ABSTRACT
The lower urinary tract has two essential functions: the low-pressure storage of urine in a
continent reservoir, and the timely expulsion of stored urine in a coordinated, efficient, and
complete fashion. These two mutually exclusive functions are ultimately determined by the
activity of the smooth and striated musculature of the bladder, urethra, and external urethral
sphincter under the control of various neural circuits in the brain and spinal cord. Although a
result of complex interplay between both the central and peripheral nervous systems, these
functions are also influenced by several anatomic factors such as integrity of the pelvic floor
support and dynamic relationship of the bladder and its outlet to various points in the bony
pelvis and adjacent organs during voiding. In addition, as our understanding of lower urinary
tract neurophysiology grows, so grows the list of neurotransmitters and receptors identified as
having a role in voiding function and dysfunction. Voiding dysfunction can occur as a result
of neurologic disease or injury, disturbance of anatomical relationships within the pelvis and
urinary organs, or as an unwanted, often unrecognized pharmacologic effect of medical
therapy for other diseases. Voiding dysfunction also occurs as a result of normal aging and
is affected by changes in the viscoelastic properties of the bladder wall. As with other
neurologic systems, innervation of the lower urinary tract is not static; it changes in
response to disease and aging. This phenomenon is known as neural plasticity. More often
than not, the etiology of voiding dysfunction is multifactorial, so a fundamental under-
standing of the neuroanatomy and neurophysiologic mechanisms of the lower urinary tract is
essential.
