This document provides information about Guillain-Barré syndrome (GBS). GBS is an acute onset of symmetrical muscle weakness and paralysis caused by damage to peripheral nerves. It is considered an autoimmune condition that can affect both motor and sensory nerves. Clinical symptoms include muscle weakness, absent reflexes, pain, and possible respiratory failure. Diagnosis involves neurological exams, cerebrospinal fluid analysis, and electrophysiological tests. Treatment focuses on plasma exchange, immunoglobulin therapy, and other supportive care. Most patients recover fully, but some have long-term weakness or neurological issues.

1. S Y N D R O M E
GUILLAIN BARRE
A S L A M A B D U L V A H I D
维 达 - 2 1 3 1 4 6 1 8 8
S C H O O L O F M E D I C I N E
S O U T H E A S T U N I V E R S I T Y

2. LEARNING
OBJECTIVES
ETIOLOGY &
PATHOGENESIS
CLINICAL SYMPTOMS &
SIGNS
DIAGNOSIS OF GBS
DIFFERENTIAL
DIAGNOSIS OF GBS
MANAGEMENT &
PROGNOSIS

3. W H A T I S G B S ?
• It is an acute or subacute onset of
generally symmetrical and progressive
lower motorneurons paralysis of limbs.
• A disease which rapidly damages
peripheral nerves.
• May hinder movement, sensation
or organ function depending on which
nerves are involved
• Named after French neurologists Georges Gullain and Jean Alexandre
Barre-1916

4. • Often the cause of GBS is unknown
• Often follows GI infection with diarrhoea or respiratory infection
• The GI infection due C.jejuni often precedes to GBS
• It occurs in all parts of the world and in all seasons, affecting
children and adults of allages and both sexes.
• Rare – only 1 -2 cases per 100,000 people world-wide each year
• Most common cause of sudden onset flaccid paralysis
E T I O L O G Y

5. C L I N I C A L M A N I F E S T A T O N
1.Muscle weakness and Flaccid paralysis
- In 25% of patients this weakness affect the respiratory muscle causes
respiratory inadequacy
2. Possible Respiaratory Failure
3. ANS Dysfunction
- Urinary Retention
- Flushing of the face
- Cardiac arrythmia-
- Orthostatic Hypotension
4. May or may not experience pain
-Pain most commonly in Back, Shoulders and Thighs

6. 2 main subtypes
1. AIDP-ACUTE INFLAMATORY DEMYELINATING POLYNEUROPATHY
2. AMAN-ACUTE MOTOR AXONAL NEUROPATHY
P A T H O P H Y S I O L O G Y

7. ACUTE INFLAMATORY
DEMYELINATING POLYNEUROPATHY

8. A M A N
ACUTE MOTOR AXONAL NEUROPATHY

11. • Symptoms are symmetrical
• progressive weakness of more than
one limb
• Absent reflex/hyporeflexia
• High levels of proteins in CSF (>0.55g/L)
• < 10 WBC per mm 3 in CSF
• Neurophysiological studies
• Nerve Conduction Study(NCS)- decreased conduction velocities
• Electromyography(EMG)- decreased muscle recruitments
D I A G N O S I S

12. • Plasmapheresis (Plasma Exchange)
• Immunoglobulin (IV)
• Corticosteroids are not given
• Mechanical Ventilation
• IV antibiotics therapy
• Manual movement of limbs
• Anticoagulent therapy – to prevent DVT
• Physical and Occupational therapy
• Pshychological therapy
T R E A T M E N T

13. • 2-5% OF GBS patients die
o Respiratory paralysis
o Cardiac arrest
• Most patients have a full recovery
• 30% of patients – residual weakness after 3 years
• 3% of patient – weakness and tingling after many years
P R O G N O S I S

14. • Peripheral neuropathy associated with GBS comes on with
a sudden onset.
• Syndrome is autoimmune
• Demyelinating
• Ascending
• Symmetrical condition
• Affect both sensory & motor neuron
• Symptoms include parasthesis, absent of reflexes, pain, muscle
weakness, may progress to  possible respiratory paralysis
S U M M A R Y

15. • ANS dysfunction (Arrhythmia, Orthostatic hypotension)
• Medical emergency
• Findings that support positive diagnosis of GBS
o Sensory & Motor symptoms
o CSF – high level of protein, low level of WBC
• Neurophysiological studies like NCS, EMG
• Treatment: Plasmapheresis, Immunoglobulin, Antibiotics &
Anti-coagulant therapy
S U M M A R Y