MICTURITION

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The storage and elimination of urine is regulated by neural circuits involving the autonomic and somatic nervous systems. The storage is facilitated by lumbosacral reflexes, while voiding involves spinal and encephalic centers.

 

 

Storage reflexes

 

The bladder distension stimulates small myelinic fibers of the pelvic nerves that reach the spinal cord and synapse on interneurons of the gray intermediate matter. Some of these interneurons stimulate somatic cholinergic neurons in the Onuf’s nucleus of the sacral segments. The axons of the cells of this nucleus form part of the pudendal nerve[1] that increases the tone of the striated urethral muscle to retain the urine. Other interneurons stimulate the preganglionic sympathetic neurons located at the level of spinal cord segments L2 to L5 in the cat and L1 to L4 in the dog. These preganglionic sympathetic neurons reach the caudal mesenteric ganglion to synapse on postganglionic neurons that form the hypogastric nerve. They allow the distension of the bladder and increase the tone of the neck.[2].

 

A group of neurons in the sacral segments, known as Gert's nucleus, receive neurons from the bladder trough the pelvic nerves, and projects to the periaqueductal gray matter in the brain stem. In turn, this center projects to the hypothalamus, cingulate gyrus and frontal cortex, to control voluntary micturition. Some authors describe that ascending pathways involve: the spinoreticular tract (in the ventral funiculus), the spinothalamic tract in the lateral funiculus and the gracile fascicle (in the dorsal funiculus).

 

During storage, descending pathways from the medulla oblongata to the Onuf nucleus, help to maintain continence by contracting the pelvic floor in situations that increase intra-abdominal pressure.

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The afferent pathways from the urine bladder are made up of myelin and myelin neurons. The first ones come from mechanoreceptors and the second from chemoreceptors. These chemoreceptors are activated in an inflammatory response. The properties of these afferent fibers are altered in spinal cord injuries and induce bladder activity by acting on efferent neurons in the sacral segments.

 

 

Voiding reflexes

 

The periaqueductal gray matter projects to the pontine micturition center to start the micturition reflex[3]. In the dog and cat two pontine micturition centers exist: the commonly known pontine micturition center (PMC) responsible for urine emptying, and a second which functions as the urine storage facilitator center. The first is located in the locus ceruleus (or coeruleus), and the second in the nucleus subceruleus (subcoeruleus). Micturition is controlled by coordination of both centers. Descending glutaminergic projections, from the micturition center, activate preganglionic parasympathetic neurons of the parasympathetic sacral nucleus.

 

The descending pathways in te CNS are facilitatory and inhibitory. Glutaminergic facilitating pathways, from the pontine micturition center, activate the preganglionic parasympathetic neurons of the sacral parasympathetic nucleus. These neurons project, through the pelvic nerve, to neurons of the pelvic plexus and intramural ganglia. The ACh induce contraction of the bladder and inhibit the release of norepinephrine from sympathetic terminals. Inhibitory pathways (GABAergic and glycinergic) act on preganglionic sympathetic neurons in the lumbar spinal segments (L1 to L5) to stop bladder distention. They also reach the Onuf nucleus to facilitate relaxation of the striated urethral muscle, allowing urination. Descending pathways form part of the pontine reticulospinal tract in the ventral funiculus although other pathways involving the corticospinal tract in the lateral funiculus have also been described.

 

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Disorders of micturition

 

Urethral obstructions can be caused by prolonged bladder distention and result in aa areflexic bladder that is difficult to recover. Old or neutered animals may present incontinence since the urethral sphincter is partially incompetent in moments of emotion and stress. Hormonal deficiencies can also affect the ability of the urethral muscle to close the urethra.

 

Lesions that affect any of the neurological pathways involved in urination produce urinary incontinence. When the lesion is located cranially to the sacral segments (injury to the upper motor neuron), the increased tone of the external urethral muscle and the inability to voluntarily urinate cause distension of the bladder. In these cases, partial voiding may occur due to the presence of a reflex pathway involving the afferent and efferent visceral components of the pelvic nerve, and the general somatic efferent component of the pudendal nerve. This reflex activates the parasympathetic sacral motor neurons and inhibits the somatic motor neurons to the urethral muscle. In these cases, light pressure on the abdominal wall triggers an uncontrolled urination reflex. In this case we talk about incontinence with overdistension. If the lesions affect the sacral segments of the spinal cord (lower motor neuron injury), the pudendal and pelvic nerves cannot retain or void urine. So the urine constantly leaks and the bladder is never distended. In this case we talk about incontinence without overdistension.

 

 

[1] Benarroch, E.E. "Neural control of the bladder. Recent advances and neurologic implications". Neurology 75, November 16, 2010.

[2] Naoki Yoshimura. "Bladder afferent pathway and spinal cord injury: possible mechanisms inducing hyperrefelxia of the urinary bladder". Progress in Neurobiology, Vol. 57, Page 583 to 606, 1999.

[3] In the dog and cat two pontine micturition centers exist: the commonly know pontine micturition center (PMC) responsible for urine emptying and a second, which functions as the urine storage facilitator center. The first is located in the locus ceruleus (or coeruleus), and the second in the nucleus subceruleus (subcoeruleus). Micturition is controlled by coordination of both centers. From Nishizawa, O, and Sugaya, K. in “Cat and dog: higher center of micturition". Neurol. Urodyn, 1994; 13 (2): 169-179.