Guillain Barre Syndrome (GBS) – Mnemonic


Required Criteria

Mnemonic: AIDP

1. Areflexia

2. Include in differential and rule out other causes

3. Duration < 4 weeks

4. Progressive weakness of 2 or more limbs due to neuropathy

Supportive criteria

Mnemonic: AIDPS

1. Afebrile

2. Involvement:

  • Mild sensory involvement
  • Facial or other cranial nerve involvement

3. Demyelinating electrophysiologic evidence

4. Protein in CSF (100-1000 mg/dl) + Low WBC (Albumino-cytologic dissociation)

5. Symmetrical distribution relatively

Why protein is increased in CSF in GBS?

Intense inflammation at the junction of the dorsal and ventral roots leads to breakdown in the blood-brain barrier and the transudation of plasma proteins into the cerebrospinal fluid (CSF).

Management of GBS

Mnemonic: AIDP

1. Supportive:

  • Analgesia: e.g. NSAIDs
  • Airway: may need ventilation in ITU
  • Autonomic: may need a urinary catheter
  • Antithrombotic: TED stockings, LMWH

2. IVIG 0.4 g/kg/day for 5 days

3. Dexamethasone (corticosteroid): No significant role

4. Plasma exchange (Plasmapheresis): Alternative to IVIG; 5 times during 2 weeks

At about 6 weeks after treatment with IVIG, 5-10% deteriorate after initial stabilization or improvement due to wearing off of therapeutic effect of IVIG in patients in whom immune response is prolonged.

3% m
ay progress to CIDP.

Variants of GBS

AIDP (Acute inflammatory demyelinating polyradiculoneuropathy): commonest; antecedent viral or bacterial infection

AMAN (Acute motor axonal neuropathy): pure motor form; 60% are seropositive for campylobacter; pediatric

AMSAN (Acute motor sensory axonal neuropathy): adults

Miller Fisher syndrome: Ophthalmoplegia + Ataxia + Areflexia

Acute panautonomic neuropathy: rarest

gbs pathophysiology

Pathogenesis of GBS

Molecular mimicry and cross-reactivity: Lipo-oligosaccharide (LOS) of C.jejuni mimic carbohydrate of ganglioside, i.e. anti-ganglioside antibodies.

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