We report the technique and early results of the Dwyer-Hartshill method for segmental fixation of the spine. This uses pedicular screws wired to a rectangular frame and is indicated after laminectomy.

Chronic pain at the donor site was reported by 25% of 290 patients who had undergone anterior lumbar spine fusion for low back pain. Donor site pain has characteristic clinical features, may be severely disabling and is stubbornly resistant to treatment. The highest prevalence was in patients who had a tricortical full thickness graft taken through a separate incision overlying the iliac crest. Patients with a clinically unsatisfactory result from the spine fusion also had a significantly higher prevalence of donor site pain.

We describe a lumbar facet syndrome in which disabling symptoms are associated with normal or near-normal plain radiographs. Local spinal fusion relieved symptoms in 12 patients; the excised facet joint surfaces showed some of the histological changes seen in chondromalacia patellae and in osteoarthritis of other large joints. The most frequent change was focal full-thickness cartilage necrosis or loss of cartilage with exposure of subchondral bone, but osteophyte formation was remarkably absent in all specimens. We suggest that there are both clinical and histological similarities between the facet arthrosis syndrome and chondromalacia patellae. Facet arthrosis may be a relatively important cause of intractable back pain in young and middle-aged adults.

The shallow lateral recesses of the trefoil shape of the lumbar spinal canal have been implicated in the production of the spinal stenosis syndrome. In the present study, 485 skeletons of South African Blacks and Whites were examined in order to establish the incidence and possible genesis of the trefoil configuration. The overall incidence was 14 per cent, with little variation between the sexes or races. The incidence was not related to increasing age, measured stenosis of the spinal canal or osteophytosis. Of 74 trefoil-shaped vertebrae, 68 (92 per cent) were found at the fifth lumbar level. It is suggested that the trefoil configuration is a common non-pathological condition, usually of the fifth lumbar vertebral canal, and is probably a developmental variation of normal anatomy.

The lumbar spines of 485 skeletons of adult South African "Whites" and "Blacks" of both sexes were examined to determine the incidence and morphology of defects in the pars interarticularis. The overall incidence was 3.5%, without significant variation between races and sexes. The incidence of lumbar spina bifida in the whole sample was 1.9%, but was 11.8% in those skeletons with spondylolysis. Some instances of unilateral spondylolysis demonstrated obvious callus formation, suggesting a capability for normal repair. It is possible that the defects in bilateral cases represent established non-union of fractures of the pars interarticularis resulting from excessive mobility, and are not due to dysplasia of bone. It is noted, for the first time, that the superior facets of affected vertebrae are abnormally enlarged, and that the inferior facets of the separate neural arch are characteristically elliptical.

Direct measurements were made on 2,166 lumbar vertebrae of 433 adult negro and caucasoid skeletons. On statistical analysis, forty-five vertebrae in twenty-seven skeletons were found to be stenotic, the mid-sagittal diameter being the significantly reduced dimension. Whereas spinal stenosis syndromes are rare in South African negroes, the lumbar canal is marginally narrower in the negro. There is a uniformity of configuration and capacity of the lumbar spinal canal, which transcends race and sex. By a new method of determining the dorsal limit of the lumbar canal on lateral plain radiography, the overall average lower limit of normal of the mid-sagittal diameter is established at 15 millimetres, and of the transverse diameter 20 millimetres. Bony degenerative changes are more likely to cause neurological compression in the nerve root tunnel than in the spinal canal. The role of skeletal narrowing of the spinal canal as an exclusive cause of the spinal stenosis syndrome may have been exaggerated.