Micturition reflex
Micturition and bladder function: nerve supply, reflex centres and neurogenic bladder
The bladder fills under sympathetic control and empties by a parasympathetic S2–S4 reflex, coordinated by the pons and held back by the frontal cortex. Covers lesions, autonomic dysreflexia, drugs that cause retention and types of incontinence.
The core idea
Storage and voiding are opposite states. In storage the detrusor is relaxed and the sphincters are closed; in voiding the detrusor contracts and both sphincters open. The sympathetic system and the pudendal nerve favour storage; the parasympathetic system drives voiding. Brain centres decide which state is active and keep the two ends coordinated.
Nerve supply
| Nerve | Segments | Effect | Receptor |
|---|---|---|---|
| Pelvic splanchnic (parasympathetic) | S2–S4 | Contracts the detrusor; relaxes the internal sphincter: voiding | Muscarinic M3 |
| Hypogastric (sympathetic) | T11–L2 | Relaxes the detrusor; contracts the internal sphincter and bladder neck: storage; prevents retrograde ejaculation | Beta-3 (detrusor), alpha-1 (neck) |
| Pudendal (somatic) | S2–S4 (Onuf nucleus) | Contracts the external urethral sphincter: voluntary control | Nicotinic |
- Afferents: stretch and fullness sensation from the bladder wall travel mainly with the pelvic splanchnic (parasympathetic) nerves to S2–S4, then up the spinal cord to the pons and cortex. The same pathway carries the sense of fullness before defecation and the sense of complete emptying. Pain from the bladder roof can travel with sympathetic fibres.
Filling and emptying
- The bladder is highly compliant: pressure barely rises until about 300–400 mL. First desire to void is felt at about 150–250 mL; normal capacity is about 400–600 mL.
- Micturition reflex: rising stretch activates afferents; above a threshold, a reflex drives parasympathetic outflow (detrusor contracts) and inhibits pudendal outflow (external sphincter relaxes). The basic reflex arc is in the sacral cord (S2–S4), the "micturition reflex centre".
- The pontine micturition centre (Barrington nucleus) is the switch that makes the reflex sustained and coordinated, so the detrusor contracts while the sphincter relaxes (detrusor–sphincter synergy). A pontine storage centre opposes it.
- Voluntary inhibition comes from the cerebral cortex, chiefly the medial frontal lobe (paracentral area), which inhibits the pontine centre and contracts the external sphincter until it is appropriate to void. Infants lack this inhibition; control develops by about 2–3 years.
- Voluntary voiding: the cortex releases inhibition, the pelvic floor relaxes, and abdominal muscles can help raise pressure.
Lesions and what the bladder does
| Lesion | Bladder behaviour | Examples |
|---|---|---|
| Frontal, above the pons | Uninhibited: urgency, frequency, urge incontinence, but coordinated complete emptying | Stroke, dementia, frontal tumour, normal pressure hydrocephalus |
| Spinal cord above S2, after spinal shock | Spastic (reflex) bladder: small capacity, involuntary contractions, detrusor–sphincter dyssynergia (high pressure, reflux, kidney damage) | Cord injury, multiple sclerosis, transverse myelitis |
| Spinal shock (days to weeks after cord injury) | Atonic: retention, needs catheter | Acute cord injury |
| Sacral cord, conus, cauda equina or pelvic nerves (S2–S4) | Atonic (flaccid): large capacity, retention with overflow incontinence, lax anal tone, saddle anaesthesia | Cauda equina syndrome, pelvic surgery, conus tumour |
| Afferent (sensory) loss | Large insensate bladder, infrequent voiding, retention and dribbling overflow | Diabetic autonomic neuropathy, tabes dorsalis (dorsal roots and columns) |
- Normal pressure hydrocephalus: dilated ventricles with the triad of gait apraxia (magnetic gait), urinary incontinence (urgency) and dementia. Stretching of periventricular fibres from the frontal lobe impairs cortical inhibition of the bladder.
- After spinal cord injury, retention and loss of voluntary voiding mean injury at or above the sacral segments; a flaccid areflexic bladder localises to S2–S4.
Autonomic dysreflexia
In cord injury at or above T6, a noxious stimulus below the lesion, most often a distended bladder (blocked catheter) or loaded rectum, triggers a massive spinal sympathetic reflex that the brain cannot inhibit. Splanchnic vasoconstriction causes severe hypertension (for example 210/115). The baroreceptors respond through the intact vagus with bradycardia, and vasodilatation above the lesion causes flushing, sweating and pounding headache. Treatment: sit the patient up and relieve the cause first (unblock or change the catheter, empty the bowel); then give a short-acting antihypertensive if pressure stays high. The bradycardia is reflex, not heart block.
Drugs and the bladder
| Drug | Receptor | Use or effect |
|---|---|---|
| Antimuscarinics (oxybutynin, tolterodine, solifenacin) | Block M3 | Overactive bladder; dry mouth, constipation, blurred vision, confusion in elderly; can precipitate retention |
| Mirabegron | Beta-3 agonist | Relaxes the detrusor; overactive bladder without anticholinergic effects |
| Tamsulosin, alfuzosin | Alpha-1 blockers | Relax bladder neck and prostate in benign prostatic hyperplasia |
| Bethanechol | Muscarinic agonist | Contracts the detrusor in atonic bladder |
| Botulinum toxin (intradetrusor) | Blocks ACh release | Refractory detrusor overactivity |
Drugs that cause retention: anticholinergics, tricyclic antidepressants (amitriptyline, a tertiary amine with strong antimuscarinic effects), antipsychotics with antimuscarinic activity (chlorpromazine, clozapine), antihistamines, opioids, alpha-agonist decongestants. A patient on such a drug with dry mouth, constipation, blurred vision and retention has anticholinergic side effects. Spinal and epidural anaesthesia block the sacral parasympathetic outflow (S2–S4), and postoperative urinary retention is now one of their commonest complications.
Incontinence types
| Type | Mechanism | Typical patient | First-line approach |
|---|---|---|---|
| Stress | Weak pelvic floor or sphincter; leak with coughing, laughing | Multiparous women; after prostatectomy | Pelvic floor muscle training |
| Urge (overactive bladder) | Involuntary detrusor contractions during filling | Elderly; neurological disease | Bladder training, then antimuscarinic or mirabegron |
| Mixed | Both | Older women | Treat the dominant type |
| Overflow | Chronic retention with dribbling | Prostatic obstruction, neuropathy, cauda equina, anticholinergic drugs | Relieve obstruction, catheterise |
| Functional | Mobility or cognition | Frail elderly | Toileting help |
Remember S2, 3, 4 empties the bladder; the pons coordinates; the frontal cortex says "not yet".
Exam trap A cord lesion above the sacral segments gives a spastic bladder with dyssynergia; sacral or cauda equina damage gives a flaccid bladder with overflow.
Exam trap In autonomic dysreflexia treat the trigger first: sit up and drain the bladder.
How FCPS asks about this
- Micturition reflex centre: sacral cord S2–S4; coordinated by the pontine micturition centre.
- Voluntary inhibition of micturition: cerebral cortex (medial frontal), acting via the pons and the pudendal nerve to the external sphincter.
- Nerve that contracts the detrusor: pelvic splanchnic parasympathetic (M3); external sphincter: pudendal.
- Sensory nerves of the bladder lost: large atonic bladder with overflow (diabetes, tabes dorsalis).
- Urinary retention, abnormal gait and dilated ventricles: normal pressure hydrocephalus.
- Retention after spinal anaesthesia or on antipsychotics or TCAs: blocked sacral parasympathetic or muscarinic transmission.
- T4 cord injury, BP 210/115, pulse 48, blocked catheter: autonomic dysreflexia; sit up and relieve the bladder.
Test yourself on this topic
5 of the 12 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
Six hours after an inguinal hernia repair under spinal anaesthesia, an elderly man cannot pass urine and has a palpable bladder. Which effect of the spinal anaesthetic mainly explains this?
Answer: Block of S2–S4 parasympathetic outflow
Detrusor contraction for voiding depends on parasympathetic fibres from S2–S4 (pelvic splanchnic nerves) and sensory feedback from the bladder. Spinal anaesthesia blocks these sacral segments, often for longer than the motor block, so the bladder fills without sensation or contraction. Opioids, anticholinergics, pain and an enlarged prostate add to the risk. Catheterisation is needed if the bladder is distended.
Post-op retention
- Voiding needs S2–S4 parasympathetic
- Spinal blocks sacral segments
- Added by opioids, anticholinergics
- Risk: older men, hernia, anorectal surgery
Remember Sacral block, silent bladder.
Exam trap A bladder over 600 mL can be damaged by overstretching; scan early.
Why the other options are wrong
- Block of T11–L2 sympathetic outflow Sympathetic block would not stop voiding.
- Direct relaxation of the prostate The block does not act on the prostate.
- Increased urine production Output is not the cause.
- Spasm of the external sphincter The external sphincter is not in spasm.
A 72-year-old man has 6 months of a slow, broad-based gait, forgetfulness and new urinary urgency with incontinence, which does not seem to bother him. CT shows ventricles enlarged out of proportion to atrophy. Why is he incontinent?
Answer: Loss of frontal cortical inhibition of voiding
Normal pressure hydrocephalus stretches periventricular fibres from the medial frontal lobes, which normally suppress the micturition reflex until voiding is socially appropriate. With this control lost, the bladder empties by an uninhibited reflex as it fills, causing urgency and incontinence, often with little concern. The pons still coordinates detrusor contraction with sphincter relaxation, so emptying is complete. Spinal cord lesions cause dyssynergia, and sacral or sensory lesions cause retention with overflow.
Cortical control of micturition
- Medial frontal cortex inhibits voiding
- Lesion: urge incontinence, unconcerned
- Pons still coordinates emptying
- NPH: gait, dementia, incontinence
Remember Frontal lobe bladder: complete but uninhibited emptying.
Exam trap Post-void residual is low in frontal lobe incontinence; a large residual points to a lower lesion or outflow obstruction.
Why the other options are wrong
- Damage to the pontine micturition centre A pontine lesion would cause poorly coordinated voiding.
- Interruption of sacral parasympathetic outflow Loss of sacral outflow causes retention, not urgency.
- Detrusor–sphincter dyssynergia from cord damage Dyssynergia follows cord lesions between the pons and the sacral cord.
- Overflow from loss of bladder sensation Sensory loss causes painless retention with overflow.
After a spinal cord injury at T6, a man's bladder contracts reflexly but the external sphincter contracts at the same time, causing high pressures. Why?
Answer: Loss of pontine coordination
Normal voiding is coordinated by the pontine micturition centre, which triggers detrusor contraction together with relaxation of the external sphincter. With a cord lesion above the sacral segments but below the pons, the sacral reflex arc survives, so the bladder contracts reflexly when it fills, but loses pontine coordination. The sphincter contracts against the detrusor (detrusor–sphincter dyssynergia), raising pressures and risking upper tract damage. A sacral or cauda equina lesion causes a flaccid, overflowing bladder instead.
Neurogenic bladder
- Coordination: pontine micturition centre
- Suprasacral cord lesion: reflex bladder + dyssynergia
- Sacral / cauda equina lesion: flaccid, overflow
- Frontal lesion: uninhibited but coordinated
Remember Below the pons, above S2: bladder and sphincter fight.
Exam trap Dyssynergia can damage the kidneys from high bladder pressure.
Why the other options are wrong
- The sacral reflex arc is destroyed The sacral arc is intact; that is why reflex contraction occurs.
- The pudendal nerve has been cut The pudendal nerve is intact.
- The detrusor muscle has degenerated The detrusor is overactive, not degenerated.
- Sympathetic outflow rises below T6 This is not the mechanism.
A 52-year-old woman with urgency, frequency and urge leakage undergoes filling cystometry. Which finding defines detrusor overactivity?
Answer: Involuntary detrusor contractions during filling
During normal filling the detrusor relaxes and accommodates urine with little rise in pressure, because of its compliance and sympathetic inhibition, and it contracts only when voiding is permitted. Detrusor overactivity is defined urodynamically as involuntary detrusor contractions during the filling phase, which may be spontaneous or provoked and cause urgency or urge incontinence. Leakage on coughing with a stable detrusor is urodynamic stress incontinence, and low flow with high pressure suggests outflow obstruction.
Detrusor overactivity
- Detrusor should be quiet during filling
- Overactivity: involuntary contractions
- Causes urgency and urge leakage
- Treated with antimuscarinics or β3 agonists
Remember Filling-phase contractions define detrusor overactivity.
Exam trap Urgency is a symptom; detrusor overactivity is a urodynamic finding.
Why the other options are wrong
- Leakage with coughing and a stable detrusor This defines urodynamic stress incontinence.
- A large post-void residual volume Suggests poor emptying or obstruction, not overactivity.
- Low urine flow rate with high voiding pressure Suggests outflow obstruction.
- Bladder capacity above 600 mL A large capacity suggests reduced sensation, not overactivity.
Once a micturition contraction starts, it builds rapidly to a strong contraction that empties the bladder, rather than staying weak. Which property of the micturition reflex explains this?
Answer: It is self-reinforcing positive feedback
The micturition reflex is self-regenerative. Stretch receptors in the bladder wall fire, the reflex causes detrusor contraction, and the contraction itself further activates the stretch receptors, increasing the afferent signal and so the strength of contraction. This positive feedback continues until the detrusor is fully contracted and the bladder empties, after which the reflex fatigues. Higher centres can inhibit or facilitate the reflex.
Micturition reflex
- Stretch receptors fire
- Detrusor contracts
- Contraction increases afferent firing
- Positive feedback to emptying
Remember Each squeeze makes the next squeeze stronger.
Exam trap The reflex then fatigues, so a second void may not start straight away.
Why the other options are wrong
- It is inhibited by detrusor stretch Stretch stimulates, not inhibits, the reflex.
- It depends only on the cortex The reflex operates at sacral and pontine level; the cortex only modulates it.
- It is a negative feedback loop It is positive, not negative, feedback.
- It needs continuous abdominal straining Normal voiding needs little straining.
Where this sits in the CPSP syllabus
- Paper 1: Renal physiology, body fluids and acid-base, Micturition and bladder function
- Surgery & Allied, Paper 2: Renal physiology, body fluids and acid-base, Micturition and bladder function
- Medicine & Allied, Paper 2: Renal physiology, body fluids and acid-base, Micturition and bladder function
Read next
Drug dose pages
Doses, cautions and practical tips for drugs in this chapter.