Mechanism to translation: Neural prostheses for the lower urinary tract

Abstract

Lower urinary tract (LUT) dysfunction is a common symptom of a wide array of neural disorders, including spinal cord injury, multiple sclerosis, and Parkinson's disease. Unfortunately, interventions to treat LUT dysfunction primarily manage symptoms without restoring coordinated bladder control. To regain this control, neural prostheses are being developed that operate through multiple neurophysiological mechanisms.

Here, we discuss recent advances that use three fundamentally different mechanisms; some systems target LUT reflexes to produce coordinated voiding or continence, others drive non-LUT circuits that indirectly influence bladder and urethral function, while others directly excite or block the motor components of the LUT. The work described here demonstrates substantial advances in the field, yet many of these advances have not been translated to clinical use. We suggest that developing devices to transform the state of clinical bladder care will require that known translational challenges are considered from the outset, even in basic mechanistic research.