The normal detrusor muscle undergoes receptive relaxation to allow urine storage, without causing a rise in intravesical pressure. When the bladder capacity is reached, sensory stimuli generate a desire to void and, when socially appropriate, the detrusor muscle contracts and voiding takes place due to the rise in intravesical pressure. If the ability for receptive relaxation is lost, the sensory stimuli are produced before the bladder is full and an intense urge to void is experienced. This recurs again as the bladder refills. The urge to void can be so intense that the patient becomes incontinent. This is known as urge incontinence and often includes the triad of symptoms:
1. urgency of micturition,
2. frequency of micturition,
These symptoms are seen in detrusor overactivity, formerly called detrusor instability, which can be proven with urody-namics (UDS). This condition may be secondary to increased stimulation of the trigone, for example bladder stone, urine infection, malignant cystitis or a neurological cause such as stroke. Alternatively, if no cause for the detrusor overactivity is identified, it is termed primary detrusor overactivity.
The term overactive bladder (OAB) is also used and can be defined from either UDS findings (e.g. detrusor overactivity) or symptoms (e.g. urgency).
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