What is the pathophysiology of urge urinary incontinence?

Updated: Sep 23, 2019
  • Author: Sandip P Vasavada, MD; Chief Editor: Edward David Kim, MD, FACS  more...
  • Print
Answer

Urge incontinence is involuntary urine loss associated with a feeling of urgency. The corresponding urodynamic term is detrusor overactivity, which is the observation of involuntary detrusor contractions during filling cystometry. [16, 17] These contractions may be voluntary or spontaneous and may or may not cause symptoms of urgency and/or urgency incontinence.

However, a study using a quality of life assessment of women with incontinence showed that women with urge incontinence from detrusor overactivity consistently had a worse quality of life than did women with other urodynamic diagnoses.

Urge incontinence may be a result of detrusor myopathy, neuropathy, or a combination of both. When the identifiable cause is unknown, it is termed idiopathic urge incontinence. When a definable causative neuropathic disorder exists, the coexisting urinary incontinence disorder is termed neurogenic detrusor overactivity. Symptoms of overactive bladder or urge incontinence in the absence of neurologic causes are known as detrusor instability.

The term overactive bladder describes a syndrome of urinary urgency, usually accompanied by frequency and nocturia, with or without urgency urinary incontinence, in the absence of urinary tract infection or other obvious pathology. Overactive bladder in adults is a disorder of unclear etiology and incompletely understood pathophysiology. For discussion of this topic, see the article Overactive Bladder.

Some researchers believe that detrusor overactivity represents the premature initiation of a normal micturition reflex. In vitro studies of bladder muscle strips from patients with detrusor overactivity have demonstrated an increase in response to electrical stimulation and an increased sensitivity to stimulation with acetylcholine. [18] These findings may indicate a higher sensitivity to efferent neurologic activity or a lower threshold of acetylcholine release needed to initiate a detrusor contraction.

A relative cholinergic denervation may explain some of these findings. This proposed mechanism is most plausible in cases of de novo detrusor overactivity, which follow hysterectomy or other pelvic surgery. The mechanism of denervation in idiopathic detrusor overactivity is less certain. Subtle obstruction and the effects of aging on smooth muscle and the autonomic nervous system are 2 possible contributors.

Another finding described in bladder muscle specimens from patients with detrusor overactivity is local loss of inhibitory medullary neurologic activity. Vasoactive intestinal peptide, a smooth muscle relaxant, is decreased markedly in the bladders of patients with detrusor overactivity. In addition, bladders of individuals with detrusor overactivity have been found deficient in smooth muscle–relaxing prostaglandins.


Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!