Nerve pain, often called neuropathic pain, occurs when disease or damage alters the normal function of pain-signalling pathways in the peripheral or central nervous system. It differs from nociceptive pain, which arises when specialised sensory receptors respond normally to actual or threatened tissue injury such as a cut, burn, fracture or inflammation. In neuropathic pain, injured or dysfunctional nerves can generate abnormal electrical activity and can transmit signals inappropriately.
The resulting sensations may include burning, shooting, stabbing, electric-shock-like or searing pain, as well as tingling, pins and needles or abnormal sensitivity. A person can experience both neuropathic and nociceptive pain simultaneously. For example, tissue inflammation can produce ordinary inflammatory pain while nerve injury in the same area produces a separate burning or shooting component. Understanding this distinction matters because treatments effective for nociceptive pain are not necessarily effective for neuropathic pain.
Peripheral nerve injury is one major mechanism. Trauma, surgery, compression, stretching or direct damage can disrupt normal nerve fibres. Entrapment disorders such as carpal tunnel syndrome compress a peripheral nerve within a confined anatomical passage and can produce pain, numbness and tingling in the nerve's distribution. Nerve roots can also become irritated or compressed by spinal disorders, including disc herniation and degenerative changes, producing radicular pain that may travel down an arm or leg.
Shingles is another important cause: reactivation of varicella-zoster virus in a sensory nerve can cause severe pain during the acute infection and, in some people, persistent post-herpetic neuralgia after the rash has resolved. The location and distribution of pain can therefore provide clues about the anatomical level at which the nervous system has been affected.
Diabetes is a particularly important systemic cause of neuropathic pain. Persistently elevated blood glucose can damage peripheral nerves and the small blood vessels that supply them, producing diabetic polyneuropathy. Pain commonly begins in the feet and may eventually involve the lower legs and hands in a length-dependent pattern. Other metabolic and nutritional disorders can also contribute. Vitamin B12 deficiency can impair normal neurological function, while thyroid, kidney and liver disorders may be associated with peripheral nerve dysfunction. Alcohol-related nerve damage can result from chronic excessive consumption and may coexist with nutritional deficiency. In each case, the mechanism is not identical, so identifying the systemic disorder is important rather than treating the pain as an isolated symptom.
Immune-mediated and inflammatory diseases can cause neuropathic pain by damaging nerves directly or by disrupting their blood supply. Conditions such as vasculitis can inflame blood vessels supplying nerves, producing nerve injury. Autoimmune disorders including rheumatoid arthritis, lupus, Sjögren's syndrome and coeliac disease can be associated with peripheral neuropathy. Certain infections can damage nerves or provoke inflammatory responses, including shingles, Lyme disease and HIV.
Some cancers can cause neuropathy directly through tumour involvement or indirectly through immune mechanisms, nutritional effects or treatment. Paraneoplastic neurological syndromes are uncommon disorders in which an immune response associated with cancer attacks nervous-system structures. Consequently, new unexplained neuropathic pain, particularly when accompanied by weakness, sensory loss or systemic symptoms, may require investigation for an underlying systemic disorder.
Medicines and toxic exposures are another important category of causes. Several chemotherapy agents can damage peripheral nerves, producing chemotherapy-induced peripheral neuropathy. Some medicines used for prolonged periods, including certain antibiotics and anticonvulsants, can also cause peripheral nerve injury in susceptible individuals. Toxic substances such as arsenic, lead and mercury can damage nerves. The probability and severity of drug-induced neuropathy depend on the particular substance, dose, duration, cumulative exposure and individual susceptibility.
Clinicians therefore consider medication history and occupational or environmental exposure when investigating unexplained neuropathic pain. If a medicine is suspected, it should not simply be stopped independently when it is medically necessary; the potential cause must be considered alongside the benefits of treatment and alternatives by an appropriate clinician.
Neuropathic pain can also arise from disorders of the central nervous system rather than peripheral nerves. Multiple sclerosis can damage myelin and neural pathways in the brain and spinal cord, producing abnormal sensory signals and pain in some people. Spinal cord injury, stroke and certain brain disorders can produce central neuropathic pain when pathways involved in sensory processing are damaged.
Central sensitisation can additionally increase the responsiveness of pain-processing systems, although the precise mechanisms differ among disorders and not every person with chronic pain has neuropathic pain. Phantom limb pain is another distinctive example in which pain is perceived in a body part that has been amputated; changes in peripheral nerves, spinal processing and brain networks can all contribute. These examples demonstrate that neuropathic pain is a mechanism rather than a single disease.
The character of nerve pain is often diagnostically informative, but symptoms alone cannot reliably establish a cause. Burning, shooting or electric-shock sensations, pins and needles, numbness and pain caused by normally harmless touch are characteristic features of neuropathic sensory dysfunction. Allodynia describes pain provoked by a stimulus that is normally non-painful, while hyperalgesia describes an exaggerated response to a normally painful stimulus.
A person may also experience sensory loss in the same region as severe pain, because damaged nerves can simultaneously fail to transmit ordinary information and generate abnormal signals. Clinical assessment commonly examines sensation, reflexes, muscle strength and the distribution of symptoms. Investigations then depend on the suspected cause and may include glucose testing, vitamin levels, thyroid assessment, nerve conduction studies, imaging or tests for inflammatory, infectious or autoimmune disease.
Treatment depends on the cause and on the nature of the pain. Correcting an underlying metabolic deficiency, treating diabetes, addressing an infection, reducing toxic exposure or treating an inflammatory disorder may prevent further nerve damage. Neuropathic pain itself may respond to medicines specifically used for neuropathic pain, whereas ordinary painkillers can be less effective.
Non-drug approaches can include physiotherapy, occupational strategies, exercise adapted to ability, psychological approaches to chronic pain management and measures that reduce injury risk when sensation is impaired. Persistent nerve pain should not automatically be attributed to stress, ageing or a previous injury without assessment, particularly when accompanied by progressive weakness, loss of sensation, balance problems or bladder and bowel changes. The prognosis varies widely: some nerve injuries recover when the cause is removed, whereas severe axonal damage may be permanent.
