Abstract
This article reviewed brain mechanism of the lower urinary tract (LUT). Among autonomic nervous systems, LUT is unique in terms of afferent pathophysiology; bladder sensation is perceived soon after the storage phase and throughout the voiding phase. Within the brain, this is measured in experimental animals by the firing of single neurons and in humans by evoked potentials/functional neuroimaging. The evidence indicates that sphincter information goes up to the precentral motor cortex and other brain areas, and bladder information goes up to the insular cortex (IC)/anterior cingulate (ACG) and further to the prefrontal cortex (PFC). Another LUT-specific phenomenon is efferent pathophysiology: detrusor overactivity (exaggerated micturition reflex) occurs in brain diseases such as stroke (focal disease) and dementia with Lewy bodies (diffuse diseases, may overlap with each other). With the turning off and on of the brain-switch of micturition (at the periaqueductal gray [PAG]), there is a bladder-inhibitory PFC-IC/ACG-hypothalamus-PAG pathway, with interconnections via the PFC with a PFC-nigrostriatal D1 dopaminergic pathway and a PFC-cerebellar pathway. Brain diseases that affect these areas may cause a loss of the brain's inhibition of the micturition reflex, leading to detrusor overactivity. This has a significant clinical impact on patients and requires appropriate management.