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The Effect of Posterior Thoracic Spine Anatomical Structures on Motion Segment Flexion Stiffness

Anderson, Andy L. MD; McIff, Terence E. PhD; Asher, Marc A. MD; Burton, Douglas C. MD; Glattes, R Christopher MD

doi: 10.1097/BRS.0b013e318198c62d
Anatomy

Study Design. This in vitro human cadaveric study tested the loss of thoracic motion segment flexion stiffness after sequential posterior upper instrumented vertebra anchor placement techniques and posterior column destabilization.

Objective. This study was designed to determine the possible destabilizing effects of upper thoracic instrumentation anchor site preparation.

Summary of Background Data. Proximal junctional kyphosis after instrumentation and arthrodesis for scoliosis and related spine deformities has recently been reported to range from 10% to 46%. The effect of posterior skeletal dissection associated with upper instrumented vertebra anchor placement on adjacent motion segment flexion stiffness has not been previously studied.

Methods. Twenty-three intact thoracic motion segments were obtained from 6 human cadavers. Biomechanical testing was performed with each motion segment flexed to approximately 3.2° at a rate of 0.1 Hz, with corresponding torques recorded. Data were collected after a series of 6 posterior procedures. Differences with P value <0.01 were considered significant and those with P value <0.05 marginally significant.

Results. Supratransverse process hook, supralaminar hook, pedicle screw placement, or pedicle screw removal done, bilaterally, produced similar, small (range, 2.09%–6.03%), nonsignificant reductions in motion segment flexion stiffness. But when totaled, these 4 procedures resulted in a significant 16.31% loss of flexion stiffness. The fifth procedure of supraspinous and interspinous process ligament transection added a marginally significant 6.59% incremental loss of flexion stiffness. Supralaminar hook site preparation combined with supraspinous and interspinous process ligament transection resulted in a marginally significant 12.62% incremental loss of flexion stiffness. Transection of the remaining posterior structures (facet joints and all other posterior soft tissue structures) produced a significant additional flexion stiffness loss of 44.72%. The anterior column alone provided only 32.39% of the total motion segment flexion stiffness. Transection of all posterior stabilizing structures, similar to a Smith-Peterson/chevron/Ponte resection, decreased motion segment flexion stiffness significantly, 67.61%.

Conclusion. Posterior thoracic skeletal structures involved in upper instrumented vertebra exposure andanchor placement were found to contribute to adjacent segment flexion stiffness. Although stiffness loss was small after individual procedures, the effects were additive for routinely used combinations.

The possible contribution of posterior skeletal structures, involved with implant anchor placement and posterior destabilization, to human cadaveric thoracic motion segment flexion stiffness was studied. Individual procedures produced small losses of flexion stiffness that, when added together, resulted in significant loss of stiffness. All posterior structures together accounted for over one-half of the motion segment flexion stiffness.

From the Department of Orthopedic Surgery, Kansas University Medical Center, Kansas City, KS.

Acknowledgment date: May 7, 2008. Revision date: September 24, 2008. Acceptance date: September 28, 2008.

The manuscript submitted does not contain information about medical device(s)/drug(s).

Foundation funds were received in support of this work. One or more of the author(s) has/have received or will receive benefits for personal or professional use from a commercial party related directly or indirectly to the subject of this manuscript: e.g., royalties, stocks, stock options, decision making position.

Supported by the J & E Berkley Foundation, Ivy, VA.

Address correspondence and reprint requests to Marc A. Asher, MD, Kansas University Medical Center, 3901 Rainbow Boulevard: Mail Stop 3017, Kansas City, KS 66160; E-mail: masher@kumc.edu.

© 2009 Lippincott Williams & Wilkins, Inc.