The question of whether people with Hansen’s disease (HD) feel pain is complex, challenging a long-held misconception. HD is the modern term for what was historically called leprosy, a chronic infectious disease. While it causes a profound loss of acute sensation, it frequently results in intense and chronic pain for patients. This neurological duality is central to understanding the disease, which is fundamentally a neuropathy.
Understanding Hansen’s Disease and Nerve Targeting
Hansen’s disease is caused by the bacterium Mycobacterium leprae, which has a specific affinity for the nervous system. The infection primarily targets the peripheral nerves, the communication lines extending from the brain and spinal cord to the rest of the body. HD is classified as a neuropathy, meaning it is a disease of the nerves.
The bacterium thrives in cooler areas of the body, concentrating in the superficial nerves of the skin and the peripheral nerves in the extremities, such as the hands, feet, face, and ears. Commonly affected nerves include the ulnar, median, peroneal, and tibial nerves. This focused attack leads to a wide range of sensory, motor, and autonomic deficits.
The Mechanism of Sensory Loss
The loss of acute sensation results from the bacterium’s interaction with specialized nerve cells. M. leprae invades and hijacks Schwann cells, the support cells that form the protective myelin sheath around peripheral nerve fibers. This invasion and the subsequent inflammatory immune response lead to the destruction of these cells.
When Schwann cells are damaged, the nerve fibers they protect become demyelinated and eventually destroyed, impairing their ability to transmit signals. The small, unmyelinated fibers responsible for transmitting pain, temperature, and crude touch sensation are often the first affected. This destruction prevents signals from an external injury—such as touching a hot surface or stepping on a sharp object—from reaching the brain. The result is the characteristic numbness and loss of protective sensation, a hallmark of the disease.
Acute Pain vs. Neuropathic Pain in HD
The belief that patients with HD feel no pain is only half true, as it confuses two different types of pain. Acute pain resulting from external injury, known as nociceptive pain, is lost due to nerve destruction. This protective function is absent in affected areas, which fuels the historical misconception.
Conversely, many patients experience intense chronic neuropathic pain. Neuropathic pain is not caused by external injury but is generated internally by the damaged, dysfunctional nerves themselves. This internal pain can be described as a burning, shooting, stabbing, or electrical sensation in areas of nerve damage. It is a direct consequence of the inflammatory process and nerve injury caused by the bacterial infection.
This chronic discomfort can occur during the active phase of the disease or years after the bacteria have been eliminated by multidrug therapy. A significant proportion of treated patients report chronic neuropathic pain that interferes with daily life and sleep. This internal pain requires specialized treatment with anticonvulsants or antidepressants, as common painkillers are often ineffective.
Secondary Damage Due to Loss of Pain Perception
The most visible and stigmatizing effects of Hansen’s disease are not caused by the bacteria actively consuming tissue. Instead, deformities and tissue loss are secondary consequences of the loss of acute pain perception. Without the protective warning signal of pain, patients repeatedly and unknowingly injure their anesthetized limbs.
Repeated, unnoticed trauma—such as minor cuts, pressure from ill-fitting shoes, or accidental burns—leads to chronic, non-healing ulcers and infections. Over time, these chronic injuries and subsequent infections cause tissue death and the slow reabsorption of bone, particularly in the fingers and toes. This process leads to characteristic physical changes, such as shortened digits, clawed hands, and foot drop, which are the result of unheeded damage.