Part of the TeachMe Series

The Storage Phase of Micturition

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Original Author(s): Oliver Jones
Last updated: 3rd May 2020
Revisions: 17

Original Author(s): Oliver Jones
Last updated: 3rd May 2020
Revisions: 17

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Micturition has two discrete phases: the storage/continence phase, when urine is stored in the bladder; and the voiding phase, where urine is released through the urethra. These phases require coordinated contraction/relaxation of the bladder and urethral sphincters, which are all under control of the sympathetic, parasympathetic and somatic nervous systems.

In this article we shall look specifically at the storage phase of micturition, its regulation and consider some clinical relevance.

Overview

The storage phase of micturition is controlled at the highest level by continence centres of the brain. These in turn control the continence centres of the spinal cord. Storage of urine requires relaxation of the detrusor muscle of the bladder, and simultaneous contraction of both the internal (IUS) and external (EUS) urethral sphincters.

The bladder and IUS are primarily under the control of the sympathetic nervous system. The EUS is under the control of the somatic nervous system.

Figure 1: The Neural Control of Micturition

Sympathetic Innervation

To stimulate storage, impulses from the cerebral cortex travel to the pons. The pons is responsible for coordinating the actions of the urinary sphincters and the bladder, and the area involved in the storage phase is the pontine continence centre (in the L-Region of the pons).

From here, signals are sent to the sympathetic nuclei in the spinal cord, and finally to the detrusor muscle and internal urethral sphincter (IUS) of the bladder.

The impulses travel from the spinal cord to the bladder via the sympathetic hypogastric nerve (nerve roots T10-L2). At the bladder, this stimulates:

  • Relaxation of the detrusor muscle in the bladder wall – via stimulation of β3-adrenoreceptors in the fundus and the body of the bladder.
  • Contraction of the IUS – via stimulation of α1-adrenoreceptors at the bladder neck

Somatic Innervation

As described above, the EUS is under voluntary somatic control. In the storage phase, impulses travel to the EUS via the pudendal nerve (nerve roots S2-S4) to nicotinic (cholinergic) receptors on the striated muscle, resulting in contraction of the sphincter.

This coordinated relaxation of the detrusor muscle and contraction of the urethral sphincters allows the bladder to fill with urine, store it for many hours. As the bladder fills, the folds in the bladder walls (rugae) flatten and the walls distend, increasing the capacity of the bladder. This means that as the bladder fills, it expands, allowing the inner (intra-vesical) pressure to remain the constant and lower than urethral pressure. This process known as receptive relaxation is vital to the storage of urine and prevents leakage during this phase.

Clinical Relevance – Incontinence

The maintenance of urinary continence is very complex, and as such urinary incontinence can arise from a multitude of different pathological processes. Here we will concentrate on the neural control of micturition, and how lesions to the spinal cord and cerebral centres can result in the disturbance of urinary storage.

Spinal Cord Lesion above T12 – Reflex Bladder

In an upper motor neurone lesion, sympathetic input to the bladder is lost, leading to an inability for the detrusor muscle to relax, or the IUS to contract.

Afferent signals via the sensory pelvic nerve are also unable to reach the brain, and so the EUS remains constantly relaxed. The result is decreased bladder capacity and detrusor overactivity. The parasympathetic system initiates detrusor wall contraction in response to bladder wall stretch, resulting in the bladder automatically emptying as it fills. This is known as a reflex bladder.  T

The causes of such spinal cord injuries include trauma and Multiple Sclerosis.

Lesion in the Pontine Continence Centre (PCC) – Incontinence

Lesions in the pons can lead to a complete loss of voiding control and the inability to store urine. In damage to the PCC, sympathetic input to the bladder is lost. This results in the same symptoms as a reflex bladder, although the damage is in a different location.

Typical causes of such brain lesions are strokes, brain tumours and the degeneration of dopaminergic neurones in Parkinson’s disease.

Treatment of Incontinence

The treatment of incontinence secondary to neurological insults is challenging. Pharmacological therapies which can be trialled include:

  • Anticholinergics(e.g. Oxybutynin, Tolterodine) which reduce parasympathetic input to the bladder. However, these are more likely to result in anticholinergic side effects such as a dry mouth or constipation, so are used less frequently. Oxybutynin particularly should be avoided in elderly frail patients due to an increased falls risk.
  • β3-adrenoceptor agonists(e.g. Mirabegron) bind to β3-receptors on the detrusor muscle and stimulate relaxation of the muscle. Therefore, these drugs can be used to increase the bladders capacity to store urine in the treatment of urge urinary incontinence.

Other possible therapies include the injection of botulin toxin A, sacral nerve stimulation, and surgical procedures such as Augmentation enterocystoplasty or urinary diversion.