The tiles make a puzzle but the single tile is not the puzzle: The need for a global assessment of the patient

The Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease of the neuromuscular transmission associated, in most patients, with antibodies against the voltage-gated calcium channel (VGCC) on the presynaptic nerve terminal (Lennon et al., 1995). The antibody attack results in a reduced influx of calcium into the presynaptic bottom, leading to a defect of acetylcholine release (Fukunaga et al., 1983 and Lang et al., 1987). As a consequence, the availability of acetylcholine at the neuromuscular junction is reduced and depolarization of the postsynaptic muscle membrane is impaired, causing weakness and fatigability.