Evaluation of Urinary Incontinence (original) (raw)

Anatomy and Neurophysiology of the Lower Urinary Tract and Pelvic Floor

Urodynamics, Neurourology and Pelvic Floor Dysfunctions, 2018

The urinary tract undergoes a very dynamic development during foetal life. Emerging from the metanephros, the human kidney begins to produce urine at 10-12 weeks of gestation [1, 2]. At this time the bladder is a cylindrical tube of cuboidal cells in a single layer. During the second trimester, 4-5 cell layers develop, forming a low compliant 'bladder' at the 21st week of gestation [3-5]. The foetal bladder handles a relatively large amount of fluid, draining to the amniotic cavity with a subsequent oral reuptake by the foetus. The salt and water homeostasis, however, is cleared by the placenta and eventually by the mother's kidneys [6]. Any deviation from this cycle may lead to a more or less pathological consequence for the foetus. In the beginning the lower urinary tract is a conduit with coordinated peristalsis propulsing the urine through the urethra, as is the case with the upper urinary tract. After the formation of the external sphincter, the lower urinary tract develops graduate filling and emptying, and the bladder wall properties change. From being a coordinated peristaltic conduit, the bladder becomes an organ with chaotic micromotions in the bladder wall.

Bladder outlet physiology in the context of lower urinary tract dysfunction

Neurourology and Urodynamics, 2011

Physiological function of the bladder outlet is complex and symptomatic consequences can result from outlet dysfunction. Within the outlet, smooth, and skeletal muscles constitute the contractile apparatus, but additional cell types include interstitial cells and neuroendocrine cells, and various transmitters are present in the innervation, raising the possibility of unrecognized functional subtleties. Key outlet functions are; maintained closure for urine storage, increased closure (guarding) during exertion, sustained opening for voiding, transient opening for territorial marking in animals and orthograde male ejaculation. These are coordinated by several spinal and higher CNS centers, with overlap of the somatic, sympathetic and parasympathetic nervous systems. During voiding, urethral afferents may be important in maintaining detrusor contraction until completion of bladder emptying. Some of the bladder outlet afferents may be shared with the anal sphincter. Dysfunction of the outlet leads to conditions such as retrograde ejaculation, Fowler's syndrome, and detrusor sphincter dyssynergia. Urethral relaxation during urine storage may lead to urinary urgency, which may be misleadingly labeled as overactive bladder. Research priorities are numerous, including; peripheral cellular integrative physiology, interactions with other pelvic organs, interconnectivity of the CNS centers at all levels of the neuraxis, and standardized animal models of outlet functions such as reflex-driven voiding.

The neural control of micturition

Nature Reviews Neuroscience, 2008

Micturition, or urination, occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. The neural circuitry that controls this process is complex and highly distributed: it involves pathways at many levels of the brain, the spinal cord and the peripheral nervous system and is mediated by multiple neurotransmitters. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary or reflex micturition, leading to urinary incontinence. This is a major health problem, especially in those with neurological impairment. Here we review the neural control of micturition and how disruption of this control leads to abnormal storage and release of urine.

The Neurophysiology of Urinary Retention In Young Women and Its Treatment by Neuromodulation

World journal of urology, 1998

Urinary retention occurring in young women as an isolated phenomenon was often thought to be psychogenic in origin. However, in 1988, Fowler et al. described a syndrome in young women in which urinary retention was the predominant feature and in which electromyography (EMG) of the striated urethral sphincter revealed a striking abnormality. This abnormality, it was postulated, would result in an inability of the sphincter to relax and retention would therefore result. Until recently there was no eective treatment for this disorder except management by clean intermittent self-catheterisation. However, preliminary results of neuromodulation using a Medtronic sacral nerve stimulator have been particularly promising in this group of patients. The response is often spectacular; a woman who has not passed urine per urethram for many months or years will frequently ®nd that within a few hours of insertion of the percutaneous nerve evaluation (PNE) lead, she can void quite normally with little or no residual urine. The precise mechanism of action is yet to be de®ned, but measurements of the latency of anal sphincter contraction on S3 stimulation during PNE are so prolonged that they can only be the result of an afferent-mediated re¯ex.

Urinary incontinence: anatomy, physiology and pathophysiology

Best Practice & Research Clinical Obstetrics & Gynaecology, 2000

Urinary continence in the female depends on urine being stored in a receptive bladder closed by a competent sphincter mechanism. Incontinence can result from a failure of storage, i.e. detrusor instability or a failure of the sphincter mechanism leading to stress incontinence. In addition there is a complex neural control which co-ordinates urethral and bladder function to alter from storage to voiding at socially acceptable times. Although the majority achieve continence early in childhood, there are a number of insults brought to bear on the continence mechanism other than advancing age. The most notable of these is childbirth with resultant neuromuscular damage to the pelvic¯oor. The onset of the menopause with oestrogen deprivation and increased risk of urinary tract infection can further compromise bladder function. Restoration of continence in those aected involves a thorough knowledge of normal functioning anatomy and physiology of the lower urinary tract as only through improved understanding of disease mechanisms can rational treatment be applied.

Comparison study of autonomous activity in bladders from normal and paraplegic rats

Neurourology and Urodynamics, 2006

Aim: To identify di¡erences in the pattern of pressure generated by isolated bladders from normal and paraplegic rats. Materials and Methods: Nine female Wister rats were made paraplegic by spinal cord transsection at the vertebral level T8-T9 and sacri¢ced between D21 and D28. A further group (n ¼ 9) was used as a control group. Each bladder was excised and placed in an organ bath where intravesical pressures were measured. Pressure changes were divided in two well-de¢ned groups: macro-transients and spikes. The e¡ects of intravesical volume load and muscarinic (M) agonists were studied. Results: We demonstrated a higher frequency, a longer duration, and a higher variance of duration in macro-transients in the neurogenic group. Intravesical volume load in£uenced the amplitude and frequency of macro-transients in both groups similarly. The e¡ects of the muscarinic (M 2 )-selective agonist areca|« dine were di¡erent in neurogenic bladder; the e¡ects of the non-selective muscarinic (M)-agonist carbachol were similar in both groups. Conclusion: We showed that the pattern of autonomous activity was signi¢cantly di¡erent between normal and neurogenic rat bladders. We also found evidence for alterations in the muscarinic response of isolated neurogenic rat bladders. This model o¡ers an exciting new research tool to evaluate the detrusor activity in neurogenic and normal conditions. Neurourol. Urodynam. 25:368^378, 2006.

Evidence of central modulation of bladder compliance during filling phase

Neurourology and Urodynamics, 2012

Aims: Bladder compliance is one expression of the pressure and volume relationship as the bladder fills. In addition to passive elements, autonomous micromotional detrusor activity contributes to this relationship. In the mouse cystometric model, compliance pressure contributes to voiding expulsive pressure. During attempts to isolate the detrusor contractile component of this filling pressurization, we found that compliance reversibly diminishes under conditions which remove central control from the micturition cycle. Methods: Ten mature female mice underwent constant infusion pressure/flow cystometry under urethane anesthesia, and five awake mature female mice underwent constant infusion pressure cystometry. Following baseline cystometry, all mice were anesthetized with isoflurane to abolish the micturition reflex, and cystometry conducted with manual emptying of the bladders. Animals were then allowed to recover from isoflurane to re-establish the micturition reflex, and cystometry again conducted. The urethane group was also studied immediately post-mortem. Repeated measures comparisons of cystometric parameters were made across conditions. Results: Compliance reversibly decreased in all mice with the abolishment of micturition responses by isoflurane anesthesia. A similar decrease was observed immediately post-mortem in the urethaned mice. Bladder filling and voiding were not different between the intact micturition segments of the testing. Conclusions: Enhanced compliance in mice with intact micturition responses suggests that autonomous micromotional activity is suppressed by central processes during normal filling. Since afferent activity during filling is also determined by the relationship between bladder pressure and volume, a feed-forward afferent signal conditioning mechanism may exist, creating novel therapeutic targets for urinary dysfunctions.

Reflex mechanisms for bladder inhibition

Acta pharmacologica et toxicologica, 1978

Continence of urine requires ability of the bladder to maintain a low intravesical pressure at increasing filling, in order to preserve a positive urethral-bladder pressure gradient. During micturition the conditions are reversed: the bladder has to generate pressures exceeding the urethral pressure, which also presupposes that the urethra opens and remains open as long as is required for all urine to be expelled. These events are made possible by a complicated pattern of central and peripheral neural responses, affecting the bladder-urethral unit. The pioneer work of determining the reflex mechanisms involved in the regulation of the lower urinary tract was done at the beginning of this century. Recently, further studies have been made and by means of electrophysiological investigations previous data have been confirmed. In this communication some important observations are reviewed and one example is given of how bladder inhibitory reflexes are utilized in therapy.