Impact of electrostimulation of neurovascular bundles and pudendal nerves on the membranous urethra in male rabbits.

PURPOSE: The pathophysiology of post-prostatectomy incontinence is supposed to be multifactorial. The impact of the neurovascular bundles on sphincter function is still under debate. We clarified the impact of cavernous nerves function on the MU. We compared MU pressure responses in male rabbits following electrophysiological stimulation trials on the neurovascular bundles vs pudendal nerve stimulation. MATERIALS AND METHODS: Six male Chinchilla Bastard rabbits were included in this study. Pudendal and cavernous nerve branches were exposed bilaterally in all animals. Randomized electrostimulation of pudendal nerve fibers and the cavernous nerves, as confirmed by erection,) were done using a biphasic signal form of 0.3 mA for 200 microseconds. Stimulation frequency was changed in a randomized pattern from 10 to 40 Hz. Changes in MU pressure were measured urodynamically via a transurethral microtip catheter placed in the MU. Stimulation responses of the 2 nerve structures were compared. RESULTS: Mean baseline pressure in the MU without stimulation was 23 cm H(2)O (range 20 to 25) in all animals. During unilateral pudendal stimulation the mean pressure response increased highly significantly to 33, 43, 59 and 60 cm H(2)O at 10, 20, 30 and 40 Hz, respectively (p <0.005). In contrast, compared to baseline pressure cavernous nerve stimulation did not result in any significant changes in proximal urethral pressure (mean 23 cm H(2)O, range 20 to 25, p >0.05). CONCLUSIONS: Our results confirm the primacy of the pudendal nerve in the external urethral sphincter innervation. In contrast, stimulation of the cavernous nerves did not produce any pressure changes in the MU. These results confirm that the neurovascular bundles have no functional impact on the MU.

Alterations of cortical electrical activity in patients with sacral neuromodulator.

OBJECTIVES: Sacral neuromodulation represents chronic stimulation of the sacral (S3) nerve. So far, the mode of action and neuro-anatomical basis is unclear. Sacral reflex mechanisms as well as pontine or cortical centers of modulation have been postulated. Our aim was to evaluate possible alterations in electroencephalogram (EEG) activity as an indicator of a supraspinally mediated mechanism of sacral neuromodulation. MATERIALS AND METHODS: We analyzed serial EEGs (apparatus: Kölner Vitaport System) using electrodes placed at Fz, Cz, Cz' and Pz in 10 patients. Subsequently, the sacral (S3) nerve was stimulated by means of an impulse generator (Medtronic, Interstim 3023) using an on-off paradigm with a 1.5s "on" interval followed by a 10s stimulation break. Raw data were analyzed using both Matlab 4.0 software and a specially developed averaging routine. RESULTS: All patients demonstrated a cortical potential complex following sacral root stimulation with an early electronegative component at 50 ms with a mean amplitude of 23 microV followed by a late potential component with a mean latency of 253 ms and a mean amplitude of 5 microV, both with a maximum at Cz, corresponding to the post-central gyrus. This finding occurred irrespective of patient's reports of actually feeling the neuromodulator being switched on and off. CONCLUSION: In neuromodulation responders, both short and long latency cortical potentials can be reproduced with a maximum at the sensory cortical area. Although these potentials are similar to cognitively mediated "event-related potentials", they are clearly distinct from any subjective sensory or even painful response since several patients of this series have not been able to feel any neuromodulator action. Therefore, this pilot study indicates a supraspinally mediated site of modulation, most probably in sensory cortex areas.