Editing Functional: Overactive Bladder (section)

== Pathophysiology ==

* No animal model of OAB because reporting of subjective symptoms in animals is not possible
* '''3 hypotheses:''' 
*#'''Neurogenic'''
*#'''Myogenic'''
*#'''Integrative'''
*#* '''Neurogenic hypothesis'''
*#** '''Suggests that DO arises from generalized, nerve-mediated excitation of the detrusor muscle.'''
*#*** Nerve-mediated detrusor excitation is normal during voiding, where it is associated synergically with relaxation of the bladder outlet.
*#*** '''Nerve-mediated detrusor excitation should not occur during urine storage because of inhibitory influences within the CNS.'''
*#**** '''Emergence of inappropriate excitation during storage implies:'''
*#***** '''Loss of inhibition'''
*#***** '''Re-emergence of primitive spinal bladder reflexes'''
*#***** '''Acquisition of new reflexes'''
*#***** '''Sensitization of afferents.'''
*#* '''Myogenic hypothesis'''
*#** '''Suggests that overactive detrusor contractions result from a combination of an increased likelihood of spontaneous excitation within the smooth muscle of the bladder and enhanced propagation of this activity to affect an excessive proportion of the bladder wall'''
*#* '''Integrative hypothesis'''
*#** '''Suggests that a range of triggers can generate localized detrusor contractions''', which can spread in the bladder wall through various routes of propagation. Consequently, '''urgency is a result of distortions in the bladder wall, and it is associated with urodynamic DO if the contractions spread to a sufficient proportion of the bladder wall'''
* '''Aging, neurologic disease, female gender, bladder outlet obstruction, and metabolic disease are potential influences on OAB etiology'''