Neurogenic Bladder and Autonomic Failure
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Direct answer
Neurogenic bladder is urinary dysfunction from a lesion of the nervous control of micturition, and its pattern depends on whether the lesion lies above or below the sacral centre. Upper motor neuron lesions cause detrusor overactivity and detrusor-sphincter dyssynergia, whereas lower motor neuron lesions cause an areflexic, overdistended bladder with retention. Autonomic failure, most often from multiple system atrophy or diabetes, adds orthostatic hypotension and sudomotor loss.
What you must remember
- Suprapontine lesions: stroke, Parkinson disease or frontal tumours cause urgency and detrusor overactivity with incontinence, while sphincter coordination is usually preserved.
- Pontine and suprasacral lesions: upper motor neuron damage causes detrusor-sphincter dyssynergia, with high detrusor pressures and a risk of upper tract damage.
- Sacral and cauda equina lesions: lower motor neuron damage gives an areflexic bladder with poor contraction, large capacity and overflow incontinence.
- Orthostatic hypotension: a sustained fall of at least 20 mmHg systolic or 10 mmHg diastolic within three minutes of standing defines it, per consensus criteria.
- Autonomic function tests: the Valsalva manoeuvre, heart rate variation with deep breathing, head-up tilt and sudomotor sweat testing assess sympathetic and parasympathetic function.
- Multiple system atrophy: a synucleinopathy with autonomic failure plus parkinsonian or cerebellar features; Shy-Drager syndrome is its older name.
- Pure autonomic failure: isolated autonomic failure, often an early form of a synucleinopathy, which may later evolve into parkinsonism.
- Intermittent catheterisation: preferred for areflexic or high-pressure bladders to prevent retention and protect the upper tract.
A lesion-level pathway for bladder dysfunction
Urological symptoms in a neurological patient are interpreted by localising the lesion along the micturition pathway.
- Suprapontine lesion: Stroke, Parkinson disease or frontal tumours cause urgency, frequency and detrusor overactivity, but the external sphincter usually coordinates with the bladder.
- Pontine and suprasacral lesion: Damage to the pontine micturition centre or spinal pathways above the sacral segments produces dyssynergia, in which the sphincter contracts during voiding and pressures rise sharply.
- Sacral reflex arc: Lesions of the sacral cord or cauda equina interrupt the parasympathetic supply, leaving an areflexic bladder with poor contraction, overflow incontinence and large residual volumes.
- Autonomic dysfunction: Diabetes, amyloidosis and multiple system atrophy damage sympathetic and parasympathetic outflow, so orthostatic hypotension and sexual dysfunction accompany the bladder symptoms.
- Measure the deficit: Post-void residuals, urodynamics and autonomic tests such as the Valsalva ratio and tilt-table testing quantify the problem.
- Choose treatment by pattern: Intermittent catheterisation protects the upper tract in areflexic bladders, alpha-blockers help dyssynergia, and anticholinergics suit overactivity but worsen retention in an underactive detrusor.
Where the exam tries to catch you
Most traps here come from giving the right drug for the wrong bladder pattern.
- Trap: Giving an anticholinergic to every incontinent patient with neurological disease Correct: anticholinergics treat overactivity but can precipitate retention and overflow in an underactive, areflexic bladder.
- Trap: Treating incontinence as simple overactivity without measuring residuals Correct: overflow from a large residual volume is a lower motor neuron pattern, so post-void residuals are measured before choosing a drug.
- Trap: Blaming postural dizziness on dehydration in a parkinsonian patient Correct: neurogenic orthostatic hypotension needs supine and standing blood pressure measurement and autonomic testing.
- Trap: Using midodrine without watching for supine hypertension Correct: midodrine is an alpha agonist that can raise supine blood pressure, so the last dose is taken well before lying down.
Frequently asked questions
Which lesion level causes detrusor-sphincter dyssynergia?
Detrusor-sphincter dyssynergia results from upper motor neuron lesions above the sacral micturition centre, classically at the pontine micturition centre or in the spinal cord above S2 to S4. The external sphincter contracts during voiding, raising intravesical pressure. This pattern risks hydronephrosis and upper tract damage if untreated.
How is orthostatic hypotension defined in autonomic failure?
Orthostatic hypotension is defined by a sustained fall of at least 20 mmHg systolic or 10 mmHg diastolic within three minutes of standing or head-up tilt. Blood pressure should be recorded lying and standing to confirm it. Tilt-table testing is used when the diagnosis is uncertain.
What is first-line bladder management in an areflexic neurogenic bladder?
Clean intermittent self-catheterisation is the preferred management for an areflexic neurogenic bladder with retention, because it empties the bladder and protects the upper urinary tract. Anticholinergic drugs are avoided, since they can worsen retention. Management is individualised by urodynamic findings.
Why is midodrine used in neurogenic orthostatic hypotension?
Midodrine is an alpha-1 agonist that constricts peripheral vessels and raises standing blood pressure in neurogenic orthostatic hypotension. It can cause supine hypertension, so the last dose is timed well before lying down. Non-drug measures such as salt intake and compression stockings are often combined with it.
Which autonomic failure syndrome combines parkinsonism with autonomic failure?
Multiple system atrophy combines autonomic failure with parkinsonian or cerebellar features and is a synucleinopathy. Its older name, Shy-Drager syndrome, is still used in some texts. Orthostatic hypotension and urinary symptoms often appear early and carry a poorer prognosis than idiopathic Parkinson disease.