All of the following are true about Guillan Barre syndrome (GBS), except
Guillain-Barre syndrome (GBS) is a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system.] The initial symptoms are typically changes in sensation or pain along with muscle weakness, beginning in the feet and hands] This often spreads to the arms and upper body, with both sides being involved. The symptoms develop over hours to a few weeks.During the acute phase, the disorder can be life-threatening, with about 15% developing weakness of the breathing muscles requiring mechanical ventilation.Some are affected by changes in the function of the autonomic nervous system, which can lead to dangerous abnormalities in hea rate and blood pressure The nerve dysfunction in Guillain-Barre syndrome is caused by an immune attack on the nerve cells of the peripheral nervous system and their suppo structures. The nerve cells have their body (the soma) in the spinal cord and a long projection (the axon) that carries electrical nerve impulses to the neuromuscular junction where the impulse is transferred to the muscle. Axons are wrapped in a sheath of Schwann cells that contain myelin. Between Schwann cells are gaps (nodes of Ranvier) where the axon is exposed. Different types of Guillain-Barre syndrome feature different types of immune attack. The demyelinating variant (AIDP, see below) features damage to the myelin sheath by white blood cells (T lymphocytes and macrophages); this process is preceded by activation of a group of blood proteins known as complement. In contrast, the axonal variant is mediated by IgG antibodies and complement against the cell membrane covering the axon without direct lymphocyte involvement. Various antibodies directed at nerve cells have been repoed in Guillain-Barre syndrome. In the axonal subtype, these antibodies have been shown to bind to gangliosides, a group of substances found in peripheral nerves. A ganglioside is a molecule consisting of ceramide bound to a small group of hexose-type sugars and containing various numbers of N-acetylneuraminic acid groups. The key four gangliosides against which antibodies have been described are GM1, GD1a, GT1a, and GQ1b, with different anti-ganglioside antibodies being associated with paicular features; for instance, GQ1b antibodies have been linked with Miller Fisher variant GBS and related forms including Bickerstaff encephalitis] The production of these antibodies after an infection is probably the result of molecular mimicry, where the immune system is reacting to microbial substances, but the resultant antibodies also react with substances occurring naturally in the body.[After a Campylobacter infection, the body produces antibodies of the IgA class; only a small propoion of people also produce IgG antibodies against bacterial substance cell wall substances (e.g. lipooligosaccharides) that crossreact with human nerve cell gangliosides. It is not currently known how this process escapes central tolerance to gangliosides, which is meant to suppress the production of antibodies against the body's own substances.Not all antiganglioside antibodies cause disease, and it has recently been suggested that some antibodies bind to more than one type of epitope simultaneously (heterodimeric binding) and that this determines the response. Fuhermore, the development of pathogenic antibodies may depend on the presence of other strains of bacteria in the bowel Ref Harrison20th edition pg 2234
Ascending paralysis
Flaccid paralysis
Sensory level
Albumino-cytological dissociation
C.N.S