After reading this chapter, the reader will be able to:
Review the neurophysiologic basis of bladder and bowel dysfunction in spinal cord injury (SCI)
Describe upper motor neuron and lower motor neuron lesions and delineate the effects of these lesions on bowel and bladder function
Discuss current management options for neurogenic bladder and bowel
Name factors to consider when developing an individualized management plan for neurogenic bowel and bladder
Apply knowledge of potential complications of neurogenic bladder and bowel to educate individuals and families about long-term management
Describe areas of controversy related to neurogenic bowel and bladder dysfunction
Neural Basis for Bowel and Bladder Dysfunction
Normal Bowel and Bladder Function and Innervation
Voluntary control of the bladder and bowel requires intact neural pathways from the S2 through S4 spinal segments through the pelvic nerves and from the sacral cord to and from the pontine level of the brain. Both organs are innervated through complex sympathetic and parasympathetic systems that operate at various levels of the spinal cord and are coordinated by centers in the brainstem.
Bladder Innervation and Control
The most important peripheral pathways affecting bladder function are the parasympathetic nerve supply to the detrusor through the pelvic nerve, the sympathetic nerve supply to the bladder neck through the hypogastric nerve, and the somatic innervation of the external urethral sphincter through the pudendal nerve. The sympathetic nerve supply is by the hypogastric postganglionic outflow from T12 to L2. The afferent and efferent neurons supplying the external sphincter via the pudendal nerve arise at the S3-S4 level. In neurologically normal individuals, the volume of the bladder and the normal voiding reflex is routed via the afferent Aδ fibers. In individuals with SCI, vanilloid receptor stimulation excites C-afferent fibers that may mediate the bladder dysfunction due to inflammatory reactions. In individuals with SCI above the sacral levels, these capsaicin-sensitive vanilloid receptors and C-afferents have a major role in the pathogenesis of bladder hyperactivity.1,2
The reflex center for the bladder lies in the pons, along with the other autonomic centers. Sensory information from the bladder wall travels through the pelvic nerve to the S2-S4 spinal segments and from there ascends to the pontine mesencephalic reticular formation. A reflex with afferent axons originating from the bladder and synapsing on the pudendal nerve nucleus at S2, S3, and S4 (Onuf's nucleus) allows inhibition of pelvic floor activity during normal voiding (micturition). Another important reflex is the local segmental innervation of the external sphincter with afferents from the urethra, sphincter, and pelvic floor and efferents in the pudendal nerve. Higher (voluntary) control over the pelvic floor is achieved through afferents that ascend to the sensory cortex. Descending fibers from the motor cortex synapse with the pudendal motor nucleus and control external urethral sphincter activity. The simple act of voiding is thus a complex ...