Normal Micturition

Diagram showing neural circuits controlling continence and micturition

 Central coordination of micturition occurs in the pontine micturition center. The parietal lobes and thalamus receive and coordinate detrusor afferent stimuli while the frontal lobes and basal ganglia provide modulation with inhibitory signals. Peripheral coordination occurs in the sacral micturition center at cord levels S2-S4. 1-Sympathetic efferents from spinal levels T11-L2 via the hypogastric nerve mediate alpha-adrenergic contraction of the urethral smooth muscle and relaxation of bladder smooth muscle (detrusor) to allow urine storage during bladder filling. 2- Sphincter closure is augmented by striated sphincter muscle contraction with cholinergic somatic stimulation from cord levels S2S4 via the pudendal nerve . 3- A fascial and muscular urethral support "hammock" compresses the urethra when there is increased abdominal pressure or when the pelvic muscles are contracted

Diagram showing neural circuits controlling continence and micturition

When detrusor afferent stimuli indicate the need to void, parasympathetic activation via the pelvic nerve from the sacral micturition center. This, in turn, causes muscarinic contraction of the detrusor muscle and preganglionic inhibition of sympathetics, leading to urethral relaxation . In addition, a variety of neurotransmitter systems in the urothelial lining of the bladder and in bladder interstitial cells likely play a role in mediating bladder contraction and relaxation via afferent signaling .

A) Urine storage reflexes.

Distension of the bladder produces low level vesical afferent firing, which in turn stimulates (1) the sympathetic outflow to the bladder outlet (base and urethra) . (2) pudendal outflow to the external urethral sphincter. These responses occur by spinal reflex pathways and represent "guarding reflexes," which promote continence. Sympathetic firing also inhibits detrusor muscle and modulates transmission in bladder ganglia. A region in the rostral pons (the pontine storage center, or "L" region) increases external urethral sphincter activity.

Diagram showing neural circuits controlling continence and micturition

(B) Voiding reflexes.

Intense bladder afferent firing activates spinobulbospinal reflex pathways passing through the pontine micturition center, which stimulate 1-the parasympathetic outflow to the bladder and internal sphincter smooth muscle 2-inhibit the sympathetic and pudendal outflow to the urethral outlet.

Ascending afferent input from the spinal cord may pass through relay neurons in the periaqueductal gray (PAG) before reaching the pontine micturition center.

Diagram showing neural circuits controlling continence and micturition

Normal voiding physiology (Panel A) and involuntary detrusor contraction commonly associated with symptoms of urge incontinence and overactive bladder (Panel B)

Patterns of neurogenic detrusor-sphincter dysfunction

The large circles represent the detrusor and the small circles the urinary sphincter. Dotted lines represent normal function, thin lines decreased function (hypo- or areflexia), and thick lines increased function (hyperreflexia). Suprapontine lesions typically result in detrusor hyper-reflexia (uninhibited contractions) with normal sphincter function. Suprasacral lesions typically result in both detrusor and sphincter hyperreflexia, with detrusor-sphincter dyssynergia. Lumbosacral lesions may result in several patterns, including (1) detrusor hyperreflexia with sphincter hyporeflexia/areflexia, or (2) impaired detrusor contractility with sphincter hyperreflexia. Complete subsacral conus lesions typically result in both detrusor and sphincter hyporeflexia. Subsacral cauda equina and peripheral nerves lesions result in detrusor hyporeflexia with intact sphincter function if the pelvic nerve plexus is damaged but the pudendal nerve is intact, and in normal detrusor function with sphincter hyporeflexia if the pudendal nerve is damaged but the pelvic nerve is intact. In rare instances, epiconal lesions may result in normal detrusor function with sphincter hyperreflexia, but impaired detrusor function with sphincter hyperreflexia is most common.

 Overflow incontinence
is a term used to describe the dribbling and/or continuous leakage associated with incomplete bladder emptying, due to impaired detrusor contractility and/or bladder outlet obstruction.

Neurogenic bladder

is a nonspecific term used to refer to conditions ranging from areflexic noncontractile bladder to detrusor overactivity (Urge incontinence).

Painful bladder syndrome/interstitial cystitis (PBS/IC)

is a disorder characterized by bladder pain of variable severity, due to urothelial abnormalities altered bladder epithelial expression of HLA Class I and II antigens, decreased expression of uroplakin , and altered integrity of the glycosaminoglycan (GAG) layer . It is likely that neurologic upregulation with central sensitization and increased activation of bladder sensory neurons during normal bladder filling . It is also possible that the increase in visceral (bladder) sensitivity is secondary to a primary somatic injury (bowel and other pelvic organs) that has sensitized central pathways that overlap with afferents from the bladder.

Age-related change.
The prevalence of involuntarydetrusor overactivity increases with aging. Detrusor overactivity has been found in 21 percent of healthy, continent.. The ability to postpone voiding decreases, and the total capacity of the bladder may diminish. Urinary flow rate decreases in both older men and women, probably due to an age-related decrease in detrusor contractility . Low estrogen levels after menopause result in atrophy of the superficial and intermediate layers of the urethral mucosal epithelium with subsequent atrophic urethritis, diminished urethral mucosal seal, loss of compliance, and irritation. Most older men have benign prostatic hyperplasia. Approximately one-half develop prostate hypertrophy with the potential for bladder outlet obstruction and voiding symptoms. The diurnal pattern of fluid excretion may shift towards increased volume of urine excreted later in the day. Possible causes include peripheral edema due to comorbid diseases and medications .

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