Fri 12, Jun 2015

The lower urinary tract (LUT) is controlled by the nervous system (central and peripheral). Therefore damage to the nervous system by illness or trauma may result in disturbance of LUT function, including incontinence. The nature of this disturbance depends on the site and extent of the neuronal injury. Thus any type of dysfunction may occur. The commonest is detrusor overactivity, but the detrusor may be underactive, or indeed both overactive and underactive.

Sensation may be diminished. In addition, if there is damage to the spinal cord above the sacral outflow there may be incoordination between the bladder and sphincter function (detrusor-sphincter dyssynergia). Especially in sacral spinal conditions compliance may be impaired, with bladder “stiffness” sometimes resulting in high bladder pressures with filling. So LUT dysfunction may range from absent to quite complex.  Stress (sphincter weakness) incontinence may also occur, but is much less common.

Neurological disorders are common, so neurogenic incontinence is also common.  However, the cause of incontinence may not be neurogenic in people with a neurological disorder, and this should always be considered in a patient’s work up.  Assessment should follow standard protocols and principles, but may be more comprehensive in neurogenic patients, including a greater use of imaging such as urinary tract ultrasound, as well as urodynamics.  It should always include assessment of bowel function, as this is often coincidentally disturbed, but also have negative impact on bladder function.

Most patients with a cerebral cause have detrusor overactivity, stroke being the commonest.  The dysfunction may be more complex in those with Parkinson’s disease.  Incontinence is usually a late feature in patients with Alzheimer’s disease. Detrusor overactivity and coincident detrusor-sphincter dyssynergia are common in patients with spinal pathology such as trauma, multiple sclerosis (MS) and cord compression.  MS is often more complex though and where detrusor underactivity may also occur, or be predominant.  Spina bifida is another complex condition with most patients having sacral cord damage resulting commonly in poor compliance as the most concerning dysfunction.  Other neurological conditions that may cause detrusor underactivity include lumbar disc prolapse (cauda equine syndrome), diabetes mellitus and radical pelvic surgery or trauma.

Management of patients with neurogenic bladders should also follow standard principles.  Those with straight forward detrusor overactivity should be treated as for idiopathic “OAB” with conservative strategies which may include pharmacotherapy with anticholinergic agents.  The beta 3 agonist mirabegron is a new agent that may also be useful, and is especially worth considering in patients with dementia as it is not expected to impact negatively on cognition.

Management of other patients with more complex LUT dysfunctions is more challenging.  While symptom control is important from the patient perspective, a fundamental principle in patients with spinal pathology is to control bladder pressure to prevent complications such as infection and renal damage.  Intensive treatment with pharmacotherapy is a strong focus, even including treatment with botulinum toxin A into the bladder wall.  Intermittent self-catheterization will be used in the many who also have impaired emptying.  Use of indwelling catheterization is avoided where possible, and the need for more major surgery is fortunately rare.

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