Abstract
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.
Lingua originale | English |
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pagine (da-a) | 1712-1713 |
Numero di pagine | 2 |
Rivista | Clinical Neurophysiology |
Volume | 124 |
DOI | |
Stato di pubblicazione | Pubblicato - 2013 |
Keywords
- Lambert-Eaton myasthenic syndrome
- myopathy