The Edward Oldfield memorial lecture
Current understanding of the pathophysiology of syringomyelia
Solving the riddle of syringomyelia pathogenesis requires an explanation of how fluid, either CSF or biochemically identical to CSF, is entrained in the spinal cord central canal, accumulates to form a syrinx, and distends the spinal cord. During syrinx expansion the volume of fluid entering the central canal (CSFin) must exceed that leaving that structure (CSFout). The late Dr Edward Oldfield and I published a study comparing transit of myelogram dye into and out of syringes among patients with syringomyelia associated with either Chiari I malformation, spinal subarachnoid lesion, or haemangioblastoma, an intramedullary tumour. We found that more dye entered syringes associated with Chiari I malformation or spinal lesions than those associated with intramedullary tumours, suggesting that syringomyelia associated with spinal subarachnoid space obstruction was maintained by fluid passing from the spinal subarachnoid space, through the spinal cord, and into the syrinx, whereas intramedullary tumours maintained their syringes through intra-tumour fluid production. Dr Oldfield and colleagues earlier published a study using contrast-enhanced FLAIR imaging to show that haemangioblastomas of the cerebellar hemisphere and spinal cord produce fluid that passes enters the surrounding extravascular spaces, creating oedema and eventual cyst or syrinx formation. Because internal fluid production has not been shown in syringes associated with spinal subarachnoid obstruction, we propose another mechanism in which enlarged subarachnoid pressure waves drive an external source of syrinx fluid, CSF, into the spinal cord to form a syrinx.
The symposium is co-organised by The Ann Conroy Trust, in association with Aesculap Academia.
The Ann Conroy Trust is Registered Charity No: 1165808.
We provide Support, Education and Research for patients living with Chiari Malformation, Syringomyelia and associated conditions.