3.8 Review

Current Knowledge and Novel Frontiers in Lower Urinary Tract Dysfunction after Spinal Cord Injury: Basic Research Perspectives

期刊

UROLOGICAL SCIENCE
卷 33, 期 3, 页码 101-113

出版社

WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/UROS.UROS_31_22

关键词

Brain-derived neurotrophic factor; detrusor overactivity; detrusor-sphincter dyssynergia; lower urinary tract; nerve growth factor; spinal cord

资金

  1. National Institutes of Health [R01DK129194]
  2. Department of Defense [W81XWH-17-1-0403]

向作者/读者索取更多资源

This review article summarizes the recent advancements in basic research on lower urinary tract dysfunction following spinal cord injury, focusing on neurophysiologic mechanisms and changes in micturition control in animal models of SCI. It discusses how SCI impairs voluntary control of voiding and normal reflex pathways, leading to bladder hyperreflexia but inefficient bladder emptying.
This review article aims to summarize the recent advancement in basic research on lower urinary tract dysfunction (LUTD) following spinal cord injury (SCI) above the sacral level. We particularly focused on the neurophysiologic mechanisms controlling the lower urinary tract (LUT) function and the SCI-induced changes in micturition control in animal models of SCI. The LUT has two main functions, the storage and voiding of urine, that are regulated by a complex neural control system. This neural system coordinates the activity of two functional units in the LUT: the urinary bladder and an outlet including bladder neck, urethra, and striated muscles of the pelvic floor. During the storage phase, the outlet is closed and the bladder is quiescent to maintain a low intravesical pressure and continence, and during the voiding phase, the outlet relaxes and the bladder contracts to promote efficient release of urine. SCI impairs voluntary control of voiding as well as the normal reflex pathways that coordinate bladder and sphincter function. Following SCI, the bladder is initially areflexic but then becomes hyperreflexic due to the emergence of a spinal micturition reflex pathway. However, the bladder does not empty efficiently because coordination between the bladder and urethral sphincter is lost. In animal models of SCI, hyperexcitability of silent C-fiber bladder afferents is a major pathophysiological basis of neurogenic LUTD, especially detrusor overactivity. Reflex plasticity is associated with changes in the properties of neuropeptides, neurotrophic factors, or chemical receptors of afferent neurons. Not only C-fiber but also A delta-fiber could be involved in the emergence of neurogenic LUTD such as detrusor sphincter dyssynergia following SCI. Animal research using disease models helps us to detect the different contributing factors for LUTD due to SCI and to find potential targets for new treatments.

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