22 Sept 2026 · Case #017

Guillain-Barré syndrome (GBS)

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Diagnosis

Guillain-Barré syndrome (GBS)

First-line treatment

IVIG (or plasma exchange)

How the diagnosis is reached

An ascending, symmetric, areflexic flaccid weakness developing over days after a diarrheal illness is the classic presentation of Guillain-Barré syndrome, most often triggered by Campylobacter jejuni through molecular mimicry between bacterial lipo-oligosaccharide and peripheral nerve gangliosides. The examination findings do the diagnostic work: global areflexia with flexor plantars and no sensory level argues against a spinal cord lesion such as transverse myelitis or compression, and preserved bladder function points the same way. Normal pupils, full eye movements and no fatigability argue against botulism and myasthenia gravis respectively. CSF showing markedly raised protein with a normal cell count, albuminocytologic dissociation, is characteristic, though it is often normal in the first week, so a normal early result does not exclude the diagnosis. Nerve conduction studies confirm a demyelinating process with conduction block and absent F waves, the latter reflecting proximal root involvement. The single most important management point is respiratory: the falling forced vital capacity is the reason this patient needs a monitored bed, since neuromuscular respiratory failure develops before hypoxia appears on pulse oximetry, and waiting for desaturation means intubating a patient in extremis. Treatment is IVIG or plasma exchange, equally effective, with nothing gained by combining them; IVIG is usually chosen on practical grounds and given over five days. Corticosteroids, notably, do not help in GBS. None of that addresses tonight, though. Elective intubation is indicated once the FVC falls to roughly 20 mL/kg, around 1.4 L in a man of his size, and at 1.9 L losing half a litre every eight hours he will reach it before morning.

Key clinical clues

The case in full

1

Presenting complaint

Patient history

A 34-year-old man has five days of progressive leg weakness that began on stairs and ascended to his thighs; since this morning he has been dropping objects. He has tingling in both feet but no numbness he can map. Three weeks ago he had bloody diarrhea after a barbecue.

2

Neurological examination

Physical examination

There is symmetric flaccid weakness, worse proximally in the legs (3/5) than the arms (4/5). Reflexes are absent throughout, plantars flexor. Sensation is preserved with no sensory level, bladder and bowel normal, pupils and eye movements unaffected.

3

Bedside respiratory monitoring

Laboratory results

Forced vital capacity is measured at the bedside on admission and repeated four-hourly. Predicted normal for his height is 4.8 L.

Measurements
ParameterValue
FVC on admission3.1 LRef ≈4.8 predicted
FVC at 8 hours2.4 LRef ≈4.8 predicted
FVC at 16 hours1.9 LRef ≈4.8 predicted
Single breath count18Ref >25
SpO₂ (room air)97 %Ref 95–100
Forced vital capacity (L)
12.253.520 mL/kg0 h4 h8 h12 h16 h
4

Cerebrospinal fluid analysis

Laboratory results

A lumbar puncture is performed on day six of symptoms.

Measurements
ParameterValue
CSF protein1.4 g/LRef 0.15–0.45
CSF white cells2 /µLRef 0–5
CSF glucose3.6 mmol/LRef 2.2–3.9
CSF opening pressure16 cmH₂ORef 10–20
Gram stain and cultureNegativeRef Negative
5

Neuroimaging

Imaging

MRI of the whole spine with contrast shows no cord compression, no intramedullary signal change, and no demyelinating plaques. There is subtle enhancement of the cauda equina nerve roots. MRI of the brain is normal.

6

Nerve conduction studies

Clinical course

Electrophysiology shows prolonged distal motor latencies, partial conduction block, temporal dispersion and absent F waves in both legs. Sensory conduction is relatively preserved, sparing the sural nerve. Serology is positive for recent Campylobacter jejuni.