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Guillain–Barré syndrome


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Guillain–Barré syndrome

  1. 1. Gullain-Barre syndrome by; Belton Winford
  2. 2. • is an acute polyneuropathy, a disorder affecting the peripheral nervous system. • Ascending paralysis, weakness beginning in the feet and hands and migrating towards the trunk • also can cause cranial nerve dysfunction
  3. 3. Epidemiology • Worldwide, the annual incidence is about 0.6–1.9 occurrences per 100,000 people • Men are one and a half times more likely to be affected than women • the incidence increasees in patients with Hodgkin disease,pregnancy or general surgery
  4. 4. Etiology • autoimmune response -The targets of such immune attack are thought to be gangliosides, compounds naturally present in large quantities in human peripheral nerve tissues - infections by bacterium Campylobacter jejun, cytomegalovirus, influenza virus,
  5. 5. Pathphysiology • focal segmental demyelination with endoneurial monocytic infiltrate
  6. 6. Variants • acute motor axonal neuropathy - motor axonal degeneration with little or no demyelination or imflammation - may follow infections with Campylobacter jejuni or parenteral injection of gangliosides • the Miller-Fisher syndrome - characterized by gait ataxia, areflexia and ophthalmoparesis; papillary abnormalities are sometimes present
  7. 7. • acute motor and sensory axonal neuropathy or neuronopathy • acute autonomic neuropathy or pandysautonomia
  8. 8. Diagnostic criteria • features required for diagnosis - progressive motor weakness of more than 1 limb [ from minimum weakness to +/- ataxia to paralysis - areflexia [usually universal but distal areflexia with difinite hyporeflexia of biceps and knee jerks sufficess if other features consistent]
  9. 9. Clinical features • progression motor weakness peaks at 2wks in 50% , 3wks 80% , 4wks > 90% • relative symmetry • mild sensory symptoms/signs eg mild paresthesias in hands or feets • cranial nerve involvment ; facial weakness , oropharyngeal muscles may be affected • recovery usually 2-4wks after progression stops , may be delayed for months
  10. 10. • autonomic dysfunction [ may flactuate] tachycardia, arrythmias, postural hypotension , HTN, vasomotor symptoms • afebrile at onset of neuritic symptoms • fever, • severe sensory loss with pain • progression >4wks • cessation of progression without recovery • sphincter dysfunction eg; bladder paralysis
  11. 11. CSF findings • protein > 55mg/dl • cells <10 mononuclear leukocytes/ml • variants - no protein rise - 11-50 monocytes/ml
  12. 12. differential diagnosis • acute polyneuropathy • acute polyneuropathy after administration of penicillin • infections affecting the anterior horn ganglion cells • myasthenia gravis • acute myopathies • albumincytologic dissociation of the CSF due to another disease • Acquired immunodeficiency syndrome
  13. 13. Treatment The patient needs to be in a unit where intensive respiratory care is available. Respiratory assistance should be instituted at the first sign of dyspnea (arterial PO2< 70 mmHg) or markedly reduced vital capacity (<12 to 15 mL/kg) • early plasaphaeresis hastens recovery and reduces the residual deficit • immunoglobulins may be helpful in severe cases
  14. 14. Prognosis • recovery may not be complete for several months • 35% of untreated patients have residual weakness and atrophy • reccurance after maximum recovery occours in 2%
  15. 15. THANK YOU