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Study Design: In vitro anatomic study investigating the degree of soft tissue disruption required to produce a subaxial cervical unilateral facet dislocation., Objectives: To develop an understanding of the relative contributions to stability of the subaxial cervical soft tissues and to define an anatomic threshold of injury necessary to produce a unilateral cervical facet dislocation., Summary of Background Data: The literature at this time is unclear regarding the precise pathomechanics of a cervical unilateral facet dislocation and the required threshold of soft tissue injury necessary for its genesis. Published clinical reports do not make any specific reference to these factors or are unclear in their objectivity., Methods: Two adjacent vertebra at a time in 10 fresh-frozen subaxial cervical spine specimens (C2-C3 to C6-C7) were transfixed in the coronal plane with 3.5-mm Schanz screws. A steady unilateral vertical distraction force resulting in lateral cervical flexion was applied to these screws as the surrounding cervical soft tissue structures were sequentially ablated. Four experimental models were developed, varying the order of soft tissue disruption., Results: The physiologic coupling of subaxial cervical unilateral distraction and rotation, because of the spatial orientation or inclination of the cervical facet joints, allowed the creation of a unilateral facet dislocation without an additional flexion moment. Disruption of the ipsilateral articular capsule, ligamentum flavum, and more than half of the anulus fibrosus was necessary for the genesis of a unilateral facet dislocation. Disruption of the supraspinous and interspinous ligaments was not necessary but appeared to facilitate or lessen the force required to dislocate a unilateral facet. Disruption of the anterior and posterior longitudinal ligaments and intertransverse ligaments was not necessary to create a unilateral facet dislocation., Conclusion: This anatomic study further supports the theory that discontinuity of the anterior and posterior longitudinal ligaments is not necessary for a unilateral facet dislocation to occur. The ipsilateral facet capsule, anulus fibrosus, and ligamentum flavum appear to be the physical soft tissue restraints that need to be disrupted to produce a unilateral facet dislocation.

116 patients with cervical spine injuries due to water sport accidents treated in eight Austrian institutions from 1991 to 1998 were reviewed retrospectively. There were 93% male, 72% were 15 to 29 years of age. 93% had injuries from diving into swimming pools or into open water. At discharge 58 patients had Frankel A lesions, 39 had incomplete cord lesions Frankel B to D, and 19 patients had no neurological injury. This data suggest that in Austria approximately one person per one million inhabitants per year sustains a spinal cord injury in a diving accident in shallow water.

The Posterior Cervical Line helps to differentiate pseudosubluxation from the true dislocation C 2/3 in children. But the line can also be used to recognize other pathologic conditions of the upper cervical spine in children, like atlanto-axial sagittal instability or rotatory dislocation.

Eleven children with a vertebral body flexion-compression fracture of the lower cervical spine were reviewed. Eight were treated non-operatively, two had a ventral interbody fusion and one a dorsal fusion. Follow-up time was 1 month to 12 years (mean 55 months). Following non-operative therapy six had a kyphotic deformity of more than 10 degrees at the last follow-up. Kyphosis cannot be prevented or cured by non-operative methods.

Unilateral locking of cervical facet joints is often misdiagnosed and inadequately treated, because it is not readily detected on plain radiographs. Primary radiographs of 17 patients were analysed to evaluate radiographical signs with reference to frequency and significance. Direct signs of locking were present in no more than 53% of cases. Of these, an abrupt change in laminar space width, seen in 88.2%, proved to be the most reliable sign. Displacement of the spinous processes above and below the lesion was found in the same percentage of cases, but it carries less diagnostic weight. While present in all cases, anterolisthesis is only diagnostic if additional oblique views show evidence of lateralized cervical anterolisthesis. Clearly less reliable indirect signs included: the bow tie sign (29.4%), dehiscence of the spinous processes (23.5%), differences in the sagittal diameters of the vertebral bodies above and below the lesion (35.2%), double facet contour (47%) and tilting of the cranial segment of the cervical spine away from the locked facets (58.8%). Abnormalities of disc shape were not seen on a.-p. projections. Those detectable in axial views are irrelevant to locking, as are empty facets. If more than one indirect sign is present and if unilateral locking is suspected but cannot be established unequivocally even on additional oblique views, computed tomography is indicated, because reduction continues to be the first step in the management of fresh injuries.

In a retrospective study of 22 patients with unilateral locked facet syndrome of the cervical spine, diagnostic and treatment problems were analysed. Diagnosis was delayed in ten patients; in two-thirds of the patients minor or major therapeutic problems were encountered. The treatment protocol advised manipulative reduction and--before 1986--posterior fusion by bone blocks and interspinous wiring; after 1986 ventral intercorporeal fusion by plates was recommended. Closed reduction manoeuvres risk dislocation of intervertebral discs, overdistraction of the spinal cord or injury to the vertebral artery. Unreduced and unfused dislocations are likely to develop chronic instability. Dorsal wiring is an inadequate form of stabilization and ventral plates or dorsal hooks are preferred. To prevent treatment problems a treatment protocol is proposed according to which open reduction following anterior discectomy, operative decompression of endangered nerve roots and stable one-level fusion is done. In non-acute injuries neural structures are decompressed; posterior fusion is done without attempts at reduction.

Ligamentous and osseous injuries of the cervical spine during growth are extremely rare and therapeutic principles for such lesions are ill-defined. In order to help solve some diagnostic and therapeutic problems a retrospective study of 30 children was carried out. There were 5 discoligamentous injuries, 5 fractures of the atlas, 1 fracture of the arcus C2, 8 fractures of the odontoid, and 11 vertebral body compression fractures. The injuries were caused by motor vehicle accident in 9, by diving into shallow water in 7, by falling from a height in 7, by a sports accident in 6, and by a direct trauma in 1 patient. Four children died, three of them due to concomitant brain injury. Two patients suffered permanent neurologic disability due to spinal cord trauma. Five patients underwent an operation. Conservative therapy of flexion-compression fractures of the vertebral bodies caused kyphotic deformity. Ventral interbody fusion in two patients had excellent long-term results. All odontoid fractures were treated by applying a plaster cast and healed promptly. Diagnostic problems were mainly caused by the hypermobility of the upper cervical spine.

In 11 patients with locked cervical spine facets after blunt injury, the patency of the vertebral arteries was evaluated by color-coded Duplex sonography (CCDS) up to 11 years after the accident. In 7 patients the dislocations had been reduced, 2 had been treated conservatively, and 9 had been fused. In 9 patients (3 of them with persistent locking) the mean systolic peak flow velocity was 55 cm/sec and the vessel diameter was 0.35 cm. Only 2 patients had an abnormal CCDS. In 1 with persistent locking the ipsilateral vertebral artery was occluded, and in the other flow signals were abnormal and the vessel diameter was smaller than on the contralateral side. The high coincidence of vertebral artery occlusions and locked dislocations, as well as fracture dislocations reported by others, was not confirmed in our series.

There is no generally accepted treatment protocol for dislocations of single articular processes of the cervical spine. However, the data in our own series and a survey of the literature show that in this type of injury the primary diagnosis rate is low (around 50%), that closed reduction maneuvers can be neurologically hazardous, and that operative fusion prevents certain complications. Among the 20 patients treated at the authors' institution the injury was located in the lower cervical spine in all but one patients and it was caused by a high-speed traffic accident in 14 patients. Four patients had no therapy at all; the others were fused by an anterior approach in 8, a dorsal approach in 6, and a combined method in 2 patients. There was one death due to intimal tearing of a vertebral artery. Closed reduction caused a transient neurological lesion in 2 patients. In 6 patients whose dislocation was neither reduced nor fused, 3 developed chronic instability. In our new treatment protocol dislocation of a single articular process is only reduced after a diskectomy to prevent extrusion of the disc. If reduction from the anterior approach fails or if it cannot be achieved due delayed treatment, the entrapped nerve root is decompressed. Fusion of the injured segments is carried out by bone blocks and plates or hooks.

In four patients with lesions of the vertebral artery resulting from cervical spine injury, two were due to unilateral facet dislocation and two to fractures of the dens. There was one arterial occlusion with minor vertebrobasilar symptoms, and an arterial lesion with thrombosis causing embolic occlusion of the basilar artery with lethal outcome. In one patient a fresh fracture of the dens caused dislocation of C1/2 with reversible occlusion of the left and stenosis of the right vertebral artery, resulting in unconsciousness. In a patient with pseudarthrosis of the dens an aneurysm of the vertebral artery could be detected. Cerebellar or cerebral symptoms associated with cervical spine injury should be investigated by vertebral angiography because vertebral arterial injury may be more common than suspected and may simulate traumatic brain damage.