Guillain-Barré syndrome is an acute inflammatory demyelinating polyneuropathy that causes progressive flaccid motor weakness. It is triggered by preceding respiratory or gastrointestinal infections in some cases. The myelin sheath surrounding nerves is damaged, blocking nerve impulse transmission. Clinical manifestations include ascending symmetrical paralysis, loss of deep tendon reflexes, and possible respiratory or autonomic involvement. Diagnosis involves clinical evaluation along with lumbar puncture, nerve conduction studies, and other tests. Treatment focuses on supportive care and immunomodulation therapies like intravenous immunoglobulins or plasma exchange.
2. Definition
• is an acute inflammatory demyelinating
polyneuropathy, with symmetrical flaccid
motor weakness and minimal sensory
involvement
3. Epidemiology
• GBS is the most common cause of acute
flaccid paralysis (AFP) in all ages.
• The estimated annual incidence of GBS is
approximately 1 case per 100,000 population.
• GBS is very rare in children younger than 1
year of age.
• Male predominance.
4. ETIOLOGY
• unclear, but an autoimmune response is
strongly suspected.
• 2 to 3 weeks preceding infections
–Respiratory viral infection (cytomegalovirus or
Epstein-Barr virus mumps measles etc)
–(Gastro intestinal infection campylobecter jajuni)
• Occasionally, vaccinations have been known
to trigger Guillain-Barré syndrome.
5. PATHOPHYSIOLOGY
• Antigen antibody reaction
• In Guillain-Barré syndrome, the myelin sheath
surrounding the axon is lost.
• Loss of the myelin sheath in Guillain-Barré
syndrome makes nerve impulse transmission
block.
9. CLINICAL MANIFESTATIONS
• 2 to 3 weeks preceding infections
• Onset is with sensory symptoms
paresthesias(numbness and tingling) of feet,
hands and back pain.
• Sudden onset of symmetrical motor weakness
of lower limbs.
• Weakness progress in ascending fashion.
10. CLINICAL MANIFESTATIONS
• Weakness is maximum by the 3rd weeks of
illness.
• Deep tendon reflexes are usually lost. A
reflexia
• Respiratory muscles can become affected,
resulting in respiratory compromise
• Autonomic disturbances
dysrhythmia hypotension.
11. CLINICAL MANIFESTATIONS
• If there is cranial nerve involvement, cranial
nerve VII, the facial nerve, is most often
affected.
• Guillain-Barré syndrome does not affect level
of consciousness, pupillary function, or
cerebral function.
12. • The level of paralysis may stop at any point.
• Motor function returns in a descending
fashion.
• Demyelination occurs rapidly, but the rate of
remyelination is approximately 1 to 2 mm per
day.
13. DIAGNOSIS
• Clinical, Mainy The history
symmetrical ascending paralysis.
• Areflexia
• lumbar puncture-albuminocytologic
dissociation (few cells high proteins).
• Nerve Conduction velocity (decrease)
• Pulmonary function tests (base line)
14. MANAGEMENT
• Supportive Care
• ( change of posture tube feedings care of
bowel and bladder)
• preventive measures
• Low molecular wt heparin to prevent DVT and
pulmonary embolism
• Artificial Ventilation (20 % Cases)
• Ammunoglobulins ( treatment of choice)
400 mg/kg/day for 5 days or 1gm/kg for 2 days
• Plasma exchange (with in 2 weeks)
• Steroids ( 2mg/kg/day for 2 weeks)
