**9. Conclusions**

The underlying pathophysiology of bladder oversensitivity in lower urinary tract disorders has not been well elucidated. However, chronic inflammation resulting in activation of the suburothelial sensory fibers, over-expression of the sensory receptors, and increased production of inflammatory proteins are likely to develop in patients with OAB, IC or bladder oversensitivity. Intravesical BoNT-A injection at the dose of 100 U can effectively reduce bladder inflammation, decrease the hyperactivity of sensory afferent nerves, restore normal urothelial barrier function, and desensitize the inflammatory printings in the central nervous system. The bladder oversensitive symptoms of OAB and IC can be improved after BoNT-A injections. However, large PVR and dysuria might develop after intravesical BoNT-A injection, especially in the elderly patients with low detrusor contractility. Liposome or LESWs can deliver BoNT-A across the urothelial barrier and have therapeutic effects on decreasing frequency and urgency episodes without compromising voiding function; these treatment modalities might have potential in treating patients with sensory bladder disorders.

**Author Contributions:** Y.-H.J.: literature search and part of manuscript writing, W.-R.Y.: literature search and part of manuscript writing, H.-C.K.: critical comment and manuscript rearrangement. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research received no external funding.

**Conflicts of Interest:** The authors declare no conflict of interest.
