Guillain-Barré Syndrome: The Sudden Paralysis That Starts in the Feet — A Neurologist Explains

Guillain-Barré syndrome (GBS) is an acute autoimmune peripheral neuropathy — the body's immune system attacks the peripheral nerves, producing progressive weakness and sensory disturbance that typically begins in the legs and ascends upward. In severe cases, it reaches the respiratory muscles and requires mechanical ventilation. It is rare — occurring in 1–2 per 100,000 people per year — but it is a neurological emergency and one of the most dramatic and frightening conditions in neurology.

How GBS Presents

The classic presentation: 2–4 weeks after a gastroenteritis (most commonly Campylobacter jejuni diarrhoea) or respiratory infection, the person notices tingling and weakness starting in the feet and toes. Over the next days, the weakness ascends — ankles, then knees, then thighs, then arms, then respiratory muscles. Tendon reflexes disappear (absent knee and ankle jerks — an important diagnostic sign). In some cases, facial weakness and difficulty swallowing develop (bulbar involvement). Back pain is common and often severe.

The ascending weakness of GBS can progress over 2–4 weeks. The nadir (worst point) is reached, then a plateau phase, then slow recovery over weeks to months. Approximately 5% of patients die despite treatment — usually from respiratory failure, autonomic instability, or secondary complications.

Red Flags: When to Call Emergency Services

• Progressive leg weakness over days, especially after a recent infection
• Difficulty breathing or speaking
• Loss of deep tendon reflexes
• Autonomic instability: wild fluctuations in blood pressure and heart rate

GBS requires emergency hospital admission — respiratory function must be monitored closely with serial vital capacity measurements.

Diagnosis

Clinical diagnosis supported by: CSF analysis (lumbar puncture) — classically showing elevated protein with normal white cell count (albuminocytologic dissociation); nerve conduction studies (NCS) and EMG showing characteristic pattern of demyelination or axonal degeneration; anti-ganglioside antibodies (anti-GQ1b in Miller-Fisher variant).

Treatment

Two treatments with good evidence: intravenous immunoglobulin (IVIG) — pooled immunoglobulin from donors that modulates the immune response; and plasma exchange (plasmapheresis) — removes the harmful antibodies from the blood. Both are equally effective. Steroids alone do NOT help in GBS (unlike most autoimmune conditions). Supportive care — respiratory monitoring, DVT prevention, pain management, physiotherapy — is equally important.

Recovery: 80% of patients eventually walk independently, though recovery can take 6–12 months or more. Approximately 20% have persistent weakness. Early treatment and early physiotherapy improve outcomes.

For GBS evaluation and neurological emergencies: Sri Anand CNC, Chanda Nagar, Hyderabad. Call +91 90633 66983.