Guillain-Barré Syndrome

Pronounced GHEE-yan bar-RAY, this acute immune-mediated polyradiculoneuropathy presents with ascending weakness and requires urgent recognition and treatment.

Topic: Peripheral neuropathy Level: Intermediate Tags: GBS, acute flaccid paralysis, neuromuscular, CSF

Overview

Guillain-Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy, often post-infectious (e.g., Campylobacter jejuni, cytomegalovirus, influenza). It is the leading cause of acute flaccid paralysis worldwide and a neurologic emergency due to risk of respiratory failure and autonomic instability.

Clinician tip: Pronounce it “GHEE-yan bar-RAY” (/ɡiːˈjɑːn bɑːˈreɪ/) to guide trainees and patients who often struggle with the French name.

Core features

  • Progressive, relatively symmetric limb weakness starting distally and ascending over hours to days.
  • Areflexia or hyporeflexia—often universal early finding.
  • Paresthesias, back pain, and possible autonomic instability (tachycardia, BP lability, urinary retention).

Key differentials

Acute myelopathy (e.g., transverse myelitis)

Usually has a sensory level and hyperreflexia or Babinski signs—features not seen in GBS.

Tick paralysis / Botulism / Myasthenia gravis

Tick paralysis improves with tick removal; botulism causes descending paralysis and pupillary changes; myasthenia shows fatigable weakness and normal reflexes.

Diagnostic work-up

  • Reflex testing: Loss of deep tendon reflexes is classic and supports diagnosis.
  • Cerebrospinal fluid: Albuminocytologic dissociation—elevated protein with normal or mildly increased cell count—after the first week.
  • Neuroimaging: MRI spine to exclude compressive or inflammatory myelopathy; may show nerve root enhancement.
  • Electrodiagnostics: Nerve conduction studies/EMG confirm demyelination (slowed conduction, prolonged distal latencies).
Red flag: Monitor respiratory function (vital capacity, negative inspiratory force); early ventilatory support may be lifesaving.

Treatment snapshot

  • Start IVIG or plasma exchange within 2 weeks of onset—both equally effective.
  • Corticosteroids are not beneficial and may worsen outcomes.
  • Provide intensive supportive care: airway monitoring, autonomic management, DVT prophylaxis, and early rehab.
Pearl: Progression beyond 4 weeks suggests an alternative diagnosis such as chronic inflammatory demyelinating polyneuropathy (CIDP).

References

  1. Hughes RA, et al. Guillain-Barré syndrome. Lancet. 2005.
  2. van Doorn PA. Diagnosis, treatment and prognosis of Guillain-Barré syndrome. Nat Rev Neurol. 2013.

Educational discussion. Not a substitute for clinical judgment. Consider local protocols and individual factors.