Sacral or cauda equinal injury due to spinal trauma results in lower motor neuron injury neurogenic bowel disorder (LMNI-NBD). Due to decreased sacral parasympathetic propulsive control of the distal colonic smooth muscle and pudendal somatomotor control of the external anal sphincter, the storage and release function of the rectum and anus are disrupted. This results in a hypocontractile bowel and sphincter, which manifests as constipation and fecal incontinence, with increased frequency of defecation and incontinence, increased use of oral medications and dietary modifications directed toward bowel care, and increased time for defecation and use of the Valsalva maneuver when defecation is the goal. The constellation of symptoms, treatments and behavioral modifications with lack of effective treatments contribute dramatically to reduction in quality of life for patients with LMNI- NBD. We have recently demonstrated the ability to impose control of function in a parallel pelvic storage and release system, the lower urinary tract, under conditions of incomplete LMNI. Our model was that of unilateral preganglionic pelvic nerve transection, as might result from pelvic surgery or trauma. In this model of neurogenic underactive bladder with detrusor underactivity, we demonstrated on-demand voiding function using proximal outlet (urethra) neural stimulation, activating positive feedback signals for evacuation. As such mechanisms are known to exist within the anorectal control system, we hypothesize that this approach may also be employed to treat LMNI-NBD by local electrical stimulation of anal canal reflex pathways in patients with incomplete LMNI.