A child falls while running across a room, strikes a knee against the floor and gets back up without crying. There is no grimace, no hesitation, not even the familiar instinct to protect the injured leg. At first, an adult might assume the child is unusually brave. But imagine the same child touching a hot pan without pulling away, breaking a bone without noticing and continuing to play while an injury quietly worsens.
Something far more unusual may be happening.
Pain is one of the body’s most important warning systems. It tells us when tissue is being damaged, when a joint needs rest and when an apparently harmless situation has become dangerous. Yet a very small number of people are born with a condition that prevents them from experiencing ordinary physical pain.
For these individuals, an injury may be real even when the suffering normally associated with it is entirely absent.
Scientists call one group of these disorders congenital insensitivity to pain. Research into this rare condition has uncovered remarkable details about how nerves communicate, how genes influence sensation and why pain is much more than an unpleasant feeling.
The discovery has implications that reach beyond rare genetic disorders. By studying people who barely feel pain—or cannot feel it at all—researchers are learning how the human nervous system works and investigating new possibilities for pain treatment.
Suggested hero image: A child with a minor injury, illustrating why the absence of a normal pain response can be medically significant.
What does it mean to rarely feel physical pain?
The phrase can describe several very different experiences, and distinguishing between them is essential.
Some people naturally tolerate discomfort better than others. An athlete may continue exercising despite a painful muscle, while another person finds the same sensation overwhelming. Expectations, attention, emotions, previous experiences and the circumstances of an injury can all influence how pain is experienced.
Others have medical conditions that alter sensation. Certain nerve disorders can reduce the ability to feel pain in particular areas of the body. Injuries to nerves, some neurological diseases and other medical problems may interfere with the transmission of sensory signals.
Then there is congenital insensitivity to pain, an exceptionally rare group of disorders in which a person has little or no ability to perceive pain from birth.
These are not interchangeable situations. Someone who tolerates pain well can still detect a burn, a fracture or a damaged tooth. Someone with genuine congenital pain insensitivity may sustain comparable injuries without receiving the warning that would ordinarily prompt protective action.
According to the US National Institutes of Health’s MedlinePlus Genetics overview of congenital insensitivity to pain, affected people can experience injuries without feeling the pain that would normally accompany them.
The condition does not necessarily mean that every sensation disappears. Some affected individuals can still recognize touch, pressure or differences between sharp and dull objects. Their ability to detect temperature may also depend on the specific genetic disorder.
That distinction is crucial: not feeling pain is not the same as being unable to sense everything happening to the body.
How the body normally creates the sensation of pain
To understand why some people cannot feel pain, it helps to follow the journey of a pain signal through the body.
Imagine accidentally touching a hot cooking pan. Specialized sensory nerve endings in your skin, called nociceptors, detect potentially damaging heat. These receptors respond to harmful mechanical, thermal or chemical stimuli and help initiate electrical signals in sensory neurons.
Those signals travel through peripheral nerves toward the spinal cord, where they are processed and relayed through neural pathways to the brain. Networks in the brain then contribute to the experience of pain, including its intensity, emotional impact and significance.
The process is not simply a wire carrying a message from the skin to the head. Signals can be amplified or suppressed at different points, and the brain combines sensory information with attention, context, memories and expectations.
This helps explain why two people can experience the same injury differently.
It also reveals several places where the system can go wrong. The sensory endings may fail to detect damaging stimuli. Nerve cells may be unable to generate electrical impulses properly. Signals may not travel effectively toward the spinal cord, or the pathways responsible for processing them may be disrupted.
In congenital insensitivity to pain, the problem often involves genes that are essential for the development or function of pain-sensing neurons.
The US National Institute of Neurological Disorders and Stroke provides a useful overview of the biology in its guide to pain.
Pain is therefore not a single switch that is either turned on or off in every person. It is the result of a complex biological system, and different genetic changes can interfere with that system in different ways.
The gene that can silence pain signals
One of the most revealing discoveries in pain research involves a gene called SCN9A.
This gene provides instructions for making part of a protein known as the NaV1.7 sodium channel. These channels help certain nerve cells generate and transmit electrical signals. They are particularly important in nociceptors, the sensory neurons involved in detecting potentially harmful stimuli.
When a person has certain loss-of-function variants in SCN9A, the NaV1.7 channel cannot function normally. As a result, pain-sensing neurons may be unable to transmit signals effectively.
The consequences can be remarkable: a person may experience little or no pain despite injuries that would ordinarily be extremely painful.
Researchers identified this connection through genetic studies of people with congenital painlessness. The findings demonstrated that a single gene involved in electrical signalling can have an extraordinary influence on how humans experience pain.
MedlinePlus Genetics explains the mechanism in its detailed entry on the SCN9A gene.
There is another intriguing detail. Some people with SCN9A-related congenital insensitivity to pain also have an inability to smell, known as anosmia. The same gene is involved in signalling in certain olfactory sensory neurons, helping explain why changes affecting pain perception can also influence smell.
This is a reminder that genes rarely operate in isolation to produce just one effect. A protein that plays an important role in one sensory pathway may also be needed in another.
However, SCN9A is not the only gene associated with congenital painlessness. Different genetic conditions can produce overlapping symptoms through different biological mechanisms.
When the problem begins before birth
Some people cannot feel pain because the sensory system does not develop normally in the first place.
One example is congenital insensitivity to pain with anhidrosis, commonly abbreviated as CIPA. It is also known as hereditary sensory and autonomic neuropathy type IV.
CIPA is commonly associated with disease-causing variants in the NTRK1 gene. This gene provides instructions for a receptor involved in nerve growth factor signalling, which helps certain sensory and autonomic neurons develop and survive.
When this pathway is disrupted, important nerve cells may fail to develop or survive as they should. The result can include an inability to feel pain and temperature, along with reduced or absent sweating.
That second feature creates an additional danger. Sweating helps regulate body temperature. Without it, affected individuals can develop dangerously high temperatures, particularly during hot weather or illness.
The condition can therefore involve more than an unusual relationship with injury. It can affect the body’s ability to detect danger and regulate essential functions.
The MedlinePlus Genetics guide to CIPA describes these features and explains how NTRK1-related changes affect the nervous system.
CIPA also illustrates why the phrase pain insensitivity covers more than one biological mechanism. In some conditions, pain signals fail because nerve cells cannot communicate normally. In others, the sensory neurons themselves may be missing or improperly developed.
The outward symptom can look similar, but the underlying biology matters for diagnosis, monitoring and care.
What happens when the body’s warning system is missing?
For most people, pain prompts an immediate response. We pull away from heat, stop putting weight on an injured ankle or seek help when a tooth begins to ache.
A person who cannot feel pain may receive none of those warnings.
A child might bite the tongue or lips without recognizing the damage. A fracture could remain undetected because walking on the injured limb does not hurt. A burn may continue to damage the skin because the person does not feel the usual warning sensation.
Repeated injuries can cause lasting damage to bones and joints. Wounds may become infected before anyone realizes that medical attention is needed. Eye injuries are particularly concerning because unnoticed damage to the cornea can threaten vision.
These are not simply hypothetical risks. They are well documented features of congenital insensitivity to pain in clinical literature.
A comprehensive medical reference, GeneReviews’ overview of congenital insensitivity to pain, describes the need for ongoing monitoring of injuries, bones, joints, eyes, dental health and temperature regulation, depending on the specific condition.
For affected families, everyday life may require a different kind of vigilance. Regular skin checks, careful examination after physical activity, routine dental visits and medical assessment of suspected injuries can become essential parts of daily care.
The absence of pain does not mean the absence of damage. In some circumstances, it means damage is more likely to go unnoticed.
Is being naturally good at tolerating pain the same thing?
Not at all—and this is where the subject becomes particularly interesting.
Someone who remains calm during a painful medical procedure may have a high pain tolerance, but that does not mean their nervous system has stopped detecting pain. They may still experience the sensation while responding to it differently.
Pain threshold and pain tolerance are also different concepts. The threshold refers to the point at which a stimulus begins to be experienced as painful. Tolerance describes how much pain a person is willing or able to endure.
Neither measure is a simple reflection of courage or character.
Research into pain shows that attention, anxiety, mood, past experiences, sleep and expectations can influence how pain is experienced. The same stimulus can feel different to the same person under different circumstances.
Chronic pain adds another layer. Some people live with persistent pain caused by conditions affecting nerves, joints or other tissues. Others experience pain that continues beyond the expected healing period, sometimes without a clear ongoing source of tissue damage.
The National Institute of Neurological Disorders and Stroke explains these distinctions in its pain information resource.
It is important not to confuse these everyday variations with a rare congenital disorder. A person who says they rarely feel pain may simply have a high tolerance, may be describing a particular kind of discomfort, or may have a medical condition affecting sensation. Their experience alone cannot establish the cause.
Could scientists use painlessness to develop better painkillers?
This is one of the most promising reasons researchers study people with congenital insensitivity to pain.
Chronic pain affects millions of people, and existing treatments do not work equally well for everyone. Some medications also carry significant risks, making the search for more targeted approaches an important area of medical research.
People with genetic pain disorders offer a rare opportunity to understand which biological pathways are essential for pain perception.
SCN9A is a particularly valuable example. If changes that disrupt NaV1.7 can dramatically reduce pain, scientists can investigate whether carefully targeting that channel might help people who experience severe or persistent pain.
But translating a genetic discovery into a safe, effective medicine is more complicated than it first appears.
A person who has lacked a functional channel from birth is not biologically identical to someone who takes a drug that blocks the channel in adulthood. Lifelong genetic changes may influence the development of neural circuits and other signalling pathways. A medication may block its target incompletely or produce different effects in different tissues.
Research has also suggested that changes in endogenous opioid signalling may contribute to the painlessness associated with loss of NaV1.7 function. This adds another layer to the mechanism and helps explain why reproducing the full effect with a drug has proved challenging.
A peer-reviewed review in the British Journal of Pharmacology explores these questions in detail: Understanding the genetic basis of congenital insensitivity to pain.
The lesson is not that scientists have discovered a simple way to switch off pain. It is that rare genetic conditions can reveal biological targets that might otherwise have remained hidden.
Future treatments may emerge from this work, but a safe and effective therapy cannot be assumed simply because a gene has been linked to painlessness.
How do doctors identify congenital insensitivity to pain?
Because the condition is rare, diagnosis requires more than noticing that someone appears unusually unfazed by injuries.
Doctors may look for a history of injuries that caused little or no pain, unexplained burns, repeated fractures, damage to the tongue or lips, and reduced sensitivity to painful stimuli. In some forms, abnormalities in temperature sensation, sweating or smell can provide additional clues.
A detailed neurological examination helps establish which sensations are affected. Depending on the findings, clinicians may recommend genetic testing to identify a causative variant.
The precise evaluation depends on the suspected condition. Someone with an inherited disorder affecting pain and sweating may need a different assessment from someone whose symptoms suggest a peripheral nerve disorder acquired later in life.
Care is also tailored to the individual. It may involve specialists in neurology, clinical genetics, orthopaedics, dentistry, ophthalmology and paediatrics.
There is currently no universal cure that restores normal pain perception across all forms of congenital insensitivity to pain. Management generally focuses on preventing injury, identifying damage early and treating complications.
For more clinical detail, the NCBI GeneReviews resource outlines diagnostic considerations and ongoing care.
An important health warning: A new or unexplained loss of pain or temperature sensation should not automatically be attributed to a rare genetic condition. It warrants medical assessment, particularly when accompanied by weakness, numbness, burns, wounds or changes in walking. Sudden neurological symptoms require urgent medical attention.
Frequently asked questions
Can a person really feel no physical pain?
Yes. Certain rare inherited disorders can prevent people from experiencing ordinary physical pain from birth. The degree of sensory loss and other symptoms vary by the underlying genetic condition.
Do people who cannot feel pain still feel touch?
Some do. Pain, touch and temperature are related but distinct sensory functions. A person may retain some forms of touch while having a severely impaired ability to perceive pain.
Can people with congenital insensitivity to pain get injured?
Absolutely. They can sustain burns, fractures, cuts, joint damage and other injuries. Without pain as a warning signal, these injuries may go unnoticed and become more serious.
Is congenital insensitivity to pain curable?
There is no established universal cure that restores normal pain perception. Care focuses on preventing injuries, detecting complications early and managing the individual’s specific symptoms.
Can studying painless people lead to new pain treatments?
Research into genes such as SCN9A has identified important pathways involved in pain signalling. Scientists are investigating how this knowledge might lead to better treatments, but developing medicines that are both safe and effective remains challenging.
The surprising value of a sensation we wish we could escape
Pain is easy to resent when a headache ruins the day, an injury interrupts a plan or a chronic condition makes ordinary activities difficult. In those moments, a life without pain can sound like a remarkable gift.
But the biology tells a more complicated story.
Pain is not perfect. It can persist long after an injury has healed, become debilitating or arise from changes in the nervous system itself. It is not always a reliable measure of how much tissue damage has occurred, and severe pain deserves appropriate medical care rather than dismissal.
Yet pain also provides information that helps protect the body. The rare people who are born without this warning system demonstrate what can happen when that protection is missing.
Their experiences have helped scientists identify genes, understand sensory neurons and investigate new approaches to treating pain. They have also revealed an important distinction: eliminating suffering and eliminating the body’s ability to detect danger are not the same achievement.
The challenge for medicine is not simply to make pain disappear. It is to relieve unnecessary suffering while preserving as much of the body’s protective function as possible.
