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28. Neurogenic Bladder
Keywords
Neurogenic bladderNeuropathic bladderSpinal cord injurySpina bifidaAutonomic dysreflexiaDetrusor sphincter dyssynergiaPoor complianceIntroduction
The lower urinary tract comprises the bladder, bladder neck and smooth muscle sphincter which are under autonomic control and also the rhabdosphincter which is somatically controlled. This provides a unique function allowing the switch between involuntary storage and voluntary voiding control. There is no agreed definition of a neuropathic bladder but a broad definition would be “lower urinary tract symptoms due to a responsible neurological lesion”. Thus a wide range of pathologies may be responsible for the neuropathic bladder. In this chapter, we categorise these lesions according to their influence on lower urinary tract function and then discuss their management.
Neuro-anatomy
It needs to be understood that the bladder spends 99% of its time storing urine in what is called the storage phase. The detrusor muscle component of the bladder is composed of smooth muscle. The urinary sphincter is composed of inner smooth muscle and outer striated muscle components [1, 2]. The urinary sphincter should not be confused with the bladder neck sphincter, which may be absent in some women. In men, it is primarily a genital sphincter with the chief role of preventing retrograde ejaculation [3]. However, it is sufficient to maintain urinary continence on its own.
Storage
During storage the bladder needs to; transmit sensation and appreciation of bladder volume to higher centres, accommodate urine without pressure change i.e. receptive relaxation and maintain continence. The healthy bladder accomplishes this with key spinal reflexes which are influenced by higher centres.
Stretch sensations from the bladder and bladder neck/urethra are transmitted to the spinal cord by the pelvic/hypogastric nerves. Bladder afferent fibres synapse in the dorsal root ganglia of S2-4 and T11-L2. Here, they synapse with interneurons that project to higher centres and to nerves involved in the “micturition reflex ” which are in the sacral micturition centre. The former travel via a delta fibres to the lateral nucleus of the pontine micturition centre (PMC) and to the peri-aquaductal grey [4]. Quiescent C-fibre afferents are part of the micturition reflex [5]. Bladder afferents containing nitric oxide synthase, glutamate, and a variety of neuropeptides enter the dorsal horn of the spinal cord where second-order neurons project rostrally to supraspinal sites including the hypothalamus, thalamus, and pons. The hypothalamus is known to coordinate autonomic activity. The thalamus processes nociceptive information. The pons is specifically involved in micturition [6].
Functional MRI studies have shown that the prefrontal cortex is active during bladder storage signifying its role in inhibition of micturition [7]. Thus during storage the efferent action is to inhibit detrusor contraction via inhibition of the parasympathetic muscarinic nerves and promote receptive relaxation via activation of B3 adrenergic sympathetic nerves. The pons is seen as the control centre for this. Stimulation of the dorsolateral pons (designated the urine storage centre) increases sphincteric activity and inhibits bladder contraction. Other brain regions implicated in bladder control include the hypothalamus, central nucleus of the amygdala, bed nucleus stria terminalis, paraventricular nucleus, and locus coeruleus indicating why stress and alertness could affect bladder function [8].
Receptive relaxation is proposed to be a spinal reflex that suppresses intrinsic bladder activity to permit bladder compliance. The sympathetic output also stimulates the alpha adrenergic receptors in the urethra and bladder neck which maintain smooth muscle tone in the bladder outflow thus preserving continence. Throughout storage, with increased filling, the striated sphincter is progressively contracted to maintain continence due to the guarding reflex [9]. The neurons innervating the external urethral sphincter and the pelvic floor arise from the anterior horn of S2-4 (eponymously termed Onuf’s nucleus) and travel in the pudendal nerve.
Voiding
Successful voiding needs to be voluntary and for the bladder to empty completely. Initiation arises in the PMC and involves input from the periaqueductal gray, inferior frontal gyrus and hypothalamus [10]. Parasympathetic nerves mediate bladder contraction through the M3 and M2 muscarinic receptors via the sacral micturition centre. Detrusor contraction needs to be sufficiently powerful and prolonged to overcome outlet resistance and to ensure near complete bladder emptying. During voiding, co-ordination is required between bladder contraction and sphincter relaxation (by switching off the guarding reflex). The smooth and striated components of the urinary sphincter are relaxed by nitric oxide and alpha adrenoreceptors respectively.
Thus it can be concluded that there are three spinal reflexes under higher centre control. The micturition reflex (parasympathetic S2-4) is inhibited during storage, receptive relaxation (sympathetic T11-L2) and the guarding reflex (parasympathetic S2-4) are active during storage. A reversal is required for voiding. These spinal reflexes are under the control from the pontine micturition centre which in turn is influenced by multiple higher centres.
In predicting the impact of neurological conditions on urinary control, it is helpful to envision a hierarchical scheme divided into suprapontine, pontine, suprasacral, sacral/peripheral and polyneuropathy.
Investigations
It is imperative that a patient with neurogenic bladder is assessed in the context of a detailed neurological history and examination. A neurologist can be invaluable in this context. Having in depth neurological information can be helpful in predicting bladder behaviour, safety of the upper tracts and determining what further urological investigation and long term follow-up is needed. The rectum is analogous to the bladder in its neurological supply and thus a neuropathic bladder is often accompanied by a neuropathic bowel which in turn can reciprocally affect the bladder. Remember the adage “a happy bladder is an empty bladder, but a happier bladder is an empty rectum!” The urologist will also be interested in the neuropathic effect on sexual function and it is worth recognising the patients’ mobility and hand function in case intermittent self-catheterisation needs to be considered in the management algorithm.
Imaging
Imaging of the neuropathic bladder necessitates imaging of the upper tracts when they are deemed at risk of high pressures; and hydronephrosis is most often easily noted on ultrasound scanning. This is relatively non-invasive and imparts no radiation and therefore has become the investigation of choice for serial assessment of the upper tracts. Due to the long term risk of renal impairment in patients at risk of high bladder pressures annual or at least biennial ultrasound assessment is recommended.
Renal scans may occasionally be required to differentiate between obstruction and a dilated renal drainage system. A diuretic renogram may be useful in this regard and in some circumstances if this is equivocal, a Whitaker test (upper tract urodynamic study) is also needed. Due to the higher than average incidence of stone formation in this cohort of patients, a plain KUB X-ray and/or CT scan may be warranted when required for monitoring and planning treatment for urinary tract calculi. The regular routine use of X-rays in patients with a neuropathic bladder, to screen for urinary tract stones, is no longer advocated due to the risks posed by the cumulative effects of radiation.
Video-urodynamics
Video-urodynamics is also crucial in investigating structural and functional abnormalities. Vesico-ureteric reflux may transfer the high pressures associated with the neuropathic bladder back to the kidneys and affect their drainage and function. In this scenario the reflux may also absorb the pressure rise in the bladder and this would not become apparent on the cytometric pressure recording and therefore concomitant cystography is obligatory to come to a correct conclusion in such patients. Video fluoroscopy also provides information on the level of obstruction, whether it be at the bladder neck, external sphincter, internal sphincter or urethra.
Simplified cystometrogram demonstrating detrusor sphincter dyssynergia (DSD) and urinary incontinence. NB- the rectal line is dampened which is often the case in spinal cord injured patients
Simplified cystometrogram demonstrating poor compliance and the detrusor leak point pressure (DLPP)
A low detrusor leak point pressure prevents the bladder from transferring pressure onto the kidneys but it usually means the patient will leak urine relatively easily and therefore when considering a procedure to reverse this leak, consideration needs to be given to what will happen to the bladder pressure should the detrusor leak point pressure rise. Thus the urodynamics study should also simulate a higher detrusor leak point pressure (by occluding the urethra) and ensure the bladder pressure does not rise after this. If it does rise then a concomitant bladder procedure is also indicated. Data from children with meningomyelocele suggests that a detrusor leak point pressure greater than 40 predicts long term renal impairment [11].
Urethral pressure profilometry and electromyography are technically difficult, not standardised and their need is currently limited as they do not impact treatment choice. Thus these are mostly limited to research studies.
Suprapontine
Suprapontine lesions such as cerebrovascular accident, Alzheimer’s, brain tumours etc. can lead to a loss of voluntary initiation and if cognition is affected, social incontinence ensues where the bladder is emptied without voluntary control. The pontine micturition centre is intact and therefore voiding efficiency is usually not compromised. There is little to no risk of poor compliance or detrusor sphincter dyssynergia and thus the bladder is considered “safe” from renal impairment. The majority of these patients are able to void spontaneously [12]. Disruption to the brains inhibitory effect on the PMC leads to neurogenic detrusor overactivity leading to urgency incontinence.
After a cerebrovascular event 29% will report incontinence which reduces to 14% at 6 months [13]. Immediately after a cerebrovascular accident, urinary retention may be evident. Later on, it is often noted that, there may be detrusor overactivity which in some cases may have been pre-existing (idiopathic) or may develop due to activation of C-fibre afferents [14]. A urodynamic study of 106 patients with incontinence found 56% to have detrusor overactivity, 15% had detrusor underactivity, 15% both detrusor overactivity with impaired contractility with the remainder having normal studies [15].
One in three patients with Parkinson’s disease (PD) have incontinence [16]. This is secondary to detrusor overactivity in 2/3 of them [17]. Nocturia is the most prevailing symptom in Idiopathic PD. Antimuscarinics are often helpful but should be used with caution due to their risk of worsening cognitive function [18]. Voiding dysfunction with incomplete bladder emptying is less common in PD and may be due to a multitude of factors including concomitant BPH, anticholinergic use and bradykinesia of the striated urethral sphincter [19, 20].
Multiple system atrophy (MSA) initially presents with similar symptoms to PD. The finding of an open bladder neck (suggestive of sphincter denervation) is suggested as a hallmark finding of MSA and differentiates from PD. [21] In addition, these patient have a lax anal tone. Other findings, which occur with greater frequency in MSA are detrusor sphincter dyssynergia and higher post void residuals. The life expectancy of those with MSA and higher post void residuals has also been shown to be worse [22]. Men with MSA who undergo a de-obstructing procedure such as a transurethral resection of the prostate are at a higher risk of post-operative incontinence than men with PD. [23] Therefore men considered for a de-obstructing procedure with symptoms of PD should have video urodynamic studies to assess for an open bladder neck and confirm bladder contractility.
With normal pressure hydrocephalus the ventricles are seen to be dilated and typical features such as gait disturbance, memory impairment and urinary incontinence are seen, with the majority (up to 95%) demonstrating detrusor overactivity [24]. A shunt will improve the symptoms in the majority of patients.
Pontine
Pontine lesions are uncommon and therefore only case reports describing bladder function after pontine injury are reported in the literature [25]. In one 5 year old with a pontine pilocytic astroctoma, urodynamic studies showed both storage and voiding dysfunctions, with detrusor overactivity, normal bladder compliance, open bladder neck and detrusor sphincter dyssynergia [26]. No recommendations can be made regarding management of such disorders as it would depend on the symptoms and urodynamic findings.
Suprasacral Spinal Cord Injury
Complete Injury
A completely transected spinal cord that leads to a cranial spinal cord segment and a caudal spinal cord segment leads to a particular lower urinary tract picture. In effect, the caudal spinal cord segment becomes autonomous and is known as the “distal autonomous cord”. Thus, muscles supplied by this segment of the cord lead to spasticity, increased tone and hyperreflexia known as upper motor neurone effects. The spinal bladder reflexes therefore also become autonomous and lose pontine co-ordination. Therefore, as the bladder fills and pressure rises it contracts automatically leading to involuntary urination. The guarding reflex (which contracts the urethral sphincter on urine entering the bladder neck) is no longer synchronised with voiding (as this is co-ordinated by the pons). This leads to neurogenic detrusor overactivity and detrusor sphincter dyssynergia i.e. concomitant contraction of the urethral sphincter during involuntary bladder contraction (Fig. 28.1). As a consequence, the bladder may not empty well.
In this group of patients, video urodynamic assessment is essential and the upper tracts are potentially at risk of high pressures. The cytometry will inform if the pressures are high and prolonged and when in the cycle they occur and if the bladder empties well or not. In a patient with non-prolonged high detrusor pressure and good bladder emptying, reflex voiding into a convene sheath may be appropriate but requires long term monitoring.
In patients with prolonged high pressures, the principle would be to ablate the pressure and make the bladder safe. Therefore the options for this include to either reduce the sphincteric resistance or reduce detrusor contractile pressure. The former is achieved with a sphincterotomy and the latter with the use of antimuscarinic agents, b3 agonists, botulinum toxin or augmentation cystoplasty [27, 28]. With a sphincterotomy, the patient needs to be prepared to wear a lifelong convene sheath and will be rendered totally incontinent. Conversely, when artificially diminishing detrusor contractility, the bladder will not empty as reliably and so another method of bladder emptying is required such as intermittent or indwelling catheterisation.
An emergency feature of this type of spinal cord injury is autonomic dysreflexia. With lesions above T6 and a distal autonomous cord, a painful stimulus below the level of the lesion leads to an aberrant sympathetic response. The painful stimulus, such as a distended bladder or impacted bowel, leads to vasoconstriction, piloerection and sweating below the level of injury. There is dumping of blood from the areas of vasoconstriction into the areas above the lesion leading to significant hypertension. Compensation occurs in the region above the lesion with vasodilatation and bradycardia. However this may be insufficient if the lesion is high (>T6) and hypertension may lead to stroke or myocardial infarction. Early recognition of the signs is essential and elimination of the painful stimulus is the first step in the management, along with use of a vasodilator such as glycerine tri-nitrate.
The crede expression manoeuvre (pressing firmly on the bladder with a fist) was previously advocated to increase bladder pressure to cause expulsion of urine. However, this technique carries a high risk of complications and can lead to renal failure due to the imbalance of pressure being applied to the bladder compared to the rest of the abdomen [29]. Also, only 2% of patients have been shown to have urethral sphincter relaxation during the manoeuvre making it grossly inefficient [30]. Voiding by Valsalva manoeuvre and tapping of the abdomen are also potentially dangerous and require long term follow up [31, 32].
Incomplete Injury
The type of injury and the amount of damage to spinal tracts can be variable and thus leads to a mixed picture. If the dorsal columns are affected then bladder sensation may be impaired [33]. The risk of neurogenic detrusor overactivity and detrusor sphincter dyssynergia is still present as is the risk to the upper tracts [34]. The management of this type of lower urinary tract dysfunction follows the same principles of those with a complete injury. A phenomenon sometimes seen with incomplete injury is neuropathic bladder pain. Urological interventions are often not helpful for this pain and instead neuropathic painkillers such as amitriptyline and gabapentin are recommended.
Sacral/Peripheral
Complete Sacral Lesions
This occurs when the conus medullaris (cauda equine) is completely destroyed resulting in lower motor neurone lesions in the distribution of the affected nerves and absent conus reflexes. Thus there is no distal autonomous cord. A high spinal lesion where the whole distal spine is damaged can also lead to this picture. The muscles usually supplied by the damaged nerves assume a flaccid state and become areflexic. This is also the case with peripheral nerve injuries.
Thus a bladder with complete sacral injury (complete cauda equina) will lead to an areflexic bladder. The sacral micturition reflex and guarding reflex are absent. Receptive relaxation will only be present in injuries below the L1 level and with injuries above this level the bladder is more likely to develop poor compliance (which is a lack of receptive relaxation). Normal bladder sensation is lost.
With an absent micturition reflex, the bladder does not contract, instead it fills and the compliance is lost gradually and eventually this overcomes sphincteric resistance leading to overflow incontinence (Fig. 28.2). Due to denervation of the urethral rhabdosphincter, stress incontinence is present and the detrusor leak point pressure is dependent on the smooth muscle component of the urethral sphincter.
Managing this type of bladder requires an in depth video urodynamic study. With a low detrusor leak point pressure, incontinence can be managed with pads or convene drainage. More commonly, the low detrusor leak point pressure is corrected with a procedure to increase outlet resistance such as an autologous sling in females or an artificial urinary sphincter in males. When doing this it is essential to ensure the bladder will be safe afterwards and can hold a good volume without a pressure rise. If not then a concomitant bladder procedure, such as a cystoplasty, is necessary [35]. With a high detrusor leak point pressure, bladder drainage prior to the development of high pressure is required and thus intermittent or indwelling catheterisation is considered.
Incomplete Sacral Lesions/Peripheral Nerve Injury
With cauda equina syndrome, patchy nerve damage to the conus may occur. Likely causes of cauda equina include disc herniation, lumbosacral fracture, tumour, spinal abscess and spinal surgery. Depending on the insult, some nerve recovery is possible over time. The likely problems in this form of nerve injury include a lack of bladder sensation (afferent nerve injury), acontractile bladder (efferent nerve injury), stress incontinence (sphincter denervation) [36]. Peripheral nerve injury or injuries may also lead to similar problems and are most commonly iatrogenic. Due to the variability in nerve damage, there are difficulties in predicting bladder behaviour and thus a video-urodynamic study is useful.
Spinal dysraphism (Spina bifida) is a congenital disorder due to failure of closure of the neural tube and non-fusion of vertebrae, most commonly affecting the lumbosacral vertebrae and nerves [37]. Of 350 individuals with spinal dysraphism, 61% described having urinary incontinence [38]. Urodynamic assessment of 36 infants with myeldysplasia revealed sphincter dyssynergia in 50% and an incompetent sphincter in 25% [39]. Most importantly, 72% of those with dyssynergia later developed hydronephrosis which only improved with better bladder drainage. Management is guided by symptoms and urodynamic findings and these patients require lifelong follow up within a multidisciplinary team [40].
Pudendal nerve neuropraxia is a recognised complication of delivery and emergency caesarean section, of which the majority of lesions recover by six months [41]. Of 14 multiparous women followed for five years after delivery, it was found five had stress incontinence with neurophysiological evidence of partial denervation of the urethral sphincter and pudendal neuropathy [42]. It should be noted, that this is not the only mechanism responsible for stress incontinence post-partum [43].
The above patients are managed by inserting a tension free vaginal tape beneath the mid urethra [44]. If there is a high degree sphincteric deficiency (which may be assessed on urodynamic studies) then a pubovaginal sling of autologous rectus fascia placed with tension beneath the bladder neck is advisable [45]. A third option is the insertion of an artificial urinary sphincter if the sphincter is significantly incompetent [46]. Conversely in men, stress incontinence is rare post surgery due to a more developed bladder neck sphincter unless the patient has had a radical prostatectomy. The artificial urinary sphincter is the gold standard and the sub-urethral sling is considered to have poorer outcomes [47].
Urinary retention has been reported to occur in <0.5% of patients undergoing rectal and uterine surgery [48]. The postulated mechanism is peripheral nerve injury and bladder de-afferentation and in these patients intermittent catheterisation is first instituted but sacral neuromodulation may be beneficial if the injury is incomplete [49]. A meta-analysis of one RCT and 13 observational studies revealed sacral neuromodulation led to increased voided volume by 299 mL and reduced residual volume by 236 mL in women with mixed non-obstructive urinary retention [50]. It is not clear from the analysis what proportion of these women had a peripheral nerve injury. If sacral neuromodulation is not feasible then the mainstay of management will be intermittent catheterisation. With peripheral nerve injury, long term risk to the kidneys is negligible if the patient manages their bladder sensibly.
Polyneuropathy
Multiple sclerosis (MS) occurs due to demyelination of white and grey matter in the central nervous system [51]. Autonomic dysfunction may be a consequence of lesions in regions responsible for autonomic regulation such as the pons [52], or due to cervical spinal cord atrophy [53]. Altogether, 97% of patients with MS will describe a urinary symptom during the course of the disease [54].
In a study of 52 patients with MS, 25% were found to have detrusor overactivity and 27% detrusor sphincter dyssynergia, whereas 65% had urinary urgency [55]. In another study when urodynamics was repeated in 22 patients, it showed worsening change in 12 and this was not associated with worsening of their MS symptoms [56]. A recent systematic review showed that 14 studies had reported on renal impairment occurring in MS patients [57]. Although this is uncommon, the mean maximum detrusor pressure, detrusor sphincter dyssynergia in men and a post void residual greater than 30% of bladder capacity were reported as risk factors for renal impairment [58, 59].
Management in MS patients is based on symptoms and urodynamics. The above reports of renal impairment have argued the case for regular follow up. Intermittent self catheterisation is recommended when there is incomplete emptying but there is no strong evidence for cut off for a post void residual but 100 mL has been suggested [57, 60]. Where antimuscarinic agents fail botulinum toxin has good success at relieving detrusor overactivity [28].
Amyotrophic lateral sclerosis causes degeneration of motor neurons responsible for skeletal muscles. Bladder and bowel function typically remains intact until the terminal stages of the illness [61]. Onuf’s nucleus is affected to a lesser degree than the other anterior horn cell groups [62]. Thus urinary problems tend to be managed conservatively with catheterisation in this group of patients as they are often at a debilitated stage when they occur.
Classification and Management
Urodynamic classification adopted by ICS
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