Meta description: Spinal cord injury can cause urgency, leakage, urinary retention and dangerous bladder pressures. Learn how upper and lower motor neuron injuries differ, how neurogenic bladder is investigated, and which treatments may protect the kidneys and improve continence.

Best treated in an organised spinal unit.

Why can a spinal cord injury affect the bladder?

Passing urine is not simply a bladder reflex. It requires communication between the brain, the spinal cord, the sacral nerves and the urinary sphincter. During normal bladder filling, the bladder muscle, called the detrusor, remains relaxed while the outlet stays closed. When it is appropriate to urinate, the detrusor contracts and the sphincter relaxes in a coordinated fashion.

A spinal cord injury (SCI) can interrupt these pathways. The resulting problem is called neurogenic lower urinary tract dysfunction, often shortened to neurogenic bladder. A person may develop urgency, leakage, difficulty emptying, urinary retention, or a combination of these.

The most important issue is not always the symptom that is most noticeable. A bladder may feel relatively quiet yet store urine at a pressure high enough to threaten the kidneys. Conversely, severe urgency may occur without dangerous pressure. Assessment therefore aims to answer two separate questions:

1. Is urine being stored and emptied at a pressure that is safe for the kidneys?
2. Does the bladder routine provide acceptable continence, independence and quality of life?

The early phase: spinal shock

Immediately after an acute SCI, the bladder commonly becomes temporarily areflexic or acontractile. It fills but does not contract effectively, causing urinary retention. Bladder sensation may also be absent. Catheter drainage is usually required in this acute phase.

This phase may last days, weeks or sometimes longer. Reflex activity can then return below a suprasacral injury and the eventual bladder pattern may be very different from the early one. For this reason, the bladder should be reassessed as the neurological situation evolves.

Upper motor neuron versus lower motor neuron bladder

The traditional distinction is useful, but it is a guide—not a substitute for urodynamic testing.

Feature	Upper motor neuron pattern	Lower motor neuron pattern
Typical injury site	Above the sacral micturition centre, often a suprasacral spinal cord lesion	Sacral cord, conus medullaris, cauda equina or sacral/peripheral nerve injury
Bladder contraction	Often involuntary detrusor contractions during filling—neurogenic detrusor overactivity	Weak or absent detrusor contraction—detrusor underactivity or acontractility
Outlet behaviour	The sphincter may contract instead of relaxing during a bladder contraction—detrusor-sphincter dyssynergia (DSD)	Outlet resistance may be reduced if sacral innervation is damaged, although obstruction from other causes can coexist
Common symptoms	Urgency, frequency, reflex voiding, urge leakage, interrupted emptying and residual urine	Reduced bladder sensation, infrequent voiding, straining, retention, overflow leakage and recurrent infection
Main safety concern	High storage or voiding pressure, poor compliance, reflux, hydronephrosis and renal damage	Chronic retention, over-distension, infection, stones and overflow incontinence
Typical emptying strategy	Often clean intermittent catheterisation, sometimes combined with bladder-relaxing treatment	Clean intermittent catheterisation is commonly required when detrusor contraction is inadequate

Upper motor neuron injury: the overactive but poorly coordinated bladder

With an injury above the sacral spinal cord, the local sacral reflex circuit may remain intact but lose normal coordination from the brain. After spinal shock resolves, the bladder may contract unexpectedly during filling. At the same time, the external urinary sphincter may fail to relax or may tighten when the bladder contracts.

This combination of detrusor overactivity and DSD can produce:

• urgency and reflex urinary leakage;
• a stop–start urinary stream or incomplete emptying;
• high bladder pressure;
• urinary tract infection and bladder stones;
• vesicoureteric reflux, hydronephrosis and, if not controlled, renal impairment.

People with SCI at or above approximately T6 can also develop autonomic dysreflexia. Bladder distension, a blocked catheter, infection or urological procedures may trigger sudden severe hypertension, a pounding headache, sweating or flushing above the injury, anxiety, nasal congestion and a slow or irregular pulse. This is a medical emergency: sit the person upright, check the catheter and drainage system promptly, and seek urgent medical assistance if symptoms or elevated blood pressure persist.

Lower motor neuron injury: the bladder that cannot squeeze effectively

Damage involving the sacral cord, conus medullaris, cauda equina or sacral nerves can interrupt the reflex pathway to the bladder. The detrusor may contract weakly or not at all. Sensation of filling may be reduced, so the bladder can become very full without the usual warning.

Possible features include:

• difficulty starting or inability to pass urine;
• infrequent voiding and a weak stream;
• abdominal straining to empty;
• a large post-void residual;
• overflow leakage;
• recurrent infection, stones or bladder over-distension.

If outlet innervation is also impaired, stress leakage can coexist with retention. A lower motor neuron lesion is therefore not automatically a “low-pressure and harmless” bladder.

Why the neurological level does not tell the whole story

Real-life bladder dysfunction does not always fit neatly into one box. An incomplete lesion can preserve some sensation or voluntary control. Injuries around the conus may affect upper and lower motor neuron pathways together. Pre-existing prostate enlargement, urethral stricture, pelvic floor dysfunction, medications, constipation and infection can further change bladder behaviour.

Most importantly, neurological examination and lesion level do not reliably predict bladder pressure or sphincter coordination. Symptoms can also change over time. Urodynamic findings, not the label alone, should guide risk assessment and treatment.

How is bladder function investigated after SCI?

Clinical assessment

Assessment usually includes:

• the level, completeness, timing and cause of the SCI;
• bladder sensation, urgency, leakage, voiding method and catheter routine;
• recurrent infections, visible blood, stones, catheter blockage and episodes of autonomic dysreflexia;
• fluid intake, urine output and a bladder diary where practical;
• bowel function and constipation;
• mobility, hand function, cognition, carer support and personal goals;
• medicines that may affect storage or emptying;
• abdominal, genital, perineal and focused neurological examination.

Basic tests

Depending on the clinical situation, these may include:

• urinalysis and urine culture when infection is suspected;
• measurement of the post-void residual by ultrasound or catheter;
• kidney function blood tests, while recognising that serum creatinine may underestimate renal impairment in people with low muscle mass;
• renal and bladder ultrasound to look for hydronephrosis, stones, bladder wall changes and residual urine;
• other renal function assessment when clinically indicated.

A urine culture should not be used to screen for and repeatedly treat bacteria in an otherwise well catheter user. Asymptomatic bacteriuria is common and generally should not be treated, apart from recognised exceptions such as pregnancy or before selected urological procedures that breach the urinary mucosa.

Urodynamic studies

Multichannel urodynamics, sometimes combined with X-ray imaging as video-urodynamics, is central when the risk is unknown or potentially significant. It can determine:

• bladder sensation and capacity;
• detrusor overactivity;
• bladder compliance and storage pressure;
• detrusor strength during attempted voiding;
• sphincter coordination or DSD;
• leakage pressure, residual urine and, with video, reflux or outlet anatomy.

The test is not merely to explain incontinence. Its crucial role is to identify a hostile, high-pressure bladder before silent upper urinary tract damage develops. Repeat testing may be required after treatment, when symptoms change, after recurrent complications, or when renal imaging deteriorates.

Other tests

Cystoscopy is not a routine screening test for every person with SCI. It is used for a specific indication, such as visible blood in the urine, recurrent catheter blockage, suspected stones, difficult catheterisation, urethral injury or another anatomical concern. CT, MRI or nuclear renal imaging may be added when ultrasound or the clinical picture warrants it.

Management: protecting the kidneys while fitting treatment to the person

Treatment should be individualised with a urologist, rehabilitation physician, continence nurse and allied health team. The aim is low-pressure storage, reliable emptying, continence where achievable, fewer complications and a routine the person can realistically manage.

1. Reliable bladder emptying

Clean intermittent catheterisation (CIC/ISC) is often the preferred method when the bladder does not empty adequately. It avoids a continuously indwelling tube and can provide predictable, low-pressure drainage. Frequency is tailored to fluid intake, catheterised volumes, bladder pressure and the treatment plan. Hand function, access to the urethra, cognition, carer assistance, work and travel must all be considered.

If intermittent catheterisation is not feasible, an indwelling catheter may be required. When long-term indwelling drainage is necessary, a suprapubic catheter is often favoured over a urethral catheter because it avoids chronic urethral pressure and erosion, although it still carries risks of infection, blockage, leakage and stones.

Reflex voiding into a sheath system may suit selected men, but only after confirming that bladder pressures and emptying are safe. Regular reliance on abdominal straining or the Credé manoeuvre is generally discouraged because it can generate high pressure and may not empty the bladder adequately.

2. Reducing overactivity and unsafe storage pressure

Options include:

• antimuscarinic medicines, which reduce involuntary bladder contractions but can cause dry mouth, constipation, blurred vision and cognitive adverse effects;
• a beta-3 agonist, which may improve storage with a different side-effect profile but requires attention to blood pressure and other contraindications;
• carefully selected combination therapy;
• intradetrusor botulinum toxin A (Botox) when tablets are ineffective or poorly tolerated. This can markedly reduce detrusor overactivity and pressure but may increase urinary retention; the person must be willing and able to catheterise if required.

Alpha-blockers may reduce outlet resistance in selected people who void spontaneously, but they do not correct every form of DSD and may cause dizziness or low blood pressure.

3. Managing sphincter dyssynergia or outlet resistance

Where DSD prevents safe emptying, management may include intermittent catheterisation, bladder-relaxing therapy, selected alpha-blocker use, sphincter botulinum toxin, or less commonly, an outlet procedure such as sphincterotomy in carefully selected men using sheath drainage. Any procedure that lowers outlet resistance may improve emptying but can trade obstruction for incontinence.

4. Treating an acontractile lower motor neuron bladder

For a bladder that cannot contract effectively, CIC is usually the mainstay. There is no consistently effective oral medicine that restores a truly acontractile detrusor. Correcting reversible contributors: constipation, medicines, infection or mechanical obstruction remains important. Outlet surgery should only be considered when a proven obstruction is present and the likely effect on continence and catheterisation has been discussed.

5. Reconstructive surgery and urinary diversion

If conservative and minimally invasive measures cannot produce safe storage or practical drainage, options may include:

• augmentation cystoplasty to increase capacity and reduce pressure;
• creation of a continent catheterisable channel, such as a Mitrofanoff-type channel;
• selected outlet continence surgery when sphincter weakness is the main problem;
• urinary diversion, with or without bladder removal, in complex or refractory cases.

These are major procedures with long-term surveillance requirements and should be undertaken in an experienced neuro-urology service.

What about sacral neuromodulation?

Sacral neuromodulation is not a routine treatment for a complete spinal cord injury with established DSD or an acontractile bladder. It may be considered in carefully selected people with an incomplete, stable neurological lesion and suitable bladder function, but evidence in SCI is more limited than it is for non-neurogenic overactive bladder or non-obstructive retention. A test phase and specialist assessment are essential.

Follow-up is lifelong

Neurogenic bladder can change even when the spinal injury itself appears stable. Follow-up intensity is based on risk, bladder management method and previous complications. It may include review of symptoms and catheter volumes, renal function assessment, upper urinary tract imaging and repeat urodynamics in moderate- or high-risk patients.

Seek earlier review for:

• new or worsening leakage;
• difficulty catheterising or repeated catheter blockage;
• recurrent symptomatic infection or fever;
• visible blood in the urine;
• flank pain, stones or hydronephrosis;
• increasing residual urine;
• new autonomic dysreflexia;
• deterioration in kidney function.

The take-home message

An upper motor neuron injury often produces an overactive bladder that may fight against a closed sphincter. A lower motor neuron injury more often produces a poorly contracting bladder with retention. Both patterns can cause leakage, infection and kidney damage, and mixed patterns are common.

The safest plan is not based on the injury label alone. It combines symptoms, neurological assessment, kidney surveillance and where indicated, urodynamic testing. With an individualised catheter, medication, Botox or surgical plan, most people can achieve safer bladder pressures and a more predictable routine.

Medical disclaimer: This article provides general education and does not replace individual medical assessment. Sudden severe headache, sweating or flushing with high blood pressure in a person with SCI—particularly with an injury at or above T6—may represent autonomic dysreflexia and requires urgent attention.

References

1. European Association of Urology. EAU Guidelines on Neuro-Urology. Current guideline edition. EAU Neuro-Urology Guidelines.
2. Ginsberg DA, Boone TB, Cameron AP, et al. The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Diagnosis and Evaluation. J Urol. 2021;206(5):1097–1105. PubMed.
3. Ginsberg DA, Boone TB, Cameron AP, et al. The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Treatment and Follow-up. J Urol. 2021;206(5):1106–1113. PubMed.
4. American Urological Association; Society of Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction. Adult Neurogenic Lower Urinary Tract Dysfunction Guideline. 2021; amended 2024. AUA/SUFU guideline.
5. NSW Agency for Clinical Innovation. Management of the Neurogenic Bladder for Adults with Spinal Cord Injuries. State Spinal Cord Injury Service. NSW ACI spinal cord injury resources.
6. Consortium for Spinal Cord Medicine. Bladder Management for Adults with Spinal Cord Injury: A Clinical Practice Guideline for Health-Care Providers. J Spinal Cord Med. 2006;29(5):527–573. Full text on PubMed Central.
7. Pannek J, Blok B, Castro-Diaz D, et al. Guidelines on Neuro-Urology. European Association of Urology; updated annually. EAU Guidelines.
8. Pannek J, Kennelly M, Kessler TM, et al. International spinal cord injury urodynamic basic data set (version 2.0). Spinal Cord Ser Cases. 2018;4:98. DOI.
9. Hooton TM, Bradley SF, Cardenas DD, et al. Diagnosis, prevention, and treatment of catheter-associated urinary tract infection in adults: 2009 International Clinical Practice Guidelines from the Infectious Diseases Society of America. Clin Infect Dis. 2010;50(5):625–663. DOI.

 

Hereditary Spastic Paraplegia (HSP) is best known for causing progressive stiffness, weakness and spasticity of the legs. However, the neurological pathways controlling the bladder travel through the same spinal cord neighbourhood, and bladder dysfunction can therefore become an important and sometimes underestimated part of HSP.

Studies of patients with HSP have reported lower urinary tract symptoms in a substantial proportion of patients, particularly urgency, urinary frequency, nocturia and urgency urinary incontinence. Difficulty emptying the bladder can also occur. Urodynamic studies frequently demonstrate neurogenic detrusor overactivity, sometimes accompanied by detrusor-sphincter dyssynergia.

The modern term for this problem is neurogenic lower urinary tract dysfunction (NLUTD) rather than simply “neurogenic bladder”, because the neurological condition may affect the bladder, bladder outlet and urinary sphincter in different ways.

For patients with HSP, treatment therefore needs to be individualised. The aim is not merely to reduce trips to the toilet. We want to achieve a bladder that stores urine safely, empties adequately, protects the kidneys and interferes as little as possible with everyday life.

How does HSP affect the bladder?

Normal bladder control requires remarkably complicated communication between the brain, spinal cord, bladder and urinary sphincter.

During filling, the bladder should remain relaxed while the urinary sphincter remains closed. When it is appropriate to urinate, the brain permits the bladder to contract while the sphincter relaxes.

HSP can disrupt these pathways.

The commonest urodynamic abnormality reported in HSP is detrusor overactivity, where involuntary bladder contractions occur during filling.

Patients may consequently experience:

• urinary urgency and frequency;
• waking repeatedly at night to urinate;
• urgency urinary incontinence;
• difficulty postponing urination;
• hesitancy or a poor urinary stream;
• incomplete bladder emptying;
• recurrent urinary tract infections; and
• occasionally significant urinary retention.

Importantly, symptoms do not always tell us exactly what the bladder is doing. Two patients saying, “I can’t hold on,” may have quite different underlying bladder physiology.

That is where urodynamic assessment can become particularly useful.

Investigating bladder dysfunction in HSP

Assessment should be tailored to the severity of symptoms and the patient’s neurological and urological risk.

It may include a detailed history, bladder diary, urinalysis, measurement of post-void residual urine, renal function assessment and ultrasound of the kidneys and bladder.

Urodynamic studies are particularly valuable when symptoms are significant, treatment has failed, bladder emptying is abnormal or invasive treatment such as Botox is being considered.

Urodynamics can identify:

Neurogenic detrusor overactivity (NDO)
The bladder contracts involuntarily while filling.

Poor bladder compliance
Bladder pressure increases excessively as the bladder fills. This is particularly important because sustained high storage pressures can potentially threaten the upper urinary tract.

Detrusor-sphincter dyssynergia (DSD)
Instead of relaxing during urination, the urinary sphincter contracts against the bladder.

Detrusor underactivity
The bladder contracts inadequately and therefore does not empty properly.

The EAU and AUA/SUFU guidelines emphasise risk-based evaluation and ongoing surveillance of patients with neurogenic lower urinary tract dysfunction rather than treating symptoms in isolation.

First-line treatment

Treatment depends upon whether the main problem is storage, emptying or a combination of both.

Lifestyle and bladder strategies

Some patients benefit from relatively simple measures such as:

• adjusting fluid intake;
• reducing excessive caffeine;
• timed voiding;
• managing constipation;
• bladder retraining where appropriate;
• pelvic-floor physiotherapy in selected patients; and
• reviewing medications that may worsen bladder function.

Mobility is an important consideration in HSP. A bladder that gives somebody 20 seconds’ warning may be considerably more disabling when that person also has difficulty walking quickly to a toilet.

Treatment goals therefore need to reflect the patient’s mobility, hand function, independence and quality of life, something specifically emphasised by neuro-urology guidelines.

Medication

For predominantly overactive bladder symptoms, treatment commonly begins with an antimuscarinic medication and/or a beta-3 adrenergic agonist.

Antimuscarinic drugs can reduce involuntary bladder contractions but may cause dry mouth, constipation, blurred vision and cognitive adverse effects in susceptible patients.

Beta-3 agonists may provide an alternative or can sometimes be combined with an antimuscarinic.

Post-void residual urine should be considered, particularly when there is already evidence of impaired bladder emptying.

Intermittent catheterisation

When significant urinary retention or incomplete bladder emptying occurs, clean intermittent catheterisation (CIC) may be required.

This can sound intimidating when first discussed, but many patients become remarkably comfortable with the technique.

HSP creates an additional consideration: progressive lower-limb disability, hand function and mobility need to be considered when deciding whether intermittent catheterisation will remain practical.

Where possible, intermittent catheterisation is generally preferable to long-term indwelling catheterisation for bladder emptying in neuro-urological patients.

Botox injections into the bladder

For patients with persistent neurogenic detrusor overactivity despite medication, Botulinum toxin A (Botox) injected into the detrusor muscle can be extremely useful.

Botox temporarily reduces excessive acetylcholine-mediated contraction of the bladder muscle.

The result is essentially a bladder that becomes a little less excitable.

How is bladder Botox performed?

Using a cystoscope, multiple small injections of Botulinum toxin A are placed into the bladder wall.

It is usually performed as a short day procedure under local anaesthetic, sedation or general anaesthesia depending upon the patient and clinical circumstances.

The treatment is temporary and therefore generally needs to be repeated when its effect wears off.

How effective is Botox?

There is strong evidence for intradetrusor onabotulinumtoxinA in neurogenic detrusor overactivity associated with spinal cord injury and multiple sclerosis.

Randomised studies in these populations show:

• fewer episodes of urinary incontinence;
• increased bladder capacity;
• reduced detrusor pressures;
• improved urodynamic storage parameters; and
• improved quality of life.

The AUA/SUFU guideline gives this treatment a Grade A evidence recommendation in MS and spinal cord injury when oral treatment has failed.

The EAU likewise recommends detrusor Botulinum toxin A injections for neurogenic detrusor overactivity when antimuscarinic therapy is ineffective.

But what about HSP specifically?

This distinction is important.

HSP-specific clinical trials of intradetrusor Botox are very limited.

HSP therefore cannot simply inherit the strength of evidence available for MS and spinal cord injury. The AUA/SUFU guideline places Botox treatment for neurogenic disorders other than MS or spinal cord injury in a lower evidence category, although it states that treatment may be offered to appropriately selected patients whose symptoms have not responded adequately to oral medication.

In clinical practice, this makes the urodynamic diagnosis particularly important.

If an HSP patient has convincing neurogenic detrusor overactivity producing significant urgency, incontinence or unsafe bladder storage pressures despite conservative and medical treatment, intradetrusor Botox is a logical treatment option.

The evidence is therefore strongest for treating the urodynamic abnormality, rather than Botox having been proven specifically for the genetic diagnosis of HSP.

What are the disadvantages of Botox?

The most important adverse effect is incomplete bladder emptying or urinary retention.

A patient who previously urinated normally may need intermittent catheterisation after treatment.

The AUA/SUFU guideline therefore specifically recommends discussing the possibility of urinary retention and intermittent catheterisation before Botox is administered to a spontaneously voiding patient.

Other possible complications include urinary tract infection, haematuria, discomfort during urination and the need for repeated treatment.

This discussion is particularly important in HSP patients whose mobility or hand function might make self-catheterisation difficult.

Sacral neuromodulation

Another intriguing option is sacral neuromodulation (SNM).

Rather than temporarily weakening the bladder muscle, SNM attempts to modulate the neurological circuitry controlling bladder storage and emptying.

A small electrode is positioned close to a sacral nerve, usually the S3 nerve root, and connected to an electrical stimulator.

Think of it less as “shocking the bladder” and more as adjusting the electrical conversation between the bladder, spinal cord and brain.

A major advantage: it can be tested first

SNM generally begins with a trial or test phase.

A temporary or tined lead is placed near the sacral nerve and connected to an external stimulator.

Symptoms are then assessed.

A clinically meaningful improvement, commonly around 50% or greater, is generally required before proceeding to implantation of the permanent pulse generator.

That provides an important advantage: the patient effectively auditions the treatment before committing to the permanent implant.

Does sacral neuromodulation work in neurogenic bladder?

The evidence is promising but considerably less robust than the Botox evidence for MS and spinal cord injury.

The AUA/SUFU guideline states that SNM may be offered to selected patients with neurogenic lower urinary tract dysfunction who have urinary urgency, frequency and/or urgency incontinence, but rates the evidence as Grade C.

Studies involving mixed neurological populations have demonstrated improvements in:

• urgency;
• urinary frequency;
• urgency incontinence;
• voided volume;
• bladder capacity; and
• quality of life.

However, these studies include heterogeneous neurological diseases, making it difficult to predict outcomes for one particular condition.

The AUA/SUFU guideline specifically advises against SNM in neurogenic bladder caused by spinal cord injury or spina bifida, but HSP is not listed as an absolute contraindication.

What about sacral neuromodulation specifically for HSP?

Here we need to be particularly careful about claims of efficacy.

There is currently very limited direct evidence specifically studying SNM in patients with Hereditary Spastic Paraplegia.

Most of the evidence supporting SNM in neurological disease comes from mixed cohorts containing conditions such as multiple sclerosis, Parkinson’s disease, stroke, incomplete spinal cord disorders and other neurological conditions.

Consequently, it would be inappropriate to tell an HSP patient that sacral neuromodulation has a proven success rate specifically for HSP.

Instead, I would regard SNM as a potential treatment for carefully selected HSP patients, particularly those who:

• continue to void spontaneously;
• have troublesome urgency, frequency or urgency incontinence;
• have failed conservative and pharmacological treatment;
• do not have dangerous high-pressure bladder physiology requiring a different strategy; and
• demonstrate a convincing response during the SNM test phase.

The test phase becomes particularly valuable when the evidence base for the underlying neurological disorder is limited.

Botox or sacral neuromodulation: which is better in HSP?

There is currently no good HSP-specific head-to-head trial demonstrating that one is superior to the other.

The choice should therefore be driven by the patient’s bladder physiology.

Botox may be particularly attractive when:

there is proven neurogenic detrusor overactivity, bladder pressures need to be reduced, medication has failed and the patient accepts the possibility of intermittent catheterisation and repeated injections.

Sacral neuromodulation may be attractive when:

urgency, frequency and urgency incontinence predominate, the patient continues to empty reasonably well, conservative and pharmacological therapy have failed, and there is no contraindication to implantation.

SNM also offers the considerable advantage of a test phase before permanent implantation.

The two therapies should therefore not necessarily be regarded as competitors. They act differently and may suit different neuro-urological phenotypes.

Why urodynamics matter before choosing treatment

For HSP, I believe one of the most useful questions is not simply:

“Does the patient have a neurogenic bladder?”

It is:

“What type of neurogenic bladder dysfunction does this particular patient have?”

An HSP patient with severe detrusor overactivity and high storage pressures is fundamentally different from an HSP patient with urgency but satisfactory storage pressures, and different again from somebody with detrusor underactivity and a large residual urine volume.

The treatment should follow the physiology.

This is particularly relevant because HSP studies confirm that detrusor overactivity is common, but voiding dysfunction and other urodynamic abnormalities also occur.

What happens when less-invasive treatments fail?

A small proportion of patients develop severe neurogenic lower urinary tract dysfunction that cannot be adequately controlled with medication, catheterisation, Botox or neuromodulation.

More invasive options can include bladder augmentation or urinary diversion, depending upon bladder pressures, continence, renal risk, mobility and the patient’s ability to catheterise.

Fortunately, these procedures are required far less commonly than the conservative, pharmacological and minimally invasive treatments discussed above.

Follow-up is important

HSP is a neurological condition that can evolve over time. Bladder function can evolve with it.

A treatment that worked well several years ago may therefore need reassessment if symptoms change.

Patients should seek review if they develop:

• worsening urinary incontinence;
• increasing difficulty emptying;
• recurrent urinary infections;
• new urinary retention;
• haematuria;
• flank pain; or
• a significant change in their usual bladder pattern.

Depending upon risk, follow-up may include post-void residual measurement, renal function, renal tract imaging and repeat urodynamics.

Current EAU guidance emphasises ongoing surveillance and reassessment in neuro-urological patients, with the intensity of follow-up determined by individual risk. The 2026 EAU Neuro-Urology Guidelines have also updated recommendations regarding diagnosis, treatment, Botulinum toxin A and follow-up.

The bottom line

Bladder dysfunction is a genuine and sometimes overlooked component of Hereditary Spastic Paraplegia.

The commonest problem is neurogenic detrusor overactivity, producing urgency, frequency, nocturia and urgency incontinence, although impaired emptying and detrusor-sphincter dysfunction can also occur.

Treatment usually progresses from conservative measures and medication to intermittent catheterisation where necessary, followed by more advanced therapies in appropriately selected patients.

Intradetrusor Botox is an effective established treatment for neurogenic detrusor overactivity, although the highest-quality evidence comes from MS and spinal cord injury rather than HSP itself. Its principal trade-off is the possibility of urinary retention and the need for intermittent catheterisation.

Sacral neuromodulation is another potential option for selected HSP patients, especially those with refractory urgency, frequency and urgency incontinence who continue to void spontaneously. However, the evidence specifically for HSP remains limited, so the temporary test phase is particularly useful in determining whether an individual patient is likely to benefit.

Most importantly, treatment should be based on the patient’s symptoms, urodynamic findings, bladder-emptying ability, mobility and individual goals rather than the diagnosis of HSP alone.

References and further reading

1. Fourtassi M, Jacquin-Courtois S, Scheiber-Nogueira MC, et al. Bladder dysfunction in hereditary spastic paraplegia: a clinical and urodynamic evaluation. Spinal Cord. 2012;50:558–562.
2. Braschinsky M, Zopp I, Kals M, Haldre S, Gross-Paju K. Bladder dysfunction in hereditary spastic paraplegia: what to expect? J Neurol Neurosurg Psychiatry. 2010;81:263–266.
3. Ginsberg DA, Boone TB, Cameron AP, et al. The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Treatment and Follow-up. J Urol. 2021;206:1106–1113.
4. Ginsberg DA, Boone TB, Cameron AP, et al. The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Diagnosis and Evaluation. J Urol. 2021.
5. European Association of Urology. EAU Guidelines on Neuro-Urology, 2026.
6. European Association of Urology. Neuro-Urology: Botulinum toxin A injections. The guideline recommends detrusor Botulinum toxin A for neurogenic detrusor overactivity when antimuscarinic therapy is ineffective.

Important note

This information is intended for general patient education and does not replace individual medical assessment. Hereditary Spastic Paraplegia encompasses multiple genetic and clinical phenotypes, and bladder treatment should be individualised following appropriate neurological and urological assessment.