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:

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

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.

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.

Introduction: The clinical condition was described as Ankylosing Hyperostosis of the Spine by Forestier (1950¹), was expanded by Resnick (1975) with the Extraspinal Manifestations². What is the nature of this unique formation, asymptomatic in 90% of cases? Several researchers questioned whether the hyperostosis was physiological or pathological. Initially, in 1985 B.M. Rotschild called it a phenomenon ³. Schlapbach in 1989 found no associated pathological condition ⁴. Hutton in his Editorial “Hyperostosis…a State not a Disease“ was doubtful ⁵.

In recent personal observations, protection by ossification was recorded in a severe trauma case and in vertebrae weakened by malignant infiltration.

Methods: A phylogenetic review of the animal world, followed by an ontogenetic study of mammals/ humans, could assist in a decision regarding the nature (physio-or pathological) of the hyperostosis.

Results: The phylogenetic lineage on one side showed the oldest record of hyperostosis in dinosaur (144 million years ago=mya). Ossifications were found in the anterior, lateral, posterior longitudinal ligaments, in C1–C2 transverse ligament. In the other phylogenetic, Hyperostosis was in historic and contemporary mammals.

The next step in this study is in the ontogenetic line of the Humans. The oldest skeleton (Ethiopia, 4.5 mya) showed “bridged vertebrae“. The first definite hyperostosis was in the Shanidar skeleton (Iraq, 40–12,000 BCE) with“flowing osteophytes”. In the historic Humans since 9500 BCE, hyperostosis was found in Europeans, Egyptians, Indians (Chile) and Incas. In the Christian era, hyperostosis was present in Roman-British/ Celt populations, Franks, Saxons, British, Swiss and N. Americans. In the 20th C, it is pandemic.

Discussion: a. Impressions from the animal world: Paleopathology was established as a scientific branch in 1912 (Ruffer), and exemplified its value in understanding the nature of diseases. Moodie questioned the function of the long spinal “bony rods”, considered them with a protective function. Others ⁶ suggested spinal hyperostosis as induced by “mechanical stress”. Shore⁷ (1936) described the spondylitis ossificans ligamentorum as due to mechanical strain.

b. Impressions from the Hominid world: The ontogenetic line shows a constant presence of hyperostosis in prehistoric and historic periods. Parallel to human migration from Africa, hyperostosis expanded globally.

c. The theory of logical probability: It is postulated that hyperostosis is a condition, as no pathology (other than inflammatory) could have expanded and persisted in many species along millions of years, as it would have been removed by the rules of the Darwinian Selection. Possibly triggered by strain in younger age, functional in the past, it is today an atavistic older age “condition“, with increased osteoblastic activity in connective tissues of ligaments and tendons. At times it is incidentally discovered and is occasionally excessive. Once presented with clinical manifestations, it becomes defined an illness and should be called the Forestier-Resnick syndrome.