Congenital insensitivity to pain

How it works

Pain starts in nerve endings that respond to damage. The signal travels along thin nerve fibres to the spinal cord and brain. In the best-studied form of CIP, one link in this chain is missing. The gene SCN9A builds a sodium channel called Nav1.7, which pain nerves need in order to fire. People with two broken copies of the gene have pain nerves that are present but silent¹². Touch, pressure, warmth, and vibration still work.

Other genes cause other forms. Changes in NTRK1 cause CIPA, in which the nerves for pain and for sweating fail to develop. People with CIPA cannot sweat, so they also overheat³. Changes in PRDM12 stop pain nerves from developing at all¹.

The condition is dangerous. Children with CIP bite through their tongues and fingertips when teething. They walk on broken bones, burn themselves without noticing, and wear out their joints because they never rest an injury¹. Eye damage is common because they do not blink or rub when something scratches the cornea. Life expectancy is often reduced¹. Pain exists for a reason.

How common it is

Around 1 in 1,000,000 people have some form of CIP¹. CIPA is rarer, at about 1 in 125 million worldwide³.

History and culture

In 2006, a team studying a family in Pakistan found the SCN9A cause. One boy in the family worked as a street performer, walking on hot coals and pushing knives through his arms¹. He died at 14 after jumping from a roof¹.

A different case is Jo Cameron, a Scottish woman whose condition was identified when doctors noticed she needed no painkillers after surgery. Her case was published in 2019, when she was 71⁴. She has a change in a gene now called FAAH-OUT, which raises the level of a natural cannabinoid in her body⁴. She feels almost no pain, heals fast, and has never felt much anxiety⁴. Her pain nerves work. The signal is dampened later. Researchers hope her case will lead to new painkillers⁴.