Abstract
Introduction: The cervical spine can be severely loaded in bending during sporting injuries and ‘whiplash’. Compressive loading could also be high if some advanced warning of impact stimulated vigorous (‘protective’) contraction of the neck muscles. Combined bending and compression can cause some lumbar discs to herniate in-vitro (1) but the outcome depends on spinal level, and may not be applicable to cervical discs. We test the hypotheses: a) that cervical discs can prolapse in-vitro, and b) that prolapse leads to irregular stress distributions inside the disc.
Material and methods: Human cervical ‘motion segments’ (two vertebrae and intervening soft tissues) were obtained from cadavers aged 51–88yrs. Specimens were secured in cups of dental stone and subjected to static compressive loading (150N) for 20s. During this time, the distribution of vertically-acting compressive ‘stress’ was recorded along the postero-anterior diameter of the disc by pulling a 0.9mm-diameter pressure transducer through it (2). Injury was induced by compressing each specimen at 1mm/s while positioned in 20 deg of flexion, 15 deg of extension, or 8 deg of lateral bending. The distribution of compressive stress within the disc was then re-measured. Specimens were sectioned at 2mm intervals in order to ascertain soft tissue disruption.
Results: In all six specimens tested to date, one or both of the apophyseal joint capsules were ruptured by the complex loading. Intervertebral disc prolapse also occurred in all six specimens, with the herniated nucleus appearing on the anterior, posterior and postero-lateral disc surface in extension, flexion and lateral bending respectively. All modes of failure affected intradiscal stresses: on average, nucleus pressure decreased by 75% (STD 7%), while stress concentrations in the annulus increased by 130% (STD 21%).
Discussion: These preliminary results confirm that severe complex loading can cause cervical discs to prolapse. No particular state of disc degeneration is required, provided the loading is sufficiently severe. Indeed, the altered stress distributions suggest that cell-mediated changes would probably follow prolapse.
Correspondence should be addressed to Mr Carlos Wigderowitz, Senior Lecturer, University Department of Orthopaedic and Trauma Surgery, Ninewells Hospital and Medical School, Dundee DD1 9SY.
References:
1 Adams MA, Hutton WC. Spine1982;7(3):184–91. Google Scholar
2 Adams et al. (1996). Spine21(4): 434–8. Google Scholar
