233 syndrome myasthenia gravis吉兰巴雷和 233综合征重症肌无力课件.ppt

Guillain-Barré Syndrome is an acute inflammatory demyelinating polyneuropathy (AIDP), a disorder affecting the peripheral nervous system. It is usually triggered by an acute infectious process. The syndrome was named after the French physicians Guillain, Barré and Strohl, who were the first to describe it in 1916. It is sometimes called Landrys paralysis, after the French physician who first described a variant of it in 1859. It is included in the wider group of peripheral neuropathies. ETIOLOGY The etiology of Guillain-Barré syndrome is unclear, but an autoimmune response is strongly suspected. There is a preceding event or trigger that is often an infection. Occasionally, vaccinations have been known to trigger Guillain-Barré syndrome. Approximately half of the people who develop Guillain- Barré syndrome have a mild febrile illness 2 to 3 weeks before the onset of symptoms. The febrile infection is usually respiratory or gastrointestinal. Approximately 25% of patients with this disease have antibodies to either cytomegalovirus or Epstein-Barr virus. PATHOPHYSIOLOGY In Guillain-Barré syndrome, the myelin sheath surrounding the axon is lost. Demyelination is a common response of neural tissue to many agents and conditions, including physical trauma, hypoxemia, toxic chemicals, vascular insufficiency, and immunological reactions. Loss of the myelin sheath in Guillain-Barré syndrome makes nerve impulse transmission is aborted. CLINICAL MANIFESTATIONS The syndrome may develop rapidly over the course of hours or days, or may take up to 3 to 4 weeks to develop. Most patients demonstrate the greatest weakness in the first weeks of the disorder. Patients are at their weakest point by the third week of the illness. In the beginning, a flaccid, ascending paralysis develops quickly. The patient is most commonly affected in a symmetrical pattern. The patient may first notice weakness in the lower extremities that may quickly extend to include weakness and abnormal sen