**2. Sensory Bladder Disorders**

Sensory bladder disorders are caused by sensation abnormality and include OAB syndrome and interstitial cystitis/painful bladder syndrome (IC/PBS). Both of these have similar irritative bladder symptoms but have different clinical features in terms of urinary incontinence and bladder pain. In OAB patients, urgency is the cardinal symptom along with urinary frequency, nocturia, and urgent incontinence. By contrast, the patients with (IC/PBS) are bothered by bladder pain, urinary frequency, and nocturia [4]. The brief description of probable sensory disturbances occurrence are illustrated in Figure 1.

**Figure 1.** Sensory bladder disorders: The sensory disturbances of an unstable bladder may elicit from activation of silence C-fibers due to noxious stimuli (1), stretching stretch-mediated receptors, and myofibroblasts (2), chemicals inducing urothelial signaling (3), and signals generated in a modulated motor-sensory system (4).

The pathophysiology of OAB is not well understood but may involve disorders of urothelial signaling, detrusor muscle instability, and nerve hyperexcitability [5]. For instance, metabolic derangement, bladder outlet obstruction, and inflammation can underlie the disturbances of these three factors of the bladder and can contribute to OAB. OAB has a high prevalence (around 16%–20%) [6], and its symptoms have detrimental effects on individual quality of life and incur societal costs for public health [7]. IC/PBS may develop due to urothelial dysfunction and cause an inflammatory reaction of the bladder and cause permanent inflammatory imprinting in the central nervous system [4]. Dysfunction of the urothelial lining may cause the activation of mast cells and the winding up of capsaicin-sensitive nerves. The release of neurotransmitters from the urothelium and nerve endings then provokes peripheral and central pain sensitization. The prevalence of IC/PBS among adult women is estimated to be between 2.7% and 6.5% [8].

The first-line therapies for OAB patients are behavioral therapies and lifestyle modifications. The second-line treatments include the monotherapy or combinations of antimuscarinics and the β3-adrenoceptor agonist. For refractory cases of OAB, intradetrusor injection of onaBoNTA or neuromodulation can be considered as third-line therapies [9].

For patients with IC/PBS, patient education and behavioral modification are essential in first-line therapy. The oral medications of amitriptyline, cimetidine, hydroxyzine, or pentosan polysulphate as well as the intravesical treatments of dimethyl sulphoxide (DMSO), heparin, or lidocaine are considered as second-line therapies. The third-line treatments include cystoscopic low-pressure hydrodistention under anesthesia and fulguration for Hunner's lesions. Intradetrusor injection of onaBoNTA is the fourth-line therapy for selective IC/PBS patients [10].
