Two patients were initially diagnosed with myasthenia gravis with elev
ated titers of acetylcholine receptor antibodies. Features including w
eakness that normalized with sustained contraction, areflexia, autonom
ic symptoms, and low-amplitude baseline compound muscle action potenti
als with abnormal increments following brief exercise and high-frequen
cy repetitive stimulation, however, suggested that these patients had
Lambert-Eaton myasthenic syndrome. One patient had antibodies directed
against presynaptic calcium channels, confirming the diagnosis. The s
econd patient was seronegative for these antibodies but had elevated t
iters of antistriated muscle antibodies. This shows that serologic stu
dies can conflict with clinical and electrodiagnostic findings in pati
ents with Lambert-Eaton syndrome. These cases also point out that acet
ylcholine receptor antibodies are not necessarily diagnostic of myasth
enia gravis in patients with Lambert-Eaton syndrome. Instead, these an
tibodies could represent a nonpathogenic epiphenomenon.