Spondylolysis may lead to spondylolisthesis, as the fracture allows one vertebral body to slip forward over the one below. This lesion is almost exclusively limited to the lower lumbar spine, usually with L5 slipping forward over S1 (Fig. 4.5). The most common cause of spondylolisthesis is an isthmic (pars interarticularis) defect in which the posterior neural arch remains stationary while the anterior body slides forward. In rare cases, neural arch dysplasia allows slippage, when facet and laminar defects insufficiently restrain forward movement. This can occur with myelomeningocele and neurofibromatosis. Degenerative and traumatic causes are rare in children. Spondylolisthesis is very unusual in the cervical spine.

Spondylolisthesis develops in less than half of those with spondylolysis. This slipping process rarely starts before age 7 and often begins or accelerates between the ages of 9 and 12, rarely increasing after age 20. While no prognostic radiographic or clinical factors can predict the progression of mild slips [13], in most cases ultimate vertebral displacement is less than 25 or 30 %.

Dysplastic spondylolisthesis is more common in girls, whereas the isthmic form is more common in boys. Most patients with spondylolysis alone are asymptomatic. When spondylolisthesis develops, low back pain and hamstring spasm are often noted.

Erect lateral radiographs may show more extensive slip than recumbent cross-table lateral examinations. Hypoplasia or scoliotic rotation of L5 can result in a false impression of spondylolisthesis. Using the lateral view, magnitude is grading from I to V: the superior surface of the sacrum is divided into four zones and the location of the slipped vertebra’s posteroinferior corner is determined (Fig. 4.8). An alternate, more reproducible assessment determines the percentage of slip by dividing the distance slipped by the width of the body below.

In long-standing spondylolisthesis, the slipped vertebral body becomes trapezoidal and its anterior face longer than the posterior due to underdevelopment of the posteroinferior corner. The superior surface of the sacrum becomes rounded because of abnormal pressure and impaired growth.

Stability of the vertebral column depends on the vertebrae; the posterior muscular, ligamentous, and capsular structures; the intervertebral disc; and the anterior and posterior longitudinal ligaments. The mechanisms that cause traumatic stress include flexion, rotation, extension, compression, and shearing. The anatomic peculiarities of various segments determine the type of lesion: horizontal facets of the cervical region promote dislocation and disc tear without fracture, whereas the more vertical lumbar facets predispose to facet fracture and slice-type fracture of the vertebral body. Dissolution of bone, for example, in the odontoid, may follow trauma.

The cervical spine is fractured in 37–80 % of pediatric spine injuries, and there is a higher incidence of neurologic injuries in younger children (less than 8 years of age) than in older children or adults [14]. Fractures in younger children are more likely to affect the upper cervical spine—from the occiput to C3. This is in part because movement occurs at a higher fulcrum, about C2–3 in young children versus C5–6 in adults and older children. It is also a consequence of their relatively large head and small body as well as increased mobility due to lax ligaments and underdeveloped neck muscles. In young children the geometry of the cervical vertebrae differs from that in adults, further predisposing them to upper cervical spine injury [15]. Elasticity of the ligaments also increases the likelihood of cord injury without osseous injury. Common upper cervical injuries include occiput-C1 injury, with possible rupture of ligaments and craniocervical separation; Jefferson fractures of the atlas; atlantoaxial separation or rotation; odontoid fractures; and hangman fracture of C2.

Older children are subject to similar fractures as adults. Most fractures involve the thoracic and lumbar spine, though the mid and lower cervical spine may be affected. Vertebral body compression fractures are most common. It is important to evaluate for additional fractures if one fracture is identified, as the presence of injury at multiple noncontiguous levels in children is associated with an increased probability of neurologic injury [16].

Flexion injury results in tears and sprains of posterior spinal muscles and ligaments, as well as vertebral body compression fractures. Rotational forces may contribute to subluxation. The cervical spine is prone to hyperextension injury caused by blows to the head, collisions, and whiplash. The thoracic and lumbar spine can suffer posterior element avulsion fractures [17].

Burst fractures, secondary to axial compressive loading, show up clearly by CT (Fig. 4.11). A retropulsed fragment may be rotated and displaced craniad or caudad. Callus extending into the spinal canal may cause late neurologic deterioration. MRI may investigate spinal cord injury. Acute intraspinal hemorrhage or cord laceration along with late myelopathy, syrinx formation, and atrophy may be evident, as well as neural injury remote from the region of skeletal injury.

The Chance fracture of the spine (Fig. 4.12) is an unstable flexion-distraction transverse disruption through the posterior elements and into the vertebral body [19]. It typically occurs at the T12–L2 level. Chance fractures are frequently associated with the lap belt injury complex: acute flexion of the abdomen over a lap belt during rapid deceleration. The abdominal viscera are compressed, possibly resulting in hollow viscus injury, as the spine flexes over the fulcrum of the belt. Sagittal reformatted CT images best show Chance fractures. Fortunately, associated spinal cord injury is rare.

Hyperflexion compression fractures may occur in children under age 2 who are subject to nonaccidental trauma [20]. These fractures may be clinically silent or associated with neurologic injury (Fig. 4.13). Subluxation and kyphosis may result. Extreme vertebral compression may suggest the dysostosis multiplex picture of mucopolysaccharidoses, and loss of disc space from traumatic intravertebral herniation may mimic pyogenic infection.