“…Locally injected, BoNT is taken up into the nerve terminal via endocytosis [12], and, by proteolytic cleavage of the SNARE proteins SNAP‐25 (BoNT/A) or Synaptobrevin (BoNT/B) which are both necessary for the acetylcholine vesicles’ fusion with the cell membrane [13,14], reduces the cholinergic peripheral neurotransmission for a limited time [15]. Therefore, a rational symptomatic therapy of hypertonia of the jaw muscles are local injections with BoNT and this was shown in single cases for a variety of conditions [16–19], and for patients with traumatic brain injury or following a stroke [5,6,8,20].…”