The most frequent urinary complaints in PD patients are frequency, urgency, urge incontinence, and nocturia. Hobson et al. (58) performed a community-based questionnaire survey in Wales, U.K., and found that bladder problems were reported in 51% of 123 PD patients returning the survey compared to 31% of 92 controls. The calculated relative risk of developing bladder symptoms in PD patients compared to controls was 2.4. Lemack et al. (59) performed a similar questionnaire-based assessment of bladder problems in PD patients, but selected early-stage patients (Hoehn and Yahr stage 2.5 or lower) to determine if bladder problems occur early in the disease. Men with early PD assessed using the American Urological Association Symptom Index had a mean score of 12 compared to the community sample of normal male volunteers whose mean score was 4.8. Significant differences were seen on questions for frequency, urgency, and weak urinary stream. Women completed the Urogenital Distress Inventory-6 where PD patients had a mean score of 4.8 compared to 2.1 for normal controls. There was no correlation between bladder dysfunction and any measure of motor severity of PD except for gait speed, which was significantly slower in patients with higher scores for bladder dysfunction. This observation suggests that neural pathways for gait and bladder control might be involved in parallel by the degenerative process of PD.
Urodynamic studies have been conducted in small samples of PD patients with persistent bladder complaints to elucidate the nature of the problem. Berger et al. (60) studied 29 patients and found that detrusor hyperreflexia was present in 90% and that incomplete sphincter relaxation during involuntary detrusor contractions as shown by EMG was present in 61%. Winge et al. (61) conducted detailed urodynamic studies in 32 PD patients without regard to whether they had bladder symptoms. Using the Danish Prostate Symptom Score (Dan-PSS), they found that 43.8% of patients met criteria for symptomatic bladder dysfunction. Irritative bladder symptoms were more commonly seen in patients with greater severity of PD as assessed by motor scoring. On urodynamic testing, bladder capacity was lower in the group with high Dan-PSS scores, and capacity increased when dopaminergic drugs were administered. Detrusor overactivity was also seen in this group, but medication administration did not impact this feature. The authors suggested that since bladder capacity improved following dopaminergic drugs, dopamine deficiency may in part underlie the irritative bladder symptoms in PD. Whether this is due primarily to central or peripheral dopaminergic cell degeneration is unknown.
The treatment of bladder dysfunction in PD is difficult due to its often multifactorial origin. For instance, in men with irritative bladder symptoms, prostatic hypertrophy may be a contributor to outlet obstruction. For this reason, patients with symptomatic bladder dysfunction should be referred to a urologist with experience in evaluating and managing the bladder problems of PD patients. Generally, treatment will be initiated only after appropriate urodynamic testing is completed. Once a significant obstructive component has been ruled out, treatment of patients with hyperactive detrusor can begin with drugs such as tolterodine (62), oxybutnin (63), or imipramine (64). Patients with nocturia should also be advised to avoid water intake in the evening.
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