Onuf's Nucleus - Involvement of Onuf's Nucleus in Stress Urinary Incontinence

Involvement of Onuf's Nucleus in Stress Urinary Incontinence

Stress urinary incontinence (SUI) is a common disease in women caused by pelvic floor muscle weakness. Coughing, laughing, sneezing, exercising or other movements that increase intraabdominal pressure, and thus increase pressure on the bladder, are common reasons for urine loss.

There are three layers of muscle that are known to control urine flow through the urethra; an inner band of longitudinal smooth muscle, a middle band of circular smooth muscle, and an external band of striated muscle called the rhabdosphincter. The urethra is controlled by the sympathetic, parasympathetic, and somatic divisions of the peripheral nervous system. The sympathetic innervation (nerve supply) comes from the sympathetic preganglionic neurons located in the upper lumbar spinal cord along the hypogastric nerve and terminates in the longitudinal and circular smooth muscle layers in the urethra. The parasympathetic nerve supply comes from the parasympathetic preganglionic neurons in the sacral spinal cord and also terminates in the longitudinal and circular smooth muscle layers. Finally the somatic nerve supply arises from the urethral sphincter motor neurons in the ventral horn of the sacral spinal cord; better known as Onuf’s nucleus. The pudendal nerve that extends from Onuf’s nucleus, connects directly to the rhabdosphincter muscle to control micturation.

The sympathetic storage reflex or pelvic-to-hypo-gastric reflex is initiated when the bladder swells. Stretch receptors cause postganglionic neurons to release norepinephrine (NE). NE causes the bladder to relax and the urethra to contract, thus preventing urine loss. The somatic storage reflex or the pelvic-to-pudendal or guarding reflex is initiated when one laughs, sneezes, or coughs, which causes increased bladder pressure. Glutamate is the primary excitatory transmitter for the reflex. Glutamate activates NMDA and AMPA receptors which produce action potentials. These action potentials activate the release of acetylcholine causing the rhabdosphincter muscle fibers to contract. When the guarding reflex does not function normally, SUI occurs.

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