8. Neurological Disease and LUTS
KeywordsNeuro-urologyNeurogenic lower urinary tract dysfunctionStrokeMultiple sclerosisParkinson’s diseaseDementia
Neurogenic lower urinary tract dysfunction (NLUTD) refers to the wide-ranging effects of neurological disease on regulation of the lower urinary tract organs, in terms of direct control of the muscle groups, and the reflex activity co-ordinating the functions. For affected patients, LUTD can be one of the worse aspects of their condition.
Some patients with NLUTD are at risk of renal damage or other serious complication such as autonomic dysreflexia. The first role of assessment in these patients is therefore to identify those at such risk. Also important is to understand the overall context in terms of loss of general function (e.g. reduced mobility, and hence difficulty reaching the toilet, or getting from a wheelchair on to the toilet seat), and the social and care situation. This then leads to treatment, ensuring that the facets of NLUTD are addressed directly, and that adaptations are made to help with the wider situation as necessary.
Several neurologic conditions have become more common in daily medical practice due to increasing life expectancy and its inherent consequences. According to the world population prospects of the United Nations, in 2017, there were an estimated 962 million people aged 60 or over in the world, comprising 13% of the global population. The population aged 60 or above is growing at a rate of about 3% per year. Currently, Europe has the greatest percentage of population aged 60 or over (25%). Globally, the number of persons aged 80 or over is projected to triple by 2050, from 137 million in 2017 to 425 million in 2050. This will have substantial implications in NLUTD, for the number of people affected, their social and medical rights, and the availability of carers.
8.2 Classification and Consequences
Time of neurological dysfunction: congenital or perinatal lesions are particularly important since the LUT function has never been normal for that person.
Likelihood of disease progression: while some neurological lesions tend to remain stable, others are at predictable risk of progression—multiple sclerosis (MS) being the archetypal example.
Severity of loss of neurological function: for example spinal cord injury (SCI) can be complete or partial.
Region of the nervous system affected  (Table 8.1):
“Suprapontine” lesions are those occurring in the brain above the level of the pons. This spans a wide range of pathologies. The pontine micturition centre (PMC) in the brainstem is controlled by the adjacent periaqueductal grey. This controls the filling and voiding cycles of the bladder, ensuring the reflex activities occurring at spinal levels are co-ordinated. Involvement of the cortex is vital for ensuring LUT functions are placed into context of social control and anticipation of commitments. The cortex is also responsible for executive decisions (e.g. deciding to initiate the voiding phase) and conscious sensation (e.g. “normal desire to void” is a sensation which derives from subconscious sensory information, modulated by context). Thus patients with suprapontine conditions have rather diverse LUTD that potentially reflects one or more of the following:
Loss of social appropriateness: Voiding dysregulation is urination in situations which are generally regarded as socially inappropriate, such as while still fully dressed, or in a public setting away from toilet facilities .
Altered sensation: some people have no awareness of bladder filling and/or urethral flow, even though the peripheral nerves and spinal cord are apparently fully functional.
Loss of decision making: some people go into retention as they are unable to transmit the conscious decision to void from their prefrontal cortex to the PMC, meaning that the PMC stays in storage mode.
Loss of top-down inhibition: normally the brain suppresses PMC and spinal centres during urine storage. Suprapontine neurology can allow the emergence of detrusor overactivity (DO). At a more extreme level, it can lead to involuntary voiding, defined as a symptom and a diagnosis of sporadic bladder emptying when awake, without intention to void . Usually the voiding reflex is preserved, and there is only lack of proper inhibition of the voiding reflex.
Pontine and suprasacral spinal cord . These tend to have similar effects on NLUTD, though brainstem lesions are rare because the role of the brainstem in vital functions means survival is unusual. Suprasacral spinal cord lesions generally leave the distal cord still functioning, but unregulated and unco-ordinated. At sacral cord level between S2 and S4, the parasympathetic nucleus and Onuf’s nucleus supply innervation to the muscles of the detrusor and the sphincter. If left to function without PMC input, the following can occur:
DO and DO incontinence.
Detrusor- urethral sphincter dyssynergia (DSD) , which is forceful bladder contraction against a closed sphincter, causing significant post-void residual (PVR) and “high pressure” bladder. The formal definition of DSD  is a detrusor contraction concurrent with an involuntary contraction of the urethral and/or periurethral striated muscle. Occasionally, flow may be prevented altogether.
Furthermore, the pons regulates the sympathetic spinal centre in the thoraco-lumbar spinal cord, responsible for blood pressure control. Thus lesions above T6 spinal cord level can lead to the emergence of autonomic dysreflexia, which is an acute elevation of blood pressure which can become life-threatening . Such activity (DSD, DO incontinence and dysreflexia) is clear in SCI. In other neurological conditions which can affect nerve transmission in the spinal cord, such as MS, elements of this can occur and these patients behave urologically like incomplete spinal cord injuries, developing neurogenic DOA and incomplete bladder emptying. DSD can arise , but it is rarely seen to have the severity present in complete SCI.
Sacral spinal cord and subsacral
Since these regions house the nerves and peripheral fibres responsible for muscle contraction, the consequences will potentially be as follows:
Detrusor areflexia (loss of parasympathetic function).
Stress urinary incontinence caused by sphincter deficiency. However, sometimes the patient may instead have a non-relaxing urethral sphincter, characterised by a non-relaxing, obstructing urethral sphincter resulting in reduced urine flow .
Impaired bladder compliance (principally for sacral lesions).
Bladder neck function in men may be preserved, provided the sympathetic nucleus (thoraco-lumbar spinal cord) can still communicate with the periphery.
Incomplete damage to peripheral nerves and the lower spinal centres can result in altered reflex activity and DO .
Archetypal lesions exemplifying the potential range of NLUTD
Stroke, head injury
Multiple system atrophya
Pons and suprasacral spinal
The issue of bladder compliance is less well understood and there are of course compliance issues associated with bladder fibrosis. However, there is thought to be a neurological element from the sympathetic system T10-L2 which allows receptive relaxation. This is particularly important to understand in patients who have had a neurological injury to the lower spinal cord, which may mean receptive relaxation cannot occur. Patients may have poor compliance which might not be recognised until a procedure is performed for stress incontinence. In this situation the patient has been converted from having a safe wet bladder into a dangerous dry bladder because the pressure rises as the bladder fills.
8.3 Assessment of LUTS in Neurological Disease
Lower Urinary Tract Symptoms
What symptoms are present and how much bother are they causing?
Storage symptoms—frequency, nocturia, urgency, urge incontinence, bladder pain
Voiding symptoms—if able to void—hesitancy, straining, poor and/or intermittent flow, sensation of incomplete emptying, double voiding
If the patient is voiding, are they able to do so on demand or only when a sense of urgency has already developed?
Incontinence—Does this occur?
When? How frequently? What volume of urine is lost? Is it urgency or stress or overflow or mixed in nature? Is there voiding dysregulation or involuntary voiding. Is there nocturnal enuresis? What impact is it having? Is it causing skin problems? Is it limiting activities? Is it impacting on care situation or disturbing sleep?
Other urinary symptoms
Has there been any haematuria?
Have there been any urinary tract infections?
If so what symptoms do these cause? Are they microbiologically proven? How have they been managed? How quickly do they resolve with antibiotics? What length of antibiotic course has been taken? How frequently are they recurring? Is the patient taking prophylactic antibiotics?
Has there been any loin pain?
If the patient is catheterised
How long for? What was the indication for catheterisation? What size and type of catheter is used? Is it urethral or suprapubic? Do they use a valve or free drainage? How often is it changed and by whom? Are there any problems—bypassing, blocking, expulsion for instance?
If the patient is performing intermittent self-catheterisation
How long have they been doing this? Why did they start? What size and type of catheter is used? Do they do it by the clock or in response to bladder sensation? How frequently do they catheterise and what volumes are drained? Are there any problems?
Neurological Symptoms and Diagnosis
What is the underlying neurological diagnosis?
How long has this been present and what is the clinical course of the neurological condition and the lower urinary tract symptoms? What is the prognosis for the neurological condition?
How has the neurological condition impacted upon the patient’s life apart from the lower urinary tract symptoms?
Has it impacted on cognitive function? Has it affected their mobility—if so to what extent? Has it affected their manual dexterity—if so to what extent? How has it affected their day-to-day life? What assistance do they now require with activities of daily living? Do they suffer with autonomic dysreflexia, and if so what provokes this? Do they experience skeletal muscle spasm?
Do they have any bowel symptoms?
Frequency, urgency, faecal incontinence, constipation, loss of rectal sensation, need to strain, loss of control over flatus
If so do these affect the lower urinary tract symptoms?
Have they received any treatment or do they have a regular bowel regime?
Are they/do they wish to be sexually active?
Are they suffering from any sexual dysfunction?
Men—erectile dysfunction, loss of ejaculation/premature ejaculation, loss of orgasm
Women—loss of arousal and lubrication, loss of sensation and orgasm, incontinence, dyspareunia
All—loss of genital sensation, skeletal spasms or pain elicited by sexual activity
Do they wish to have children/further children?
Past Medical History
Are there any significant comorbidities?
Details of past urological, obstetric, gynaecological and surgical history
Previous trials of medication relevant to bladder and bowel dysfunction
Who do they live with? What is the type and size of the property? Where are the toilet facilities? Who provides their care?
What work did/do they do? What are their plans regarding work in the future? Are they in receipt of benefits?
Validated symptom and condition-specific questionnaires such as the tools from the International Consultation on Incontinence Questionnaires (ICIQ) system are ideally suited to these patients
Generic symptom scores such as the International Prostate Symptom Score can be a useful way to quantify the symptoms and their impact on quality of life.
Examination should be focused on the aspects of the neurological condition that may affect the bladder function and/or its management.
This should start with simple observations of the patient during the preceding interview.
How mobile/immobile are they? Are they using a wheelchair, if so is it self-propelling or motorised? What assistance do they require to get on/off the examination couch? Are they able to manipulate buttons and zips or are they wearing clothing free of these?
Inspection for scars, palpation for organomegaly (in particular the bladder) and any tenderness, check for palpable renal masses or loin tenderness. Are there any hernias?
Inspection for any excoriation or skin problems due to urinary or faecal incontinence and any pressure sores. Is there any phimosis or catheter hypospadias? Is there any visible vaginal prolapse?
In women, palpation should include a full bimanual pelvic examination. Are there any pelvic masses? Is vaginal sensation normal, reduced or painful? Is there demonstrable stress incontinence? Is there senile vaginal atrophy? Is there good pelvic floor tone and can they generate a voluntary squeeze?
Digital rectal examination is also required to assess for anal sensation, anal tone and voluntary squeeze and to assess the contents of the rectum.
In men, digital rectal examination is important to assess the prostate gland—is it tender? Is it enlarged? Is it smooth and symmetrical or irregular and hard?
Focused Neurological Examination
Assess manual dexterity—is the patient able to hold a pen, use cutlery, do up and undo buttons, etc.?
Test for sensation in the saddle area, perineum and over the external genitalia—e.g. the lumbar and sacral dermatomes
Assess the bulbocavernosus and anal reflexes to check on integrity of the relevant segments of the sacral spinal cord (S2-4)
Investigations are required to answer specific questions rather than as “routine” and should be selected on an individual basis.
Dipstick urinalysis should be carried out to exclude significant infection or haematuria and glycosuria. MSU or CSU specimens should be sent as indicated but will need to be interpreted carefully in the light of the likelihood of bacteriuria in patients with catheters or who are using ISC.
A simple serum creatinine and eGFR will give a good guide to renal function but will need to be interpreted carefully in patients with reduced muscle bulk (spina bifida or muscle wasting diseases), since this will mean a lower reference range of normality for creatinine.
Formal 24-hour creatinine clearance or 99 m DTPA clearance may be required for an accurate assessment in some cases.
If indicated by the DRE and after appropriate discussion a PSA may be required.
Post Micturition Residual Bladder Scan
In patients who are capable of voiding, a simple post micturition bladder scan will give an indication of voiding efficiency. Single measurements may not be representative so repeated assessment preferably at different times of the day and in the patient’s home environment may be more useful 
Frequency Volume Chart
In all patients who are voiding or using intermittent self-catheterisation, a 3-day bladder diary is a vital tool for assessing the volume and nature of all fluids consumed, the urinary frequency including nocturia, frequency of incontinence episodes, degree of urgency and functional capacity. The nocturnal polyuria index can be calculated.
Renal Tract Ultrasound Scan
The primary responsibility of the urologist caring for patients with neuropathic bladder dysfunction is to prevent renal damage. A baseline renal tract ultrasound is vital to assess for hydronephrosis, scarring and stones. Regular renal ultrasonography is a cornerstone of follow-up in these patients. These scans can be undertaken seated in a wheelchair (Fig. 8.1).
Not generally recommended and possibly contraindicated in patients with poor perineal sensation due to risk of skin damage.
May be required in selected patients to assess renal scarring, split function and renal drainage. It is important to choose the correct scan for the question asked and to interpret them in the light of normal bladder function for the patient, e.g. to make an assessment before and after ISC.
Should be used selectively to answer diagnostic questions, guide management and to allow stratification of the risk of renal damage as a result of neuropathic bladder behaviour.
Simple urodynamic tests, such as uroflow rate, may be useful in some circumstances. Generally videourodynamics is the urodynamic assessment of choice in neurological patients.
The decision to perform invasive urodynamics should be based on the need to assess the risk of upper tract damage. It is therefore generally agreed that patients with a high risk of such damage, e.g. those with SCI  or Spina Bifida, do require videourodynamics, whilst others at a low risk of renal complications such as patients with MS can be safely managed without this invasive investigation .
Filling cystometry will enable the collection of important data reflecting bladder behaviour during filling—is there normal sensation? Is there normal bladder compliance? Is there neurogenic detrusor overactivity? If so, is there associated incontinence and/or DSD? What is the bladder capacity and how does this relate to bladder sensation and the functional capacity from the frequency volume chart?
The use of concomitant X ray screening (Videourodynamics) will also allow further questions to be answered—Is there urodynamic stress urinary incontinence? If so what type is it? Is there ureteric reflux? Is the bladder heavily trabeculated and/or are there significant diverticula?
If voiding occurs, either intentionally or spontaneously, then this can be assessed and further questions be answered—is emptying complete? Are voiding pressures high? If so why—is there outflow obstruction due to stricture, benign prostatic hyperplasia, or DSD, or fixed sphincteric resistance?