**2.2.1.1 Suprapontine lesions**

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 reducing suprapontine inhibition. (Koelbl et al, 2009)

#### **2.2.1.2 Spinal cord lesions**

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

#### **2.2.2 Non-neurogenic etiologies**

#### **2.2.2.1 Outflow obstruction**

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 obstruction causes OAB and detrusor overactivity includes partial denervation.

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 is a reduction of blood flow due to increased intravesical pressure during voiding or the increased tissue pressure of hypertrophied bladder wall during filling. (Azadzoi et al, 1996) (Greenland & Brading, 2001)
