The neural control of micturition

Abstract

The lower urinary tract is innervated by a complex system of autonomic and somatic nerves, the former of which control the smooth muscle of the bladder and the urethra and the latter of which activate the striated sphincter. Afferent fibres travel with the parasympathetic, sympathetic and somatic nerves. The recent discovery of the sensory properties of the urothelium has triggered an intensive investigation into the importance of neural–urothelial interactions in health and disease states. Multiple CNS pathways that carry information between the brain and the spinal cord are involved in the regulation of the lower urinary tract. The neural organization that controls bladder filling and maintains continence through the guarding reflex is organized within the spinal cord. However, voluntary voiding, a central part of human behaviour, is dependent on complex neural pathways in the brain that have been identified with functional brain-imaging techniques. The periaqueductal grey (PAG) receives sensory input from the bladder and seems to have a central role in both registering the extent of bladder fullness and controlling the initiation of voiding. The PAG makes multiple connections with many other brain areas, including the pontine micturition centre (PMC), the thalamus, the prefrontal cortex and the insula. During urine storage, the PAG relays bladder filling information to higher centres, and might participate in the tonic suppression of voiding. During voiding, PMC suppression is interrupted by activity in the prefrontal cortex and the hypothalamus. Excitation of the PMC then activates descending pathways to the spinal cord that cause sequential urethral relaxation and contraction of the detrusor. During postnatal development, the maturation of central neural pathways leads to the downregulation of reflex voiding and the emergence of voluntary voiding mechanisms. However, primitive voiding reflexes can re-emerge following neural injury. A full understanding of the pathophysiological changes and neuroplasticity that underlie idiopathic detrusor overactivity, cystitis and painful bladder conditions has yet to be elucidated, although recent progress has been made. New therapies for the treatment of detrusor overactivity include vanilloids and, most recently, detrusor injection of botulinum toxin A.