**1. Introduction**

Urethral sphincter dysfunction (USD) is one of the functional causes of voiding dysfunction (VD), which leads to slow or incomplete micturition in both males and females [1]. The condition can be either neurogenic or non-neurogenic. While detrusor sphincter dyssynergia (DSD) commonly stands for the well-known neurogenic cause [2], dysfunctional voiding (DV), Fowler's syndrome (FS), and poor relaxation of the external urethral sphincter (PRES) during voiding comprise the non-neurogenic causes [3,4]. Management of these functional disorders can be challenging if conventional treatment fails.

The introduction of a botulinum toxin A (BoNT-A) injection at the external urethral sphincter (EUS) was first performed in 1988 by Dykstra et al. [5]. Paralysis of the urethral sphincter and decreased urethral resistance were anticipated following the BoNT-A injection. The authors indeed found the signs of sphincter denervation and an improvement in voiding efficiency in patients with spinal cord injury (SCI) and DSD. Since then, extended use of BoNT-A in various urinary tract dysfunctions has been reported [6], however, the currently approved indications for BoNT-A for the lower urinary tract are neurogenic detrusor overactivity and overactive bladder [7]. To date, there have been only a handful of studies demonstrating the application of BoNT-A injections into the EUS, especially in the case of VDs other than DSD [8,9]. This review is an attempt to summarize the pathophysiology of BoNT-A and its therapeutic effects among different types of USD.
