Congenital analgesia is a rare condition in which people do not sense physical pain coming in from outside stimuli.
Scientists at Jena University Hospital in Germany compared the gene sequence of a girl with the disorder against those of her parents, and identified a mutation in a gene called SCN11A.
This gene controls the development of channels on pain-sensing neurons. Sodium ions travel through these channels, creating electrical nerve impulses that are sent to the brain, which registers pain, 'New Scientist' reported.
"The outcome is blocked transmission of pain signals," said researcher Ingo Kurth.
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In mice studies, researchers inserted a mutated version of SCN11A into the creatures and tested their ability to perceive pain.
They found that 11 per cent of the mice with the modified gene developed injuries similar to those seen in people with congenital analgesia, such as bone fractures and skin wounds.
The control group of mice with the normal SCN11A gene, did not develop such injuries, researchers said.
The team is now searching for drugs that block the SCN11A channel.
"It would require drugs that selectively block this but not other sodium channels, which is far from simple," said Kurth.