The urinary bladder has only two functions, to store urine and to eliminate it from the body at socially convenient times. These functions depend on total integrity of the nervous system from brain to bladder. Many different neurotransmitter pathways are involved, modulating proper voluntary control over the reciprocal relationship between the storage function of the bladder and the outlet sphincters of the urethra. When voluntary control is lost or disrupted through neurological disease or damage then aberrant reflexes can take over resulting in incontinence. Such reflexes often involve the loss of those inhibitory mechanisms which normally suppress bladder contractions during the filling phase or sphincter contractions during the emptying phase. Treatment of incontinence by applied neuromodulation probably utilizes residual reflex pathways by which electrical stimulation can inhibit unwanted detrusor contractions or suppress the overactive urethral sphincter. With improvements in our understanding of the pathophysiology of voiding dysfunction, better diagnosis and the latest technical advances, for example, combining neuromodulation for detrusor hyper-reflexia with sacral anterior root stimulation for emptying the paralysed bladder (Brindley, 1988), we might hope to develop a new generation of implantable devices for treating people with incontinence (Craggs, 1997).There are still many gaps in our knowledge of neuromodulation of the lower urinary tract, for example we know little about the cerebral control of micturition in man. Such knowledge may be important for a better understanding of the many conditions we currently label 'idiopathic'. Future opportunities offered by functional magnetic resonance imaging and spectroscopy may help us to identify pathways and neurotransmitters in the brain of humans to complement the latest animal studies using transneuronal virus tracing to identify central micturition pathways.