Guillain Barre Syndrome

This is caused by a process known as molecular mimicry.  This is when antibodies produced to defend against a real pathogen cross react with proteins in the body, initiating an autoimmune attack.  In Guillain Barre, this commonly occurs after a Campylobacter jejuni infection (GI) where antibodies cross react with myelin proteins.

There are many subtypes of GBS, the most common of which is known as Acute Inflammatory Demyelinating Polyneuropathy (AIDP).  The common features of GBS include:

  • Weakness- usually symmetrical and ascending in nature (lower limb extremities first- usually spreads up involving upper limbs too- can reach proximal muscles and respiratory muscles)
  • CN dysfunction- (commonly CNIII-VII, IX-XII) Facial droop; diploplia; dysarthria; dysphagia etc
  • Change in sensation- usually paraesthesia and/or numbness although pain can occur.  May precede weakness and usually starts at the extremities progressing upwards
  • ANS dysfunction- (both sympathetic and parasympathetic) Tachy-/brady-cardia; Facial flushing; paroxysmal hypertension; postural hypotension; diaphoresis/anhidrosis (excess/little sweating)

This is usually a clinical diagnosis but electrophysiology (to show demyelination) and CSF (high protein, low/normal WBC)/imaging (inflammation of the sacrolumbar plexus) (to exclude other causes) may be useful.

It is usually self limiting but can be disabling and can last up to a year.  Symptomatic treatment may therefore be used.

see also neurology problem: peripheral neuropathy

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