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Guillain – Barre syndrome

It is a post infectious polyneuropathy that causes demyelination in mainly motor but sometimes also sensory nerve.

The peripheral lymphocytes are sensitized to a protein component of the myelin (p2 neuritogenic peptide) the basic myelin protein may be altered and rendered immunogenic by infection and this leads to demyelination

The paralysis usually follows a non specific viral infection by about 10 days. The original infection may have been caused by gastrointestinal (especially Campylobacter jejuni) or respiratory tract (especially Mycoplasma pneumoniae) symptoms


Clinical features

  1. Weakness begins usually in the lower extremities and progressively involves the trunk, the upper limb and finally the bulbar muscles. The onset is gradual and progresses over days or weeks
  2. Tendon reflexes are diminished planter is normal and there is hypotonia
  3. Cranial nerve involvement occurs in 50-75% of cases and most common facial nerve is involved
  4. Autonomic dysfunction marked by urinary retention: lability of blood pressure and heart rate
  5. Spontaneous recovery begins within 2 – 3 weeks; most patients regain full muscular strength. The tendon reflexes are usually the last function to recover
  6. Improvement usually follows the direction of involvement with recovery of bulbar function first and lower extremities weakness resolving last 

Diagnosis / Lab finding

  1. CSF protein is elevated to more than twice the upper limit of normal, glucose level is normal there is no pleocytosis
  2. MCV – decreases



- Patient in early stage of this acute disease should be admitted to the hospital for observation because the ascending paralysis may rapidly involve respiratory muscles during the next 24 hours

- Patient with slow progression may be observed for stabilization and spontaneous remission without treatment

- Rapidly progressively ascending paralysis is treated with intravenous immunoglobin (IV Ig)

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