Synopsis
Localise peripheral nerve symptoms by fibre type and distribution, identify rapidly progressive or vasculitic emergencies, and choose focused metabolic, neurophysiological, genetic or biopsy investigation.
- Localise before listing causes: decide whether symptoms fit length-dependent polyneuropathy, focal mononeuropathy, mononeuritis multiplex, plexopathy, radiculopathy, neuromuscular junction or myopathy.
- Large-fibre loss causes vibration and joint-position impairment, sensory ataxia and reduced reflexes; small-fibre loss causes burning pain and temperature or pinprick change with preserved routine nerve conduction.
- A symmetrical stocking pattern progressing slowly from toes upward suggests length-dependent axonal polyneuropathy, commonly metabolic, toxic, nutritional or idiopathic.
- Painful, stepwise, asymmetric involvement of separate named nerves suggests mononeuritis multiplex and can represent treatable vasculitis, infection or infiltrative disease.
- Weakness with upper motor neurone signs, a sensory level or sphincter dysfunction points to spinal cord disease, while dermatomal pain and myotomal weakness suggest radiculopathy.
- Core tests commonly include FBC, renal and liver profile, glucose or HbA1c, B12, thyroid function, inflammatory markers and serum protein electrophoresis or immunoglobulins, adjusted to history.
- Nerve-conduction studies and EMG classify axonal versus demyelinating, sensory versus motor and focal versus diffuse disease but can be normal in pure small-fibre neuropathy.
- Ask about alcohol, chemotherapy, metronidazole, nitrofurantoin, amiodarone, excess vitamin B6, occupational toxins, bariatric surgery, vegan diet and family foot deformity.
- Do not treat a neuropathic pain score alone: protect insensate feet, address falls and weakness, remove the cause where possible and select analgesia by function and adverse effects.
Key red flags
Prominent weakness, diffuse areflexia and neurophysiological slowing, conduction block or temporal dispersion raises acquired or hereditary demyelinating neuropathy.
Painful acute or subacute deficits in separate individual nerves, such as foot drop followed by wrist drop, suggest vasculitic or infiltrative nerve injury.
Hyperreflexia, extensor plantar response, sensory level, new bladder dysfunction or saddle anaesthesia shifts localisation to cord or cauda equina and changes urgency.
Investigation priorities
Map modalities, weakness and reflexes to a fibre type, nerve, root, plexus or length-dependent distribution.
Management branches
Numbness, pain, weakness or imbalance could arise from peripheral nerve disease.
- Define onset, tempo, symmetry, proximal versus distal distribution, pain, autonomic symptoms and exposure or family history.
- Map pinprick, temperature, vibration, joint position, power and reflexes, while checking gait, cranial nerves and central long-tract signs.
- Classify length-dependent, focal nerve, multiple nerve, root, plexus, small-fibre, motor-predominant or demyelinating phenotype before ordering tests.
- Escalate immediately for respiratory, bulbar, sphincter, rapidly progressive motor or painful asymmetric vasculitic patterns.
A stable peripheral neuropathy pattern is established without an emergency.
- Review diabetes, alcohol, diet, surgery, cancer treatment, infection, systemic autoimmunity, renal disease and a complete medicine and supplement list.
- Order core metabolic, haematological, thyroid, nutritional and paraprotein testing, adding infection or autoimmune assays only where pre-test probability supports them.
- Refer for nerve-conduction and EMG assessment when weakness, atypical distribution, progression or diagnostic uncertainty will change management.
- Use imaging, small-fibre testing, genetics or biopsy only after the remaining anatomical and causal question is explicit.