Role of botulinum neurotoxin–A in cerebral revascularization graft vasospasm prevention: current state of knowledge

Abstract

<jats:p>Graft stenosis and occlusion remain formidable complications in cerebral revascularization procedures, which can lead to significant morbidity and mortality. Graft vasospasm can result in early postoperative graft stenosis and occlusion and is believed to be at least partially mediated through adrenergic pathways. Despite various published treatment protocols, there is no single effective spasmolytic agent. Multiple factors, including anatomical and physiological variability in revascularization conduits, patient age, and comorbidities, have been associated with graft vasospasm pathogenesis and response to spasmolytics. The ideal spasmolytic agent thus likely needs to target multiple pathways to exert a generalizable therapeutic effect. Botulinum toxin (BTX)–A is a powerful neurotoxin widely used in clinical practice for the treatment of a variety of spastic conditions. Although its commonly described paradigm of cholinergic neural transmission blockade has been widely accepted, evidence for other mechanisms of action including inhibition of adrenergic transmission have been described in animal studies. Recently, the first pilot study demonstrating clinical use of BTX-A for cerebral revascularization graft spasm prevention has been reported. In this review, the mechanistic basis and potential future clinical role of BTX-A in graft vasospasm prevention is discussed.</jats:p>

Botulinum Toxin A for the Treatment of Sympathomimetic Pressor-Induced Digital Hand Ischemia in the Critically Ill Intensive Care Unit Patient

“…This occurs through cleavage of the SNAP-25 protein, thereby preventing vesicular fusion with the cell membrane. 1…”

“…This occurs through cleavage of the SNAP-25 protein, thereby preventing vesicular fusion with the cell membrane. 1 Despite being one of the most potent peptide toxins described, Botox has a favorable safety profile and effectively treats several disorders, including infantile strabismus, overactive bladder, cervical dystonia, and chronic migraines. [2][3][4][5] Furthermore, because of its large molecular size, it has a low diffusion rate and has a long active halflife at sites of injection.…”