Mobility of lumbar segments instrumented with a ProDisc II prosthesis: a two-year follow-up study.Spine (Phila Pa 1976). 2006 Jul 01; 31(15):1726-33.S
STUDY DESIGN
Longitudinal prospective study on a sample of 41 consecutive disc prosthesis patients, covering a postoperative time period of at least 2 years.
OBJECTIVES
To document the rotational and translational range of segmental motion of patients instrumented with ProDisc II prostheses in the lumbar spine and to compare motion between instrumented and untreated adjacent segments with respect to a normative database. To discuss potential causes of the low range of rotational motion observed after instrumentation with a Prodisc II prosthesis.
SUMMARY OF BACKGROUND DATA
Disc replacement is intended to restore physiologic motion and height of the affected levels. Published reports show, however, that the goal of restoring motion at the operated segment is missed in the majority of cases. The cause of this failure is unresolved.
METHODS
Rotational and translational segmental motion in the sagittal plane, disc height, and posteroanterior displacement were measured from lateral radiographic views taken standing (before surgery) and in flexion and extension (1 year and 2 years after surgery) by Distortion Compensated Roentgen Analysis (DCRA). The protocol permits to take measurements from all segments imaged on the radiographic views and compensates for variations in stature, magnification, and posture. Data from instrumented and untreated segments can be compared and related to a previously determined normative database.
RESULTS
The rotational range of motion of segments instrumented with a ProDisc II prosthesis was low, especially at L4-L5 and L5-S1. In the majority of cases, it amounted to less than 45% of the normal range. Virtually no improvement occurred between 1 and 2 years after surgery. Malalignment of the axis of rotation of the prosthesis with respect to the anatomic axis, persisting clinical symptoms, or the significant increase of intervertebral space documented after instrumentation are unlikely to cause the low range of motion. As the range of rotational motion of the untreated segments was low with respect to normal as well, it is conjectured that tissue adaptation during the preoperative symptomatic time period might have caused the postoperative motion deficit. This conjecture complies with fragmentary previous observations of a low postoperative segmental range of motion from untreated segments of fusion patients.
CONCLUSIONS
Disc replacement in the lumbar spine by a ProDisc II implant fails to restore normal segmental rotational motion in the sagittal plane, specifically at levels L4-L5 and L5-S1. As segmental motion of the untreated segments was lower than normal as well, though not quite as conspicuous as that of instrumented segments, adaptation of soft tissue taken place during the preoperative symptomatic time period is conjectured to cause the observed motion deficit. Postoperative physical therapy might be considered if restoration of a normal range of rotational motion is desired.
