MICTURITION

 

The storage and elimination of urine are 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

 

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 nucleus of the sacral segments. The axons of the cells of this nucleus form part of the pudendal nerve 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.[1].

 

A group of neurons in the sacral segments, known as Gert's nucleus, receive neurons from the bladder trough the pelvic nerves, project 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 (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's nucleus, help to maintain continence by contracting the pelvic floor in situations that increase intra-abdominal pressure.

 

 

Voiding

 

The periaqueductal gray matter projects to the pontine micturition center to start the micturition reflex. Descending glutaminergic projections, from the micturition center [2], activate preganglionic parasympathetic neurons of the gray intermediate matter. These neurons project, via the pelvic nerve, to postganglionic neurons in the pelvic plexus and to intramural ganglia. The descending pathways also inhibits preganglionic sympatetic neurons in the spinal lumbar segments to stop distension of the bladder. The ACh of the parasympathetic fibers induces contraction of the bladder and inhibits release of norepinephrine from sympathetic terminals. Also descending inhibitory GABAergic and glycinergic pathways reach the Onuf nucleus to facilitate the relaxation of the striated urethral muscle, allowing voiding. 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.

 

 

Disorders of micturition

 

Urethral obstructions can cause prolonged bladder over-distension, developing an areflexic bladder difficult to recover. In older or neutered animals, incontinence can be observed as 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. In these cases, the bladder can be emptied easily with a gentle abdominal massage.

 

            Lesions that affect any of the neurological pathways involved in micturition produce urinary incontinence. When the lesion is located cranially to the sacral segments (upper motor neuron lesion), the increase in the external urethral muscle tone and the incapacity of voluntary emptying causes bladder distension. In a few days, partial emptying may develop due to the presence of a reflex pathway involving the general visceral afferent (GVA), the general visceral (GVE) components of the pelvic nerve, and the general somatic efferent component (GSE) of the pudendal nerve. This reflex activates the motor parasympathetic sacral neurons and inhibit the somatic motor neurons to the urethral muscle. In these cases, a slight pressure on the abdominal wall triggers a micturition reflex. If the lesions affect the sacral spinal cord segments (lower motor neuron lesion) then, pelvic and pudendal nerves are unable to neither hold nor evacuate urine. So urine leaks constantly and the bladder is never distended.

 

[1] 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.

[2] 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.

 

[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.