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limb muscles such as the extensor digitorum communis, with a lower yield in limb muscles in general than expected in other MG populations83,87 The diagnostic yield in any patient suspected to have MG studied electrodiagnostically can be improved upon by withdrawing cholinesterase inhibitors for 12 hours or more prior to testing and by warming tested limbs adequately It must be emphasized that none of the aforementioned electrophysiological tools are speci c for either MG or any other DNMT Any of them can be abnormal in any nerve disease in which active reinnervation and immature NMJs occur ALS is a notable example of this305 The electrical ndings in transient neonatal MG are analogous to those found in adults102,105,306 A decremental CMAP response is typically demonstrable at low rates of stimulation, which can be minimized with postactivation excitation and augmented with postactivation exhaustion Frequently, a decrement occurring at high rates of stimulation occurs as well, depending on the severity of the disease Tapering anticholinesterase medication and assessing the degree of decrement can be used in an attempt to determine safe medication withdrawal The absence of a decrement indicates adequate (and permanent) recovery
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AChR antibodies are detected in the majority but not in all patients with MG307 There are three types of detectable antibodies directed speci cally at the AChR receptor These are also described in more detail in 2 AChR-binding antibodies, AChR-modulating antibodies, and AChR-blocking antibodies are all commercially available tests228,308 Elevation of one or more of these three antibody levels identi es 80 90% of patients with all grades of MG The sensitivity is estimated at 70 80% in MG clinically restricted to extraocular muscles In patients who have generalized disease, a sensitivity of over 90% is expected There does not appear to be signi cant differences in phenotype, EDX signature, natural history of disease, or response to treatment between patients who are seropositive and seronegative66 AChR-binding antibodies are the most frequently tested and identi ed Most patients have both the binding and the modulating antibodies present, but approximately 8% will have only one of these antibodies detected71,228,308 AChR-modulating antibodies also have value as a surveillance tool for thymoma, as 73% of patients with thymoma and MG will have modulating antibodies producing a >90% receptor loss71 AChRblocking antibodies are present in approximately half of patients with generalized MG but only 30% of patients with ocular disease228,308 As <1% of patients will have blocking without detectable binding or modulating antibodies, this particular test has limited pragmatic value
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AChR-binding antibodies are highly speci c for MG, but these can also be detected in patients with autoimmune liver disorders, approximately 13% of patients with LEMS, and about 3% of patient with lung cancer without an apparent neurological disorder228 It is important to emphasize that the value of any of these tests is strictly in initial diagnosis, or in the case of modulating antibodies, as a potential marker for thymoma The serum titer of any of these antibodies does not correlate with disease severity Following titers is generally not considered an accurate means to judge treatment response, although in some patients, a falling antibody titer following thymectomy seems to correlate with clinical improvement309 In 2001, the rst report of antibodies directed against MuSK antibodies in MG was published310 Currently, it is estimated that 40% of patients with MG who do not have one or more of the aforementioned AChR antibodies will be found to be MuSK seropositive Most studies have suggested no overlap between MuSK and AChR antibodies in patients with MG,85,310 although exceptions to this rule at least in Japanese patients occur118 Unlike AChR antibodies, there appears to be a correlation between anti-MuSK titers, disease severity, and the application of immunomodulatory therapy311 On the other hand, thymectomy does not signi cantly alter antiMuSK levels Striated muscle antibodies refer to a class of antibodies directed against components of skeletal muscle including titin, the ryanodine receptor, myosin, and -actinin312 These are discoverable in approximately 30% of adult patients with MG without thymoma, 24% of patients with thymoma without MG, and 70 80% of patients who have both71,228,313,314 These antibodies may also occur in high titer in individuals who do not appear at the time of testing to have either MG or thymoma Their ultimate signi cance in these situations is unknown In some patients, striated muscle antibodies may be the only serological marker of autoimmunity in patients with MG Unlike AChR antibodies, striational antibodies can be of value in monitoring the disease course Persistence or recurrence of high titers of these antibodies may suggest incomplete resection or recurrence of thymoma, respectively There is also a known association between MG and certain HLA genotypes Some studies have noted a predilection for HLA types A1, A3, B7, B8, and DRw3 in patients with MG315 These HLA subtypes may somehow predispose patients to autoimmune diseases HLA genotyping is not routinely used in the evaluation of patients suspected to have MG Antibodies directed against the Kv14 subunit of voltage-gated potassium channels have been described to occur in a percentage of patients with MG but not in patients with thymoma, in ammatory myopathy, or in healthy controls93 These were found exclusively in
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