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.

Background: Our understanding of the neural circuits controlling micturition and continence is constrained by a paucity of techniques for measuring voiding in awake, behaving mice. New method:To facilitate progress in this area, we developed a new, non-invasive assay, micturition video thermography (MVT), using a down-facing thermal camera above mice on a filter paper floor.Results: Most C57B6/J mice void infrequently, with a stereotyped behavioral sequence, and usually in a corner. The timing of each void is indicated by the warm thermal contrast of freshly voided urine. Over the following 10-15 min, urine cools to ~3 °C below the ambient temperature and spreads radially in the filter paper. By measuring the area of cool contrast comprising this "thermal void spot," we can derive the initially voided volume. Thermal videos also reveal mouse behaviors including a home-corner preference apart from void spots, and a stereotyped, secondslong pause while voiding. Comparison with existing methods and Conclusions:MVT is a robust, non-invasive method for measuring the timing, volume, and location of voiding. It improves on an existing technique, the void spot assay, by adding timing information, and unlike the cystometrogram preparation, MVT does not require surgical catheterization. Combining MVT with current neuroscience techniques will improve our understanding of the neural circuits that control continence, which is important for addressing the growing number of patients with urinary incontinence as the population ages.

The upper brainstem tegmentum is dense and complex, making it difficult to localize functions to specific subregions. In particular, the precise location and possible laterality of subregions supporting basic functions like consciousness and urinary continence remain unclear. Here, we describe a patient who presented with a right pontine tegmental syndrome caused by intraparenchymal hemorrhage. Despite hemorrhage extension into the fourth ventricle and expansion of both hemorrhage and edema into a large region of the caudal midbrain and right-sided pontine tegmentum, this patient did not lose consciousness. Instead, he developed new and total urinary retention, with residual bladder volumes of more than 1,000 mL. We conclude that injury to the right pontine tegmentum is sufficient to disrupt the micturition reflex pathway.

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