Pediatr Nephrol (2008) 23:541–551 detrusor sphincter dyssynergy (5%), is invariably present, but lower motor neuron injury with sphincter denervation due to spinal cord involvement can be seen as well (11%) [61] (Tables 5 and 6). Volitional control over sphincter function is present, and affected children have some ability to prevent leaking from an overactive detrusor by tighten- ing the muscle for a variable period of time. Children with milder forms of dysfunction, with just learning disabilities without spasticity, have an overactive detrusor leading to either urgency (with or without incontinence) and nocturia, or day and night wetting. Therefore, modulating the overactivity with anticholinergic medication is the treat- ment of choice. However, this must be done judiciously, with careful monitoring of residual urine to prevent the development of retention. Trauma Traumatic injuries to the spine Fortunately, spinal cord injuries in children are rare (2.6 per million) [62]. The incidence tends to increase geometrically with age [63]. When an injury does occur, it is more likely to happen in a boy than in a girl, and it is usually the result of a motor vehicle or bicycle accident (24–52%), a fall from a high place, a gunshot wound, or a diving or sports incident. Injuries may also occur iatrogenically after surgery to correct scoliosis, kyphosis or other intraspinal processes, congenital aortic anomalies, or patent ductus arteriosus operations [62, 64–67]. Newborns are particularly prone to a hyperextension injury during high forceps delivery [68]. Spinal cord injuries in children are intrinsically different from those in adults, owing to a variety of factors, including the mechanism of injury and the difference in configuration of the cord in children compared with that in adults. In addition, the horizontal versus vertical orientation of the facet joints in vertebral bodies that predisposes to ante- roposterior subluxation in children, the delayed supportive effect of the paraspinous musculature and ligaments, and the relative heaviness of the head, which causes a fulcrum of maximal flexion of the upper cervical region in infants and young children, all contribute to a high degree of hypermobility that places the child’s spinal cord at risk for ischemic necrosis [65]. Table 5 Lower urinary tract function in cerebral palsy Type Upper motor neuron lesion Mixed upper + lower motor neuron lesion Incomplete lower motor neuron lesion No urodynamic lesion Number 49 5 1 2 547 Table 6 Urodynamics findings in cerebral palsy (some patients had more than one finding) Type of Lesion No. of Patients Upper motor neuron (detrusor or sphincter) Detrusor overactivity Detrusor sphincter dyssynergy Overactive sacral reflexes No voluntary control Smaller than expected bladder capacity Poorly compliant Lower motor neuron (abnormal motor unit potentials) Excessive polyphagia of sphincter ↑ Amplitude + ↑ duration potentials 35 7 6 3 2 2 5 4 The lower urinary tract dysfunction that ensues is not likely to be an isolated event but is usually associated with loss of sensation and paralysis of the lower limbs. Radiologic investigation of the spine may not reveal any bony abnormality, although momentary subluxation of osseous structures resulting from the elasticity of the vertebral ligaments can result in a neurologic injury. This condition has been seen only in children (usually younger than 8 years old) and has been labeled SCIWORA (spinal cord injury without radiologic abnormality) [69]. Overall, SCIWORA can account for up to 38% of spinal cord injuries in children [70]. Often, what appears to be a permanent lesion initially turns out to be a transient phenomenon with time. Although sensation and motor function of the lower extremities may be restored relatively quickly, the dysfunction involving the bladder and rectum may persist considerably longer. During the acute phase of the injury, the bladder is often acontractile and the urethral sphincter nonreactive, although normal-appearing bioelectric potentials can be recorded on sphincter EMG (spinal shock). Over a variable but unpredictable period of time, detrusor contractility and sphincter reactivity return as spinal cord edema subsides. With this return of function, an overactive detrusor and bladder-sphincter dyssynergy may develop if the lateral reticulospinal cord pathways to and from the brainstem have been disrupted. When the lesion affects the cauda equina, there is probably little to no return of bladder or sphincter function. Sacral sensation and peripheral reflexes are not good indicators of ultimate lower urinary tract function [71]. Over time, the predominant urodynamic pattern in patients with a thoracic-level lesion is an overactive detrusor with sphincter dyssynergy, high voiding pressures, eventual hydronephrosis and vesicoureteral re- flux. Patients with an upper thoracic or cervical lesion are likely to exhibit autonomic dysreflexia with a spontaneous discharge of α1 stimulants during bladder filling and with contractions of the detrusor that require careful monitoring of their blood pressure during any investigational studies of the lower urinary tract [72, 73].