Subthalamic Stimulation and Urinary Function

Abstract & Commentary

Source: Seif C, et al. Effect of subthalamic deep brain stimulation on the function of the urinary bladder. Ann Neurol. 2004;55:118-120.

With the approval and widespread use of deep brain stimulation (DBS) of the subthalamic nucleus (STN) in Parkinson’s disease (PD), there has been increasing awareness of non-motor effects of DBS. Recent reports have illustrated that DBS may induce mania and even impair executive function in PD, despite its often dramatic and clinically meaningful improvement in motor performance. In this elegant study, Seif and colleagues asked a simple question: does DBS alter urodynamic parameters in patients with PD? Urologic symptoms are common in PD, usually expressed as urinary urgency, increased frequency, or frank incontinence. Urodynamic studies typically show detrusor hyper-reflexia, resulting in a reduced bladder capacity and early desire to void.

Seif et al selected 16 patients with PD who had undergone bilateral STN implantation 6-29 months before. All patients experienced a significant improvement in motor disability from STN stimulation. Patients were examined 12 hours after taking their last dose of antiparkinsonian medication, in order to evaluate the effects of DBS. Two videourodynamic examinations were performed 20 minutes apart—one in the stimulation off state and one with stimulators on. These studies measured desire to void, maximum bladder capacity, detrusor pressure, and urine flow while the bladder was filled with warm isotonic saline.

In the off stimulation state, initial desire to void occurred at a bladder capacity of 135 mL, while in the on stimulation state, desire to void was noted at 199 mL. Unstable detrusor contractions were observed in 5 patients in the stimulator off state and in none when stimulators were on. The maximum capacity of the bladder was 174 mL with simulators off and 302 mL with simulators on. These changes occurred quickly, as only 20 minutes separated the stimulator off from on measurements, and were statistically significant.


This study adds another important feature to the list of symptoms improved by STN stimulation. The patients did not have symptoms of urinary distress, and none had incontinence. The effect of STN stimulation on such patients is not yet known; however, one could envision that normalizing bladder urodynamics might reduce the risk of urinary tract infections and also improve patients’ comfort and quality of life.

The mechanism by which STN stimulation improves micturition is unknown. The central control of micturition is complex, involving cingulate and prefrontal cortex, the pontine micturition center, and sacral parasympathetic preganglionic neurons. Loss of dopaminergic activity in the substantia nigra leads to excitation of the STN and possibly activation of direct STN projections to the brainstem. Alternately, stimulation of the STN disinhibits thalamocortical projections to the cingular and prefrontal cortex, which might re-establish their normal role in controlling micturition. — Steven Frucht

Dr. Frucht, Assistant Professor of Neurology, Movement Disorders Division, Columbia-Presbyterian Medical Center, is Assistant Editor of Neurology Alert.