Next Lesson - Diuretics
Core
Micturition is the process of passing urine. It can be split up into storage and voiding phases. These phases work antagonistically meaning they are constantly working in opposition.
During the filling phase volume increases gradually, and initially pressure stays at the same low level. After around 150 ml of urine in the bladder, the brain often becomes aware of bladder filling. As filling continues, typically beyond 300 ml, intra-vesical pressure begins to rise more noticeably. At volumes of around 400 to 600 ml, the urge to void is usually strong, although this varies between individuals.
During the voiding phase, the detrusor muscle contracts in waves. This means that pressure increases and decreases multiple times until the full volume of the bladder is voided.
The graph below shows the relationship between intra-vesical pressure and volume.
Diagram - Graph showing the relationship between increasing intra-vesical volume and pressure
SimpleMed original by Dr. Joshua Sturgeon
Diagram - Neural control of storage and voiding. The detrusor receives parasympathetic input; the external urethral sphincter is skeletal muscle under somatic control. A minus sign denotes inhibition and a plus sign denotes stimulation.
SimpleMed Original by Dr. Maddie Swannack, with contributions from Dr. Joshua Sturgeon
Stretch receptors in the bladder detect the level of filling. Sensory neurones synapse in the cortex and cause the feeling of the bladder filling.
Sensory neurones also synapse with sympathetic neurones in the spinal cord. The sympathetic neurones act to stimulate the internal urinary sphincter (IUS) through alpha-1 adrenoceptors. The sympathetic neurones also directly inhibit the detrusor muscle through beta-3 adrenoceptors - this causes progressive relaxation of the bladder during storage meaning the pressure remains constant initially.
The lateral micturition centre (often referred to as the pontine storage centre) is located in the brain stem. It continually sends excitatory action potentials down the cord and synapses with the pudendal nerve. The pudendal nerve is a somatic motor neurone from the nerve roots S2, S3, and S4 and acts on the external urinary sphincter (EUS) through nicotinic acetylcholine receptors (nAChR). The pudendal nerve stimulates the EUS to contract, meaning the lateral micturition centre acts to retain urine.
The voiding phase involves a large amount of input from the cerebral cortex - this allows for voluntary control over voiding, but it is important to recognize that in certain situations, such as emergencies, voiding may not be postponed.
The paracentral lobules in the cortex send inhibitory and excitatory action potentials to the medial micturition centre in the brain stem. The medial micturition centre directly inhibits the lateral micturition centre in order to relax the IUS and EUS, and it also stimulates parasympathetic neurones in the spinal cord.
Stretch receptors in the bladder also send excitatory action potentials to the parasympathetic neurones as well as directly stimulating the medial micturition centre when the bladder becomes full.
These parasympathetic neurones synapse with other parasympathetic neurones in the bladder. These act via stimulatory M3 muscarinic receptors and cause contraction of the detrusor muscle. This means that the medial micturition centres and parasympathetic nervous system act to encourage micturition but can be overridden by the cerebral cortex.
Cauda equina syndrome (CES) is a medical emergency which arises due to compression of the spinal nerves that exist in the spinal column below the bottom of the spinal cord (below the spinal level L2). Symptoms include bilateral sciatica, perianal anaesthesia, and loss of urinary or faecal continence.
CES can cause incontinence through a number of mechanisms:
- Damage to Sacral Parasympathetic Pathways - parasympathetic efferent fibres supply the detrusor muscle. Damage to these pathways can impair bladder contraction and emptying, causing urinary retention with possible overflow incontinence.
- Damage to Sensory Neurones - this means patients cannot feel how full the bladder is, again leading to overflow incontinence.
- Pudendal Nerve Damage - the pudendal nerve supplies the external urethral sphincter through somatic motor fibres. Injury can weaken sphincter closure and contribute to leakage. It does not necessarily leave the sphincter permanently open or cause constant leakage; the pattern depends on the combined effects on bladder sensation, detrusor function and outlet control.
- Disruption of Sympathetic Function - while sympathetic neurones arise from the thoracolumbar region of the cord, there can be secondary effects on sympathetic function due to the overall disruption of spinal cord pathways in CES. This means the bladder is continually relaxed so cannot void properly. This will cause stagnation of urine so patients often require catheterisation as a supportive measure, alongside urgent imaging and neurosurgical assessment to address the underlying cause.
It is important to note a sacral spinal cord lesion will have very similar effects as CES.
A complete transection of the mid-spinal cord initially results in loss of supraspinal inhibition to parasympathetic neurones. After a period of spinal shock with urinary retention, this typically leads to a reflex bladder with involuntary detrusor contractions. Coordination with sphincter relaxation is lost, so effective voiding does not occur. This patient needs to be catheterised to relieve the pressure.
Edited by: Dr. Maddie Swannack
Reviewed by: Dr. Thomas Burnell
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