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POST-TRAUMATIC SAGITTAL IMBALANCE: THE ORIGIN OF PAIN.



Abstract

Introduction: Flat Back is a syndrome of sagittal imbalance often associated with back pain commencing in the lumbar region and progressively ascending. It is noted after posterior instrumentation to the lumbosacral junction, with various arthropathies and following compression fractures of the dorsolumbar and lumbar spines. In an attempt to maintain vertical posture, muscle fatigue causes back pain which persists until the condition is rectified. A compensatory pelvic tilt produces hip/hamstring pain and is relieved once lumbar correction is established. The cause of pain is unknown. The aim of this radiological study is to identify abnormal parameters which may contribute to sagittal imbalance and back pain.

Methods: Seven fully mobile subjects without fractures served as normal cohorts. Thirty-four consecutive patients aged 18 to 83 years with vertebral compression fractures were studied. There were 28 males. CT scout views of the full length spine in prone and supine positions provided functional scanograms for the Cobb measurement of thoraco-lumbar kyphosis and lumbar lordosis. Degrees of sagittal imbalance were graded as I, II and III, in accordance with the presence of dorsolumbar kyphosis, loss of lumbar lordosis and rigidity in functional views. Previous CT, MRI, Bone Scans were used to exclude other sources of pain such as protruding discs, annular tears, listhesis or un-united fractures. No patients with neurological signs were included. Three sets of measurements were taken:

  1. Dorsolumbar angulation: On prone films, Cobb angle was measured at upper T12 and lower L1 end plates (normal 0°; with standard deviation +3/−3).

  2. Lumbosacral angular motion: On functional films, lines were drawn on the upper end plates of L5 and S1. The resulting differences [(+)-(−)] between functional angles were compared with the normal values obtained from the literature (i.e. in excess of 26° of combined motion). The difference between standing lateral functional radiography and the prone/supine scanography was accepted.

  3. Sacral inclination: On supine films, the angle between a vertical line (a perpendicular to horizontal baseline) and the upper S1 endplate.

Results: There wasÊsignificant reduction in the radiation dose for CT scanograms when compared to conventional radiography: with sparing of bone marrow by 74–80%. The frequency of the abnormal radiological parameters was as follows:

  • Dorsolumbar angulation: 26 showed (positive) kyphotic angles up to 30°−40°.

  • Lumbosacral angular motion: In view of the spinal rigidity found in most cases, a compensatory excess mobility was expected at 5/1 level, but the opposite was confirmed. Indeed, 27 patiens showed exaggerated (negative) extension shift (of −5°−10°); amongst these 10 were with complete loss of flexion; 12 were with partial flexion (a forward shift of up to 15°), but 5 with full flexion, permitted by a lumbar kyphosis.

  • Sacral inclination: twenty-eight patients showed a shift to a diminished angle of 25°–35° as compared to 35°–55° in 15 control spines.

The patients were grouped according to the number of selected abnormal radiological parameters present. The cases were graded: Grade I (1 abnormality) – 2 cases, Grade II -13 cases and Grade III – 19 cases. The threshold for imbalance was (1) at least one severe thoracolumbar compression (or an equivalent combination of multiple minor thoraco-lumbar compression fractures) for D/L kyphosis and (2) a single lumbar fracture with at least 50% compression.

Discussion: The cause of pain in post-traumatic sagittal imbalance remains unclear. This study suggests three possible sources of pain, individually or in combination, namely altered angulation at the dorsolumbar junction, reduced motion at L/S level and sacral verticalisation. A more extensive study will be required for verification and interpretation of these preliminary data. It is important to expand the study to variants other than loss of lumbar lordosis.

The abstracts were prepared by I. B. McPhee. Correspondence should be addressed to the Spine Society of Australia Secretariat, The Adelaide Centre for Spinal Research, Institute of Medical and Veterinary Science, PO Box 14, Rundle Mall, Adelaide SA 5000, Australia.