The detrusor is the smooth muscle of the bladder wall responsible for both bladder storage (by relaxing during filling) and emptying (by contracting during micturition). Its unique three-layer interlacing architecture allows uniform spherical contraction to maximise voiding efficiency. Overactive detrusor (overactive bladder) is one of the most common urological conditions, affecting up to 16 percent of adults and producing urgency, frequency, and urgency urinary incontinence.
| Origin | Bladder wall, three interlacing smooth muscle layers (inner longitudinal, middle circular, outer longitudinal) that cannot be separated anatomically |
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| Insertion | Bladder base and urethral junction. The muscle forms the trigone and internal urethral sphincter at the bladder neck |
| Nerve Supply | Parasympathetic: pelvic splanchnic nerves (S2, S3, S4), acting on muscarinic (M3) receptors to drive contraction; Sympathetic: hypogastric nerves (T11-L2), relaxing the detrusor through beta-3 receptors during filling and contracting the bladder neck through alpha-1 receptors |
| Blood Supply | Superior and inferior vesical arteries |
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The coordination of detrusor contraction with external sphincter relaxation is mediated by the pontine micturition centre and requires intact spinal pathways, its disruption in spinal cord injury above the sacral segments produces the dyssynergia that characterises neurogenic bladder.
Overactive bladder from involuntary detrusor contractions produces urgency, frequency and urgency incontinence, managed stepwise with bladder training, antimuscarinic drugs (oxybutynin, solifenacin, tolterodine), beta-3 agonists (mirabegron), intradetrusor botulinum toxin injection and sacral neuromodulation. Neurogenic detrusor overactivity occurs in multiple sclerosis, Parkinson disease and spinal cord injury. Cord injury above the sacral segments can cause detrusor-sphincter dyssynergia, in which the detrusor contracts against a closed external sphincter, generating high bladder pressures that can damage the kidneys; intermittent catheterisation with antimuscarinics or botulinum toxin protects the upper tracts. Detrusor underactivity from neuropathy (for example diabetes) causes incomplete emptying and overflow incontinence.
Not directly palpable. Assessed by urodynamic testing (cystometry) measuring bladder pressure during filling and voiding.
Involuntary detrusor contractions producing urgency, frequency, and urgency incontinence managed with antimuscarinic drugs, beta-3 agonists, and bladder botulinum toxin injection.
Underactive detrusor from neuropathy producing incomplete bladder emptying and overflow incontinence managed with clean intermittent self-catheterisation.
