Abstract
BACKGROUND: The etiopathogenesis of syringomyelia is still an enigma. The authors present a novel theory based on fluid dynamics at the craniovertebral (CV) junction to explain the genesis of syringomyelia (SM). The changes in volume of spinal canal, spinal cord, central canal and spinal subarachnoid space (SSS) in relation to the posterior fossa have been analysed, specifically during postural movements of flexion and extension. The effect of fluctuations in volume of spinal canal and its contents associated with cerebrospinal fluid (CSF) flow dynamics at the CV junction have been postulated to cause the origin and propagation of the syringomyelia. The relevant literature on the subject has been reviewed and the author's theory has been discussed. CONCLUSION: Volume of spinal canal in flexion is always greater than that in extension. Flexion of spine causes narrowing of the ventral subarachnoid space (SAS) and widening of dorsal SAS while extension causes reverse changes leading to fluid movement in dorsal spinal SAS in flexion and ventral spinal SAS in extension. Cervical and lumbar spinal region with maximum bulk hence maximum area and volume undergo maximum deformation during postural changes. SSS CSF is the difference between the volume of spinal canal and spinal cord, varies in flexion and extension which is compensated by changes in posterior fossa (CSF) volume in normal circumstances. Blocked SAS at foramen magnum donot permit spinal SAS CSF exchange which during postural changes is compensated by cavitatory/cystic (syrinx) change at locations in cervical and lumbar spine with propensity for maximum deformation. Augmentation of posterior fossa volume by decompression helps by normalization of this CSF exchange dynamics but immobilizing the spinal movement theoretically will cease any dynamic volume changes thereby minimizing the destructive influence of the fluid exchange on the cord. Thus, this theory strengthens the rational of treating patients by either methodology.