Neurourology

Physiology — Storage & Emptying

Filling (Storage)

1. Accommodation

• Compliance
• Sympathetic stimulation
• Parasympathetic inhibition

2. Closed bladder outlet

• Sympathetic stimulation → increases involuntary smooth sphincter tone
• Onuf's nucleus stimulation → increases voluntary striated sphincter tone

Emptying (Voiding)

1. Open bladder outlet

• Relaxation of the pelvic muscle
• Sympathetic inhibition
• Onuf's nucleus inhibition

2. Detrusor contraction

• Parasympathetic stimulation
• Sympathetic inhibition

Pathways & Receptors

System	Level	Nerve	Receptor
Sympathetic	T10–L2	Hypogastric	β₃
Parasympathetic	S2–S4	Pelvic	M₃
Somatic	S2–S4	Pudendal (Onuf's nucleus)	—

• Central control by the pontine micturition center
• M₂ is the predominant receptor, but M₃ is the primary (functional) receptor

Treatment Options — by Functional Category

Storage

A — Bladder related

• Behavioral → education, bladder training, timed voiding, pelvic floor
• Medication → antimuscarinic, β₃ agonist, Botox (presynaptic)
• Neuromodulation → sacral, posterior tibial
• Augmentation

B — Outlet related (sphincter)

• Behavioral therapy → bladder training, timed/fluid restriction, pelvic floor
• Sling procedure
• Artificial urinary sphincter

Voiding

A — Bladder related

• Credé maneuver
• Neuromodulation

B — Outlet related (sphincter / BPH / stricture)

• α-blocker
• Prostate surgery
• Urethral stricture repair
• Sphincterotomy
• CIC
• Indwelling catheter

EAU 16 (2025) discourages Credé / Valsalva / triggered reflex voiding: they raise intravesical pressure and provoke reflex sphincter contraction → hazardous to the urinary tract unless UDS confirms pressures stay within safe limits. All assisted emptying requires low outlet resistance + close urodynamic surveillance. Triggered voiding can induce AD in lesions at or above T6. The penile clamp is absolutely contraindicated in NDO or low compliance.

Evaluation

• Detailed history — including neurological and bowel history
• Physical exam — including sensory, reflexes, anal tone
• Voiding diary & QoL
• Labs & PVR
• Pad test & uroflow (optional)

→ After this, the patient is categorized as Low risk vs Unknown risk

Risk Stratification

Framework: AUA/SUFU 2021 NLUTD. Not present in EAU 16 (2025), which uses only an informal low- vs high-risk split.

Click the algorithm to open it full size.

Category	Defining features
Low risk (must meet all)	Suprapontine lesion or lesion distal to the spinal cord · spontaneous void · low PVR · no hydronephrosis · normal renal function
Unknown risk	Suprasacral lesion, MS · elevated PVR · recurrent UTI → these need upper tract imaging + UDS
Moderate risk	UDS shows BOO or DO · high PVR · no hydronephrosis · normal renal function
High risk	Poor bladder compliance · elevated detrusor pressure · DSD · hydronephrosis · abnormal renal function

• Low risk → no routine upper tract imaging, renal function testing, or UDS
• Not clearly low risk → unknown risk until worked up, which then reclassifies as moderate or high

The four goals in a spinal cord injury patient:

1. Preserve and protect the upper tracts
2. Minimize lower urinary tract complications
3. Treat incontinence
4. Produce a management plan that is both safe and compatible with quality of life

To assess the upper tracts: a renal scan is preferred, with renal ultrasound as the alternative.

Patterns of LUT Following Neurological Disease

Key: I = impaired · OV = overactive · N = normal · S = synergic · D = dyssynergic · OP = open/incompetent · A = areflexia · CNR = competent, non-relaxing · F = fixed tone

Disorder	Detrusor activity	Compliance	Smooth sphincter	Striated sphincter	Comment
CVA	OV	N	S	S	Suprapontine
Cerebral palsy	OV	N	S	S / 25% D	25% have DSD
Parkinson	OV	N	S	S	Bradykinesia
Multiple system atrophy	OV	N	OP	S (denervation)	No TURP — open bladder neck
MS	OV	N	S	S / 30–65% D	30–65% have DSD; 20–40% areflexia
Suprasacral cord injury	OV	N	S / D	D	Smooth sphincter DSD if lesion above T6
Autonomic dysreflexia	OV	N	D	D
Sacral SCI	A	N	CNR	F	Compliance may be decreased
Myelodysplasia / spina bifida	A	N (may be ↓)	OP	F	10% have DSD
Disk	A	N	CNR	S
Tabes dorsalis / pernicious anemia	I	N	S	S	Loss of sensation is the primary problem
Pelvic surgery	I or A	↓ or N	OP	F
Diabetes	I or A or OV	N or ↑	S	S

Sensation is not tabulated above but is recorded for three: CVA — may be reduced · suprasacral cord injury — absent · tabes dorsalis — loss of sensation is the primary problem.

Pattern mnemonics — which disorders cluster where:

Finding	Mnemonic	Disorders
Areflexia	SIDS MD	Sacral SCI · Iatrogenic (post-op) · DM · Spina bifida · MS (20–40%) · Degenerative disk disease
Poor compliance	SIMS	Sacral SCI · Iatrogenic · MSA · Spina bifida
DSD	SMCS-T	Suprasacral SCI · MS (30–65%) · Cerebral palsy (25%) · Spina bifida (10%) · Transverse myelitis
Open smooth sphincter	IMS	Iatrogenic · MSA · Spina bifida
Competent, non-relaxing smooth sphincter	SD	Sacral SCI · Degenerative disk disease
Fixed external sphincter	ISS	Iatrogenic · Spina bifida · Sacral SCI

Causes of detrusor overactivity:

1. Idiopathic
2. Neurogenic — supraspinal: stroke, Parkinson's, hydrocephalus, brain tumor, traumatic brain injury, MS · suprasacral spinal: SCI, cord tumor, MS, myelodysplasia, transverse myelitis · plus diabetes
3. Non-neurogenic — UTI · BOO (men: BPH, bladder neck stricture; women: POP, post-incontinence surgery, primary bladder neck, stricture) · bladder tumor · bladder stones · foreign body · aging

Cerebral shock — the early period after a stroke: urinary retention from detrusor areflexia, lasting 6–12 weeks and occasionally 1–2 years. The cerebral counterpart of spinal shock.

Brain tumor — the superior frontal lobe is the site most often associated with voiding dysfunction; incontinence is the usual picture, while retention is commoner with posterior fossa tumors.

Parkinson's disease — mainly detrusor overactivity, but a minority have acontractility, so TURP may not help. Motor onset precedes LUTS by about 3 years, so the patient is already known to have PD.

Parkinsonism is not only PD — it is the syndrome of tremor, rigidity and bradykinesia, also produced by multiple system atrophy, progressive supranuclear palsy and Lewy body dementia.

Tethered cord — often declares itself at a growth spurt; detrusor overactivity is the commonest urodynamic finding, which is the reverse of the usual spina bifida pattern.

Lumbar disc disease and cauda equina syndrome both cause retention.

Multiple System Atrophy

Urinary symptoms — urgency, frequency and urge incontinence — can precede the diagnosis by up to 4 years. The bladder neck is open. Treating the incontinence pharmacologically may worsen emptying, so the goal is to facilitate storage and use CIC; an indwelling catheter is considered only in advanced cases who cannot manage CIC. Desmopressin helps predominant nocturia.

Urogenital features favoring MSA over PD:

• Urinary symptoms, or erectile dysfunction, preceding or coinciding with the parkinsonism
• Urinary incontinence · high post-void residual · open bladder neck
• Striated sphincter denervation on EMG
• Worsening lower urinary tract function after urological surgery — unlike PD, where most patients do not deteriorate after surgery

Autonomic Dysreflexia

• Lesion above T6–T8 — an acute, massive, disordered sympathetic response to a noxious stimulus below the level of the lesion. It occurs only after the spinal shock phase has passed and requires a viable, intact distal cord.
• Mechanism — uninhibited sympathetic outflow below the lesion (splanchnic vasoconstriction) with reflex parasympathetic outflow above it.
• Commonest trigger is bladder distension. Others: constipation, instrumentation, catheter change, stone, sexual activity, long-bone fracture pain, pressure sores.
• Pounding headache · hypertension · sweating and flushing above the lesion · cool skin below it · reflex bradycardia — though tachycardia or arrhythmia can occur instead.
• Urodynamics during an episode: detrusor overactivity + smooth sphincter dyssynergia + DSD.

Prophylaxis in an at-risk patient:

• Identify the at-risk patient and remove potential noxious stimuli beforehand (retention, constipation, pressure sores)
• Spinal anesthesia
• Nifedipine 10 mg, 30 minutes before the procedure — 20 mg before electroejaculation
• Labetalol · terazosin

Treatment — the sequence matters:

1. Remove the noxious stimulus — stop the cystoscopy, check the catheter — then sit the patient up and loosen tight clothing. These steps alone may abort the episode.
2. Drugs come only after the bladder has been emptied.
3. Monitor observations every 2–5 minutes.
4. Topical 2% nitroglycerin paste above the level of the lesion — standard of care. Alternatives: nifedipine 10–20 mg, or a beta- plus alpha-blocker.
5. Atropine 1 mg IV as needed for reflex bradycardia.
6. IV nitroprusside if still refractory.

For dysreflexia refractory to oral agents, ablative options exist — sympathectomy, dorsal root ganglionectomy, sacral neurectomy, sacral rhizotomy, cordectomy. Sacral rhizotomy with CIC is the one usually favored, being moderately invasive and relatively low risk.

EAU defines AD as an SBP rise > 20 mmHg from baseline, with headache, blurred vision, flushing/sweating above the lesion and pallor/cold skin below it. It is more common in cervical (60%) than thoracic (20%) SCI; bradycardia is typical, though only 23% were actually bradycardic in one series. Triggers: bladder/bowel distension, cystoscopy, urodynamics, any noxious stimulus (ingrown toenail, pressure sore), sexual stimulation. Drugs: 2% nitroglycerin paste above the lesion is first-line; sublingual nifedipine 10–20 mg works but is prohibited in many centers (rapid, non-reversible BP drop); IV nitroprusside if refractory. Prophylaxis: terazosin 1–10 mg daily. EAU (Strong): BP + HR monitoring is mandatory during UDS and other invasive procedures in at-risk patients; empty the rectal ampulla first.

DSD — Detrusor Sphincter Dyssynergia

• Suprasacral SCI
• MS (30–65%)
• Cerebral palsy (25%)

Management

The goal is to lessen abnormal external sphincter activity or to circumvent it. Drugs used for detrusor overactivity do not relax the external sphincter — that is the central point.

1. CIC
2. Sphincterotomy
3. Stent across the external sphincter
4. Botulinum toxin into the external sphincter
5. Continuous catheterization — urethral or suprapubic
6. Urinary diversion

By site of dyssynergia: bladder neck → an alpha-blocker (tamsulosin); external sphincter → a skeletal muscle relaxant — baclofen, diazepam or dantrolene.

Indications for sphincterotomy:

• Autonomic dysreflexia caused by DSD
• DSD itself
• Risk of upper tract deterioration in a high-risk patient (DLPP > 40 cmH₂O)
• Difficulty performing CIC
• High-pressure voiding with severe hydronephrosis or VUR
• To gain the patient independence

How to decrease the rate of bladder stones in SCI with a Foley catheter

1. Long-term antibiotics
2. Acidify urine
3. Increase fluid intake
4. Routine bladder lavage

Fowler Syndrome

• Urinary retention with no neurological disease in a young female
• Associated with PCOS
• Capacity over 1 L with no urge sensation
• UDS → impaired sphincter relaxation
• Highly responsive to sacral neuromodulation — around 70% success, the best response of any indication

Impaired sphincter relaxation is the concentric-needle EMG finding (decelerating bursts / complex repetitive discharges). The urodynamic finding is detrusor acontractility.

CIC vs Indwelling Catheter

Benefits of CIC over indwelling catheter

• Improved quality of life
• Facilitates sexual activity
• Maintenance of bladder compliance — over 80% is lost with an indwelling catheter
• Reduced risk of pyelonephritis
• Reduced risk of stones, upper and lower tract
• Reduced risk of prostatitis, epididymitis, orchitis and Fournier's gangrene
• Reduced risk of urethral stricture
• Reduced risk of traumatic hypospadias (both sexes) and the "lead-pipe" urethra in women

Bladder cancer in SCI with chronic catheter

• Incidence 1% → surveillance after 8 years

Underactive Bladder (DUA)

• Difficult to diagnose — overlaps with OAB and is associated with BOO
• Diagnosis by urodynamics → measure BCI

BCI = Pdet@Qmax + 5(Qmax)

• < 100 → underactive / acontractile bladder

Management

• Behavioral, timed voiding, pelvic physiotherapy
• CIC, indwelling catheter, urinary diversion
• Bladder outlet obstruction surgery
• Neuromodulation

Neuromodulation — positive results found in

1. Non-obstructive urinary retention
2. DUA

OAB

OAB = urgency, with or without UUI, usually with increased daytime frequency and nocturia, in the absence of UTI or other obvious pathology.

Evaluation

• Hx + physical exam + UA + PVR + QoL + voiding diary
• Urodynamics should be done if a neurological etiology is suspected
• Urodynamics & cystoscopy should be done when surgery for UUI is considered

Treatment Pathway

1. Behavioral, timed voiding, fluid restriction
2. Pelvic floor muscle therapy
3. OAB medication (antimuscarinic / β₃ agonist)
4. Botox or neuromodulation
5. Urinary diversion / augmentation

Management of MS for LUTS

• Hx + physical exam + voiding diary + QoL + UA + US KUB + PVR + UDS
• High PVR → CIC
• Low PVR → 1st behavioral therapy · 2nd OAB medication · 3rd Botox · 4th neuromodulation · 5th indwelling catheter · 6th augmentation

Antimuscarinics

Divided into tertiary or quaternary.

A — Tertiary (lipophilic)

• Cross BBB → CNS side effects
• Oxybutynin (non-selective)
• Tolterodine
• Darifenacin (highest M3 selectivity)
• Solifenacin

B — Quaternary (lipophobic)

• Safe on CNS
• Trospium (safe, but watch the renal profile)

Contraindications

• Urinary retention
• Closed-angle glaucoma — precisely: untreated narrow-angle; treated narrow-angle is not a contraindication
• Myasthenia gravis
• cognitive impairment

Side effects

• Constipation, dry mouth, blurry vision, headache, retention

β₃ Agonist

• Mirabegron (50 mg PO daily)
• Effect at 4 weeks to 3 months
• Contraindicated → severe uncontrolled hypertension

OnabotulinumtoxinA (Botox)

• MoA → inhibits release of ACh at the presynaptic terminal
• Indications → ① OAB with incontinence · ② decrease DLPP
• Efficacy → 30% complete resolution · 60% have a 50% reduction in symptoms
  • Retreatment often needed after 6 months
  • Do not reinject within 3 months
• Complications → UTI (most common), high PVR, transient retention requiring CIC
• Contraindications → UTI, pregnancy, myasthenia gravis, not accepting catheterization

Steps

1. Map the bladder — except the trigone, don't inject it
2. 100 U / 10 mL → inject 0.5 mL × 20 sites
3. Increase to 200 U / 30 mL → inject 1 mL × 30 sites — for neurogenic overactivity

Sacral Neuromodulation

• MoA → modifies the voiding reflex — stimulation of the S3 afferent nerve

2-stage procedure

1. Stage 1 → insertion of the electrode at the S3 root, test for 2–4 weeks; if symptoms improved →
2. Stage 2 → connection of the electrode to a subcutaneous generator

How to know if placement is accurate

Root	Response
S3 (target)	Bellows of the pelvic floor + plantar flexion of the great toe
S2 (move down)	Anus contraction + plantar flexion of the whole foot
S4 (move up)	Bellows of the pelvic floor without plantar flexion

EAU 16 (2025) Strong: "Consider sacral neuromodulation in selected neuro-urological patients" (LE 1b) — MS with NDO are often good responders. MRI is no longer a barrier — current generators/leads are 1.5-T and 3-T conditional. SNM is not FDA-approved for neurogenic bladder (off-label) despite its efficacy — RCT success 76% on vs 42% off.

Percutaneous Tibial Nerve Stimulation

• Insertion 5 cm cephalad to the medial malleolus and 2 cm posterior to the tibia
• Stimulates S3 through the tibial nerve
• Proper placement → patient feels sensation at the bottom of the foot

Polyuria

• Polyuria = > 40 mL/kg
• Nocturnal polyuria = 33% of the volume at night (NPI > 33%)

Evaluation

• Hx (DM, OSA, neuro) + physical + FVC (frequency-volume chart)

Click the algorithm to open it full size.

FVC finding	Next step	Result
Low volume	Look for a urological cause	Treat
Nocturnal polyuria (NPI > 33%)	Look for CHF, DM, OSA, excessive PM fluid intake	Treat the cause
Polyuria (> 40 mL/kg)	Overnight water deprivation	Urine osmolality > 800 → primary polydipsia; Urine osmolality < 800 → renal concentration test
Renal concentration test	Normal → central DI	Abnormal → nephrogenic DI
Mixed	Both patterns

Treatment for nocturnal polyuria (NPI)

• Control the underlying cause
• Desmopressin — watch for hyponatremia

Contraindicated in:

• CrCl < 50
• Hyponatremia
• vWD

Spinal Shock

• Decreased excitability of cord segments at and below the lesion → areflexic, acontractile bladder; urinary retention is the rule
• Duration → 6–12 weeks in complete suprasacral lesions; may last 1–2 years
• Resolution → begins with return of the bulbocavernosus reflex, alongside return of lower-limb DTRs
• First UDS within 3 months of SCI (EAU); repeat after spinal shock resolves
• Do not perform irreversible interventions based on symptoms during this period

Urodynamics during spinal shock:

• Detrusor areflexia; radiologically a smooth-contoured bladder without trabeculation
• Synergic smooth sphincter; closed, competent bladder neck
• Reduced but still synergic external sphincter tone — no voluntary control, and the guarding reflex is absent
• Hypercompliance
• Absent sensation

Expected urodynamic findings by lesion:

Lesion	Detrusor	Bladder neck	External sphincter
Complete suprasacral SCI, above T6	Overactive	Dyssynergic	DSD
Complete suprasacral SCI, below T6	Overactive	Normal	DSD
Complete sacral SCI	Areflexic (± poor compliance)	Tight	Fixed
Peripheral lesion (pelvic surgery)	Areflexic (± poor compliance)	Open	Fixed

Radical Pelvic Surgery

The inferior hypogastric plexus, lying alongside the rectum and vagina, is the structure at risk.

Operation	Voiding dysfunction
Abdominoperineal resection	20–70%
Radical hysterectomy	16–80%
Low anterior resection	20–25%
Proctocolectomy	10–20%

Injury is permanent in 15–20%.

• Presentation — a combined storage and emptying failure: inability to empty, plus stress incontinence.
• Urodynamics — impaired detrusor contractility or areflexia · open smooth sphincter · fixed external sphincter (loss of voluntary control, obstructing) · reduced compliance, though it may be normal.
• Recovery takes 6–12 months. Avoid early intervention such as TURP, which can worsen the incontinence. Treatment is CIC.
• Mechanisms: denervation/decentralization · tethering or encasement of nerves in scar · direct bladder or urethral trauma · bladder devascularization.

Storage Pressure & the Upper Tract

• DLPP = lowest Pdet at which leakage occurs without a detrusor contraction or raised abdominal pressure
• DLPP > 40 cmH₂O → hydronephrosis or VUR in 85%
  • A cut-off of 20 cmH₂O is more sensitive (91.5%) for upper tract damage
  • Aim for as low a pressure as reasonably achievable, well < 40 cmH₂O — the 40 figure is not a validated "safe" line
• Impaired compliance → < 20 mL/cmH₂O (no consistent definition; 10–20 range used)

VUR in neurogenic bladder

• Incidence 17–25% in SCI; more common with suprasacral injury
• Driven by high storage/voiding pressures + infection — no discrete VUR pressure threshold is stated
• Best initial treatment → normalize urodynamics (lower storage pressure, lower outlet resistance) before considering surgical correction
• Upper tract deterioration 51% with urethral catheters vs lower with voiding/CIC

Risk factors for upper-tract damage in SCI: bladder overdistension · loss of compliance · high DLPP · DSD. Complications: VUR · infection (UTI, pyelonephritis) · stones, upper and lower · renal failure.

Bladder Augmentation

• Aim → low-pressure reservoir; improves compliance, abolishes/reduces NDO
• EAU (Strong): "Offer bladder augmentation in low bladder compliance and/or refractory neurogenic detrusor overactivity" — only when all less-invasive methods have failed
• Supratrigonal cystectomy → indicated with a severely thick, fibrotic bladder wall; CIC may become necessary
• Caution with pre-operative renal scars → metabolic acidosis
• Auto-augmentation (detrusor myectomy) → low surgical burden, does not preclude further intervention
• Transplantation into a defunctionalized bladder succeeds if capacity is > 100 mL and voiding pressure < 100 cmH₂O

Long-term complications

Complication	Rate
Bowel dysfunction	15%
Mucus production	12.5%
Stone formation	10%
Metabolic abnormalities	3.35%
Bladder perforation	1.9%

• Lifelong follow-up is essential — stabilizes renal function and prevents anatomical deterioration, but morbidity is significant
• Any bowel-segment reconstruction → annual history, physical, metabolic panel (electrolytes/acid-base), renal function, upper tract imaging (AUA/SUFU)

Follow-up & Surveillance

No high-level evidence; intervals are largely unspecified. Flagged as such rather than invented.

EAU 16 (2025)

• Interval between baseline and control investigations should not exceed 1–2 years; much shorter in high-risk
• High risk → upper tract ultrasound every 6 months
• High risk → physical exam + urine labs yearly
• UDS → mandatory baseline in high-risk, repeated at regular intervals — no numeric interval given
• Any significant clinical change → further specialized investigation (Strong)

AUA/SUFU 2021

• Low risk → no routine yearly surveillance unless symptoms, imaging, or renal function change
• Moderate / high risk → yearly history, physical, symptom check + yearly renal function + upper tract imaging every 1–2 years
• UDS → repeat for a change of symptoms or when clinically indicated — no fixed interval
• Stone history or high stone risk → imaging every 1–2 years