GBS (Guillain-Barré Syndrome)

I'll assume you mean Guillain-Barré syndrome, the most common medical use of "GBS" (if you meant Group B Streptococcus instead, let me know and I'll cover that separately).

What it is

GBS is a rapidly progressive, immune-mediated acute polyneuropathy affecting the peripheral nervous system. It's one of the most common life-threatening diseases of the peripheral nerves and needs urgent recognition (Robbins & Kumar Basic Pathology, p. 809-ish; Bradley and Daroff's Neurology in Clinical Practice).

Pathophysiology

About two-thirds of cases are triggered by a preceding infection (commonly 1-3 weeks before onset) that provokes microbe-specific T cells and antibodies which cross-react with nerve sheath antigens (molecular mimicry). Both T-cell- and antibody-mediated responses are involved, with T cells thought to play the dominant role. Common triggering infections include:

Campylobacter jejuni
Epstein-Barr virus
Cytomegalovirus
HIV
Zika virus
SARS-CoV-2

The injury is most extensive in nerve roots and proximal nerve segments, with mononuclear infiltrates rich in macrophages causing multifocal inflammatory demyelination (the classic form is acute inflammatory demyelinating polyradiculoneuropathy, AIDP). Axonal variants (acute motor axonal neuropathy/AMAN, acute motor-sensory axonal neuropathy/AMSAN) also exist, where axons themselves are damaged rather than just myelin.

Robbins & Kumar Basic Pathology, p. 809
Bradley and Daroff's Neurology in Clinical Practice

Clinical features

Original 1916 description (Guillain, Barré, Strohl): motor weakness, areflexia, paresthesias with mild sensory loss, and elevated CSF protein without pleocytosis (albuminocytological dissociation).

Diagnostic criteria (required):

Progressive weakness of both legs and arms
Areflexia or hyporeflexia

Supportive features:

Progression over days to 4 weeks, then plateau, then recovery beginning 2-4 weeks after progression stops
Relative symmetry
Mild sensory symptoms
Bifacial palsies, autonomic dysfunction
Absence of fever at onset
Elevated CSF protein with <10 cells/uL
Nerve conduction slowing or block on electrodiagnostics

Symptoms typically progress ascendingly (legs then arms/trunk) over about 2 weeks, with nadir reached by 4 weeks in most patients.

Bradley and Daroff's Neurology in Clinical Practice, Box 106.10

Treatment

Plasmapheresis (plasma exchange) - removes offending antibodies
IVIG (intravenous immunoglobulin) - suppresses immune response through mechanisms not fully understood
Supportive care - critical, including ventilatory support for respiratory failure, autonomic monitoring, DVT prophylaxis
Modern critical care has cut mortality from ~33% (pre-positive-pressure-ventilation era) down to roughly 1-5% today

Most patients who survive the acute phase recover over time, though some are left with residual weakness.

Related condition

CIDP (chronic inflammatory demyelinating polyneuropathy) is immune-mediated like GBS but follows a chronic relapsing-remitting or progressive course (2+ months) rather than a monophasic one.

Recent evidence check

A 2024 systematic review found retreatment with a second IVIG cycle showed some benefit in patients who responded poorly to the initial cycle, though evidence quality was limited (PMID: 38553651). This nuances the standard single-IVIG-course approach mentioned in the textbooks above - worth discussing with a neurologist if a patient isn't responding to first-line IVIG. No findings contradict the core diagnostic or pathophysiologic picture above.

If you actually meant Group B Streptococcus (the perinatal pathogen relevant to maternal-fetal medicine and neonatal sepsis screening) or something else GBS could stand for in your context, tell me and I'll pull that up instead.

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