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Gullian barre syndrome


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autoimmune disease

autoimmune disease

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  • 2. INTRODUCTION o Popularly known as “French polio” is an acute inflammatory demyelinating polyneuropathy characterized by progressive muscle weakness and areflexia. o All forms of Guillain–Barré syndrome are autoimmune disease, due to an immune response to foreign antigens. o It has an annual incidence of 0.6 to 2.4 cases per 100,000 population and occurs at all ages and in both sexes. o With the marked decline in the incidence of polio, GuillainBarré syndrome is now the most common cause of acute flaccid paralysis in healthy people.
  • 3. TYPES o ACUTE INFLAMMATORY DEMYELINATING POLYNEUROPATHY(AIDP)- autoimmune response directed against Schwann cell membranes. o MILLER FISHER SYNDROME (MFS)- Anti-GQ1b antibodies are present in 90% of cases. o ACUTE MOTOR AXONAL NEUROPATHY (AMAN) also known as Chinese paralytic syndrome- Anti-GD3 antibodies are found more frequently in AMAN. o ACUTE PANAUTONOMIC NEUROPATHY- associated with a high mortality rate, owing to cardiovascular involvement, and associated dysrhythmias.
  • 4. CAMPYLOBACTER INFECTION o Campylobacter infection is the most commonly identified precipitant of Guillain-Barré syndrome. o A case-control study involving 103 patients with the disease found that 26% of affected individuals had evidence of recent C. jejuni infection compared with 2% of household and 1% of age-matched controls. o Seventy percent of those infected with C. jejuni reported a diarrheal illness within 12 weeks before the onset of the neurologic illness.
  • 5. o The main lesions are acute inflammatory demyelinating neuropathy and, particularly in patients with Campylobacter-associated disease, acute axonal degeneration. o These changes may be caused by cross-reacting antibodies to GM1 ganglioside (present in high concentrations in peripheral nerve myelin) formed in response to similar epitopes expressed by the infecting Campylobacter strain. o However, mechanisms other than molecular mimicry may be associated with the production of antibodies to GM1 ganglioside.
  • 6. ANTIBODIES AGAINST GANGLIOSIDES o Anti-GD3-Anti-GD3 antibodies have been found in association with specific forms of Guillain-Barré syndrome. o In vivo studies of isolated anti-GM1 and GD3 antibodies indicate the antibodies can interfere with motor neuron function. o Anti-GD1a antibodies were highly associated acute motor axonal neuropathy while high titers of anti-GM1 were more frequent indicating that GD1a possibly targets the axolemma and nodes of ranvier. .
  • 7. o Anti-GM1-Levels of anti-GM1 are elevated in patients with various forms of dementia & correlate with more severe Guillain-Barré syndrome. o Titers to GM1 in other diseases (rheumatoid arthritis, primary Sjögren's syndrome and systemic lupus erythematosus) was also elevated. o The autoimmune role of anti-GM1 is still unclear.
  • 8. o Anti-GQ1-Anti-GQ1b are found in MillerFisher syndrome. o Studies of these antibodies reveal large disruption of the Schwann cells. o Anti-GQ1b IgG levels were elevated in patients with ophthalmoplegia in GuillainBarré syndrome.
  • 9. PATHOGENESIS o In Guillain-Barré syndrome, the myelin sheath surrounding the axon is lost. o Demyelination is a common response of neural tissue to many agents and conditions, including physical trauma, hypoxemia, toxic chemicals, vascular insufficiency, and immunological reactions. o Loss of the myelin sheath in Guillain-Barré syndrome makes nerve impulse transmission is aborted.
  • 10. CLINICAL MANIFESTATION o The syndrome may develop rapidly over the course of hours or days, or may take up to 3 to 4 weeks to develop. o Most patients demonstrate the greatest weakness in the first weeks of the disorder. o Patients are at their weakest point by the third week of the illness. o In the beginning, a flaccid, ascending paralysis develops quickly.
  • 11. o The patient may first notice weakness in the lower extremities that may quickly extend to include weakness and abnormal sensations in the arms. o Deep tendon reflexes are usually lost, even in the earliest stages. o The trunk and cranial nerves may become involved. o Respiratory muscles can become affected, resulting in respiratory compromise.
  • 12. DIAGNOSIS o The history of the onset of symptoms can be revealing because symptoms of Guillain-Barré syndrome usually begin with weakness or paresthesias of the lower extremities and ascend in a symmetrical pattern. o A lumbar puncture may be performed and reveal increased protein. o Also, nerve conduction studies record impulse transmission along the nerve fiber.
  • 13. TREATMENT o The main modalities of therapy for Guillain-Barré syndrome include – Plasmapheresis – Administration of intravenous immune globulin o The first therapy proven to benefit patients with Guillain-Barré syndrome is plasmapheresis. o This procedure mechanically removes humoral factors.
  • 14. o Plasma exchange is recommended for patients who – Are unable to walk unaided – Demonstrate worsening vital capacities – Require mechanical ventilation – Have significant bulbar weakness o Intravenous immunoglobulin (IVIG) is also useful in managing Guillain-Barré syndrome.
  • 15. REFERENCE o Davids, H. "Guillain-Barre Syndrome". Medscape Reference. Retrieved 3 Jan 2012. o Jump up Mori, M; Kuwabara, S; Fukutake, T; Hattori, T (2002). "Plasmapheresis and Miller Fisher syndrome: analysis of 50 consecutive cases". Journal of neurology, neurosurgery, and psychiatry 72 (5). o Thomas J.Kindt,Barabara A.Osborne,Richard A.Goldsby.Kuby Immunology 6th edition.
  • 16. American actor Andy Griffith developed GuillainBarré syndrome in 1983. Griffith is seen here receiving an award at the White House in 2005.