Dr. Kevin Yip

Dr Kevin Yip
Orthopaedic Surgeon
MBBS(UK), FRCS(EDIN), FAM(SING), FHKCOS(ORTHO)

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Catastrophic Cervical Spine Injuries-Unstable Fractures and Dislocations

As expected, unstable fractures and/or dislocations make up the majority of catastrophic spinal injuries in athletes. An osseous or ligament injury is considered to be unstable when it results in loss of the ability of the spine, under physiological loads, to maintain its premorbid patterns of motion, so there is no initial or additional damage to the spinal cord or nerve roots, no major deformity, and no incapacitating pain.

Spinal column damage occurs when the force and resistance balance of the normal motion of the spine is exceeded. Injury patterns often can help to illustrate the mechanism of cervical motion and damage.In football and hockey, the injury vector most frequently associated with cervical spinal cord injury is compression (axial loading).

A smaller percentage of injuries result from excessive flexion. Finally, extension, lateral stretch, and congenital instability also have been reported in cervical spine injury.

Initial loading most often occurs at the vertex of the collision athlete’s helmet. The cervical spine is then left to compress between the mass of the oncoming body, which represents the instantly decelerated head, and the mass of the remaining body.

Perhaps most influential in determining specific injury patterns is the neck position at the time of impact. Neutral alignment leaves the cervical spinal column slightly extended because of the normal lordotic posture.

Compressive forces in this position are dissipated by the anterior paravertebral musculature and vertebral ligaments (anterior longitudinal ligament). Slight flexion will eliminate cervical lordosis and direct force along the spine’s longitudinal axis.

This will result in large forces being transferred directly to the vertebrae as opposed to the surrounding soft tissues. Cadaveric studies have shown that the cervical spine, when straight and colinear with the applied load, responds to compression by buckling.

Most fractures and dislocations in injured athletes occur in the lower cervical spine. Two major patterns of compressive spinal column damage exist. Most often, evidence of a compressive–flexion injury is present as a result of a combination of axial force and a bending moment.

The anterior column shortens under loading. We then see compressive failure of the vertebral body and tensile failure of the posterior spinal ligaments. This pattern can be highly unstable both anteriorly and posteriorly, with displacement of the anterior fracture and widening of the posterior elements, and it often may be associated with spinal cord injury.

Pure vertical compression (the cervical spine is slightly flexed, eliminating the normal lordosis) results in equal force on the anterior and posterior columns, which may result in an axial loading fracture (“burst”).

Intradiscal pressure rises such that the adjacent end plate fractures and fails. Bone fragments often can displace in all directions secondary to forced, extruded disc material within the vertebral body. In fact, these burst fractures are notable for retropulsion of osseous material into the spinal canal.

During most normal neck motion, the cervical spine remains in slight extension (or lordosis). Flexion vectors, however, can be created either by a direct blow to the occipital region or by a rapid deceleration of the torso.In this situation, spine flexion subjects the posterior ligamentous structures of the involved motion segment to tensile forces.

These are characterized as flexion–distraction injuries, and the most common specific injury pattern to result in spinal cord dysfunction is a bilateral facet dislocation. An axial rotation force in conjunction with the flexion–distraction injury may produce a unilateral facet dislocation (spinal cord injury in up to 25% of cases).

The spectrum of neurological dysfunction with cervical fractures or dislocations often can be highly variable. Syndromes include complete quadriplegia, with total loss of sensory or motor function below the level of the cord lesion, versus partial spinal cord injury, with incomplete loss of sensory or motor function in the extremities and torso.

The most common clinical entity of partial spinal cord injury is central cord syndrome, followed by anterior cord syndrome. Maroon et al.It reported a variant of the central cord lesion that was characterized by dysesthesias in both hands without loss of strength or sensation.

Although the etiology is not entirely clear, this “burning hands” syndrome is thought to result from a vascular insufficiency. This may affect the medial portion of the somatotopically arranged spinothalamic tracts.

Upper cervical spinal fractures and dislocations, although significant injuries, rarely cause spinal cord damage. The spinal canal in the upper cervical region has a much greater proportion of space to spinal cord.

Therefore, even with displacement, cord compression is unlikely in relation to upper cervical spinal injury. In fact, a burst fracture of the atlas (Jefferson fracture) and traumatic spondylolisthesis of the axis (Hangman fracture) expand the dimensions of the spinal canal, making cord compression and neurological injury improbable.

Some scenarios may place the upper cervical cord at increased risk for injury. Odontoid fractures or ruptures of the transverse ligament will destabilize the atlantoaxial joint. Typically, high cervical cord injuries can cause respiratory compromise secondary to high-cord/low-brainstem injury as well as diaphragmatic paralysis from trauma to the anterior horn cells of the phrenic nerve.

Thus far, we have discussed primarily upper motor neuron damage from cervical injury. Occasionally, a lower motor neuron finding will be the only sign. For instance, a unilateral facet dislocation may compress the dislocated side at the foraminal opening. This phenomenon certainly can cause isolated nerve root symptoms (monoradiculopathy).

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