BACKGROUND The pathogenesis of the central cord syndrome is still unclear. While there is a consensus on hyperextension as the main traumatic mechanism leading to this condition, there is yet… Click to show full abstract
BACKGROUND The pathogenesis of the central cord syndrome is still unclear. While there is a consensus on hyperextension as the main traumatic mechanism leading to this condition, there is yet to be consensus in studies regarding the pathological features of the spine (intervertebral disc bulging or ligamentum flavum hypertrophy) that could contribute to clinical manifestations. METHODS A comprehensive finite element model of the cervical spine segment and spinal cord was used to simulate high-speed hyperextension. Four stenotic cases were modelled to study the effect of ligamentum flavum hypertrophy and intervertebral disc bulging on the von Mises stress and strain. FINDINGS During hyperextension, the downward displacement of the ligamentum flavum and a reduction of the spinal canal diameter (up to 17%) led to a dynamic compression of the cord. Ligamentum flavum hypertrophy was associated with stress and strain (peak of 0.011 Mpa and 0.24, respectively) in the lateral corticospinal tracts, which is consistent with the histologic pattern of the central cord syndrome. Linear intervertebral disc bulging alone led to a higher stress in the anterior and posterior funiculi (peak 0.029 Mpa). Combined with hypertrophic ligamentum flavum, it further increased the stress and strain in the corticospinal tracts and in the posterior horn (peak of 0.023 Mpa and 0.35, respectively). INTERPRETATION The stenotic typology and geometry greatly influence stress and strain distribution resulting from hyperextension. Ligamentum flavum hypertrophy is a main feature leading to central cord syndrome.
               
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