ABSTRACT
This chapter aims to review the pathophysiology of neurogenic detrusor overactivity (NDO), starting within the bladder urothelium and ending at the brain. Some NDO mechanisms may be common regardless of the site of the neurologic lesion, whereas some NDO mechanisms are neurologic lesion specific. Investigators have studied which urodynamic variables might help discriminate between NDO and idiopathic detrusor over-activity (IDO) in multiple sclerosis (MS) patients. Compared to IDO, NDO had greater peak detrusor pressures and greater first detrusor overactivity contraction pressure. In NDO bladder urothelial tissues from spinal cord injury and MS patients, adenosine triphosphate was significantly elevated by mechanical stretch and electrical field stimulation compared to control urothelial tissues. The contribution to NDO by the myofibroblasts within suburothelial lamina propria of the bladder has also been studied. The use of harvested detrusor smooth muscle from human and animal “neurogenic bladder” to study NDO pathophysiology has been ongoing for many years.
