and Mikolaj Przydacz1
(1)
Department of Urology, Jewish General Hospital, McGill University, Montreal, QC, Canada
Keywords
Benign prostatic hyperplasiaBladder outflow obstructionRetentionα-blockersα-adrenoreceptor antagonists5-α reductase inhibitorsTransurethral resection of the prostate (TURP)Introduction
Proper diagnosis and treatment of benign prostatic hyperplasia (BPH) in neurogenic individuals remains a challenge for urologists. On the one hand, the assumption that reported lower urinary tract symptoms are fixedly due to the underlying neurological pathology may result in inadequate treatment of BPH [1]. Furthermore, bladder outflow obstruction secondary to BPH, considered as a progressive disease, may further increase the risk of complications to the lower and upper urinary tract with severe renal damage. On the other hand, disregarding the underlying neurological disorder may exacerbate symptoms and dramatically worsen quality of life. Therefore, clinicians should carefully balance all circumstances in choosing proper management, as surgical treatment for BPH in some patients may result in urinary incontinence instead of retention .
Epidemiology
BPH is the most common male urological disease. It has been shown that 10% of men of 40 years of age and 90% of those 80 years of age can be diagnosed with BPH [2–4]. A small study of 28 men (mean age 66.4 years) revealed that BPH patients, particularly those >65 years of age, commonly have neurogenic bladder dysfunction [5]. Multiple cerebral infarction (upper neuron disorder) and lumbar spondylosis (lower neuron disorder) might contribute to neurogenic detrusor overactivity and neurogenic detrusor underactivity, respectively. Epidemiological data of BPH among neurogenic patients with confirmed and specific neurological diagnosis are sparse. As some neurological disorders commonly appear in middle-aged and elderly men (e.g., Parkinson and Alzheimer disease), it can be assumed that a significant percentage of these patients suffer from BPH.
Diagnosis
Comprehensive guidelines for the diagnosis and treatment of BPH have been developed and they can be applied to patients with neurogenic lower urinary tract dysfunction. These include Guidelines of the European Association of Urology (EAU) [6], the American Urological Association (AUA) [7], and the Canadian Urological Association (CUA) [8]. However, in those with bothersome symptoms of bladder outflow obstruction and concomitant neurological disorder, further evaluation is necessary. BPH in men with neurogenic bladder dysfunction may be indicated by increasing difficulty or pain during intermittent catheterizations, growing residual urine volumes in those who void by Valsalva or Crede maneuvers, and higher rates of urinary tract infections. Difficulty with catheterization has been reported as the most suspicious symptom of BPH in the neurogenic population [9–11]. Patients typically report that they feel increasing difficulty in passing a catheter into the bladder while using catheters that previously passed smoothly. A carefully conducted medical history will elicit that this has developed over time. Patients may also complain of hematuria (either spontaneous or in combination with catheterization) due to the increased size of the prostate and neovascularity of the enlarged gland [12–14]. Those who void by Valsalva or Crede maneuver may report an increase in the feeling of incomplete emptying, a weaker stream than usual, or a complete inability to void [10]. Further evaluation should include cystourethroscopy to assess the contour of the prostate and, in cases of hematuria, to rule out bladder malignancy [15].
Urodynamic study in neurogenic patients suspected of BPH is recommended. Whereas BPH represents an organic obstruction, urodynamic testing can substantially support the differential diagnosis of functional bladder obstruction presented as detrusor-sphincter dyssynergia (see Chap. 8). In some patients, these two conditions may coexist. Video urodynamics with electromyography seems to be the optimal diagnostic modality to diagnose this discoordination. Urodynamic study is also the gold standard to differentiate retention resulting from bladder outlet obstruction and retention due to underactive detrusor [16]. Calculation of the bladder outlet obstruction index (BOOI) helps clinicians reach the proper diagnosis. The BOOI (BOOI = P det Q max − 2Q max) is derived from the Abrams–Griffiths nomogram [17] and divides patients into three different groups according to their degree of obstruction:
BOOI > 40: obstructed
BOOI = 20–40: equivocal
BOOI < 20: unobstructed
The true cause (neurogenic vs. non-neurogenic) of detrusor overactivity in neurogenic patients with concomitant BPH is often difficult to establish. Nevertheless, coexistence of detrusor-sphincter dyssynergia and detrusor overactivity typically indicates a neurological cause of overactive detrusor [1]. Of note, treatment of BPH in these patients should be especially considered because the increased outlet resistance in combination with an overactive detrusor can lead to extremely high bladder pressures with elevated residual urine volumes and urinary retention , significantly increasing the risk of renal failure [10].
Treatment
Pharmacological Treatment
Experts indicate a conservative approach as the first-line treatment option of BPH in patients suffering from neurogenic lower urinary tract dysfunction [18]. The use of α-blockers (α-adrenoreceptor antagonists ) in mild/moderate obstruction has shown significant voiding improvement [19, 20] but clinicians should expect poor results in those with more severe neurological impairments [21, 22]. Combining this with a 5-α reductase inhibitor in order to reduce the size of the prostate, decrease symptoms, and allow for continued catheterization (if performed), may be taken into account [10, 23–25].
It is important to emphasize that it is sometimes impossible to discriminate between lower urinary tract symptoms resulting from BPH and those secondary to neurological disease. Symptoms secondary to BPH such as poor urine flow, frequency, urgency, and nocturia may also be induced by neurogenic bladder dysfunction. Urodynamic study may also present ambiguous findings. In these settings, conservative treatment is preferable to irreversible surgical intervention [1].
Surgical Treatment
Surgical treatment of BPH in patients suffering from retention with concomitant neurological disorder remains a matter of dispute. The main concern includes post-surgical appearance or exacerbation of urinary incontinence instead of retention . Unfortunately, there is a paucity of long-term and randomized studies performed on large cohorts. Existing data are limited to single studies or case reports and do not allow one to make reliable conclusions and recommendations.
It has been proposed that patients who do not suffer from sacral/infrasacral lesions and peripheral denervation involving the pudendal nerve responsible for the activity of the external sphincter (these lesions typically leads to neurogenic detrusor underactivity and/or neurogenic sphincter deficiency—see Chap. 3) should have no negative consequences (especially stress urinary incontinence) from prostatic surgery and might benefit from removal of bladder outflow obstruction [18].
Some data are available for patients suffering from Parkinson disease. Because Parkinson disease and BPH are common in late middle-aged males, their concurrence is probable and often seen. A retrospective study of 23 men suffering from Parkinson disease who underwent transurethral resection of the prostate (TURP) due to bladder outlet obstruction secondary to BPH and were followed for 3 years after surgery demonstrated interesting findings [26]. According to the preoperative Abrams–Griffiths nomograms 52% of patients were obstructed, 22% equivocal, and 26% unclassified, as they could not void but did demonstrate increase in detrusor pressure. Of the 14 patients with a preoperative indwelling urinary catheter, TURP restored voiding in 9 (64%), and only 5 (36%) required catheterization postoperatively. Of the 10 patients with preoperative urge urinary incontinence, continence was restored in 5 and improved in 3 following TURP. There were no cases of de novo urinary incontinence after transurethral prostate resection. To summarize, at a median postoperative follow-up of 3 years TURP was successful in 16 of the 23 patients (70%). Authors concluded that TURP for BPH in patients with Parkinson disease may substantially improve lower urinary tract function and the risk of de novo urinary incontinence is minimal. They added that Parkinson disease should no longer be considered a contraindication for TURP, provided that preoperative investigations including urodynamic assessment indicate prostatic bladder outflow obstruction. In view of these findings, multiple experts propose that patients with Parkinson disease and BPH can be considered for appropriate surgery and that preoperative investigations, including urodynamic assessment, should be used to confirm the diagnosis of BPH in such patients [18, 27, 28]. On the other hand, a retrospective study on post-TURP continence in 50 parkinsonian patients revealed a high incidence of incontinence following the procedure [29]. However, authors emphasized the fact that some of these patients were likely to have had multiple system atrophy, a disease with frequent denervation of the external urinary sphincter resulting in neurogenic sphincter deficiency [30]. Therefore, accurate differentiation between Parkinson disease and multiple system atrophy (more severe, rapidly progressive, multisystemic and fatal disease classified as a form of atypical parkinsonism—see Chap. 3) is critical before surgical intervention for BPH [1]. In patients with a diagnosis of Parkinson disease but who have clinical symptoms that are more aggressive and extensive, including pyramidal or cerebellar signs, erectile dysfunction, severe postural hypotension, and marked urinary incontinence, a diagnosis of multiple system atrophy should be suspected and investigated before proceeding to surgery [31].
A series of 39 patients with a history of one or more cerebrovascular accidents and who underwent TURP for BPH showed less encouraging results [32]. Only 50% had a satisfactory result from the operation and 11.7% died within 3 months of surgery. Better results were achieved in those under the age of 70 and who had their operation more than 1 year after the stroke. Authors also indicated that the degree of neurological deficit at the time of operation has a significant influence on final outcomes.