Background
Recently dopaminergic drugs are the main therapy for patients with Parkinson's disease (PD). However, exact effects of L-dopa on micturition are not ascertained. Animal experiments showed the fact that selective D2 receptor agonist quinpirole reduced bladder volume threshold for the micturition reflex in MPTP lesioned parkinsonian monkeys. We evaluated that an effect of L-dopa (D1/D2 receptor agonist) on micturition disturbance in patients with PD by using urodynamic studies.

Methods
We recruited 10 patients with PD (including 5 men, 5 women), mean age 64 years. All patients have been taking dopaminergic drugs including only L-dopa / carbidopa in 3 and L-dopa / carbidopa with other antiparkinsonian drugs in 7. All patients showed marked 'on' (alleviation) and 'off' (worsening of motor performance) phenomenon in a day depending on the time of L-dopa medication. We performed detailed questionnaire of urinary symptoms and urodynamic assessments before ('off' period) and one hour after taking 100 mg of L-dopa / carbidopa ('on' period). No patient had apparent prostate hypertrophy on rectal examination and ultrasonography.

Results
Comparing the 'on' period to the 'off' period, three complained exacerbation in urinary urgency in filling phase, however seven noticed improvement of voiding difficulty. Urodynamic study in the 'off' period showed that seven had detrusor hyperreflexia (DH) and none had detrusor sphincter dyssynergia (DSD). In the 'on' period, DH did not disappeared in any patients, but bladder capacity was decreased in 9 (-15 %) and increased in 1 patient. Bladder capacity of all three patients without DH was also decreased. Maximum value of watts factor (WFmax) was increased in all patients (+8.4 %). Residual urine volume (RV) was decreased in 5 (-85 %), unchanged in 4 and increased in 1 patient. All cases with unchanged RV had originally little residual urine volume (0-20 ml). DSD did not appeared in any patients, however maximum flow rate (Qmax) was decreased in 6, unchanged in 3 and increased in 1 patient and AG number (Pdet at Qmax - 2Qmax) was increased in 7, unchanged in 1 and decreased in 2 patients. Maximum urethral closure pressure (UPmax) was measured in 2 patients, and both patients showed UPmax was increased.

Conclusion
Comparing urinary function in the 'on' and 'off' periods of L-dopa treatment, the results showed that L-dopa decreased bladder capacity in most of our patients, even without DH. In the voiding phase, L-dopa augmented detrusor contractility but also L-dopa increased urethra obstruction, and overall lessened post-micturition residuals in most patients. These findings may reflect central and peripheral dopaminergic action of L-dopa or its metabolite.