**2.2.2.2 Aging**

164 Urinary Incontinence

For coordinated micturition to occur, parasympathetic stimulation of the detrusor occurs via cholinergic muscarinic receptors. Urethral smooth muscle contraction occurs chiefly by stimulation of alpha-adrenerigic receptors. (Fowler et al, 2008) In addition, a variety of neurotransmitter systems in the urothelial lining of the bladder and in bladder interstitial cells likely play a role in mediating bladder contraction and relaxation via afferent signaling. (Andersson, 2002) This complex interplay results in socially appropriate and effective voiding. Any disruption in this pathway can lead to storage and/or emptying disorders.

The presumed etiology of OAB is uninhibited bladder contractions, but overactivity is not sufficient to cause incontinence (e.g. OABdry). In addition, leakage symptoms may be due to factors outside of the lower urinary tract such as failure of compensatory mechanisms in the lower urinary tract (e.g. fascial and muscular urethral support "hammock" that compresses the urethra when there is increased abdominal pressure or when the pelvic muscles are

Patients with suprapontine lesions such as cerebrovascular disease and Parkinson's disease can present with detrusor overactivity. These patients lose voluntary inhibition of micturition most likely secondary to uninhibited detrusor contractions. (Fall, et al, 1989) (Fall, et al, 1995) The cerebral cortex and the basal ganglia are theorized to suppress the micturition reflex. Therefore, damage to the brain results in bladder overactivity by

Spinal cord disruption below the level of the pons leads to unsustained and uncoordinated detrusor contractions. (Koelbl et al, 2009) Impairment or loss of bladder sensation usually occurs. Patients with spinal cord lesions above the lumbosacral level lose voluntary and supraspinal control of micturition. Bladder overactivity in these patients is mediated by

Outflow obstruction is associated with detrusor overactivity. (Koelbl et al, 2009) Up to 50% of patients with symptomatic benign prostatic enlargement exhibit bladder outlet obstruction. ( de Nunzio et al, 2003) However, OAB symptoms can occur independently of bladder outlet obstruction. One hypothesis that has been proposed to explain how outflow

Denervation injury has been shown to increase detrusor supersensitivity to acetylcholine. (Harrison et al, 1987) This may be the basis of unstable bladder activity. However, it is not clear how denervation develops in patients with outflow obstruction. It is possible that there

obstruction causes OAB and detrusor overactivity includes partial denervation.

Bladder overactivity may be related to neurogenic, myogenic, or idiopathic origins.

contracted) , and functional impairments in some patients.

reducing suprapontine inhibition. (Koelbl et al, 2009)

spinal reflex pathways (deGroat et al, 1993) (Bros & Comarr,1971)

**2.2 OAB etiology** 

**2.2.1 Neurogenic etiologies 2.2.1.1 Suprapontine lesions** 

**2.2.1.2 Spinal cord lesions** 

**2.2.2 Non-neurogenic etiologies** 

**2.2.2.1 Outflow obstruction** 

The prevalence of OAB in both men and women increases with age. In addition, storage symptom scores increase with age while bladder compliance decreases. (Koelbl et al, 2009) This implies that bladder function in both sexes has age related alterations. (Araki et al, 2003) There can be difficulty however, in determining in the elderly, the difference between neurogenic and non-neurogenic causes.

### **2.2.2.3 Estrogen deficiency**

Menopause and estrogen deficiency have been implicated in the etiology of OAB symptoms. (Koelbl et al, 2009) Estrogen receptors (ERs) have been identified in the bladder and urethra. (Blakeman et al, 2000) The effect estrogen has on bladder contractility has yet to be elucidated.

However, it has been shown that estrogen replacement therapy can significantly improve the symptoms of frequency, urgency and urge incontinence. (Eriksen & Rasmussen,1992) In addition, a metaanalysis of the effects of estrogen therapy on symptoms of OAB in postmenopausal women showed that estrogen therapy was associated with significant improvements in all symptoms of OAB. (Cardoza et al, 2004b) Thus it appears that menopause plays role in the development of bladder overactivity and OAB symptoms in women.
