Early endoscopic detection and subsequent removal of sphincter penetrating anastomotic sutures may prevent irreversible urinary incontinence after radical prostatectomy.

BACKGROUND AND PURPOSE: Iatrogenic sphincter lesions are possible reasons for sphincteric incompetence and postprostatectomy urinary incontinence. The aim of this study was to identify early possible sphincter injuries as causes for urinary incontinence after radical prostatectomy by endoscopic evaluation of the anastomotic region. PATIENTS AND METHODS: Among 374 patients who had undergone radical prostatectomy from 2005 to 2009 at our institution, we investigated patients with early postoperative urinary incontinence. Nineteen incontinent patients were identified with the symptomatic triad of early incontinence, reduced urinary flow, and post-void residual (PVR) volume after catheter removal. Patients were examined endoscopically, and the clinical effect of early suture removal in patients with sphincter penetration was evaluated. RESULTS: Urethrocystoscopic evaluation revealed an isolated sphincter penetration as reason for early postoperative incontinence in 15/19 cases. The suture penetration was observed predominantly in the 3-degree (7/19) and 9-degree (8/19) positions and less frequently in the 12-degree (2/19) and 6-degree (2/19) positions. Four of (21%) 19 patients did show an additional sphincter transection. The penetrating sutures of the urethrovesical anastomosis were removed during the endoscopic procedure, and initial urinary incontinence could be corrected in all cases of isolated sphincter penetration. CONCLUSION: Early severe urinary incontinence, reduced urinary flow, and PVR volume after radical prostatectomy may indicate sphincter penetration by anastomosis sutures. In our patients, early transurethral punctual removal of the penetrating sutures could decrease the early postoperative incontinence rate.

High frequency oscillations in the subthalamic nucleus: a neurophysiological marker of the motor state in Parkinson's disease.

Increasing evidence suggests that abnormal oscillatory activity in basal ganglia and cortex plays a pivotal role in the pathophysiology of Parkinson's disease. Recordings of local field potentials from subthalamic nucleus of patients undergoing deep brain stimulation have focused on oscillations occurring at frequencies below 100 Hz in the alpha, beta and gamma range and suggested that, in particular, an increase of beta band oscillations underlies slowing of movement in Parkinson's disease. Recent findings showing that the amplitude of high frequency oscillations (>200 Hz) couples with the phase of beta activity have raised the important question about the role of subthalamic high frequency oscillations in Parkinson's disease. To investigate functional characteristics and clinical relevance of high frequency oscillations, we recorded local field potentials from 18 subthalamic nuclei of 9 akinetic-rigid Parkinsonian patients with implanted deep brain stimulation electrodes and still externalised leads before and after intake of levodopa. We identified two distinct bands of high frequency oscillations, one centred around 250 Hz and another one around 350 Hz that show characteristic levodopa dependent amplitude and coupling behaviours. Administration of levodopa changed the power ratio between the two high frequency bands towards the component centred around 350 Hz in all 18 nuclei under study (p<10(-4)). Moreover, this power ratio correlated significantly with the Unified Parkinson's Disease Rating Scale hemibody akinesia/rigidity subscore (r=0.3618, p=0.015), but interestingly not with beta peak power (p=0.1) suggesting that levodopa induced changes in high frequency and beta oscillations are at least potentially independent of each other. Accordingly, a combined parameter composed of power ratio of high frequency oscillations and beta peak power significantly increased the correlation with the motor state (r=0.45, p=0.004). These results indicate that a shift from slower to faster frequencies of the spectrum greater than 200 Hz represents a prokinetic neurophysiological marker underlying levodopa induced motor improvement in Parkinson's disease.