The Brain and the Bladder: Forebrain Control of Urinary (In)Continence

Abstract

Neural circuits extending from the cerebral cortex to the bladder maintain urinary continence and allow voiding when it is socially appropriate. Injuries to certain brain regions produce a specific disruption known as urge incontinence. This neurologic symptom is distinguished by bladder spasticity, with sudden urges to void and frequent inability to maintain continence. The precise localization of neural circuit disruptions responsible for urge incontinence remains poorly defined, partly because the brain regions, cell types, and circuit connections that normally maintain continence are unknown. Here, we review what is known about the micturition reflex circuit and about forebrain control of continence from experimental animal studies and human lesion data. Based on this information, we hypothesize that urge incontinence results from damage to a descending pathway that normally maintains urinary continence. This pathway begins with excitatory neurons in the prefrontal cortex and relays subcortically, through inhibitory neurons that may help suppress reflex micturition during sleep and until it is safe and socially appropriate to void. Identifying the specific cell types and circuit connections that constitute the continence-promoting pathway, from the forebrain to the brainstem, will help us better understand why some brain lesions and neurodegenerative diseases disrupt continence. This information is needed to pave the way toward better treatments for neurologic patients suffering from urge incontinence.

Shunt Surgery Efficacy Is Correlated With Baseline Cerebrum Perfusion in Idiopathic Normal Pressure Hydrocephalus: A 3D Pulsed Arterial-Spin Labeling Study

“…The higher brain’s net effect on micturition is thought to be inhibitory. Moreover, the micturition reflex passes through the dorsolateral frontal cortex, anterior cingulate cortex, and hypothalamus ( Tish and Geerling, 2020 ) as a part of the frontal-subcortical pathway and is closely related to the urinary control function. Preoperative perfusion in the cingulate gyrus being associated with recovery of bladder function is likely to predict the functional restoration of the descending cingulate pathway or cingulate cortex after shunt surgery.…”

The intracerebroventricular injection of lipopolysaccharide may induce neurogenic detrusor overactivity symptoms in mice

“…The descending neural projections from forebrain to pontine micturition center (PMC) may be responsible for the inhibition and activation of the micturition reflex in time to maintain continence. 27 When it is time to void, PMC is released from the suppression of cortex and subcortical central of the brain, and the storage phase changes to F I G U R E 8 Nissl staining of the prefrontal cortex in mice (Nissl staining, ×40, ×400). (A) The prefrontal cortex sections of the control and the i.c.v.…”

Urinary Incontinence and Alzheimer’s Disease: Insights From Patients and Preclinical Models

“…In addition to the autonomic signals between the brain and bladder, the CNS plays a role in bladder contraction and voluntary release of urine when acceptable (i.e., when on a toilet). This conscience decision to void requires coordination with the relaxation of the internal sphincter, controlled by efferent input from autonomic nervous system, and the external sphincter, controlled by the somatic nervous system through the PMC (Lim, 2017;Tish and Geerling, 2020).…”

“…Neurologic lesion in nerve centers of the micturition pathway can lead to neurogenic bladder incontinence. The most common conditions that experience UI are Alzheimer's disease, birth defects of the spinal cord, brain or spinal cord tumors, cerebral palsy, multiple sclerosis, Parkinson's disease, traumatic brain injury, and spinal cord injury (Ginsberg, 2013;Tish and Geerling, 2020). Less common cause of neurogenic bladder incontinence are autonomic neuropathy due to diabetes mellitus, pelvic surgery complication, and cauda equina syndrome (Ginsberg, 2013).…”

“…These lesions alter the signal sent between the brain and bladder, resulting in dysfunction. Similarly in AD patients, damage to the brain occurs in more than one location so pinpointing the region(s) causing UI is elusive (Tish and Geerling, 2020).…”