Epidemiology and pathophysiology of neurogenic bladder after spinal cord injury.

Abstract

Spinal cord injury (SCI) usually affects younger age groups with male preponderance. The most common traumatic cause is road traffic accident followed by sports accidents and gun-shot injuries. Infections and vascular events make up non-traumatic causes. There is regional variance in incidence and prevalence of SCI. Most systematic reviews have been undertaken from USA, Canada, and Australia with only few from Asia with resultant difficulty in estimation of worldwide figures. Overall, the incidence varies from 12 to more than 65cases/million per year. The first peak is in young men between 15 and 29years and second peak in older adults. The average age at injury is 40years, with commonest injury being incomplete tetraplegia followed by complete paraplegia, complete tetraplegia, and incomplete paraplegia. The bladder function is reliant on both central and peripheral nervous systems for co-ordination of storage and voiding phases. The pathophysiology of bladder dysfunction can be described as an alteration in micturition reflex. It is postulated that a new spinal reflex circuit develops which is mediated by C fibers as response to reorganization of synaptic connections in spinal cord. This is responsible for the development of neurogenic detrusor overactivity (NDO). Various neurotrophic hormones like nerve growth factor affect the morphological and physiological changes of the bladder afferent neurons leading to neuropathic bladder dysfunction. A suprasacral SCI usually results in a voiding pattern consistent with NDO and sphincter dyssynergia. Injury to either the sacral cord or cauda equina results in detrusor hypoactivity/areflexia with sphincter weakness.