Specialised nerve conduction studies for inflammatory neuropathy — Dr Ron Granot, FRACP, Bondi Junction. Same-day reports.
Phone (02) 9388 0615If you or your patient cannot walk independently, has shortness of breath, has weakness progressing within hours rather than days, or has bulbar symptoms (difficulty swallowing or speaking), attend the nearest Emergency Department or call 000. Suspected GBS in a deteriorating patient requires hospital admission for respiratory monitoring and immediate treatment — not outpatient testing.
Outpatient nerve conduction studies are appropriate for stable, ambulant patients where the diagnosis is uncertain, and for monitoring of established CIDP.
Inflammatory neuropathies are autoimmune disorders in which the immune system attacks peripheral nerves. The two best-recognised forms are:
Guillain-Barré syndrome. Develops over days to four weeks, often after a recent infection. Usually monophasic — patients deteriorate, reach a nadir, and recover (with treatment). Most common cause of acute flaccid paralysis in adults.
Chronic inflammatory demyelinating polyneuropathy. Develops over more than eight weeks. Runs a progressive or relapsing course. Requires long-term treatment (IVIG, plasma exchange, corticosteroids).
Multifocal motor neuropathy. Asymmetric motor weakness without sensory involvement. Often mistaken for motor neurone disease early. NCS shows characteristic conduction block.
Miller Fisher syndrome (ophthalmoplegia, ataxia, areflexia), MADSAM (multifocal acquired demyelinating sensory and motor neuropathy), DADS (distal acquired demyelinating symmetric neuropathy). NCS phenotype guides classification and treatment.
Progressively unsteady gait, weakness rising from a chair or climbing stairs.
Grip weakening, dropping objects, difficulty with buttons or keys.
Numbness, tingling or unsteadiness, often more prominent in CIDP than in pure MMN.
Ankle and knee reflexes typically lost early — a critical clinical finding that distinguishes inflammatory neuropathy from many alternatives.
Swallowing difficulty, slurred speech, or facial weakness — features of more severe or atypical GBS. Requires emergency assessment.
GBS commonly follows a recent viral or bacterial infection (Campylobacter, CMV, EBV, hepatitis), surgery, or rarely vaccination. CIDP rarely has a clear trigger.
Inflammatory neuropathies produce characteristic findings that distinguish them from axonal neuropathies (e.g. diabetic) — the difference matters because demyelinating neuropathies often respond well to immunomodulatory treatment.
| Feature | Demyelinating (GBS / CIDP) | Axonal neuropathy |
|---|---|---|
| Conduction velocity | Markedly slowed (often <75% of normal) | Normal or mildly reduced |
| Distal motor latency | Prolonged | Normal |
| F-waves | Prolonged or absent (early sign in GBS) | Normal |
| Conduction block | Present | Absent |
| Temporal dispersion | Present | Absent |
| CMAP amplitude | Variable, may be reduced | Reduced (primary finding) |
| Treatment response | IVIG, plasma exchange (CIDP also corticosteroids) | Treat underlying cause |
Dr Granot reviews the symptom timeline, examines for reflex changes and weakness pattern, and assesses whether outpatient testing is appropriate or hospital referral is needed.
Motor and sensory studies in multiple nerves of upper and lower limbs. F-wave studies to detect proximal demyelination — particularly important in early GBS where peripheral findings may still be mild.
Sampling of selected muscles to assess for active denervation (axonal involvement), motor unit recruitment, and chronicity. Adds important prognostic information.
Findings discussed immediately, classification (demyelinating vs axonal, GBS vs CIDP) explained. Formal report to your referring doctor the same day. Direct phone discussion for urgent or complex cases.
Phone the rooms to discuss timing • Same-day reports • Direct neurologist line for urgent cases
Call (02) 9388 0615