Guillain–Barré syndrome and CIDP

Lesion

After an infection, antibodies and T cells attack nerve roots: weakness climbs over days (Guillain-Barré). A slower form relapses for months (CIDP).

Updated Nov 12, 2026

What it is

Guillain–Barré syndrome is an acute, immune-mediated polyradiculoneuropathy and the commonest cause of acute flaccid paralysis now that polio is rare. It usually follows an infection (Campylobacter jejuni, CMV, EBV, Mycoplasma, influenza, Zika) by one to three weeks. In the demyelinating form, T cells and macrophages strip myelin from roots and nerves; in the axonal forms, antibodies against gangliosides such as GM1 attack the axolemma at the nodes. The Miller Fisher variant has anti-GQ1b antibodies. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) evolves over more than two months, relapses or progresses and responds to steroids.

Structure

Endoneurial and perivenular infiltrates of lymphocytes and macrophages, most marked in roots and proximal nerves.
Macrophages penetrate the Schwann cell basement membrane and strip myelin lamellae from intact axons (segmental demyelination).
In axonal forms, antibody and complement at the nodes of Ranvier lead to axonal degeneration with little inflammation.
CIDP: inflammation with demyelination and remyelination, onion bulbs and enlarged roots on MRI.

Step by step

An infection or, rarely, vaccination exposes antigens that resemble nerve gangliosides or myelin proteins.
Cross-reactive antibodies and T cells form (molecular mimicry).
Antibodies bind gangliosides at nodes and paranodes and fix complement; macrophages are recruited.
Macrophages strip myelin or the node is damaged, and conduction blocks in roots and nerves.
Weakness peaks within four weeks; remyelination over weeks to months brings recovery, slower if axons were lost.

Acute vs chronic immune demyelinating neuropathy

Feature	Guillain–Barré syndrome	CIDP
Onset to peak	Days to four weeks	Over more than eight weeks
Course	Monophasic, recovers	Relapsing or progressive
Preceding infection	Common	Uncommon
Respiratory failure	Up to about a quarter need ventilation	Rare
Treatment	IVIG or plasma exchange; steroids do not help	Steroids, IVIG or plasma exchange
Biopsy	Inflammation, acute demyelination	Onion bulbs, chronic demyelination

Clinical notes

Respiratory failure and autonomic instability (arrhythmias, blood pressure swings) cause most deaths; vital capacity is monitored.
Treatment with intravenous immunoglobulin or plasma exchange shortens the illness.
Recovery takes weeks to months; a minority keep disability.

In the lab

CSF: high protein, normal cell count (cells raise the possibility of HIV, Lyme or lymphoma).
Anti-GQ1b antibodies in Miller Fisher syndrome; anti-GM1 in axonal forms.

Test yourself

Think of the answer, then tap the question to see it.

What is albuminocytologic dissociation?

High CSF protein with a normal cell count, typical of Guillain-Barré syndrome.

Which bacterium is most linked to Guillain-Barré, and by what mechanism?

Campylobacter jejuni, through molecular mimicry with nerve gangliosides.

Which antibody is linked to the Miller Fisher variant?

Anti-GQ1b.

What separates CIDP from GBS in time course?

CIDP progresses for more than eight weeks or relapses; GBS peaks within four weeks.

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Elsewhere in DurgiPedia

Connections

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: Guillain-Barre Syndrome (StatPearls (NCBI Bookshelf), 2025); Zika virus disease, microcephaly and Guillain-Barré syndrome in Colombia: epidemiological situation during 21 months of the Zika virus outbreak, 2015-2017 (Archives of public health, 2025).

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Representative model, for educational purposes only.