Spinal Lipomas

Jeffrey P. Blount, MD, and Scott Elton, MD, Division of Neurosurgery, University of Alabama at Birmingham, Children's Hospital of Alabama, Birmingham, Alabama

Neurosurg Focus. 2001;10(1) 

In This Article

Blood Flow

To study blood flow in a model of TCS, Yamada, et al.,[74] used hydrogen clearance on the dorsal surface of the cat spinal cord that was placed under a stretching condition. In this model blood flow decreased gradually as a traction weight was increased. When the weights were released, blood flow returned to normal. Kang, et al.,[31] similarly shown the development of impaired blood flow when longitudinal traction was applied on the spinal cord in a feline model of tethered cord. Schneider, et al.,[63] have recently reported that release of a tethered spinal cord is associated with increased spinal cord blood flow as demonstrated by laser Doppler flowmetry.

Although these hypotheses are in keeping with the progressive loss of function seen in most patients with untreated lipomyelomeningocele, there remain several clinical observations for which these concepts do not account.

First, in some patients with lipomyelomeningocele progressive neurological decline is not shown. Whereas it is widely recognized that older patients have more symptoms (thus supporting the general notion that early surgical untethering is appropriate), it is also noted that there is significant variability in the degree of symptoms manifested by patients of differing ages.[42,52] Indeed, there are isolated case reports of adults with lipomyelomeningocele and no apparent neurological deficit. It is emphasized that we do not consider these rare cases as indicative of a benign natural history of untreated lipomyelomeningocele, nor do such cases justify a conservative approach to the management of spinal lipomas. They do, however, attest to variability in the extent to which different patients are affected and prompt us to consider whether an additional mechanism could be causing injury to the cord.

Second, the majority of patients who undergo an untethering procedure experience significant prolonged benefit. In many patients late-onset neurological deterioration is demonstrated (months to years following untethering) that is attributed to retethering. Why all patients do not experience immediate retethering as a result of normal scar tissue formation is uncertain. If fibrosis occurs following tethered cord release, as it does in a similar fashion following other operative procedures, one could reasonably anticipate a period of weeks or months in which the untethered cord was truly free. Neurological deterioration in such a short time, however, is remarkably rare. This suggests that the pathophysiological event is acting apart from simple connection-related traction.

Third, patients presenting with delayed-onset neurological deterioration following an untethering procedure are thought to have a retethered cord and are often offered repeated surgery in another attempt to untether the cord. Such procedures are recognized to be more difficult, carry higher risks of neurological insult, and have a lower success rate in preventing neurological decline. During some such repeated procedures, a complete anatomical untethering occasionally cannot be accomplished because the apparently intact neural structures, which are integrally related to a mass of scar tissue, must not be put at risk. However, even in the absence of complete anatomical untethering, significant clinical improvement often is sustained in many such patients. If the anatomical tether is not disconnected, the current hypotheses cannot account for such improvement of the pathophysiology in the TCS.


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