Scientists have discovered the gene potentially responsible for ‘congenital analgesia’; a disorder preventing individuals from feeling pain.
The collaborations of academic institutes across the globe have found that mutations at the ‘SCN9A’ gene can be linked with the inability of rare individuals to experience pain. Thus providing massive insight into the causes of pain within the body, and opening up a field of research into new pain management pharmaceuticals.
The study in which this research is stated was recently published in the prestigious ‘Nature’ journal on the 14th of December 2006.
Pain is an essential evolutionary mechanism. It helps to minimise damage to the body, and facilitates the learning of behaviours which help avoid future affliction. Studying this disorder has allowed massive insight into the complex workings of pain within the body, and the insight gained may provide massive leaps forward in the development of new treatments.
The sensation of pain is a major role of neurons within the body. DNA provides the code for the building blocks which make up these neurons. In response to pain these neurons become ‘excited’ and ‘fire’ a signal to the brain. The ‘SCN9A’ gene codes for the part of the neuron which is responsible for this firing of a signal. Patients with congenital analgesia have mutations at this gene, which is thought to prevent the firing of a signal. Hence the individual does not feel pain.
The first intensely studied instance of congenital analgesia was displayed in a young boy from northern Pakistan. He was found performing on the streets by walking over hot coals, and even sticking knives into his arms. All the while claiming not to feel pain. This phenomena was found in three other families also part of the Qureshi bidari/ clan. With some children from the three families had this disorder, whilst their siblings did not.
Many tests were performed to try and distinguish any other loss of sensation. Was this inability to feel pain be linked to some other physiological disorder? Researchers found this not to be case, in that all other function was normal.
The information that the non-presence of pain is an isolated defect in patients with mutations at this gene, could prove to be an interesting target. This calls for further research as blocking the part of the neuron newly identified as firing painful signals could provide more effective and potentially safer analgesia.