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J. Harley Astin, Christopher G. Wilkerson, Andrew T. Dailey, Benjamin J. Ellis, and Douglas L. Brockmeyer

OBJECTIVE

Instability of the craniocervical junction (CCJ) is a well-known finding in patients with Down syndrome (DS); however, the relative contributions of bony morphology versus ligamentous laxity responsible for abnormal CCJ motion are unknown. Using finite element modeling, the authors of this study attempted to quantify those relative differences.

METHODS

Two CCJ finite element models were created for age-matched pediatric patients, a patient with DS and a control without DS. Soft tissues and ligamentous structures were added based on bony landmarks from the CT scans. Ligament stiffness values were assigned using published adult ligament stiffness properties. Range of motion (ROM) testing determined that model behavior most closely matched pediatric cadaveric data when ligament stiffness values were scaled down to 25% of those found in adults. These values, along with those assigned to the other soft-tissue materials, were identical for each model to ensure that the only variable between the two was the bone morphology. The finite element models were then subjected to three types of simulations to assess ROM, anterior-posterior (AP) translation displacement, and axial tension.

RESULTS

The DS model exhibited more laxity than the normal model at all levels for all of the cardinal ROMs and AP translation. For the CCJ, the flexion-extension, lateral bending, axial rotation, and AP translation values predicted by the DS model were 40.7%, 52.1%, 26.1%, and 39.8% higher, respectively, than those for the normal model. When simulating axial tension, the soft-tissue structural stiffness values predicted by the DS and normal models were nearly identical.

CONCLUSIONS

The increased laxity exhibited by the DS model in the cardinal ROMs and AP translation, along with the nearly identical soft-tissue structural stiffness values exhibited in axial tension, calls into question the previously held notion that ligamentous laxity is the sole explanation for craniocervical instability in DS.