MS vs GBS vs CIDP — the myelin is leaving, but the pattern tells you who's stealing it and where
Three diseases that strip myelin. Three completely different patterns. The trick is knowing where (CNS vs PNS), how fast (acute vs chronic), and which direction the damage goes.
CNS only — brain and spinal cord. Never touches peripheral nerves.
Relapsing-remitting (85%) — episodes come and go, separated by time. Dissemination in time AND space is the diagnostic requirement. 🔑 Multiple Sclerosis = Multiple Spots, Multiple times. If it only happened once or in one place, it's not MS.
Oligoclonal bands (IgG) present in CSF but NOT serum. Normal glucose, mildly elevated protein.
Periventricular white matter plaques — perpendicular to ventricles (Dawson fingersNamed after James Walker Dawson. The plaques form around the small veins that run perpendicular to the ventricles — so the lesions follow the veins and appear as "fingers" radiating outward. Pathognomonic for MS on MRI.). Enhancing = active. Non-enhancing = old.
Acute flare: IV methylprednisolone. Disease-modifying: interferon-beta, natalizumab, ocrelizumab, fingolimod.
PNS only — peripheral nerves and nerve roots. Never the brain.
Acute ascending paralysis — starts in the feet, climbs up over days to weeks. Symmetric weakness that ascends is the giveaway. 🔑 GBS = Goes Bottom-up, Symmetric. Starts at the feet, climbs. If it starts in the face or one side, think something else.
Albuminocytologic dissociation — elevated protein with NORMAL cell count. Protein is up because inflamed nerve roots leak protein into CSF. Cells stay normal because the immune attack is in the peripheral nerves, not the CSF space itself.
Respiratory failure. Monitor FVCForced Vital Capacity — the total volume of air you can forcefully exhale. In GBS, you monitor FVC every 4-6 hours. If it drops below 20 mL/kg (or 1 liter in an average adult), intubate. Don't wait for the patient to look like they're struggling — by then it's too late. every 4-6 hours. Intubate if FVC < 20 mL/kg.
IVIG or plasmapheresis. NOT steroids (they don't help GBS — boards loves this trap).
PNS only — same as GBS, different timeline.
Chronic and progressive — symptoms develop over >8 weeks (vs GBS which peaks in 4 weeks). Think of CIDP as "chronic GBS" — same location, slower burn.
Same as GBS: albuminocytologic dissociation
Timeline. GBS = acute (peaks <4 weeks). CIDP = chronic (>8 weeks). Same CSF, same nerve damage location, different speed.
IVIG, plasmapheresis, AND steroids work here (unlike GBS). The chronic nature means the immune process responds to chronic immunosuppression.
| MS | GBS | CIDP | |
|---|---|---|---|
| Location | CNS (brain + cord) | PNS (peripheral nerves) | PNS (peripheral nerves) |
| Timeline | Relapsing-remitting (years) | Acute (days to 4 weeks) | Chronic (>8 weeks) |
| Reflexes | Hyperreflexia (UMN) | Areflexia (LMN) | Areflexia (LMN) |
| CSF | Oligoclonal bands | High protein, normal cells | High protein, normal cells |
| Imaging | Brain MRI: white matter plaques | Nerve conduction: demyelination | Nerve conduction: demyelination |
| Steroids help? | Yes (acute flares) | NO | Yes |
| Trigger | Autoimmune (HLA-DR2) | Post-infectious (C. jejuni, CMV) | Autoimmune (often idiopathic) |
The classic. Attacks come, damage happens, symptoms partially or fully recover, then another attack months or years later. Most patients start here.
Starts as RRMS, then transitions to steady decline without clear relapses. Most untreated RRMS patients convert to SPMS within 10-15 years. The relapses stop but the disability doesn't.
Progressive decline from the start. No relapses. No remissions. Just a steady downhill. More common in older males (MS overall is more common in young women). Treated with ocrelizumab.
Neuromyelitis optica (NMO / Devic disease)Previously called Devic disease. An autoimmune attack on aquaporin-4 water channels, primarily in the optic nerves and spinal cord. It was once thought to be a variant of MS — it's not. Completely different antibody, different treatment, different prognosis. looks like MS but it's a different disease with a different antibody and a different prognosis. Boards will try to trick you.
| MS | NMO | |
|---|---|---|
| Antibody | Oligoclonal bands (CSF) | Anti-aquaporin-4 (AQP4) |
| Optic neuritis | Usually unilateral | Often bilateral, more severe |
| Spinal cord | Short lesions (<3 segments) | Longitudinally extensive (≥3 segments) |
| Brain MRI | Periventricular plaques | Often normal (or atypical lesions) |
| Demographics | Young white women | More common in non-white populations |
| Treatment | Interferon-beta, natalizumab | Rituximab, eculizumab (interferon-beta can WORSEN NMO) |
The GBS variant boards loves most. Classic triad:
Associated with anti-GQ1b antibodies. It's "GBS that starts at the top instead of the bottom."
AIDP (acute inflammatory demyelinating polyneuropathy) = the classic form. Demyelination. Slowed conduction velocity on nerve studies.
AMAN (acute motor axonal neuropathy) = axonal variant. Motor only. More common with Campylobacter. Anti-GM1 and anti-GD1a antibodies.
AMSAN = axonal variant with sensory AND motor involvement. Worst prognosis.
Each scenario gives you clues one at a time. Eliminate the wrong diagnoses as you go.