Guillain-Barré Syndrome is a life-threatening, demyelinating, autoimmune condition in which the body’s immune system attacks the myelin of the peripheral nervous system. Guillain-Barré Syndrome is characterized by ascending motor weakness and acute flaccid paralysis. Demyelination results in nerve inflammation, numbness, tingling, muscle weakness, structural damage to the myelin sheath, and possible respiratory system complications. The annual incidence rate is 1.1 to 1.8 per 100,000 persons worldwide. Guillain-Barré Syndrome is thought to be triggered by an antecedent infection such as a viral, gastrointestinal, or bacterial infection, food poisoning, or reaction to a vaccine. Approximately 9-11% of cases result in severe disability or death. The acute phase can vary in length from a few days to several months, although over 90% of patients begin rehabilitation within four weeks. Patient care involves a team of neurologists, physiatrist, internist, nurses, physical, occupational, and speech therapists, social worker, psychologist and family physician. Elevated cerebrospinal fluid protein, symmetrical muscle weakness, the rate and order at which symptoms appear, and the absence or prolonged latency of reflexes are hallmarks for diagnosing Guillain-Barré Syndrome. A lumbar puncture to test for protein levels in the brain and spinal cord, and nerve conduction velocity test may aid in proper diagnosis, critical for optimizing treatment options and minimizing further progression. Although there is no cure, treatment may consist of plasmapheresis, typically performed four times during hospitalization, or intravenous immunoglobulin. Intravenous immunoglobulin combined with plasmapheresis should be avoided. Although glucocorticoids could repair damage to the blood-nerve barrier, oral corticosteroids could delay recovery.