524 CHAPTER 13 Neuropathic bladder
Bladder dysfunction in multiple sclerosis, in Parkinson disease, after stroke, and in other neurological disease
Multiple sclerosis (MS)
MS is a neurological disease caused by focal demyelination of white matter in the brain and spinal cord. Urological manifestations are the presenting complaint in about 2.5% of MS patients.
Three-quarters of patients with MS have spinal cord involvement and, in these patients, bladder dysfunction is common. Detrusor hyperreflexia with urge incontinence is the most common GU symptom present in 78% of patients with voiding dysfunction.
DSD is present in 30% to 65% of patients, leading to poor emptying and possible upper tract damage.
Parkinson disease (PD)
PD is a cause of Parkinsonism, a clinical complex of tremor, rigidity, and bradykinesis, and is due to degeneration of dopaminergic neurons in the substantia nigra in the basal ganglia. Mild intellectual deterioration may occur, and frequency, urgency, and urge incontinence are common.1
The most common urodynamic abnormality is DH (the basal ganglia may have an inhibitory effect on the micturition reflex). L-dopa seems to have a variable effect on these symptoms and DH, improving symptoms in some and making them worse in others.
LUTS in Parkinson disease may simply be due to benign prostatic obstruction or to the PD itself. Many PD patients have coexisting detrusor overactivity with impaired bladder contractility.
Consider combining intermittent catheterization with antimuscarinic drugs initially (e.g., oxybutynin 5 mg PO tid or tolterodine LA 4 mg PO qd). Second-line medical therapy can include tricyclic antidepressants such as imipramine 10–25 mg PO bid/tid.
Traditionally, patients with PD have had a poorer outcome after TURP than those without PD, but if the patient has urodynamically proven BOO, TURP is a treatment option.
Multiple system atrophy (MSA; formerly Shy–Drager syndrome)
MSA is a cause of Parkinsonism characterized clinically by postural hypotension and detrusor areflexia. Loss of cells in the pons leads to DH (symptoms of bladder overactivity). Loss of parasympathetic neurons due to cell loss in the intermediolateral cell column of the sacral cord causes poor bladder emptying, and loss of neurons in Onuf nucleus in the sacral anterior horns leads to denervation of the striated sphincter causing incontinence.
1 Winge K. Skau AM. Stimpel H, et al. (2006). Prevalence of bladder dysfunction in Parkinson’s disease. Neurourol Urodyn 25(2):116–122.
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The presentation is usually with DH (i.e., symptoms of bladder overactivity), followed over the course of several years by worsening bladder emptying.
Cerebrovascular accidents (CVAs)
DH occurs in 70%, DSD in 15% of patients. Detrusor areflexia can occur.2 Frequency, nocturia, urgency, and urge incontinence are common. Retention occurs in 5% in the acute phase.
Incontinence within the first 7 days after a CVA predicts poor survival.3 Common urodynamic findings with CVA include the following:4,5
•Normal bladder and normal sphincter
•Bladder overactivity and a normal sphincter
•Detrusor-sphincter dyssynergia is rare after a CVA.
•Diminished bladder contractility (often due to preexisting conditions)
Initial goals are adequate bladder drainage by CIC or Foley catheter until the patient resumes voiding. Long term, attain adequate bladder drainage and maintain urinary continence while preventing complications.
Anticholinergic/antimuscarinics may be used as needed in an attempt to decrease the frequency and force of involuntary bladder contractions. There are many medication choices and individual response is idiosyncratic, so several medications often have to be tried.
Botulism toxin and sacral neuromodulation have been used in this population with promising results.
Other neurological disease
Frontal lobe lesions (e.g., tumors, AVMs)
These may cause severe frequency and urgency (frontal lobe has inhibitory input to the pons).
Brainstem lesions (e.g., posterior fossa tumors)
These can cause urinary retention or bladder overactivity.
Transverse myelitis
Also known as acute inflammatory demyelinating polyneuropathy, this is an inflammatory demyelinating disorder of the autonomic and peripheral nervous system. It is thought to be immune related triggered by a bacterial or viral infection.
Symptoms may include muscle weakness, respiratory difficulties, autonomic neuropathy, cardiac, bowel, bladder, and sexual dysfunction. Lower urinary tract dysfunction can range from urge and stress incontinence to
2 Sakakibara R, et al. (1996). Micturitional disturbance after acute hemispheric stroke: analysis of the lesion site by CT and MRI. J Neurol Sci 137:47–56.
3 Wade D, et al. (1985). Outlook after an acute stroke: urinary incontinence and loss of consciousness compared in 532 patients. Quart Med J 56:601–608.
4 Pettersen R, Stien R, Wyller TB (2007). Post-stroke urinary incontinence with impaired awareness of the need to void: clinical and urodynamic features. BJU Int 99(5):1073–1077.
5 Chandiramani VA, Palace J, Fowler CJ (1997). How to recognise patients with prostatism who should not have urological surgery. Br J Urol 80:100–104.
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