In Spain, neuropathic Pain is managed by pain medicine & palliative cares. Neuropathic pain is chronic pain caused by damage or disease of the somatosensory nervous system itself, rather than ongoing tissue injury. It affects an estimated 7-10% of the general population, with diabetic peripheral neuropathy, postherpetic neuralgia, sciatica, post-stroke central pain, and chemotherapy-induced neuropathy accounting for most cases.
Neuropathic pain (ICD-10: G89.4 chronic pain syndrome; G62.9 polyneuropathy, unspecified; G63 polyneuropathy in diseases classified elsewhere) is defined by the International Association for the Study of Pain (IASP, 2017) as pain caused by a lesion or disease of the somatosensory nervous system. The lesion can sit anywhere along the pain pathway — peripheral nerve, dorsal root ganglion, spinal cord, brainstem, thalamus, or cortex — and produces aberrant signalling rather than appropriate detection of tissue damage. Pathophysiology involves peripheral sensitisation through ectopic firing of injured axons and dorsal root ganglion neurons, upregulation of sodium channels Nav1.7 and Nav1.8, microglial activation in the dorsal horn, central sensitisation via NMDA-receptor potentiation, and loss of descending inhibitory control from brainstem nuclei. The 2015 NeuPSIG grading algorithm (Finnerup, Lancet Neurology) classifies a patient as having possible, probable, or definite neuropathic pain based on pain distribution in a plausible neuroanatomical territory, a relevant lesion on history, sensory signs on examination, and confirmatory testing.
The key symptoms of Neuropathic Pain are: Constant or near-constant burning pain in the affected territory, often worst at night and interfering with sleep — described by patients as 'on fire' or 'sunburned from the inside'., Brief, paroxysmal electric-shock-like or shooting pains lasting seconds, occurring spontaneously or triggered by minor stimuli such as touch or movement., Allodynia — pain provoked by stimuli that should not be painful, such as the brush of clothing, a bedsheet, or a light breeze across the skin., Hyperalgesia — disproportionately severe pain to mildly painful stimuli, such as a pinprick feeling like a deep stab., Numbness, hypoesthesia, or 'wooden' sensation coexisting with the pain in the same area, with the paradoxical pattern of feeling both numb and intensely painful at once., Tingling, pins-and-needles, or crawling sensations (paresthesia) and unpleasant abnormal sensations (dysesthesia) such as ants under the skin., Symmetric distal distribution in length-dependent neuropathies — beginning in the toes and progressing upward in a stocking pattern, later involving the fingertips in a glove pattern..
Diagnosis of neuropathic pain is primarily clinical, anchored on the 2015 NeuPSIG grading algorithm (Finnerup, Lancet Neurology). The clinician first establishes whether the pain has a plausible neuroanatomical distribution — does the territory correspond to a peripheral nerve, dermatome, plexus, spinal cord level, or central pathway. Step two is a history of a relevant lesion or disease that can explain the distribution, such as long-standing diabetes, a previous shingles rash, a known disc herniation, a stroke, or recent neurotoxic chemotherapy. Step three is a focused sensory examination — testing for hypoesthesia and hyperalgesia with pinprick, allodynia with a soft brush, thermal hypoesthesia with warm and cool objects, and vibration loss with a 128 Hz tuning fork. Reflex changes and motor signs are documented when present. Confirmatory testing depends on the suspected lesion. Nerve conduction studies and electromyography document large-fibre neuropathy and localise mononeuropathies and radiculopathies but are normal in pure small-fibre disease. Skin biopsy for intraepidermal nerve fibre density confirms small-fibre neuropathy. MRI defines structural lesions of brain, spinal cord, and roots. Quantitative sensory testing has a research role and helps phenotype patients for trial enrolment. Validated screening tools — the painDETECT, DN4, and LANSS questionnaires — distinguish neuropathic from nociceptive pain in primary care with sensitivities of 80-85%. Three certainty levels emerge from this workflow: possible (criteria 1-2 met), probable (criteria 1-3 met), and definite (criteria 1-4 met, with confirmatory testing). Most treatment guidelines apply once probable status is reached.
Pain medicine specialist referral is warranted when two or more first-line agents at adequate dose and duration have failed, when an interventional option such as a nerve block or spinal cord stimulator is being considered, when pain involves a complex distribution (CRPS, central pain), or when high-risk medication combinations (opioids, multiple sedating agents) are being layered. A neurologist should be involved when the diagnosis is uncertain, when central nervous system disease is suspected, or when small-fibre neuropathy needs skin biopsy confirmation. Spine surgery referral is appropriate for radicular pain with progressive neurological deficit or imaging-concordant compressive lesions.
Find specialists →Pharmacotherapy effects take time to assess. Gabapentin and pregabalin show benefit within 1-2 weeks of reaching an adequate dose. Duloxetine and tricyclic antidepressants typically need 4-6 weeks at target dose for full analgesic effect. Topical 5% lidocaine produces relief within hours but plateaus over days. A single 8% capsaicin application produces stable analgesia from week 2 through week 12 in responders. Spinal cord stimulator trials are usually 5-7 days; permanent implants show stable response by 3 months. Following recommended care, expect the first meaningful improvement at 2-6 weeks and a realistic stable endpoint at 3-6 months; treatment then continues to maintain that response.
Look for fellowship training in pain medicine, board certification, and access to image-guided injection, neuromodulation, and a structured multidisciplinary pain programme that includes a clinical psychologist and physical therapist. Ask whether the clinic uses validated outcome measures (Brief Pain Inventory, neuropathic pain scale, PROMIS) and follows current guidelines rather than defaulting to opioid prescribing. Continuity matters — neuropathic pain is a long-term condition managed over years, and abrupt provider changes degrade outcomes.
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Long-term outlook depends heavily on the underlying cause and how quickly effective treatment begins. Postherpetic neuralgia improves in roughly 50% of patients within 12 months even without intervention, with a smaller fraction having persistent pain at 5 years. Diabetic peripheral neuropathy progresses slowly when glycaemic control is poor and stabilises in many patients with tight control plus first-line pharmacotherapy. Radicular pain from disc herniation resolves in roughly 70% of patients within 6-12 weeks of conservative care. Central post-stroke pain and chronic post-surgical neuropathic pain are more persistent — only about 30-40% achieve substantial long-term relief on pharmacotherapy alone, and many require neuromodulation. Across all causes, around 30% of patients reach a 50% pain reduction on first-line monotherapy, another 20-30% improve with combination therapy, and the remainder need interventional or multidisciplinary pain programme support. Even when pain intensity is only modestly reduced, structured care improves function, sleep, mood, and quality of life — the outcomes patients value most. The single strongest predictor of a poor trajectory is delay of more than 6 months between symptom onset and the start of evidence-based treatment.
Graded aerobic exercise (walking, cycling, swimming) for 30 minutes most days plus 2 sessions of resistance training weekly improves neuropathic pain intensity, sleep, mood, and small-fibre nerve density in diabetic neuropathy. Begin at a level you can sustain without a 24-hour pain flare and progress by no more than 10% per week. For patients with significant loss of protective sensation in the feet, pool-based exercise and stationary cycling reduce ulceration risk. Stop and reassess any activity that produces sharp shooting pain, new weakness, or unsteady gait.
Medically reviewed by AIHealz Medical Editorial Board · May 12, 2026