Stimulation of the pudendal nerve or the anal sphincter could provide therapeutic options for fecal incontinence with little involvement of other organs. The goal of this project was to assess the effects of pudendal nerve and anal sphincter stimulation on bladder and anal pressures.
Ten virgin female Sprague Dawley rats were randomly allocated to control (n = 2), perianal stimulation (n = 4), and pudendal nerve stimulation (n = 4) groups. A monopolar electrode was hooked to the pudendal nerve or placed on the anal sphincter. Aballoon catheter was inserted into the anus to measure anal pressure, and a catheter was inserted into the bladder via the urethra to measure bladder pressure. Bladder and anal pressures were measured with different electrical stimulation parameters and different timing of electrical stimulation relative to spontaneous anal sphincter contractions.
Increasing stimulation current had the most dramatic effect on both anal and bladder pressures. An immediate increase in anal pressure was observed when stimulating either the anal sphincter or the pudendal nerve at stimulation values of 1 mA or 2 mA. No increase in anal pressure was observed for lower current values. Bladder pressure increased at high current during anal sphincter stimulation, but not as much as during pudendal nerve stimulation. Increased bladder pressure during anal sphincter stimulation was due to contraction of the abdominal muscles.
Electrical stimulation caused an increase in anal pressures with bladder involvement only at high current. These initial results suggest that electrical stimulation can increase anal sphincter pressure, enhancing continence control.
1 Department of Biomedical Engineering, Cleveland Clinic, Cleveland, Ohio
2 Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, Ohio
3 Advanced Platform Technology Center, Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio
4 Department of Colorectal Surgery, Cleveland Clinic, Cleveland, Ohio
5 American Medical Systems Inc., Minnetonka, Minnesota
6 Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, Ohio
Funding/Support: This research was supported in part by American Medical Systems, The Cleveland Clinic Foundation, and the Rehabilitation Research & Development Service of the Department of Veterans Affairs.
Financial Disclosure: Dr Damaser acted as a consultant to American Medical Systems in 2008 when this work was performed.
Correspondence: Massarat Zutshi, M.D., Cleveland Clinic Foundation, 9500 Euclid Ave, A30, Cleveland, OH 44195. E-mail: email@example.com