Botulinum Neurotoxin Type A: The Poison that Can Treat the Sick

Abstract

Lower urinary tract symptoms (LUTS) are typical of several neurologic conditions, including spinal cord injuries, multiple sclerosis, Parkinson disease, and stroke. Specifically, storage LUTS (ie, daytime and nighttime frequency, urgency, and urge incontinence) sustained by neurogenic detrusor overactivity [DO] can significantly affect patients’ quality of life (QoL), increasing the disability associated with the primary disease and jeopardizing upper urinary tract function [1]. Anticholinergic drugs are currently used as the first-line pharmacologic therapy for storage LUTS, both in neurogenic and idiopathic overactive bladder (OAB) syndrome. Although cholinergic receptor antagonists have proven to be effective treatments for both neurogenic and idiopathic OAB [2,3], some patients can experience insufficient relief of the symptoms, even after dose escalation, as well as intolerable adverse events. Traditionally, those patients have been considered candidates for invasive surgical treatments, such as sacral rhizotomy, autoaugmentation, enterocystoplasty, or even urinary diversion [4]. During the last decade, the use of botulinum neurotoxin has gained wide diffusion in the treatment of neurogenic and, subsequently, idiopathic OAB. Botulinum neurotoxin has been a known cause of food poisoning since the 19th century, but it was isolated in crystal form only in 1946. Two serotypes of botulinum neurotoxins are available, but the