Neurosurgery

Dorn Spinal Therapy

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Lipomeningocele

Fig. 27.2. a Lumbar lipomeningocele. Sagittal T1-weighted MR scan, demonstrating a low-lying conus associated with a lipomeningocele. The spinal cord ends in a lipoma, which itself is continuous with the subcutaneous tissues and is coupled with a defect in the lumbar laminae. b Lumbar lipomeningocele. Axial T1-weighted MR image, revealing the relationship between the conus and the lipoma itself.

Fig. 27.2. a Lumbar lipomeningocele. Sagittal T1-weighted MR scan, demonstrating a low-lying conus associated with a lipomeningocele. The spinal cord ends in a lipoma, which itself is continuous with the subcutaneous tissues and is coupled with a defect in the lumbar laminae. b Lumbar lipomeningocele. Axial T1-weighted MR image, revealing the relationship between the conus and the lipoma itself.

prevent re-tethering by local scar tissue. Surgery is generally carried out through a midline incision, although plastic surgical considerations may need to be taken into account in large lesions. The first normal lamina above the lesion is identified and the dura here exposed. The dura is then opened to expose the attachment of the lipoma to the cord and the opening continued around the exiting fatty defect. The line of fusion of the lipoma with the cord can then be identified and, with the exiting nerve roots anterior to this line, the lipoma can be detached. The bulk of the lipoma can then be removed and the dura closed, ensuring that the mobility of the conus is not compromised by the closure. The frequent difficulty in obtaining a satisfactory dural closure leads to the two chief complications of the procedure: CSF leakage and re-tethering. The former is generally manageable with CSF drainage and re-suturing, if need be. The latter may become apparent within months or many years of the initial surgery and is characterized by the onset of neurological deterioration or pain. Since the conus, following even successful surgery, may not change position on MRI studies, re-tethering can be difficult to prove radiologically and re-exploration may be necessary on clinical grounds alone (see above).

Surgery carries a low risk for neurological deterioration (less than 5%) and appears to prevent the subsequent development of neurological deficits. In those with clinical signs of tethering, surgery appears to be effective at preventing further deterioration and, for early intervention, may reverse some of the neurological dysfunction. For long established deficits with orthopedic deformity, surgery will not lead to improvement but can effectively prevent a worsening deficit.

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