Re: The Passive and Active Contractile Properties of the Neurogenic, Underactive Bladder

for this article http://dx.doi.org/10.1016/j.juro.2013.07.029 available at http://jurology.com/ Editorial Comments: Urinary retention and incomplete bladder emptying are common forms of voiding dysfunction, particularly in older adults. Recently the concept of the underactive bladder has received increased research attention. Previously held beliefs that this type of voiding dysfunction was caused solely by poor detrusor contractility are being challenged by emerging data. The interactions between detrusor muscle, supporting connective tissues and matrix structures, and bladder innervation are complex. The role of the bladder epithelium in this process is also a focus of intense research. This particular study is important because the authors have created an animal model of the neurogenic, highly compliant bladder. Urodynamic and other physiological tests showed no evidence of contractile failure in this pilot study. This animalmodel has potential usefulness in the study of various forms of bladder underactivity. Such translational research may help to advance our understanding of voiding dysfunction in subjects ranging from geriatric patients with urinary retention and overflow incontinence to individuals with spinal cord injuries and other neurological conditions. Tomas L. Griebling, M.D., M.P.H. This is a translational article on a topic that is receiving increased attention. Detrusor underactivity is defined as a bladder contraction of either reduced strength and/or insufficient duration to complete voiding within a normal time span (International Continence Society definition). It is a prevalent condition especially in elderly patients. The prevailing thought has been that this is primarily a problem of contractile failure. This article suggests that detrusor contractility per se is not impaired, and reduced passive bladder wall stiffness and an enhanced rate of stress relaxation comprise changes in passive wall mechanical function, which, at least in this model, result in the “underactivity.” This implies that some sort of agonist might be effective for improving bladder function (unfortunately to date they have not), or improvement may be achieved by “reversing the changes to passive bladder wall mechanical function,” although exact mechanisms for accomplishing this are not suggested. Alan J. Wein, M.D., Ph.D. (hon.)