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Syringomyelia - Pathogenesis
The pathogenesis of canine CM/SM is not fully understood. An important contributory factor is thought to be the mismatch in size between the brain and skull volume.
Studies in the Griffon Bruxellois have suggested that CM is characterised by a shortening of the basicranium and supraoccipital bone with a compensatory lengthening of the cranial vault especially the parietal bone. This has led to the hypothesis that the condition may be due to insufficiency of the bone and /or craniosynostosis of the lambdoid (occipitoparietal) and cranial base sutures.
The precise pathogenetic mechanism of development of syringomyelia is much debated.
A popular theory is that obstruction of CSF flow results in relative increase in spinal cord pressure and decrease in pressure in the CSF space around the spinal cord, the consequence of which is repeated mechanical distention of the spinal cord. This in turn results in dilatation of the central canal and accumulation of tissue fluid which eventually coalesces into cavities.
In this MRI image of a Cavalier with Syringomyelia you can see the hindbrain poking down through the foramen magnum, clear overcrowding of the cranial structures, and brainstem 'kinking'. Several wide syrinxes can be seen in the cervical spinal cord (in white)
Almost all Cavaliers have CM. One of the enigmas of CM/SM is the difficulty of predicting or explaining which dogs with CM will subsequently develop SM.
The cause of SM is a mismatch between brain and skull size. Cavaliers have a similar skull volume to other Toy breeds but more brain tissue within the skull.
Skull volume is significantly smaller for CKCS with early onset SM. The volume of brain within the skull is greater for CKCS with SM, especially in those dogs with early onset SM.
A large syrinx is associated with larger brain ventricles.
This is an MRI image of the brain and spinal cord of a five-year-old female Cavalier without Syringomyelia. Note the solid black normal spinal cord.
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