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Guillain barre syndrome
Acute inflammatory demyelinating
Polyradiculoneuropathy (Guillain-
Barre syndrome, GBS)
Introduction
• Acute/subacute onset
• Inflammatory demyelinating polyradiculoneuropathy
• Symmetrical, progressive lower motor neurons
paralysis of limbs.
Commonly preceded by viral infection, vaccination to
1-4 weeks.
• It appears to be an immunological basis.
• Pathological lesion are demyelinating on anterior
roots and peripheral nerves sometimes with axonal
degeneration.
3. Cranial nerves involvement: produce ophthalmologic,
facial palsy, bulbar palsy that predisposes to aspiration
pneumonia.
oculormotor nerve: Ⅲ、Ⅳ、Ⅵ
facial nerve: Ⅷ
bulbar palsy: Ⅸ、Ⅹ
4. Autonomic dysfunction: tachycardia, cardiac
irregularities, labile blood pressure, disturbed
sweating, sphincter disturbance are rare.
5. CSF: albuminocytologic dissociation: a characteristic
abnormality, with increased protein concentration but
a normal cell count.
Diagnosis
• Progressive weakness of more than one limb
• Distal or proximal hyporeflexia
• Relatively symmetrical deficit
• Mild sensory involvement
• Cranial nerve involvement
• Recovery beginning within 4 weeks after progression stops
• Autonomic dysfunction
• No fever at onset
• CSF albuminocytologic dissociation
• Nerve conduction slowing or block by several weeks
Treatment
1. Plasmapheresis. May reduce the time required for recovery or
decrease the likelihood of residual neurologic dificits.
2. Intravenous large dose of immunoglobulin 0.4g/kg/d for
persistent 5~7 days appears to be equally effective. The two
therapies are not additive.
3. Symptomatic therapy:
closely monitor and assist respiration. If patient is short of
breath, the vital capacity falls below about 1L, blood oxygen
saturation declines to 80% or oxygen pressure lower 70mmHg.
The tracheotomy is necessary for patients with respiratory canal
blocked by secretion or sputum.
Sometimes treatment with pressor agents is required
to counter hypotension
Low-dose heparin may help to prevent pulmonary
embolism.
4. Corticosteroids may affect the outcome adversely
or delay recovery, and are not indicated.
• Self-limiting and cease to progress by about 4 weeks,
improvement occurs over weeks or months following
onset.
• 70-75% of patients recover completely, 25% are left
with mild neurological deficits, and 5% die,usually as
a result of respiratory failure.
• Poor prognosis: Campylobacter jejuni infection,
axonal degeration,more rapid onset of symptoms,
the need for ventilatory support.

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GBS.pptx

  • 2. Acute inflammatory demyelinating Polyradiculoneuropathy (Guillain- Barre syndrome, GBS) Introduction • Acute/subacute onset • Inflammatory demyelinating polyradiculoneuropathy • Symmetrical, progressive lower motor neurons paralysis of limbs.
  • 3. Commonly preceded by viral infection, vaccination to 1-4 weeks. • It appears to be an immunological basis. • Pathological lesion are demyelinating on anterior roots and peripheral nerves sometimes with axonal degeneration.
  • 4.
  • 5. 3. Cranial nerves involvement: produce ophthalmologic, facial palsy, bulbar palsy that predisposes to aspiration pneumonia. oculormotor nerve: Ⅲ、Ⅳ、Ⅵ facial nerve: Ⅷ bulbar palsy: Ⅸ、Ⅹ 4. Autonomic dysfunction: tachycardia, cardiac irregularities, labile blood pressure, disturbed sweating, sphincter disturbance are rare. 5. CSF: albuminocytologic dissociation: a characteristic abnormality, with increased protein concentration but a normal cell count.
  • 6. Diagnosis • Progressive weakness of more than one limb • Distal or proximal hyporeflexia • Relatively symmetrical deficit • Mild sensory involvement • Cranial nerve involvement • Recovery beginning within 4 weeks after progression stops • Autonomic dysfunction • No fever at onset • CSF albuminocytologic dissociation • Nerve conduction slowing or block by several weeks
  • 7. Treatment 1. Plasmapheresis. May reduce the time required for recovery or decrease the likelihood of residual neurologic dificits. 2. Intravenous large dose of immunoglobulin 0.4g/kg/d for persistent 5~7 days appears to be equally effective. The two therapies are not additive. 3. Symptomatic therapy: closely monitor and assist respiration. If patient is short of breath, the vital capacity falls below about 1L, blood oxygen saturation declines to 80% or oxygen pressure lower 70mmHg. The tracheotomy is necessary for patients with respiratory canal blocked by secretion or sputum.
  • 8. Sometimes treatment with pressor agents is required to counter hypotension Low-dose heparin may help to prevent pulmonary embolism. 4. Corticosteroids may affect the outcome adversely or delay recovery, and are not indicated.
  • 9. • Self-limiting and cease to progress by about 4 weeks, improvement occurs over weeks or months following onset. • 70-75% of patients recover completely, 25% are left with mild neurological deficits, and 5% die,usually as a result of respiratory failure. • Poor prognosis: Campylobacter jejuni infection, axonal degeration,more rapid onset of symptoms, the need for ventilatory support.