Introduction A very specific group within the 80 percent of the population that suffers from low back pain at some stage in life are young cricket fast bowlers. Amongst them a high occurrence of unilateral L4 pars interarticularis fractures exists, which shows a strong statistical correlation to the presence of a contralateral volumetric increase in the Quadratus Lumborum (QL) muscle. However, there is no clear physical link between these two phenomena. To investigate this relationship, we have combined a mathematical model of the lumbar spine muscles with a finite element model of the fourth lumbar vertebra and analysed the stresses occurring in the L4 vertebra throughout the bowling motion.

Methods A mathematical model of the lumbar spine muscles has been developed previously at QUT. It contains 170 fascicles representing all major muscles in the lumbar region and allows for analysis of the forces and moments on the intervertebral joints caused by these muscles in any given posture. A Finite Element Model (FEM) of an L4 vertebra and intervertebral disc (IVD) was developed based on one created by Theo Smit and obtainable from the Internet through the BEL Repository of the Istituti Ortopedici Rizzoli, Bologna, Italy. Material properties were obtained from literature, while muscle forces, directions and attachment locations in the different postures came from the mathematical model. Six postures occurring in right-handed fast bowling were modelled to determine the differences in stresses between having symmetric and asymmetric QL muscles. The asymmetric condition consisted of a 30% increase in Physiological Cross-Sectional Area (PCSA) on the right side. In all cases it was assumed the left facet joints were ‘locked up’, to create a presumed worst-case scenario for the stress build-up in the pars.

Results It was found that when using muscle activation levels from literature an enlarged right-side QL did not increase the stresses in the left pars noticeably, in fact in some cases it even slightly reduced those stresses. When only the right-side QL muscle was activated, while all other muscles only provided passive muscle force, a 30% PCSA increase of this muscle produced an increase in maximum Von Mises and principal stresses in the left-side pars from typically 30 MPa to 40 MPa but only in the postures close to upright stance. In more extreme postures where the maximum stresses in the pars are higher, the increased PCSA of the right QL only led to small stress increases from typically 125 to 129 MPa.

Discussion Even in the worst-case scenario where only the right-side QL is active and the left-side facet joint is locked up, a PCSA increase of that muscle does not cause a large increase in stresses in postures where the stresses are high. Hence, this study has not demonstrated a clear physical link between asymmetric hypertrophy of QL and pars fractures. It may even suggest the hypertrophy is a response to postural overload attempting to reduce stresses in the pars. To clarify this, an improved FEM of the L3 and L4 vertebrae and IVDs, including all ligaments, is currently being developed. We believe that in the future this combination of models can be used for many more purposes where the influence of posture and musculature on the lumbar spine biomechanics needs investigation.

Assessment of the appropriateness of tendon transfer procedures and the necessity for excising the posterior tibial tendon (PTT) in stage II PTT dysfunction.

12 patients undergoing surgical treatment for unilateral PTT dysfunction underwent magnetic resonance imaging of the tibialis posterior (TP) and flexor digitorum longus (FDL) muscle bellies.

All patients had atrophy of the TP muscle compared to the normal leg (mean 10.7%, p = 0.008). In those patients with a complete rupture of PTT there was replacement of the TP muscle by fatty infiltration. Conversely, the FDL muscle showed a compensatory hypertrophy (mean 17.2%, p< 0.002).

Treatment of stage II posterior tibial tendon (PTT) dysfunction remains controversial. These findings support the use of FDL as the tendon of choice for augmentation of PTT in stage II disease. This study also demonstrates that in the presence of a complete rupture, excision of the PTT is a reasonable surgical procedure and pure tenodesis will fail because the TP muscle belly undergoes fatty infiltration. In patients with a diseased but intact PTT there was no fatty infiltration and the TP muscle volume was at least 83% of the normal side in all cases. We therefore suggest that in the presence of an intact PTT the TP muscle may provide some useful function if used to augment the FDL transfer when the diseased tendon is excised.