Tethering of the spinal cord has been a recognized cause of neurological symptoms in pediatric patients and is increasingly being recognized as a cause of symptoms in adults as well. The pathophysiology surrounding spinal cord tethering has begun to be understood in the pediatric population but is still unclear in adult patients.
Using a PubMed database literature search, the authors reviewed the pathology and pathophysiology surrounding the tethered spinal cord, focusing particularly on the pathophysiology of adult tethered cord syndrome (TCS).
Experimental data obtained in pediatric patients at surgery and in animal models indicate that spinal cord tethering causes a reduction in spinal cord blood flow and dysfunction of neuronal mitochondrial terminal oxidase. Retrospective analyses of patients undergoing surgery for adult TCS show that many adults developed symptoms following an event that could stretch the spinal cord, while others did not. Many patients also were found to have structural lesions in addition to a tethered spinal cord at diagnosis.
Both adult and pediatric TCSs are likely the result of a relative lack of blood flow to the spinal cord, causing dysfunction in mitochondrial oxidative phosphorylation. The likely reason the syndrome present later and differently in adults is that a secondary threshold of tension or a cumulative effect of repetitive, transient tension is placed on the cord before symptoms are recognized.