What is chronic pain?
The three pain mechanisms — nociceptive, neuropathic, nociplastic — and why the distinction drives treatment.
Nerve pain has a distinctive voice — burning, electric, shooting — and a distinctive cause: the wiring that carries sensation is itself damaged. That makes it different from other chronic pain. But even here, the pain system's sensitivity shapes how much you suffer, and that part is trainable.
What is neuropathic pain?
Neuropathic pain is pain caused by damage or disease of the nerves themselves — the somatosensory nervous system. It often feels burning, electric, or shooting, and even light touch can hurt. Common causes include diabetic neuropathy, shingles, nerve compression, and chemotherapy. Treatment combines nerve-targeted medications with graded activity and brain-based retraining, because the pain system itself usually becomes sensitized over time.
That two-part picture — a genuine nerve problem plus an amplifying pain system — explains why purely peripheral treatments often underdeliver, and why layered care works better.
Most pain begins with nociceptors — sensory endings reporting genuine or threatened tissue trouble. Neuropathic pain is different: it arises when the reporting system itself is damaged or diseased. The formal definition is pain caused by a lesion or disease of the somatosensory nervous system — the network that carries touch, temperature, and pain signals from body to brain.
A damaged nerve doesn't go quiet; it misfires. That produces a characteristic set of experiences:
Two features help distinguish it from other pain: it usually follows the territory of a specific nerve or nerve pattern (a stocking-and-glove distribution in the feet and hands, one side of the chest, one leg below the knee), and it often pairs pain with sensory loss — the same region can be both numb and painful.
Anything that damages sensory nerves — from bloodstream to spinal cord to brain — can cause it. The most common culprits:
Identifying the cause matters because some are treatable at the source — better glucose control slows diabetic neuropathy, decompression can relieve a trapped nerve root, and phantom limb pain responds to feedback-based retraining designed for it specifically.
Modern pain medicine distinguishes three mechanisms, and neuropathic pain occupies a distinctive position among them: it's the category with the clearest physical driver.
| Mechanism | What's driving the pain | Feels like | Examples |
|---|---|---|---|
| Nociceptive | Ongoing tissue damage or inflammation, reported by healthy nerves | Aching, throbbing, worse with use of the damaged part | Rheumatoid arthritis, advanced osteoarthritis |
| Neuropathic | Damage or disease of the nerves themselves | Burning, electric, shooting; numbness and allodynia in a nerve's territory | Diabetic neuropathy, post-herpetic neuralgia, true sciatica |
| Nociplastic (neuroplastic) | A sensitized pain system with no matching tissue or nerve damage | Widespread or moving pain that flares with stress and varies day to day | Fibromyalgia, most chronic back and neck pain |
The crucial caveat: these mechanisms mix. When a nerve misfires for months or years, the spinal cord and brain typically adapt by amplifying — central sensitization layers a nociplastic component on top of the neuropathic one. Pain that spreads beyond the nerve's territory, tracks stress and sleep, or persists after the nerve problem is fixed is telling you the amplifier is now part of the story.
This layering is why purely peripheral treatments — nerve blocks, decompression surgery, medications aimed only at the damaged nerve — often underdeliver in long-standing neuropathic pain. Treating the nerve without turning down the amplifier addresses only half the circuit.
Neuropathic pain is one area where specific medications have solid trial evidence — a contrast with nociplastic pain, where drugs generally perform poorly. Guidelines consistently recommend three first-line classes:
Honest expectations matter. Average effects are modest: in trials, these drugs help a minority of patients substantially while many get partial or no relief, and side effects like drowsiness or dizziness are common. The practical approach is a systematic trial — one medication at a time, adequate dose, several weeks, tracked against your goals — done entirely in partnership with your prescriber. Never start, stop, or adjust doses on your own. Second-line options (topical lidocaine or capsaicin, and others) exist when first-line drugs fall short; long-term opioids are discouraged for chronic neuropathic pain. See our guide to non-opioid treatment options.
Because medications help only modestly on average, non-drug care isn't an afterthought in neuropathic pain — it's the other half of treatment, and it targets the amplification the drugs don't reach.
Good care also means tracking what matters. A simple record of pain intensity and function — see our guide to the chronic pain scale — makes medication trials and activity progress measurable instead of guesswork, and our guide to living with chronic pain covers the daily-life side: sleep, pacing, and flare planning.
Most neuropathic pain warrants a timely — not emergency — medical evaluation to identify the cause. But some patterns need urgent attention:
If red flags are absent, the right path is an unhurried work-up with your clinician: an exam mapping the affected territory, targeted tests where they'll change management, and a treatment plan that addresses both the nerve and the pain system around it.
M79.2 covers neuralgia and neuritis, unspecified — but cause-specific codes are usually preferred where the cause is known.
Common ones: E11.42 for type 2 diabetic polyneuropathy, B02.29 for post-herpetic neuralgia, G50.0 for trigeminal neuralgia, G54.6 for phantom limb pain with pain, and G89.4 where chronic pain syndrome is also documented. Coding is your clinician's call.
Clues include burning, electric, or shooting qualities; pins and needles or numbness in the same region; pain from light touch; and a distribution matching a nerve's territory — both feet in a stocking pattern, one band of the chest, one leg below the knee. Clinicians confirm the picture with a sensory exam and sometimes screening questionnaires or nerve tests. Aching pain that moves around the body and tracks stress points instead toward a nociplastic mechanism.
True sciatica — a compressed or inflamed nerve root sending pain, tingling, or numbness down the leg in that root's territory — is neuropathic. But much leg pain labeled 'sciatica' is actually referred pain from back structures or a sensitized pain system, without real nerve root involvement. The distinction matters because true radicular pain sometimes benefits from targeted interventions, while most chronic back-and-leg pain responds better to movement and retraining.
No. They're first-line for neuropathic pain and genuinely help some people, but average effects are modest, many patients get little relief, and side effects like drowsiness, dizziness, and weight gain are common. They also tend to work poorly for pain that isn't truly neuropathic, which is one reason a correct mechanism diagnosis matters. Whether to try one — and when to stop an unhelpful trial — is a decision to make with your prescriber.
Often, partially — peripheral nerves can regrow slowly, over months to years, especially when the cause is removed: blood sugar controlled, a compression relieved, a neurotoxic drug finished. Some damage is permanent. Importantly, pain relief doesn't require full nerve healing: calming the misfiring, strengthening descending inhibition, and de-amplifying the central pain system can all reduce pain even while the nerve remains imperfect.
Two common reasons. First, nerves injured long enough can keep misfiring even after decompression — the wiring itself was changed. Second, months of pain typically sensitize the spinal cord and brain, so the central pain system continues generating pain after the peripheral trigger is gone. That second, centralized component is real, common, and treatable — with the retraining approaches covered in our chronic pain treatment guide.
It can help with the part of the problem that lives centrally. Brain-retraining approaches don't repair a damaged nerve, and no honest program claims they do. But because long-standing neuropathic pain almost always includes central amplification — and because fear, guarding, and disuse feed that amplification — approaches like VR embodiment training and graded activity target a component that nerve-focused treatment leaves untouched. Ask a pain clinician whether your picture includes that centralized layer.
Not necessarily. Some causes resolve substantially — post-herpetic neuralgia often fades over months to a couple of years, chemotherapy neuropathy frequently improves after treatment ends, and compressed nerves can recover once freed. Even when a nerve problem persists, pain levels are not fixed: systematic medication trials, graded activity, and treatment of the centralized component regularly move people from disabling pain to manageable background noise.
Talk with our care team about your pain, your history, and whether KVET™ is right for you — free, and from the comfort of home.