Guillain Barre

Question 1

Def

Answer 1

acute immune-mediated polyneuropathy that typically manifests with bilateral ascending flaccid paralysis and sensory involvement, e.g., paresthesia.

autoantibodies against antigens in the myelin sheath, other Schwann-cell antigens, and axon membranes

Question 2

Pathogenesis

Answer 2

65% of patients have an upper respiratory tract or gastrointestinal infection up to 6 weeks prior to onset of GBS symptom

Campylobacter enteritis is the most common disease associated with GBS.
Cytomegalovirus (CMV)
HIV
Influenza
Zika virus
Epstein-Barr virus
SARS-CoV-2
Mycoplasma pneumoniae

Postinfectious autoimmune reaction that generates cross-reactive antibodies (molecular mimicry)
autoantibodies against gangliosides (e.g., GM1, GD1a) or other unknown antigens of peripheral Schwann cells → immune-mediated segmental demyelination → axonal degeneration of motor and sensory fibers in peripheral and cranial nerves (CN III–XII)

Question 3

CSF

Answer 3

albuminocytologic dissociation - elevated protein, normal cells

Question 4

Tx

Answer 4

IVIg
Plasmapheresis

+ cardiac and respiratory monitoring

Question 5

Presentation

Answer 5

typically bilateral and ascending from the lower limbs
Progressive flaccid paresis or paralysis
Paresthesia: stocking‑glove distribution
Hyporeflexia or areflexia typically begins in the lower limbs.
Back and limb pain (often an early symptom)
Involves nociceptive and neuropathic pain
Cardiac arrhythmias, blood pressure fluctuations [2]
Urinary retention and/or intestinal dysfunction
Respiratory muscle involvement: may lead to respiratory failure.
Cranial nerve involvement
Facial diplegia: due to bilateral facial nerve involvement (most frequently affected cranial nerve in GBS)
Bulbar dysfunction

Question 6

Types

Answer 6

Acute inflammatory demyelinating polyneuropathy

Acute motor axonal neuropathy (AMAN)
Acute motor and sensory axonal neuropathy (AMSAN)

Question 7

Diff dx

Answer 7

Transverse myelitis