Discectomy, decompression, and fusion are traditionally used to manage cervical disc disease accompanied by neural element compression that is refractory to conservative management. Concerns regarding stress at levels adjacent to fusion and possible adjacent-level degeneration as well as a desire to maintain a more normal biomechanical environment have led to investigation of cervical disc replacement as an alternative to fusion procedures. Cervical disc prostheses currently under investigation are constructed of predominantly metal-on-polyethylene or metal-on-metal bearing surfaces, and use roughened titanium surfaces and osteoconductive coatings to facilitate fixation. The unique anatomy and biomechanics of the cervical spine must be considered when extrapolating from the experience of appendicular arthroplasty and lumbar disc replacement.
Harvey E. Smith, David W. Wimberley and Alexander R. Vaccaro
Philip A. Saville, Abhijeet B. Kadam, Harvey E. Smith and Vincent Arlet
The aim of this study was to evaluate the segmental correction obtained from 20° and 30° hyperlordotic cages (HLCs) used for anterior lumbar interbody fusion in staged anterior and posterior fusion in adults with degenerative spinal pathology and/or spinal deformities.
The authors report a retrospective case series of 69 HLCs in 41 patients with adult degenerative spine disease and/or deformities who underwent staged anterior, followed by posterior, instrumentation and fusion. There were 29 females and 12 males with a mean age of 55 years (range 23–76 years). The average follow-up was 10 months (range 2–28 months). Radiographic measurements of segmental lordosis and standard sagittal parameters were obtained on pre- and postoperative radiographs. Implant subsidence was measured at the final postoperative follow-up.
For 30° HLCs, the mean segmental lordosis achieved was 29° (range 26°–34°), but in the presence of spondylolisthesis this was reduced to 19° (range 12°–21°) (p < 0.01). For 20° HLCs, the mean segmental lordosis achieved was 19° (range 16°–22°). The overall mean lumbar lordosis increased from 39° to 59° (p < 0.01). The mean sagittal vertical axis (SVA) reduced from 113 mm (range 38–320 mm) to 43 mm (range −13 to 112 mm). Six cages (9%) displayed a loss of segmental lordosis during follow-up. The mean loss of segmental lordosis was 4.5° (range 3°–10°). A total complication rate of 20% with a 4.1% transient neurological complication rate was observed. The mean blood loss per patient was 240 ml (range 50–900 ml).
HLCs provide a reliable and stable degree of segmental lordosis correction. A 30° HLC will produce correction of a similar magnitude to a pedicle subtraction osteotomy, but with a lower complication rate and less blood loss.
Ossama Al-Mefty, H. Louis Harkey, Isam Marawi, Duane E. Haines, Dudley F. Peeler, Harvey I. Wilner, Robert R. Smith, Howard R. Holaday, Joseph L. Haining, William F. Russell, Brent Harrison and Troy H. Middleton
✓ A canine model simulating both cervical spondylosis and its results in delayed progressive myelopathy is presented. This model allowed control of compression, an ongoing assessment of neurological deficits, and evaluation using diagnostic images, frequent electrophysiological tests, local blood flow measurements, and postmortem histological examinations. Subclinical cervical cord compression was achieved in 14 dogs by placing a Teflon washer posteriorly and a Teflon screw anteriorly, producing an average of 29% stenosis of the spinal canal. Four dogs undergoing sham operations were designated as controls. Twelve of the animals undergoing compression developed delayed and progressive clinical signs of myelopathy, with a mean latent period to onset of myelopathy of 7 months.
Spinal cord blood flow studies using the hydrogen clearance method showed a significant transient increase in blood flow immediately after compression and a decrease before sacrifice. Somatosensory evoked potential studies indicated progressive deterioration during the period of compression. Magnetic resonance images revealed intramedullary changes. Histological studies showed abnormalities overwhelmingly within the gray matter, including changes in vascular morphology, loss of large motor neurons, necrosis, and cavitation. Axonal degeneration and obvious demyelination were rarely seen. The most profound morphological changes occurred at the site of greatest compression. It is proposed that a momentary arrest of microcirculation occurs during extension of the neck because of loss of the reserve space in the compromised spinal canal. This microcirculatory disturbance is predominant in the watershed area of the cord and mainly affects the highly vulnerable anterior horn cells, leading to neuronal death, necrosis, and eventual cavitation at the junction of the dorsal and anterior horns. Additional supportive evidence of this hypothesis was derived from the literature.