Micturition is the process of eliminating water and electrolytes from the urinary system, commonly known as urinating. It 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 co-ordinated contraction/relaxation of the bladder and urethral sphincters, which are controlled by 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.
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 urethral sphincters (IUS) and external urethral sphincters (EUS).
The bladder and IUS are under the control of the autonomic nervous system. The EUS is under the control of the somatic nervous system. This means only the EUS can be voluntarily opened or closed to control micturition, the others are controlled automatically.
To stimulate storage, impulses from the cerebral cortex travel to the pons. The pons is responsible for co-ordinating the actions of the urinary sphincters and the bladder, and the area involved in the storage phase is the pontine continence centre (on the left-hand side of the pons).
From here, signals are sent to sympathetic nuclei in the spinal cord (nerve roots T10-L2), 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 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 neck of the bladder
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 EUS. This prevents any urine from leaking out.
The co-ordinated relaxation of the detrusor muscle and contraction of the urethral sphincters allows the bladder to fill and store urine 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.
Urinary incontinence is the inability to maintain a storage phase of micturition. Incontinence can arise from a multiple different pathological processes, or can simply caused by normal events, such as pregnancy or holding urine for too long. Different causes of urinary incontinence include:
- Stress incontinence – urine leakage when pressure is exerted on the bladder. This is common in pregnancy and can sometimes happen when laughing or sneezing, due to increased intra-abdominal pressure
- Urge incontinence – urine leakage as soon as the urge to urinate arise. This is seen in urinary tract infections (UTIs) and can also be caused by medications, alcohol or caffeine.
- Overflow incontinence – urine leakage due to the bladder being overfilled. Causes of this include bladder stones and chronic urinary retention.
- Neurological incontinence – urine leakage caused by nerve lesions or neurological conditions, such as multiple sclerosis or spinal cord compression
Here we will focus on neurological causes of incontinence, such as lesions to the spinal cord and cerebral centres.
Spinal Cord Lesion above T12 (Reflex Bladder)
In an upper motor neuron 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, 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.
The causes of such spinal cord injuries include trauma and multiple sclerosis.
Pontine Continence Centre (PCC) lesions
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 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) – these reduce parasympathetic input to the bladder. However, anticholinergics can cause side effects such as a dry mouth or constipation, therefore are not used frequently. Oxybutynin in particular should be avoided in frail patients, due to an increased risk of falls.
- β3-adrenoceptor agonists (e.g. Mirabegron) – these drugs bind to β3-receptors on the detrusor muscle to cause relaxation. By doing so, these drugs increase the bladder’s capacity to store urine. β3-receptors are particularly useful for treating urge urinary incontinence.
Other possible therapies include the injection of botulinum toxin A, sacral nerve stimulation, and surgical procedures such as Augmentation enterocystoplasty or urinary diversion.