Urological problems in Parkinson's disease: clinical aspects

Jost, Wolfgang
April 2013
Journal of Neural Transmission;Apr2013, Vol. 120 Issue 4, p587
Academic Journal
Bladder dysfunctions are quite common in Parkinson's disease. They may occur at any stage of the illness and get worse with advancing and aggravating disease. The most prominent dysfunction is the so-called overactive bladder. Control of bladder function is part of a highly complex system subject to the interaction of predominantly the frontal and pontine micturition or continence center and the spinal cord. Besides there are some other anatomic structures involved in the complex control loop of bladder regulation. Regarding central regulation, dopamine is the essential neurotransmitter that inhibits bladder activity. All dopaminergic substances are capable of influencing automatic control systems. This also holds true for many other classes of other medications such as anticholinergics, antidepressants, and beta-blockers. The chief clinical problem of this patient consists in reduced inhibition with consequentially resulting overactivity of the detrusor muscle, meaning the urge to urinate in the absence of adequate bladder filling. The patients mostly complain of an imperative urge to urinate, of pollakisuria, nocturia and even incontinence of urine (urge incontinence). The objectives of diagnosis and therapy focus on controlled bladder evacuation and continence of urine. The most important diagnostic clues are provided by the patient's medical history. Only in rare cases urodynamic studies are indicated as well. For treatment we can avail ourselves of a number of anticholinergic drugs. We must watch out though that the medication ordered is not going to impact on cognition.We recommend tolteradine, not passing the blood brain barrier, or M3-specific antimuscarinics such as solifenacin and darifenacin. Positive therapeutic outcomes are limited. A new alternative at hand, albeit not approved for the time being, is the local injection of botulinum toxin into the detrusor muscle.


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