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Ceftriaxone in amyotrophic lateral sclerosis
Author(s) -
Ettore Beghi,
Maria Laura Presti,
Cristina Manzoni,
Tiziana Mennini,
Cinzia Cavestro,
M. Poloni,
A Micheli,
P Pinelli,
Roberto Mai,
D. Facchetti,
D. Testa,
F. Cornelio,
Letizia Mazzini,
Carla Baizarini,
Gabriele Mora,
Adriano Chiò,
Davide Schiffer,
P. Tonali,
Mario Sabatelli,
T Mignogna,
G Lippi,
M. Manfredi,
Maurizio Inghilleri,
Massimo Musicco
Publication year - 1996
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.1996.tb00220.x
Subject(s) - amyotrophic lateral sclerosis , medicine , ceftriaxone , glutamate receptor , neurochemical , spinal cord , anesthesia , neuroprotection , excitatory amino acid transporter , pharmacology , antibiotics , disease , psychiatry , microbiology and biotechnology , biology , receptor
One hundred and eight patients with amyotrophic lateral sclerosis (ALS) received ceftriaxone 2 g daily i.v. (62) or i.m. (34) or by both routes (12), for 21‐day cycles on an open basis. Baseline MRC and Norris scores were similar to those at the end of the first 21‐day cycle of therapy. Seven patients showed remarkable clinical improvement, mostly segmental, which started during the first week of treatment and lasted up to 2 months after its completion. Improvement was also noted in seven out of 21 cases given a subsequent cycle of treatment. Based on these findings, the drug is supposed to act by altering the neurochemical transmission at the neuromuscular junction and/or by facilitating the presynaptic uptake of glutamate at the synaptic junction. This hypothesis positively correlates with the results of in vitro experiments showing that ceftriaxone increases 3 H‐glutamate uptake in rat spinal cord synaptosomes.