Commentary

Mr. Fox and colleagues present a well-written and well-illustrated case report along with a thorough review of the literature highlighting the potential for tumor-associated hindbrain herniation to lead to secondary spinal cord syrinx formation. While a rare association, it is one that should be recognized by skull base surgeons, particularly to avoid the mistake of initiating direct treatments for the syrinx, which almost always resolves over time once the hindbrain herniation has been reduced and normal flow of cerebrospinal fluid (CSF) and pressure equilibration dynamics have been restored.

Indeed, we are increasingly recognizing that spinal cord syrinxes are almost always secondary phenomena. They usually improve or resolve after successful treatment of their primary cause. This holds true for lysing spinal canal arachnoid adhesions for post-traumatic or postmeningitic syrinxes; releasing caudal cord tension for tethered cord syrinxes (e.g., thickened filum, lipomeningocele, or scarred myelomeningocele repair); removing the spinal cord tumor for tumor-associated syrinxes; posterior fossa decompression of Chiari malformation-induced syrinx; anterior decompression for ventral compression or instability-induced syrinx (e.g., platybasia, C1-C2 rheumatoid arthritis); removing the shunt for lumboperitoneal shunt-induced syrinxes; and shunting the ventricles for hydrocephalus-induced hindbrain herniation leading to spinal cord syrinx. Removing a mass lesion (e.g., tumor) leading to hindbrain herniation should now be added to that list. Restoring normal flow of CSF and pressure equilibration dynamics throughout the craniospinal axis should be the goal. Primarily shunting or fenestrating a spinal cord syrinx should become a rare procedure, reserved for the small subset of cases where chronicity of the condition does not allow sufficient spontaneous resolution.