Posterior short fusion without neural decompression using pedicle screws and spinous process plates: A simple and effective treatment for neurological deficits following osteoporotic vertebral collapse.

BACKGROUND

The optimal treatment of neurological deficits following osteoporotic vertebral collapse (OVC) is controversial, owing to complications that result from fragile bone quality. In the present study, we assessed surgical results following posterior spinal fusion without decompression. We achieved stable fusion over a short segment of the spinal column using pedicle screws and spinous process plates, maximizing the use of the preserved posterior elements.

METHODS

We reviewed surgical data, perioperative complications, clinical outcomes, and radiographic data of 20 consecutively recruited patients with delayed neurological deficits following OVC, who experienced posterior short fusion without neural decompression. The average follow-up period was 24.3 months. The spine was typically stabilized with pedicle screws and spinous process plates from one level above to one level below the collapsed vertebrae, without using neural decompression or considerable correction of kyphosis.

RESULTS

All patients experienced relief from back pain and neurological improvements of at least one modified Frankel grade. Bone unions of the collapsed vertebrae were achieved in all patients, and spinal fusions of the instrumented segments were achieved in all but one patient. The mean loss of correction was 5.9°, and the average spinal canal compromise by bone fragments was 32.4% before surgery as against 26.0% at the final follow-up time point. Fractures in adjacent or upper instrumented vertebrae were observed in four cases (20%).

CONCLUSIONS

Rigid augmentation by spinous process plates and an enough bed for the bone grafts were available in patients with severe osteoporosis, without neural decompression. All patients had satisfactory neurological recovery regardless of the extent of spinal canal remodeling, demonstrating that dynamic factors are the primary contributor to neurological deficits following OVC.