11.1 Introduction

The term ‘neurogenic’ bladder is non-specific and applies to any lower urinary tract (LUT) dysfunction which is a consequence of neurological disease. A neurogenic bladder can result in disruption of storage and voiding functions of the LUT depending on the associated neurological pathology, which often (but not always) leads to the LUT symptoms and requires prompt evaluation. Urodynamic testing is frequently undertaken to evaluate such patients, as their disease or injury to the nervous system can have profound consequence. The sequelae of neurological LUT dysfunction can include chronic urinary infection, formation of urinary tract calculi, incontinence, vesico-ureteric reflux, acute kidney injury and chronic kidney disease. There is, therefore, a low threshold for urodynamic investigation within this patient group.

11.2 Patterns of Urodynamic Abnormality

Examples of neurological conditions associated with bladder dysfunction are shown in Table 11.1 [1]. The pattern of LUT dysfunction can often be predicted by the anatomical location of neurological disease or injury. There are three main patterns of LUT dysfunction (Figure 11.1):

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  Suprapontine

  
  
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  Suprasacral (can also be termed Spinal or Infrapontine-Suprasacral)

  
  
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  Infrasacral

Figure 11.1 Patterns of lower urinary tract dysfunction following neurological disease.

(Reproduced from Panicker et al. [2], with permission from Elsevier). Note the common findings from clinical history, ultrasound scanning and urodynamics. The likely pattern of bladder and sphincter activity is also shown (PVR = Post Void Residual).

In order to comprehend how the level of lesion impacts on LUT function, it is important to understand the basic processes of filling and voiding. In normality, the bladder stores urine at low pressure with sufficient sphincter activity to maintain continence, and during voiding, the co-ordination of detrusor contraction and sphincter relaxation allows efficient bladder emptying to completion. These functions are complex and require both central and peripheral nervous system involvement. The micturition process can be viewed as specific, important contributions from three distinct central nervous system locations: the higher cerebral cortex which is involved with sensation and decision-making; the brainstem (specifically the pontine micturition centre) which coordinates storage and voiding; and the sacral micturition centre which is involved in detrusor muscle and urinary sphincter contraction/relaxation. Peripheral nervous system contribution is via the parasympathetic, sympathetic and somatic nerves. Parasympathetic nervous system involvement from S2 to S4 spinal cord segments is via pelvic nerves which are responsible for excitatory input to the bladder and lead to detrusor contraction. Sympathetic nervous system input is primarily from T11 to L2 spinal cord segments and causes relaxation of the bladder via the hypogastric nerves. The most important somatic nerves involved in LUT function are the pudendal nerves which supply the striated muscle of the urinary sphincter and also originate from the S2 to S4 spinal cord level.

Supra pontine lesions – disruption to neuronal circuitry above the brain stem.

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  Loss of the central inhibition to voiding.

  
  
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  Reduction in bladder capacity.

  
  
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  Detrusor overactivity during the filling phase of urodynamic studies.

  
  
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  If connections between the pontine micturition centre, sacral micturition centre and peripheral nervous system remain intact, then voiding will be normal with unaltered co-ordination of detrusor contraction and sphincter relaxation.

  
  
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  Sphincter activity is usually normal in these patients.

Suprasacral lesions eliminate both the central inhibition of voiding, as seen in suprapontine lesions, and local reflex activity below the lesion.

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  Detrusor overactivity seen on urodynamic evaluation.

  
  
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  Possible disturbance to voiding as pontine coordination of detrusor contraction and urethral sphincter relaxation is lost (detrusor–sphincter dyssynergia).

  
  
  
  
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    very high voiding pressures

    
    
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    hydronephrosis and renal dysfunction

    
    
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    secondary changes in the bladder becomes hypertrophic and stiffer (urodynamics as loss of compliance)

    
    
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    elevated pressures at the end of the filling is an indicator of risk to upper urinary tract.

  
  
  
  
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  Uncoordinated voiding large post-void residual volumes/incomplete bladder emptying.

Infrasacral lesions – trauma to the sacral and subsacral regions.

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  Loss of sensation during bladder filling.

  
  
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  Detrusor acontractility.

  
  
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  Sometimes, a decrease in bladder compliance which may not be evident in the short to medium term.

  
  
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  Urethral function dependent on the severity of nerve damage as injury to the pudendal nerve may result in an incompetent urethra which can manifest as urodynamic stress incontinence.

Almost always following a spinal cord injury, there will be a period of acute spinal shock whereby the parasympathetic innervation of the bladder is disrupted rendering the bladder atonic and consequently the patient will experience a period of urinary retention. In these cases, the priority is to ensure patient’s upper tracts are safe and this is usually achieved with an indwelling catheter or preferably via the early establishment of intermittent catheterisation. Urodynamics are normally delayed until the period of spinal shock has subsided (6–12 weeks).