Since its initial approval in 1989 by the US Food and Drug Administration for the treatment of
blepharospasm and other facial spasms, botulinum toxin (BoNT) has evolved into a …

Tetanus and botulinum neurotoxins cause the neuroparalytic syndromes of tetanus and
botulism, respectively, by delivering inside different types of neurons, metalloproteases …

Botulinum toxins (BoNTs) are a product of the bacteria Clostridium botulinum. By entering
nerve endings, they cleave and inactivate SNARE proteins, which are essential for …

Botulinum neurotoxins (BoNTs) are potent inhibitors of synaptic vesicle fusion and
transmitter release. The natural target of BoNTs is the peripheral neuromuscular junction …

Recent animal experiments suggested that centrally transported botulinum toxin type A
(BoNT-A) might reduce an abnormal muscle tone, though with an unknown contribution to …

Peripheral nerve section with subsequent disconnection of motor neuron (MN) cell bodies
from their skeletal muscle targets leads to a rapid reactive response involving the …

Despite the expanding clinical utility of botulinum neurotoxins, there remain problems to be
solved for attaining the best outcome. The efficacy and safety need to be reconsidered for …

Background and Purpose Botulinum toxin type A (BoNT/A) injections into hyperactive
muscles provide effective treatment for spasticity and dystonias, presumably due to its local …

Overt muscle activity and impaired spinal locomotor control hampering coordinated
movement is a hallmark of spasticity and movement disorders like dystonia. While botulinum …

Apart from the known efficacy of Botulinum Neurotoxin Type A (BoNT/A) in hyperactive
striated and smooth muscles, different pain states have become potential targets of toxin …