On the Pathogenesis of Syringomyelia: A Review

Abstract

Discussion of the pathogenesis of syringomyelia involves considering the origin of the fluid and also the forces which cause that fluid to break down the structure of the cord. When cerebrospinal fluid (CSF) appears to be the destructive element, it commonly enters through a patent central canal running from the fourth ventricle to the inside of the syrinx. In both clinical and experimental situations pressure differences may be measured which suck on the hindbrain, particularly the cerebellar tonsils, producing deformities. These pressure differences may also suck fluid into the syrinx. In other cases, even when a communication does not appear to be patent, the hindbrain abnormalities are usually present and suck effect may usually be demonstrated and its correction be accompanied by clinical improvement. Other sources of fluid within a syrinx include liquefaction of haematomata after traumatic paraplegia and transudation of fluid from intrinsic spinal tumours. Once fluid is present within a cord cavity it may pulsate upwards and downwards in response to fluid movements in the subarachnoid space, the most energetic of which result from venous influences. Such movement, ‘slosh’, may cause the cavities to extend at either end giving rise to upward and downward extension from a post-traumatic cord cyst and sometimes to syringobulbia. Cord ischaemia, venous congestion and transport of fluid along perivascular spaces may all play a part in the maintainance of cord cavities or the progression of the clinical disabilities.