Guillain-Barre Syndrome
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Direct answer
Guillain-Barre syndrome (GBS) is an acute, post-infectious, immune-mediated demyelinating polyradiculoneuropathy — the commonest cause of acute flaccid paralysis in Indian adults — presenting days to weeks after a diarrhoeal (Campylobacter jejuni) or respiratory infection with symmetric, ascending, areflexic weakness progressing over days to four weeks, often with back pain and minimal sensory signs. Cerebrospinal fluid shows albuminocytological dissociation — raised protein with few or no cells — and nerve conduction studies confirm demyelination (the AIDP subtype) or the axonal variants (AMAN, AMSAN) that Indian series report frequently. Treatment is intravenous immunoglobulin 2 g/kg over 5 days (or plasma exchange, equal efficacy, never both routinely); corticosteroids are NOT beneficial. The life-threatening issues are respiratory (serial vital capacity, intubate below 15-20 mL/kg), autonomic instability and thromboembolism prophylaxis — GBS kills by ventilatory failure.
What you must remember
- Diagnostic pattern: symmetric leg-origin weakness ascending over days (nadir by 4 weeks), absent reflexes, minimal sensory findings, often bilateral facial weakness; bladder involvement rare — a persistent catheter-bound bladder argues against GBS.
- CSF phrase: albuminocytological dissociation — protein elevated (often 100-1000 mg/dL, rising after the first week) with fewer than 10-50 white cells; cells beyond that suggest infection (HIV, tuberculosis) or another diagnosis.
- Subtypes to name: AIDP (demyelinating, commonest worldwide), AMAN (motor axonal, linked to Campylobacter and common in Indian series), AMSAN (axonal motor-sensory, slower recovery), Miller Fisher syndrome (ophthalmoplegia, ataxia, areflexia — the triad to quote — with anti-GQ1b antibodies).
- Antecedent infection ladder: Campylobacter jejuni diarrhoea (the strongest association), respiratory viruses including influenza and SARS-CoV-2, mycoplasma, HIV, surgery, and historically rabies vaccine — Indian exams love the post-diarrhoeal stem.
- Treatment specifics: intravenous immunoglobulin 0.4 g/kg daily for 5 days (2 g/kg total) — first choice in most Indian centres; plasma exchange (200-250 mL/kg over 5 exchanges) equally effective; neither is combined routinely; steroids (including high-dose methylprednisolone) have proven no benefit — a classic negative trial to quote.
- Respiratory surveillance numbers: serial bedside vital capacity every 4-6 hours; intubate when it falls below 15-20 mL/kg or earlier with bulbar weakness, aspiration or a falling trend — do not wait for desaturation.
- Supportive care set: deep-venous-thrombosis prophylaxis with low molecular weight heparin, chest physiotherapy, neuropathic pain analgesia, monitoring for autonomic arrhythmia and blood-pressure swings — recovery takes weeks to months.
- Differential anchors: acute flaccid paralysis in India also means poliomyelitis (asymmetric, febrile at onset, CSF pleocytosis), hypokalaemic periodic paralysis (reflexes preserved, K+ low, resolves with potassium), diphtheritic neuropathy (slower, palatal paralysis first), botulism (descending, cranial first), cord compression (a sensory level, sphincter involvement, reflexes may be brisk) — and transverse myelitis, the great mimic.
A fortnight on the neurology ward
A 34-year-old man develops tingling in both feet and unsteadiness ten days after bloody diarrhoea; within three days he cannot climb stairs, within six he has bilateral facial weakness and weak grip. Power is 3/5 distally, reflexes absent throughout, plantars flexor, bladder intact — AIDP-pattern GBS. Lumbar puncture shows protein 180 mg/dL with 3 lymphocytes; nerve conduction studies show prolonged distal latencies, conduction block and slowed velocities. IVIG 0.4 g/kg daily for five days begins the same day, alongside enoxaparin 40 mg daily, chest physiotherapy, and vital capacity measured four times daily.
On day 9 his vital capacity trends from 28 to 19 mL/kg with a weak cough — elective intubation, decided on the trend rather than the number alone. Extubation comes after three weeks; power recovers proximally first over months, and most patients walk within six months, though fatigue and distal weakness can persist. Every element of that arc, from the diarrhoea to the trend-based intubation, is a mark-earning sentence.
Where students slip
The first error is waiting for desaturation before intubating — the answer is the falling vital capacity below 15-20 mL/kg with a poor cough, an elective airway. Second, the steroid reflex: GBS is one of the few acute neurological emergencies where corticosteroids are explicitly not recommended, and the option list baits you with methylprednisolone. Third, protein high with cells high is NOT albuminocytological dissociation — a pleocytosis redirects towards HIV, poliomyelitis or other infections. Fourth, GBS ascends (legs to arms to face), botulism descends (eyes and bulbar first), and Miller Fisher stays at the top. Fifth, every acute flaccid paralysis case in India is reported under polio eradication surveillance, and GBS is its commonest non-polio cause in adults.
Frequently asked questions
What CSF finding supports Guillain-Barre syndrome?
Albuminocytological dissociation — markedly raised protein with few or no cells (typically under 10-50), usually after the first week of illness.
What is the first-line treatment and its dose?
Intravenous immunoglobulin 0.4 g/kg daily for five days (total 2 g/kg), or plasma exchange within 2-4 weeks of onset; both are equally effective and corticosteroids are not beneficial.
When should a GBS patient be intubated?
When vital capacity falls below 15-20 mL/kg, or earlier with bulbar weakness, weak cough, aspiration or a rapid declining trend.
What distinguishes Miller Fisher syndrome?
The triad of ophthalmoplegia, ataxia and areflexia, with anti-GQ1b antibodies, often following Campylobacter infection.
How does GBS differ from hypokalaemic periodic paralysis?
GBS shows areflexia, slow progression and raised CSF protein, whereas periodic paralysis has preserved reflexes, low serum potassium and rapid resolution with potassium correction.