Sensory neuropathy
Exam Tips
- In OSCEs, describe the pattern first: "symmetrical distal stocking-glove sensory loss suggests distal symmetrical polyneuropathy."
- Large-fibre clues: reduced vibration/proprioception, sensory ataxia, absent ankle jerks; small-fibre clues: burning pain/allodynia with relatively preserved reflexes and possible normal NCS.
- Always screen for common reversible causes early: HbA1c/fasting glucose, B12, and serum protein electrophoresis with immunofixation.
- Red flags for urgent specialist input: rapid progression (weeks-months), asymmetry, non-length-dependent onset (face/upper limbs early), marked motor weakness, or prominent autonomic failure.
- Diabetes exam pearl: loss of protective sensation predicts ulcer/amputation risk; demonstrate structured foot inspection and safety-net advice.
- Image reference for revision: use a peripheral nerve fibre-type schematic (small vs large fibre functions) and a stocking-glove sensory map from your neurology textbook figures.
Definition
Sensory neuropathy is a peripheral nerve disorder in which sensory fibres are damaged, causing symptoms such as numbness, tingling, burning pain, altered temperature perception, and sensory ataxia. It is commonly length-dependent (distal symmetrical polyneuropathy), so symptoms usually begin in the toes and progress proximally in a stocking-glove pattern, with small-fibre, large-fibre, or mixed involvement.
Pathophysiology
Most cases reflect axonal injury in the longest peripheral nerves ("dying-back" neuropathy), so distal symptoms appear first. Small-fibre damage (A-delta and C fibres) impairs pain/temperature and can generate spontaneous ectopic firing, producing burning pain, hyperalgesia, and allodynia; autonomic fibres may also be affected. Large-fibre damage (A-beta, heavily myelinated) disrupts vibration and proprioception, causing sensory ataxia, reduced ankle reflexes, and falls. Mechanisms vary by cause: metabolic toxicity (diabetes, uraemia), nutritional deficiency (B12 and others), immune-mediated inflammation, paraprotein-related injury, infection, toxins/drugs, and inherited channel/myelin/axonal defects (for example CMT). Central sensitisation may amplify persistent neuropathic pain even after the peripheral trigger is treated.
Risk Factors
- Diabetes mellitus and pre-diabetes
- Vitamin B12 deficiency and malnutrition (including alcohol-related deficiency states)
- Paraproteinaemia/monoclonal gammopathy
- Advancing age (higher prevalence in older adults)
- Female sex (slightly higher prevalence)
- Alcohol misuse
- Drug exposure (for example chemotherapy, metronidazole, nitrofurantoin, fluoroquinolones, phenytoin, statins, leflunomide, reverse transcriptase inhibitors)
- Toxin or occupational exposure (lead, arsenic, mercury, organophosphates, thallium, nitrous oxide, vibration/cold)
- Family history of inherited neuropathy (for example Charcot-Marie-Tooth disease)
- Systemic disease (CKD, liver disease, hypothyroidism, amyloidosis)
- Autoimmune/inflammatory disease (Sjögren syndrome, SLE, sarcoidosis, vasculitis, coeliac disease)
- Infections (HIV, hepatitis C, Lyme, VZV, HTLV-1, leprosy risk exposure)
Clinical Features
Symptoms
- Distal numbness in a stocking-glove distribution
- Paraesthesia (tingling, pins and needles, electric-shock sensations)
- Burning or shooting neuropathic pain
- Reduced temperature perception
- Hyperalgesia and/or allodynia
- Imbalance, unsteady gait, frequent trips or falls
- Possible autonomic symptoms (postural dizziness, bowel/bladder disturbance, erectile dysfunction, altered sweating) in some causes
Signs
- Symmetrical distal sensory loss (pinprick, temperature, vibration, proprioception depending on fibre type)
- Reduced or absent Achilles tendon reflexes
- Sensory ataxia (worse with eyes closed, positive Romberg)
- Mild distal weakness in advanced distal symmetrical polyneuropathy (for example toe extension or ankle dorsiflexion weakness)
- Foot deformities suggesting hereditary neuropathy (pes cavus, hammer toes)
- Skin injury/ulceration from loss of protective sensation
Investigations
Management
Lifestyle Modifications
- Treat the underlying cause early (glycaemic optimisation, alcohol reduction/cessation, toxin and neurotoxic drug review, nutritional correction)
- Daily foot care and footwear advice; prompt treatment of skin breaks to prevent ulcer/infection (especially in diabetes)
- Falls prevention: physiotherapy for balance/proprioception, strength work, home hazard reduction, mobility aids if needed
- Sleep and mental health review, with support for chronic pain impact
- Patient education on red flags (rapid progression, asymmetry, early upper-limb/face involvement, prominent autonomic symptoms) requiring urgent reassessment
- Image reference: review a "stocking-glove distribution" and diabetic foot-risk diagram in your neurology teaching atlas
Pharmacological Treatment
Tricyclic antidepressant (neuropathic pain)
- Amitriptyline 10 mg at night initially, titrate gradually (commonly to 25-75 mg at night; higher only with specialist input)
Usually first-line option for neuropathic pain if tolerated. Avoid/caution in significant cardiac conduction disease, recent MI, severe liver disease, glaucoma, urinary retention, and high anticholinergic burden; overdose is dangerous.
SNRI (neuropathic pain)
- Duloxetine 30 mg once daily initially, then 60 mg once daily (usual effective dose 60 mg/day)
Useful especially with diabetic neuropathic pain. Avoid with MAOIs and severe hepatic impairment; caution in uncontrolled hypertension, risk of serotonin syndrome, and withdrawal if stopped abruptly.
Gabapentinoid (neuropathic pain)
- Gabapentin 300 mg on day 1, 300 mg twice daily day 2, 300 mg three times daily day 3, then titrate; usual range 900-3600 mg/day in 3 divided doses
- Pregabalin 75 mg twice daily initially, increase after 3-7 days to 150 mg twice daily; max 600 mg/day in divided doses
Adjust dose in renal impairment. Counsel on dizziness, sedation, ataxia, peripheral oedema, dependence/misuse potential, and additive respiratory depression with opioids/other sedatives.
Topical options for focal peripheral neuropathic pain
- Capsaicin 0.075% cream applied 3-4 times daily
- Lidocaine 5% medicated plaster (typically up to 12 hours on, 12 hours off) in selected localised neuropathic pain under specialist/indication-specific use
Useful when pain is localised and systemic adverse effects are problematic. Capsaicin can initially worsen burning; avoid broken/inflamed skin.
Cause-specific replacement therapy
- Hydroxocobalamin 1 mg IM on alternate days for 2 weeks for B12-deficiency neuropathy, then maintenance 1 mg IM every 2-3 months if ongoing cause persists
Do not delay treatment when neurological deficits are present. Also correct contributory folate/other deficiencies once B12 treatment is started.
Surgical / Interventional
- No routine surgery for most sensory polyneuropathies
- Orthopaedic bracing/corrective foot surgery may help selected inherited neuropathies (for example CMT with deformity)
- Surgical decompression only if a coexisting focal entrapment neuropathy is clearly identified
Complications
- Chronic neuropathic pain with sleep disturbance, anxiety/depression, and reduced quality of life
- Loss of protective sensation leading to burns, trauma, retained foreign bodies, cellulitis, and severe soft-tissue infection
- Diabetic foot ulceration and increased lower-limb amputation risk
- Falls, fractures, and functional decline due to sensory ataxia
- Progressive disability in hereditary neuropathies
Prognosis
Outcome depends mainly on cause, severity, and delay before treatment. Metabolic, toxic, and deficiency-related neuropathies may stabilise or partly improve when the cause is corrected early, whereas hereditary neuropathies (for example CMT) are usually chronic and progressive. Prognosis is improved by pain control, foot protection, falls prevention, and active management of mood/sleep comorbidity.
Sources & References
🏥BMJ Best Practice(4)
✅NICE Guidelines(1)
- Sensory neuropathy[overview]