Drug Delivery Approaches for OAB

Overactive bladder (OAB) syndrome is characterised by “urinary urgency, usually accompanied by frequency and nocturia, with or without urgency urinary incontinence, in the absence of urinary tract infection (UTI) or other obvious pathology” [1]. The etiological factors of OAB can be neurogenic, myogenic and urotheliogenic [2][3]. Abnormal afferent excitability and central sensory processing are the neurogenic causes, and it is prevalent in patients suffering from Parkinson’s disease, multiple sclerosis and cerebrovascular disease [3]. Abnormal transmission of nonadrenergic noncholinergic neurotransmitter is another neurogenic factor that can also cause OAB [4]. The spontaneous contraction of the detrusor muscle (Figure 1) and hypersensitivity to incoming signals is a myogenic factor, whereas changes in ion channel, urothelial signalling and increased afferent activity are urotheliogenic factors [5][6][7]. Changes or disturbances in any of these factors, including any combinations, can cause OAB. Additionally, metabolic derangement, bladder inflammation (interstitial cystitis), and bladder obstruction due to benign prostatic hyperplasia may also cause OAB. These factors typically increase the excitability of the nerve, the detrusor muscle and alter the barrier and sensory functions of the urothelium [2][3].