Transcript Diagram showing neural circuits controlling continence and micturition

This lecture was conducted during the Nephrology Unit
Grand Ground by Medical Student rotated under
Nephrology Division under the supervision and
administration of Prof. Jamal Al Wakeel, Head of
Nephrology Unit, Department of Medicine and Dr.
Abdulkareem Al Suwaida, Chairman of Department of
Medicine. Nephrology Division is not responsible for the
content of the presentation for it is intended for learning
and /or education purpose only.
Normal Micturition
Presented by:
Rinda Mousa
Medical Student
July 2008
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 .
Thank you