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Biomechanics of the Cervical Spine
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The determination of spine stability and instability is a challenge. It depends on the definition of the anatomic elements involved and the determination of the extent to which they are injured. The study of the biomechanics of the spine encompasses many controversial topics and continues to evolve. The goals of this chapter are to introduce the basic biomechanical principles of the intact and diseased cervical spine, to define the most accurate parameters regarding the definition of spine stability, and, through biomechanical scientific evidence, to assist treating physicians in crafting the optimal strategy for management of the unstable spine.
Spine Biomechanics
More important than biomechanical instability itself is the definition of clinical instability. In their classic biomechanical textbook, White and Panjabi introduced the most widely accepted definition of clinical spine instability: “Clinical instability is the loss of the ability of the spine, under physiologic loads to maintain relationships between vertebrae in such a way that there is neither initial or subsequent damage to the spinal cord or nerve roots, and in addition, there is neither development of incapacitating deformity nor severe pain.” Spine instability may be caused by trauma leading to bony or ligamentous injury, by infection, by tumor, or by iatrogenic resection of the spinal elements. Multiple in vitro and in vivo studies have been performed with the goal of defining the stability of the spine segment in question, and the results of these studies aid in treatment decisions.
Upper Cervical Spine Stability: Principles and Biomechanical Evidence
Unique bone and ligamentous anatomica features form the elements responsible for the stability of the upper cervical spine. Heller and colleagues tested the isolated biomechanical properties of the transverse ligament of C1 by simulating an anteroposterior shear injury mechanism. Eleven specimens failed in the midsubstance of the ligament, and 2 failed by bony avulsion. The mean load to failure was 692 N (range, 220 to 1590 N), and the mean displacement to failure was 6.7 mm (2 to 14 mm). These investigators concluded that anteroposterior translation of the C1 transverse ligament in relation to the C2 dens is essential for its fracture, and the rate of loading affects the type of injury (the greater the rate, the more probable it is a ligamentous injury, as opposed to a fracture). When the transverse ligament-dens complex fails, either by midsubstance tear or by dens fracture, the greatest increase in instability is in flexion and extension (42% or 22 degrees), followed by lateral bending (24% or 8 degrees), and least in axial rotation (5% or 5 degrees).
The alar ligaments have been extensively studied, and although the involved mechanics is more complex, the alar ligaments have been shown mainly to limit axial rotation. Their transection increases contralateral axial rotation by approximately 15%; as in the transverse ligament, alar ligament rupture is rate dependent. In one report, these ligaments failed at 13.6 Nm at 4 degrees per second and at 27.9 Nm at 100 degrees per second. Radiographically, occipitoatlantal instability should be considered when the patient has more than 2 mm of translation or 5 degrees of rotation between the occiput and C1. Significant variability exists from patient to patient, and patients with rheumatoid arthritis perhaps should be assessed by more lenient parameters. Radiographic instability is seen between C1 and C2 when the atlantodens interval (ADI) is greater than 3 mm in adults and 5 mm in children. When the ADI is greater than 5 mm, the transverse ligament is considered ruptured, and when the ADI is greater than 9 mm, both the transverse and alar ligaments are deemed incompetent. More than 50% of rotation between C1 and C2 is also considered a radiographic sign of instability.
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