A patient presents with quadriparesis. CSF shows protein 1 g%, sugar 40 mg% and no cells. He should be treated with:
There is convincing evidence that GBS at least in some patients is caused by an infection-induced aberrant immune response that damages the peripheral nerves. Four key factors were identified that control this process Anti-ganglioside antibodies In up to 50% of patients, serum antibodies to various gangliosides present in human peripheral nerves, including GM1, GD1a, GalNAc-GD1a, and GQ1b, can be demonstrated. Other antibodies may bind to mixtures or complexes of different gangliosides instead of individual ones. Interestingly, most of these antibodies are related to defined clinical subgroups of GBS. Molecular mimicry and cross-reactivity C. jejuni isolates from GBS patients express lipooligosaccharides (LOS) that mimic the carbohydrates of gangliosides. The type of ganglioside mimic in C. jejuni seems to determine the specificity of the anti-ganglioside antibodies and the associated variant of GBS. Antibodies in these patients usually are cross-reactive; they recognize LOS as well as gangliosides or ganglioside complexes. GBS after Campylobacter infection in anti-GM1/GD1a/GQ1b antibody-related cases is considered to be true example of molecular mimicry-related disease. Complement activation Postmoem studies demonstrated that local complement activation occurs at the side of nerve damage. A mice model for GBS showed that some anti-ganglioside antibodies are toxic for peripheral nerves and can cause blockade of nerve transmission and paralysis of the nerve-muscle preparation. Additionally, there is destruction of the nerve terminal and perisynaptic Schwann cells . Antibodies to GM1 affect the sodium channels at the nodes of Ranvier of rabbit peripheral nerves All of these effects appear to be dependent on complement activation and formation of the membrane attack complex. The neurotoxic effects of these antibodies can be inhibited by IVIG and the complement inhibitor eculizumab Treatment for Gillian barre syndrome: IVIG is applied in a regimen of 2 g/kg bodyweight, usually as 0.4 g/kg bodyweight per day for five consecutive days. IVIG has replaced PE as the preferred treatment in many centers, mainly because of its greater convenience and availability The combination of PE followed by IVIG was not significantly better than PE or IVIG alone . It appeared that oral steroids and, surprisingly, intravenous methylprednisolone 500 mg/day for five consecutive days alone is not beneficial in GBS . The combination of IVIG and intravenous methylprednisolone was not significantly more effective than IVIG alone. Although when a correction was made for known prognostic factors, the combined treatment shows some sho-term effect These trials show that there is an effect of immunotherapy on the course of GBS, but new studies with different regimens or another therapy that is directed toward improving the prognosis and outcome of GBS are needed Ref Harrison20th edition pg 2345
Antisnake venum
5% dextrose
Intravenous immunoglobulin
I.V. Potassium chloride
C.N.S