Faecal incontinence in women is often related to damage to the pudendal nerve during traumatic childbirth (Snooks et al., 1984). The precise pathophysiology of this disorder is not well understood. Chronic electrical stimulation of sacral nerve roots decreases the frequency of soiling episodes in patients with faecal incontinence (Melenhorst et al., 2007), but the scientific basis of this therapy is unknown. For these reasons, animal models of neuropathic faecal incontinence may offer unique insights into this debilitating disorder and lead to more rational and successful application of neurostimulators. In order to examine the central nervous system adaptations to obstetric related pudendal nerve injury, two animal models have been created using female virgin Wistar rats (Healy et al., 2008). The first involves a direct crush bilaterally of the inferior rectal nerve (IRN), a terminal branch of the pudendal nerve. The IRN supplies the external anal sphincter (EAS). The second involves retro-uterine inflation of two balloon catheters to increase pelvic pressure and mimic the compressive forces of labour. Both models lead to significant EAS atrophy, denervated motor endplates and electromyographic evidence of renervation one week following injury. The IRN is not purely a motor nerve but contains small diameter fibres with cell bodies in dorsal root ganglia L6-S2. This was demonstrated by examining fluorogold labelling of axons and immunocytochemistry for activating transcription factor 3, a marker of axonal injury. Electrical stimulation of this mixed nerve evokes potentials in the contralateral somatosensory cortex and these potentials are significantly reduced in both animal models four weeks after injury (Peirce et al., 2009). The working hypothesis that emerges from these results is as follows: childbirth may damage the pudendal nerve and the sensory component of the nerve is more susceptible to damage, leading to loss of cortical awareness of the pelvic floor. In more recent studies a finer exploration of the somatosensory cortex and anorectal representation is being conducted using multi-electrode array and functional magnetic resonance imaging. The lumbosacral nerve roots will be electrically stimulated in future experiments to test whether the cortical control of continence is plastic and susceptible to re-modelling by this intervention.