-tactile afferents) and they are believed to subserve the affective components of touch. Patients with large-fibre sensory neuropathies exhibit skin sympathetic responses to stroking, and report the stimuli as feeling pleasant. Moreover, the posterior insula is activated. Patients with small-diameter sensory neuropathies, specifically those with congenital insensitivity to pain, suffer from cumulative injuries that can lead to joint degeneration. There is evidence that the nociceptive (and sympathetic) axons die because nerve growth factor is not being produced by the target tissues; patients with congenital insensitivity to pain have mutations in the NTRK1 gene, the gene responsible for producing the TrkA receptor, but there is also evidence for mutations in the SCN9A gene, which codes for a specific subunit of the voltage-gated sodium channel. Specific mutations, leading to clusters of cases of congenital insensitivity to pain, have been found in several geographical locations, with several genetic mutations having been documented. Interestingly, even patients with congenital insensitivity to pain, despite having never experienced pain, can still empathise with the pain in others-we do not need to feel pain in order to empathise, but we do need to feel pain in order to ensure that our body looks after itself.