Introduction: Vertebral bodies and intervertebral discs resist most of the compressive force acting on the spine. However, experiments on lumbar spines have shown that apophyseal joints can resist more than 50% of applied compression, and that the proportion varies with spinal level, disc narrowing, and posture. In the cervical spine, the situation is likely to be complicated by the presence of uncovertebral joints on the lateral margins of the disc. Load-sharing is important because it influences injury risk, and predisposition to degenerative changes. The present study aims to characterise compressive load-sharing in the cervical spine.

Methods: Sixteen cervical motion segments, consisting of two vertebrae and the intervening disc and ligaments, were dissected from nine cadaveric spines, aged 48-77 yrs (mean 63 yrs) which had been stored at -17degC. Specimens were subjected to 200N of compression while the distribution of compressive ‘stress’ was measured along the mid-sagittal diameter of the disc, using a pressure transducer side-mounted in a 0.9mm-diameter needle. ‘Stress profiles’ effectively were integrated over area to calculate the total compressive force acting on the disc. Experiments were performed with each specimen in flexion, extension and neutral posture. They were repeated after creep compressive loading (2 hrs at 150N) to simulate diurnal loading in life, and again following removal of the apophyseal joints. Eight specimens were re-tested following bi-lateral removal of the uncovertebral joints.

Results: Creep loading reduced disc height by an average 0.64mm (approximately 12%). Creep reduced overall computed disc loading by 14% and 25% in neutral and extended postures respectively (P< 0.005). Apophyseal joint removal increased disc loading in extension (only) by 14% (P< 0.05). Uncovertebral joint removal further increased disc loading in flexed, neutral and extended postures by 28%, 33% and 21% respectively (P< 0.05).

Conclusion: Creep loading of the cervical spine transfers loading to the apophyseal joints and uncus. The former effect is small, and significant only in extended postures. The latter effect is larger, and is greatest in flexed and neutral postures.

Introduction: Back pain can be associated with erratic and/or excessive movements between adjacent vertebrae. Such movements are normally resisted by intervertebral ligaments, and yet few back pain patients report traumatic rupture of ligaments prior to their onset of symptoms. We suggest that two other mechanisms can lead to ligamentous slack and therefore to spinal instability. The first of these is the age-related dehydration of intervertebral discs, which reduces disc volume and height, bringing the vertebrae closer together. The second mechanism is disc decompression following vertebral endplate fracture, which is a common injury but one which is difficult to detect. Decompression allows the disc to bulge and lose height, increasing ligamentous laxity. In the present experiment, we simulated disc dehydration and endplate injury in cadaveric spines, and compared their effects on spinal (in)stability.

Methods: Cadaveric thoraco-lumbar motion segments were subjected to complex, continuous loading using a hydraulic materials testing machine (Zwick-Roell, Leominster, UK) to simulate full flexion and extension movements in vivo. Vertebral movements were recorded at 50 Hz using the optical “MacReflex” video capture system (Qualisys AB, Sweden). Experiments were repeated following 2 hours of compressive “creep” loading at 1500 N, which reduced disc water content by an amount similar to the aging process, and again following compressive overload sufficient to fracture a vertebral endplate. Bending moment-rotation curves were used to quantify the “neutral-zone” (NZ), range of motion (ROM), and bending stiffness (BS).

Results: Preliminary results (10 motion segments) showed that specimen height was reduced by 1.0 mm (STD 0.3 mm) following creep, and by a further 1.5 mm (STD 0.5 mm) following endplate fracture. Mean ROM in flexion increased from 6.5 deg initially, to 8.9 deg after creep and 12.6 deg after fracture. Corresponding values for NZ in flexion were 4.6 deg, 6.6 deg and 9.5 deg. BS decreased from 28.9 to 23.0 to 15.2 Nm/deg. All changes were statistically significant (p< 0.03). NZ, ROM and BS values in extension were initially 1.6 deg, 4.0 deg and 32.7 Nm, respectively, but no significant changes were noted following creep and endplate fracture. Total ROM (flexion + extension) increased from 10.5 deg to 16.7 deg degrees following both interventions.

Discussion: Results suggest that disc dehydration, which is a normal feature of aging, increases NZ and ROM in flexion, presumably because accompanying disc height loss allows more slack to the posterior intervertebral ligaments. Endplate fracture, which can occur under physiological loads in osteoporotic elderly spines, has an even greater effect. Extension movements were little affected, presumably because loss of disc height also increases the risk of impaction between neural arches.

Conclusion: We conclude that age-related disc dehydration, and relatively minor endplate injury, can increase segmental motion and cause substantial mechanical instability to the thoraco-lumbar spine.

Introduction : We have shown previously that, in the presence of severe disc degeneration, the neural arch can resist up to 80% of the compressive force acting on the spine. We hypothesise that the inferior articular processes can then act as a “pivot” during backward and lateral bending movements.

Materials and Methods: Twenty-one motion segments (T8–9 to L4–5) were obtained from spines aged 48–90yrs. Specimens were loaded rapidly to simulate flexion, extension and lateral bending, while vertebral movements were tracked using an optical MacReflex system. The varying position of the centre of rotation (CoR) during these movements was calculated. Experiments were repeated after a treatment designed to simulate two effects of severe disc degeneration: creep loading to dehydrate the disc, and compressive overload to fracture a vertebral endplate and decompress the nucleus.

Results: In flexion, the CoR was usually located just below the inferior endplate of the disc, close to the antero-posterior midline, and in extension it moved an average 4.6 mm posteriorly. The additional “disc degeneration” treatment increased the variability of the CoR within and between specimens. It also moved the CoR an average 10.7mm posteriorly during extension movements (P< 0.001), so that in some specimens it was near the tip of the inferior articular processes.

Discussion: Severe disc decompression and narrowing increase translational (gliding) movements between adjacent vertebrae so that the effective CoR becomes more variable. During extension movements, the CoR can move so far posteriorly that the vertebrae can effectively “pivot” about the inferior articular processes.

Introduction: We hypothesise that disc degeneration is a major cause of segmental instability in elderly spines. Accordingly, we simulated two mechanical features of disc degeneration on cadaveric spines, and measured their effects on spinal movements.

Methods: Twenty-one motion segments (T8–9 to L4–5) were obtained from spines aged 48–90yrs. Specimens were loaded rapidly to simulate full spinal bending movements in vivo, while vertebral movements were tracked using an optical MacReflex system. Intradiscal stresses were investigated using “stress profilometry”. Experiments were repeated following compressive creep loading (which reduced disc water content by an amount similar to the aging process) and again following a compressive overload cycle which fractured a vertebral endplate and decompressed the nucleus. MacReflex data were used to quantify the neutral-zone (NZ), the range of motion (ROM), and the range of translational (gliding) movements.

Results Creep and endplate fracture both reduced disc height, and generated stress concentrations within the posterior annulus. Both treatments increased NZ, ROM and translational movements in flexion and lateral bending, but not in extension. Endplate fracture markedly increased the “instability index” (NZ/ROM) in flexion.

Discussion Disc “degeneration” increased all measures of spinal instability during flexion and lateral bending. Disc decompression in particular created a large NZ in which the spine had negligible resistance to bending. In life, muscle action would prevent the spine “wobbling” within this range of movement. Results in extension suggest impaction between the neural arches. Back pain associated with spinal instability could arise from stress concentrations in the annulus and neural arches, or from abnormal muscle activity.