TY - JOUR
T1 - The tiles make a puzzle but the single tile is not the puzzle: The need for a global assessment of the patient
AU - Caliandro, Pietro
AU - Padua, Luca
AU - Evoli Stampanoni-B, Amelia
PY - 2013
Y1 - 2013
N2 - 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.
AB - 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.
KW - Lambert-Eaton myasthenic syndrome
KW - myopathy
KW - Lambert-Eaton myasthenic syndrome
KW - myopathy
UR - http://hdl.handle.net/10807/53815
U2 - 10.1016/j.clinph.2013.03.011
DO - 10.1016/j.clinph.2013.03.011
M3 - Article
SN - 1872-8952
VL - 124
SP - 1712
EP - 1713
JO - Clinical Neurophysiology
JF - Clinical Neurophysiology
ER -