Faecal incontinence in women is associated with pudendal nerve damage sustained during traumatic childbirth (Snooks et al. 1984). Sacral nerve stimulation (SNS) and tibial nerve stimulation (TNS) are used as treatments for this condition. SNS has been employed as a therapy since 1995 (Matzel et al. 1995), but it is quite invasive and costly. Recently clinical trials have taken place using TNS as a treatment for faecal incontinence. There are a small number of trials using TNS, but the results to date have been promising (Mentes et al. 2007; Queralto et al. 2006; Vitton et al. 2009). The exact mechanism of action of SNS or TNS remains unclear. It is possible that affected individuals with pudendal nerve damage develop a sensory deprivation syndrome and that sacral neuromodulation increases the sensory input to the cortex. The aim of this experiment was to study evoked potential following anal canal stimulation before and after acute SNS and TNS. Twenty one female virgin Wistar rats (body mass: 200-250g) were used. Three groups were constructed, group 1: control, group 2: SNS and group 3: TNS. Animals were anaesthetised with urethane (1.5g/kg i.p.). The femoral artery and vein were cannulated and the animals were ventilated with supplemental O2. Arterial blood gases and respiration rate were monitored thoughout the experiment. A unilateral craniotomy was performed over the right hemisphere. An extradural recording array (FlexMEA, multi-channel systems) was placed over the right somatosensory cortex. A cathode placed in the anal canal was used to provide triggered stimulation at 1Hz (amplitude: 10volts and pulse duration 0.1ms). Four trials of 500 sec sweeps were recorded in each group. Following the first trial in group 2, SNS was applied (amplitude: 6 volts, frequency 15Hz and duration 1ms) and in group 3, TNS (amplitude: 20 volts, frequency 15Hz and duration 1ms). After stimulation 3 consecutive trials were run. In all groups the amplitude of the first trial was designated 100%, each trial was normalised against this. The amplitude of the somatosensory evoked potential in group 1 was stable over all four trials. Following the application of SNS in group 2, there was an increase in amplitude from 100% to 158.9 ± 10.60%. This amplitude increase was sustained in all 3 trials following SNS. Group 3 also resulted in an increase in amplitude following TNS, the SEP increased from 100 % to 148.1 ± 22.56% following stimulation. As seen in group 2, the amplitude increase following stimulation to the tibial nerve remained constant until the conclusion of the experiment. The findings support the hypothesis that even brief SNS and TNS can increase sensory input from the anal canal to the somatosensory cortex. These results indicate a similar mechanism of action of both therapies.