Nerve Pain (Neuropathic Pain) — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Neuropathic pain (nerve pain) is defined as pain arising as a direct consequence of a lesion or disease affecting the somatosensory nervous system — either the peripheral nervous system (peripheral neuropathic pain) or the central nervous system (central neuropathic pain). It is fundamentally different from nociceptive pain (pain caused by tissue injury, inflammation, or mechanical stimuli) — neuropathic pain persists after the initiating injury has healed, is driven by abnormal nervous system signalling, and typically responds poorly to conventional analgesics such as NSAIDs and paracetamol. Neuropathic pain affects 6-8% of the general adult population, is often severe and chronic, and profoundly impacts quality of life, sleep, and mental health. Common descriptors include burning, shooting, electric shock-like, stabbing, and tingling pain. The hallmark clinical features are allodynia (pain from a normally non-painful stimulus, such as light touch or clothing) and hyperalgesia (exaggerated pain from a mildly painful stimulus).

Peripheral neuropathic pain causes: Diabetic peripheral neuropathy (DPN) — most common globally, affecting up to 50% of diabetic patients over their lifetime; caused by metabolic damage and microvascular changes in peripheral nerves. Postherpetic neuralgia (PHN) — persistent pain after shingles (herpes zoster) reactivation along a dermatome; more common and severe with advancing age. Trigeminal neuralgia — severe paroxysmal facial pain in the trigeminal nerve distribution (typically triggered by touching the face, eating, or speaking); most common in older women; often caused by vascular compression of CN V. Chemotherapy-induced peripheral neuropathy (CIPN) — common with paclitaxel, vincristine, cisplatin, oxaliplatin. HIV sensory neuropathy. Radiculopathy from lumbar or cervical disc disease (sciatica). Carpal tunnel syndrome (median nerve entrapment). Complex Regional Pain Syndrome (CRPS). Central neuropathic pain causes: central post-stroke pain (thalamic pain), multiple sclerosis, spinal cord injury, syringomyelia, and phantom limb pain after amputation.

Neuropathic pain has distinctive characteristics that differ from musculoskeletal or inflammatory pain: quality — burning, scalding, electric-shock, shooting, stabbing, lancinating, or freezing pain; spontaneous (unprovoked) pain occurring without any stimulus; allodynia — pain evoked by gentle stimuli that are normally non-painful (light touch, temperature change, clothing contact); hyperalgesia — exaggerated, disproportionate pain from mildly painful stimuli; dysaesthesia — unpleasant abnormal sensations (crawling, tingling, itching); hypoaesthesia or anaesthesia — numbness and reduced sensation in the affected area. The combination of positive symptoms (pain, allodynia, hyperalgesia) and negative symptoms (numbness, sensory loss) in the same distribution is characteristic of neuropathic pain. Distribution: typically follows a dermatomal (shingles, radiculopathy) or stocking-and-glove (peripheral neuropathy) pattern. Sleep disruption and depression are almost universal in chronic neuropathic pain — the combination creates a vicious cycle of worsening pain and mood.

Clinical assessment using validated neuropathic pain screening tools: DN4 questionnaire (Douleur Neuropathique 4 — sensitivity 83%, specificity 90%), PainDETECT, and LANSS (Leeds Assessment of Neuropathic Symptoms and Signs). Detailed neurological examination: sensory testing (light touch, pinprick, temperature, vibration, proprioception), motor function, and reflexes to characterise the extent and pattern of neurological deficit. Quantitative Sensory Testing (QST): standardised testing of thresholds to various stimuli — detects allodynia and hyperalgesia objectively. Nerve conduction studies (NCS) and electromyography (EMG): assess peripheral nerve function — identify neuropathy type (demyelinating vs. axonal), location, and severity. Skin punch biopsy (intraepidermal nerve fibre density): highly sensitive for small fibre neuropathy — diagnoses neuropathy not detectable on standard NCS. MRI spine: identifies disc herniation, cord lesions, or spinal canal stenosis causing radiculopathy. Blood tests to identify underlying causes: HbA1c (diabetes), B12, folate, TSH, HIV, SPEP (paraprotein), renal function, liver function, autoimmune screen (ANA, ANCA, anti-ganglioside antibodies). CSF examination if inflammatory or CNS cause suspected.

NeuPSIG (International Association for the Study of Pain) and NICE guidelines recommend a stepwise approach. First-line treatments: Duloxetine (60-120mg daily) — SNRI antidepressant, particularly effective for diabetic neuropathy and chemotherapy-induced neuropathy; reduces pain by 50% in 50% of patients. Amitriptyline (10-75mg nightly) — tricyclic antidepressant; broad evidence across neuropathic pain conditions; limited by anticholinergic side effects (dry mouth, sedation, constipation). Gabapentin (900-3600mg daily in divided doses) — anticonvulsant blocking voltage-gated calcium channels; effective for PHN and DPN. Pregabalin (150-600mg daily) — similar mechanism to gabapentin; superior pharmacokinetics; licensed for DPN, PHN, and post-operative neuropathic pain. Topical treatments (limited systemic side effects — preferred in elderly): topical lidocaine 5% patches (effective for PHN); topical capsaicin 8% patch (QUTENZA — single application, pain relief up to 12 weeks; depletes substance P from nociceptors). Second-line: tramadol (opioid agonist + SNRI activity). Third-line (specialist initiation): strong opioids (morphine, oxycodone — limited long-term efficacy), tapentadol. Interventional pain management: epidural steroid injections for radiculopathy; nerve blocks; spinal cord stimulation (SCS) — highly effective for CRPS, failed back surgery syndrome, and refractory DPN; dorsal root ganglion stimulation. Trigeminal neuralgia: carbamazepine first-line (200-1200mg/day); oxcarbazepine, lamotrigine as alternatives; microvascular decompression surgery (Jannetta procedure) or gamma knife radiosurgery for refractory cases.

Chronic neuropathic pain causes extensive functional impairment beyond the pain itself. Sleep disturbance is almost universal — burning, electric-shock, or allodynic pain is frequently worse at night, severely impairing sleep quality and creating a vicious cycle where sleep deprivation amplifies pain perception and reduces pain tolerance. Psychological complications: depression affects 30–50% of patients with chronic neuropathic pain — chronic, poorly controlled pain profoundly reduces quality of life, causes social isolation, and interferes with work, relationships, and daily activities; anxiety and fear-avoidance behaviours further limit function. Diabetic peripheral neuropathy leads to loss of protective sensation in the feet — patients cannot perceive injury or pressure ulceration, leading to diabetic foot ulcers (affecting 15–25% of diabetic patients over their lifetime), Charcot neuroarthropathy, and in severe cases limb amputation (diabetes accounts for 60–70% of non-traumatic lower limb amputations). Postherpetic neuralgia (PHN) following shingles causes severe, often disabling pain lasting months to years in elderly patients — significantly impairing daily activities and causing depression. Falls: peripheral neuropathy causing lower limb numbness, ataxia, and proprioceptive loss dramatically increases fall risk in the elderly, leading to fractures, hospitalisation, and loss of independence. Medication complications from long-term treatment: amitriptyline causes anticholinergic effects (urinary retention, constipation, falls from orthostatic hypotension in elderly); gabapentinoids (gabapentin, pregabalin) cause dizziness, sedation, weight gain, and carry a recognised risk of dependence and misuse. Allodynia and hyperalgesia can develop secondary to central sensitisation, where the nervous system becomes progressively more sensitive over time without effective early treatment.

Optimal glycaemic control in diabetes (HbA1c below 53 mmol/mol / below 7%) is the single most effective measure to prevent diabetic peripheral neuropathy — reduces risk by 60% in Type 1 diabetes (DCCT trial). Shingles vaccination (Shingrix — recombinant zoster vaccine, 2 doses, over 97% efficacy) prevents varicella zoster reactivation and dramatically reduces postherpetic neuralgia incidence. Recommended for all adults aged 50+ and immunocompromised adults from 18. Regular foot inspection in diabetic patients — prevents Charcot neuroarthropathy and foot ulceration from sensory loss. Physiotherapy and graded exercise improve pain scores and function in chronic neuropathic pain conditions. Psychological therapies: cognitive-behavioural therapy (CBT) and acceptance and commitment therapy (ACT) are effective adjuncts for chronic neuropathic pain — address pain catastrophising and improve coping. Sleep hygiene measures to address insomnia associated with neuropathic pain. Transcutaneous electrical nerve stimulation (TENS) provides short-term relief in some patients.

See your GP promptly for: persistent burning, shooting, or electric-shock pain lasting more than 4 weeks, particularly if associated with numbness or tingling in a dermatomal or glove-and-stocking distribution; allodynia (pain from clothing or gentle touch); painful feet in a known diabetic patient; severe facial pain triggered by talking or chewing (possible trigeminal neuralgia — may respond well to carbamazepine). Seek urgent assessment for: sudden onset severe shooting pain down one or both legs with bladder or bowel dysfunction, or saddle anaesthesia (numbness around the perineum) — these are red flags for cauda equina syndrome requiring emergency MRI and neurosurgical assessment. See a pain specialist or neurologist if first-line treatments have failed after adequate trials or if the diagnosis is uncertain.