El síndrome de Guillain-Barré es una polineuropatía aguda inmunomediada que causa debilidad muscular progresiva. Se asocia con infecciones previas como Campylobacter jejuni. Los síntomas incluyen debilidad simétrica ascendente, arreflexia y disautonomía. El tratamiento con plasmaféresis o inmunoglobulina intravenosa mejora los resultados. Algunos pacientes requieren soporte ventilatorio en la UCI debido a la debilidad respiratoria o arritmias causadas por la disaut
Guillain-Barré syndrome is an autoimmune disorder where the immune system attacks the peripheral nervous system, causing muscle weakness and sometimes paralysis. It is usually triggered by a bacterial or viral infection. While most patients recover fully within a few months with treatment like intravenous immunoglobulin or plasmapheresis, it can in rare cases lead to respiratory failure or even death if not properly managed. The exact mechanisms are not fully understood but involve the immune system mounting an attack against nerve antigens, damaging the myelin sheath surrounding nerves.
Guillain Barre Syndrome (GBS) is an acute immune-mediated inflammatory neuropathy. It is the most common cause of acute flaccid paralysis worldwide. Recent decades have seen progress in understanding the epidemiology, pathogenesis, and prognosis of GBS. The pathogenesis involves molecular mimicry between gangliosides and antigens from preceding infections like Campylobacter jejuni, leading to anti-ganglioside antibody production and complement-mediated nerve damage. Different GBS subtypes are associated with different antiganglioside antibodies and clinical courses.
Guillain-Barré syndrome is an acute autoimmune disease marked by inflammation of the peripheral nerves affecting the arms and legs. It involves destruction of the myelin sheath surrounding the largest sensory and motor fibers, resulting in weakness and disrupted proprioception. While the cause is unknown, it is thought to be an inappropriate immune response, possibly linked to certain vaccines. It affects about 2 per 100,000 people annually in a nondiscriminatory manner. Signs and symptoms include numbness, tingling, muscle weakness and diminished reflexes that progress distally. Most patients experience complete recovery within 2 months to 2 years through intravenous immunoglobin therapy or plasmapheresis.
Guillain-Barré syndrome is an acute inflammatory demyelinating polyneuropathy characterized by progressive muscle weakness. It is an autoimmune disorder caused by the immune system attacking the peripheral nervous system. Campylobacter infection is the most common precipitant of Guillain-Barré syndrome. There are different types including acute inflammatory demyelinating polyneuropathy and Miller Fisher syndrome. Treatment involves plasmapheresis or intravenous immunoglobulin to remove antibodies and improve symptoms.
El síndrome de Guillain-Barré es una polineuropatía aguda inmunomediada que causa debilidad muscular progresiva. Se asocia con infecciones previas como Campylobacter jejuni. Los síntomas incluyen debilidad simétrica ascendente, arreflexia y disautonomía. El tratamiento con plasmaféresis o inmunoglobulina intravenosa mejora los resultados. Algunos pacientes requieren soporte ventilatorio en la UCI debido a la debilidad respiratoria o arritmias causadas por la disaut
Guillain-Barré syndrome is an autoimmune disorder where the immune system attacks the peripheral nervous system, causing muscle weakness and sometimes paralysis. It is usually triggered by a bacterial or viral infection. While most patients recover fully within a few months with treatment like intravenous immunoglobulin or plasmapheresis, it can in rare cases lead to respiratory failure or even death if not properly managed. The exact mechanisms are not fully understood but involve the immune system mounting an attack against nerve antigens, damaging the myelin sheath surrounding nerves.
Guillain Barre Syndrome (GBS) is an acute immune-mediated inflammatory neuropathy. It is the most common cause of acute flaccid paralysis worldwide. Recent decades have seen progress in understanding the epidemiology, pathogenesis, and prognosis of GBS. The pathogenesis involves molecular mimicry between gangliosides and antigens from preceding infections like Campylobacter jejuni, leading to anti-ganglioside antibody production and complement-mediated nerve damage. Different GBS subtypes are associated with different antiganglioside antibodies and clinical courses.
Guillain-Barré syndrome is an acute autoimmune disease marked by inflammation of the peripheral nerves affecting the arms and legs. It involves destruction of the myelin sheath surrounding the largest sensory and motor fibers, resulting in weakness and disrupted proprioception. While the cause is unknown, it is thought to be an inappropriate immune response, possibly linked to certain vaccines. It affects about 2 per 100,000 people annually in a nondiscriminatory manner. Signs and symptoms include numbness, tingling, muscle weakness and diminished reflexes that progress distally. Most patients experience complete recovery within 2 months to 2 years through intravenous immunoglobin therapy or plasmapheresis.
Guillain-Barré syndrome is an acute inflammatory demyelinating polyneuropathy characterized by progressive muscle weakness. It is an autoimmune disorder caused by the immune system attacking the peripheral nervous system. Campylobacter infection is the most common precipitant of Guillain-Barré syndrome. There are different types including acute inflammatory demyelinating polyneuropathy and Miller Fisher syndrome. Treatment involves plasmapheresis or intravenous immunoglobulin to remove antibodies and improve symptoms.