Botulinum toxin A, brain and pain

Botulinum toxin type A in motor nervous system: unexplained observations and new challenges

“…For now there is no experimental evidence for that. In experiments by Antonucci et al (2008) (Bach-Rojecky et al, 2005, 2010a, 2010b, Bach Rojecky and Lacković 2009Matak and Lacković 2014;Drinovac et al, 2016) and the group of Pavone and Luvisetto (Luvisetto et al, 2006(Luvisetto et al, , 2007(Luvisetto et al, , 2015Marinelli et al, 2012;Pavone and Luvisetto 2010;Mika et al, 2011) Mazzocchio and Caleo 2015). Similar findings were obtained in quadriceps muscle of stroke-related spastic patients after BoNT/A injection into soleus muscle .…”

“…Intoxication with neurotoxin causes botulism, the disease characterized by prevention of acetylcholine release at neuromuscular junctions resulting in flaccid paralysis of skeletal muscle, and paralysis of autonomic cholinergic synapses (Matak and Lacković, 2014). BoNT/A targets synaptosomal associated protein SNAP-25, an integral part of heterotrimeric soluble Nethylmaleimidesensitive factor attachment protein receptor (SNARE) complex of proteins required for synaptic vesicle exocytosis (Blasi et al, 1993).…”

Botulinum toxin type A versus botulinum toxin type B for cervical dystonia

“…In addition to this, recent research has also suggested that Bt is active at the level multiple levels, namely sensory nerve terminals, and muscle spindles, which leads to a reduction in sensory input and fewer muscle contractions (Matak 2014;Filippi 1993;Rosales 1996;). …”

Botulinum Neurotoxin a for Chronic Migraine Headaches: Does it Work and How?

“…The light chain of BoNTA binds to and cleaves SNAP-25, part of the structure responsible for vesicular docking to the membrane that permits neurotransmitter release [10]. This results in a long lasting, reversible inhibition of neurotransmitter release from the terminal due to the stability of the BoNTA light chain in the cytosol [11]. As a result, injected BoNTA blocks neurotransmission from motor and autonomic nerve terminals, leading to muscle paralysis and inhibition of autonomic function, respectively [12].…”

“…Intramuscularly injected BoNTA has been shown to significantly decrease muscle interstitial glutamate concentration [14,15]. BoNTA may also block the normal cycling of receptors (e.g., glutamate receptors) from inside the axon to the axon membrane surface [11]. Through these mechanisms, BoNTA would directly attenuate nociceptive input from the muscles.…”