Micturition is controlled by a combination of autonomic and somatic innervation. Sympathetic innervation to the bladder
via the hypogastric nerve is composed of preganglionic fibers exiting the lumbar spinal cord from the L1-4 spinal cord segments
and synapsing in the caudal mesenteric ganglion. Beta-adrenergic fibers terminate in the detrusor muscle; stimulation results
in detrusor muscle relaxation and facilitates bladder filling. Alpha-adrenergic fibers innervate the smooth muscle fibers
in the trigone and urethra, resulting in contraction of these muscle fibers to form a functional internal urethral sphincter.
The normal storage phase is created by sympathetic autonomic domination, which results in detrusor muscle relaxation and urethral
sphincter contraction created by alpha-adrenergic stimulation. Voiding is consciously inhibited by voluntary contraction
of striated urethral muscles and is reflexly inhibited by a spinal reflex, which tightens the external urethral sphincter
when there is a sharp increase in intra-abdominal pressure (e.g., barking, coughing, sneezing, or retching).
Parasympathetic innervation to the bladder is provided by the pelvic nerve, which arises from the sacral spinal cord segments
S1-3. Parasympathetic innervation predominates during the voiding phase of micturition; stimulation of the pelvic nerve
results in depolarization of pacemaker fibers throughout the detrusor muscle. The subsequent spread of excitation to adjoining
muscle fibers through tight junctions of smooth muscle cells leads to contraction of the detrusor muscle. The sacral
spinal cord segments S1-3 are also the source of the somatic innervation to the external urethral sphincter via the pudendal
nerve. Stimulation of the pudendal nerve causes contraction of the striated skeletal muscle of the external urethral sphincter.
As the bladder fills and intramural tension exceeds the threshold, stretch receptors in the bladder send impulses via the
sensory portion of the pelvic nerve through spinal cord pathways to the thalamus and cerebral cortex. When it is appropriate
to void, impulses are sent from the cerebral cortex to the pons and then down the reticulospinal tract to the sacral nuclei.
Parasympathetic activity via the motor portion of the pelvic nerve causes the detrusor muscle to contract and there is simultaneous
inhibition of the sympathetic stimulation that closes the internal urethral sphincter. When the bladder has emptied, the
normal sympathetic domination resumes; the outflow tract closes and the detrusor muscle relaxes for filling. The normal
residual volume of urine after complete voiding is 0.2 - 0.4 ml/kg for both the dog and cat.
Clinical Signs and Diagnosis
Clinical signs associated with micturition disorders will often help one discern the underlying problem. In cases with small
or normal-sized bladder disorders, urinary incontinence is usually caused by either increased detrusor contractility/irritability
or decreased outflow resistance. Continuous urinary incontinence present from birth is likely associated with a congenital
abnormality and may be a combination of anatomic and functional abnormalities. Incontinence associated with hematuria, pollakiuria,
dysuria/stranguria, breaking of normal house training behavior usually indicates there is inflammation of the bladder and/or
urethra (increased detrusor contractility/irritability). Urinary incontinence that is most pronounced when the patient is
laying down, relaxed and/or asleep is most likely associated with urethral sphincter mechanism incompetence (decreased outflow
On the other hand, in cases with large, distended bladders, urine retention is usually caused by either decreased detrusor
contractility or increased outflow resistance. Increased outflow resistance may be caused by anatomic obstruction (e.g.,
urethral calculi) or by functional outflow resistance (e.g., reflex dyssynergia). Reflex dyssynergia results in urine retention
associated with increased outflow resistance during attempts to void due to failure of the alpha-adrenergic input to the internal
urethral sphincter to be reflexly inhibited. Physical examination findings are often helpful in differentiating the underlying
cause. A distended bladder that is easy to express is usually associated with decreased detrusor contractility. Distended
bladders that are difficult to express are usually associated with increased outflow resistance; the ease of urethral catheterization
can then often be used to differentiate anatomic from functional outflow resistance problems. Urethral catheterization is
usually easy to perform in cases of increased urethral sphincter tone (e.g., reflex dyssynergia and upper motor neuron lesions).
In contrast, passage of a urethral catheter is relatively difficult if anatomic obstructive lesions are present (e.g., urethral
calculi and urethral masses).