Pathogenesis of urinary dysfunction

To understand the pathogenesis of urination and defecation disorders with different levels of damage to the systems that regulate them, it is necessary first of all to focus on the innervation mechanisms of the bladder and rectum.

The function of stretching the urinary bladder during accumulation of urine and its contraction during emptying is performed by the smooth muscle detrusor. The synergists of the detrusor during emptying are the muscles of the abdominal press and perineum. The outlet of the urinary bladder into the urethra is closed by two sphincters - smooth muscle internal and striated external. The detrusor and sphincters function reciprocally: when emptying the urinary bladder, the detrusor contracts and the sphincters relax, when the bladder closes, the relationship is reversed, i.e. the detrusor relaxes and the sphincters contract.

Control of bladder function is predominantly parasympathetic. The spinal parasympathetic center of the bladder is located in the conus medullaris, in the nuclei of the lateral horns of the sacral segments SII-SIV.

The nuclei fibers initially pass as part of the pudendal plexus, then go along both sides of the rectum and, joining the hypogastric sympathetic nerves, form the vesical plexus. Postganglionic parasympathetic fibers innervate the smooth muscles of the bladder, its neck, and the urethra. Some of the preganglionic nerves end in the intramural ganglia in the thickness of the bladder, causing automatic urination with partial or complete denervation of the bladder. In general, parasympathetic stimulation is accompanied by contraction of the detrusor and relaxation of the internal sphincter. As a result, the bladder is emptied. Damage to the parasympathetic pathways leads to atony of the bladder.

Preganglionic sympathetic nerve fibers originate in the intermediolateral nuclei of the lateral horns of spinal segments TXI, TXII, LI, LII. Some of them, after passing through the sympathetic trunk, terminate in the inferior mesenteric and hypogastric plexuses. Postganglionic neurons are directed from here to the smooth muscles of the bladder wall and the internal sphincter. Another part of the preganglionic sympathetic nerves terminate in the vesical plexus around the neck of the bladder or in the intramural ganglia of the bladder wall.

Histochemical studies have revealed a large number of adrenergic nerve endings throughout the bladder and urethra, especially numerous at the base of the bladder and proximal urethra (a-adrenergic receptors), and fewer in the bladder body (alpha-adrenergic receptors). Stimulation of alpha-adrenergic receptors causes an increase in outlet resistance (contraction of the internal sphincter), and stimulation of beta-adrenergic receptors leads to relaxation of the bladder body (relaxation of the detrusor). Animal experiments have demonstrated the presence of alpha-adrenergic receptors in the parasympathetic ganglia of the detrusor. It is assumed that sympathetic control of the bladder is mediated by sympathetic effects on transmission in the parasympathetic ganglia. Thus, sympathetic stimulation causes relaxation of the detrusor and contraction of the internal sphincter, which leads to an increase in filling of the bladder and inhibition of evacuation of urine from it. It is believed that damage to the sympathetic nerves does not lead to significant urination disorders.

The external sphincter of the bladder is a striated muscle and receives somatic innervation from the anterior horn cells of the sacral segments (SII-SIV). Although it is under voluntary control, it opens only when urine passes through the internal sphincter, and it remains open until the bladder is completely empty.

Afferent impulses from the urinary bladder are conducted by the hypogastric nerves, the sensitivity of the urethral part of the mucous membrane is determined by the pelvic and pudendal nerves. Some of these fibers go to the posterior horns of the spinal cord, participating in the formation of the spinal reflex arc (at the level of SII-SIV), some rise as part of thin bundles (Goll's bundles) to the brain, providing a sensation of the urge to urinate and its voluntary existence.

The cortical center of urination, according to most authors, is localized in the paracentral lobule. There is also an opinion about its localization in the anterior central gyrus, in the area of the center of the thigh muscles. Corticospinal fibers pass in the anterior and lateral columns of the spinal cord and have a two-way connection with the spinal nuclei. Subcortical centers are located in the thalamus, hypothalamic region and some other sections. Research in this area is not yet complete.

Thus, the function of the urinary bladder is based on spinal reflexes, which are in reciprocal relationships during emptying and closing. These unconditioned reflexes are subject to cortical influence, which, according to the principle of a conditioned reflex, causes voluntary urination.

The anatomical and functional relationships of the act of defecation are similar to urination. The exit from the rectum is closed by a smooth-muscle internal sphincter, which functions involuntarily, and a striated external sphincter, which acts voluntarily. The muscles of the perineum, especially m.levator ani, play an auxiliary role in this. Getting into the rectum, feces reflexively cause peristalsis due to the contraction of its longitudinal circular muscles and the opening of the internal sphincter, which receives parasympathetic innervation from the nuclei of the II-IV sacral segments. These fibers are part of the pelvic nerves. Sympathetic nerves, originating in the intermediolateral nuclei of the lateral horns of the I-II lumbar segments, approach the smooth-muscle internal sphincter. Sympathetic stimulation leads to inhibition of peristalsis. The external voluntary sphincter of the rectum receives impulses from the anterior corneal apparatus of the spinal cord via the pudendal nerve.

In the wall of the rectum, as well as in the urinary bladder, there is an intramural plexus, due to which the autonomous function of the rectum can be carried out under conditions of its denervation.

Sensory fibers from the rectum pass into the spinal cord through the posterior roots. One part of these fibers participates in the formation of the spinal reflex arc, the other rises to the brain, causing a sensation of the urge to defecate. The cortical center of defecation, according to most authors, is localized in the upper part of the anterior central gyrus. Conductors from the cortex to the spinal centers pass in the anterior and anterolateral columns of the spinal cord. The subcortical apparatus is located in the hypothalamus, nuclei of the brain stem. Afferent impulses entering the cortex arise when feces pass into the rectum and move toward the anus. Defecation can be voluntarily delayed by contraction of the striated muscles of the pelvic floor and the external sphincter. Voluntary defecation occurs under conditions of peristalsis of the rectum, relaxation of the smooth muscle internal sphincter and opening of the external one. At the same time, the abdominal muscles contract synergistically.

The unconditional reflex activity of the spinal reflex arc during defecation, as well as during urination, is under constant control of more complex higher mechanisms, in particular the cortical center, the function of which is determined by the corresponding conditions. The pathogenesis of urination disorders consists in the disruption of the considered relationships as a result of structural defects in various lesions of the nervous system, which lead to urination and defecation disorders, combined in pathological conditions.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ], [ 7 ]