Introduction
Since the innervation of the lower urinary tract (LUT) is both complicated and subtle, it is no surprise that LUT dysfunction occurs in many neurological conditions to a variable degree. The symptoms are related to the disease, dysfunction, or injury type which must be further classified according to the site of origin and extent (central versus peripheral and complete versus incomplete). Often the LUT dysfunction involves the bladder, the sphincter complex and the synergy between both elements (pontine micturition center). The most common neurological diseases that are associated with voiding dysfunction are multiple sclerosis, spinal cord injury, Parkinson’s disease, stroke, dementia and neuropathy. Though not considered neurological diseases per se, diabetes mellitus and alcohol abuse both affect the nervous system and are commonly associated with voiding abnormalities. Usually clinicians try to differentiate brain and spinal cord lesions, as impact on kidney preservation may be different.
Signs and Symptoms
In order for normal urinary elimination to occur, there must be coordination between the bladder and urethra known together as the vesico-urethral unit and both organs must also be functionally competent. Incontinence may be due to overactivity of the bladder muscle (detrusor) as seen in spinal cord injuries above the sacral level or following a stroke. It may also be due to detrusor hypocontractility with overflow incontinence, as seen in lower spinal cord lesions. Incontinence also occurs if the external urinary control mechanism (sphincter muscle) is weak. This occurs in nerve injuries below the spinal cord such as spina bifida.
Assessment
The diagnosis of neurogenic urinary dysfunction is based on detailed information gathered from a full clinical assessment including history (with particular reference to clinical symptoms and signs), a physical examination with neurological testing and analysis of the urine. A bladder diary provides essential information on symptoms as well.
In order to complete the diagnostic evaluation in these patients, urodynamic testing is often necessary. Urodynamics encompasses a number of measurements of bladder and urethral function. Often these are done with concomitant x-ray imaging so that the nature of the dysfunction is actually visualised (eg videourodynamics). Upper tract evaluation by ultrasonography is obtained in all patients to look for scarring of the kidneys or dilation of the collecting system, both evidence of injury from a neurogenic bladder. In some cases, a neurogenic bladder may be suspected but without a clear diagnosis of neurological disease, in which case specialised tests including neurophysiologic evaluation or imaging of the nervous system may be helpful.
Treatment
Treatment of neurogenic vesicourethral dysfunction must be tailored to the individual patient. It will depend on many factors including the patient’s age and severity or progression of the neurologic problem. Additionally, the patient’s mobility, including hand function, mental status, motivation and family support may need to be considered. As specific therapies for primary neurogenic disease are not available in most cases, the treatment of neurogenic vesicourethral dysfunction is focused on urinary symptoms and the degree of bother reported by the patients.
One of the primary goals of treatment is to restore continence by producing a low-pressure bladder or reservoir that stores adequate amounts of urine and allows regular emptying of urine at a socially convenient time. The bladder must remain at low pressures during filling and the bladder neck and urethra must open in a coordinated fashion to allow free passage of urine. Emptying must also be efficient and occur at low pressure. Failure to achieve these factors may predispose to upper urinary tract complications and urinary infection.
Conservative treatment, which must be exhausted before considering invasive therapy, may consist of behavioural therapy, the use of drugs that promote both storage (antimuscarinics or beta-3 agonists) and emptying (alpha adrenergic antagonists), intermittent catheterisation and electrical stimulation.
Behavioural therapies include timed voiding, habit retraining and prompted voiding. Clean intermittent catheterisation (CIC) is safe and effective for both short-term and long-term management and is recommended the first choice of treatment for those with the inability to empty their bladder adequately. In those with neurogenic detrusor overactivity (NDO) as well as impaired emptying, a combination of antimuscarinics and CIC must be used. When antimuscarinic medications are ineffective, botulinum toxin A can be injected into the detrusor to produce the necessary detrusor relaxation. Sacral neuromodulation may be indicated in some selected cases. There is increasing interest in the use of various neuromodulatory techniques to bypass or correct neurologic urinary dysfunction. These include posterior tibial nerve stimulation (transcutaneous electrical current delivered via needle electrode), sacral neuromodulation (spinal implant) and sacral nerve stimulation, usually with concomitant sacral rhizotomy.
For patients unable to perform CIC, the bladder may need to be drained continuously. Suprapubic catheter drainage is preferred, as urethral catheters may cause devastating urethral damage.
If NDO cannot be controlled with medication or botulinum toxin A and bladder capacity is functionally low, then the pressure in the bladder can be decreased and its capacity increased by augmentation enterocystoplasty – enlarging the bladder with a patch of bowel.
Urethral overactivity can be addressed with medication such as alpha-adrenergic antagonists that relax the bladder outlet. Botulinum toxin A injections can also be used in male patients to treat spasticity of the external urinary sphincter. Endoscopic Incision of the urethral sphincter, external sphincterotomy, has largely fallen out of favour due to frequent recurrence of dysfunction and/or problematic incontinence. However it is the preferred choice to improve trigger voiding in high quadriplegic patients. In select cases, urethral stents have been placed to improve emptying.
In the rare instance that urethral closure is a problem, injection of a bulking agent, fascial sling, or placement of an artificial urinary sphincter can be used to alleviate incontinence. Neurogenic stress urinary incontinence is always a challenge for physicians and more research has to be done to improve minimally invasive techniques in this type of dysfunction.
In intractable incontinence, in which the abovementioned options have failed, it may be appropriate to divert the urine away from the bladder entirely. In these situations, the urine is usually diverted to the abdominal wall using a short segment of ileum (ileal conduit). Urine is collected externally in a specialised pouch appliance attached to the abdominal wall. In selected circumstances, an internal reservoir may be constructed out of bowel, with the patient emptying this pouch with a catheter through a constructed continent catheterisable channel. Continent cutaneous diversion is gaining greater favour with patients as it combines continence objectives and quality of life improvement for disabled patients.
Conclusion
In general, patients with vesicourethral dysfunction associated with neurologic disease, following appropriate assessment and management, can expect associated improvement in overall well-being and prolonged survival. Emphasis must be given to improving quality of life, with surgical intervention used only when all conservative options have been exhausted.
References
- Rosier PF, Szabó L, Capewell A, et al; International Consultation on Incontinence 2008 Committee on Dynamic Testing. Executive summary: The International Consultation on Incontinence 2008--Committee on: “Dynamic Testing”; for urinary or faecal incontinence. Part 2: Urodynamic testing in male patients with symptoms of urinary incontinence, in patients with relevant neurological abnormalities, and in children and in frail elderly with symptoms of urinary incontinence. Neurourol Urodyn. 2010; 29(1):146-52. Review.
- Wein AJ. Pathophysiology and classification of lower urinary tract dysfunction: Overview. Campbell-Walsh Urology, 10th ed. 2012. Ch 61: 1834-1846.
- Wein AJ, Dmochowski R. Neuromuscular dysfunction of the lower urinary tract. Campbell-Walsh Urology, 10th ed. 2012. Ch 65: 1909-1946.
- Wyndaele JJ, Kovindha A, Madersbacher H, et al. Neurologic urinary incontinence. Neurourol Urodyn. 2010; 29(1):159-164.
- EAU guidelines 2015, http://uroweb.org