Intradiscal Pressure Changes during Manual Cervical Distraction: A Cadaveric Study.

The objective of this study was to measure intradiscal pressure (IDP) changes in the lower cervical spine during a manual cervical distraction (MCD) procedure. Incisions were made anteriorly, and pressure transducers were inserted into each nucleus at lower cervical discs. Four skilled doctors of chiropractic (DCs) performed MCD procedure on nine specimens in prone position with contacts at C5 or at C6 vertebrae with the headpiece in different positions. IDP changes, traction forces, and manually applied posterior-to-anterior forces were analyzed using descriptive statistics. IDP decreases were observed during MCD procedure at all lower cervical levels C4-C5, C5-C6, and C6-C7. The mean IDP decreases were as high as 168.7 KPa. Mean traction forces were as high as 119.2 N. Posterior-to-anterior forces applied during manual traction were as high as 82.6 N. Intraclinician reliability for IDP decrease was high for all four DCs. While two DCs had high intraclinician reliability for applied traction force, the other two DCs demonstrated only moderate reliability. IDP decreases were greatest during moving flexion and traction. They were progressevely less pronouced with neutral traction, fixed flexion and traction, and generalized traction.

Primary and coupled motions after cervical total disc replacement using a compressible six-degree-of-freedom prosthesis.

This study tested the hypotheses that (1) cervical total disc replacement with a compressible, six-degree-of-freedom prosthesis would allow restoration of physiologic range and quality of motion, and (2) the kinematic response would not be adversely affected by variability in prosthesis position in the sagittal plane. Twelve human cadaveric cervical spines were tested. Prostheses were implanted at C5-C6. Range of motion (ROM) was measured in flexion-extension, lateral bending, and axial rotation under ± 1.5 Nm moments. Motion coupling between axial rotation and lateral bending was calculated. Stiffness in the high flexibility zone was evaluated in all three testing modes, while the center of rotation (COR) was calculated using digital video fluoroscopic images in flexion-extension. Implantation in the middle position increased ROM in flexion-extension from 13.5 ± 2.3 to 15.7 ± 3.0° (p < 0.05), decreased axial rotation from 9.9 ± 1.7 to 8.3 ± 1.6° (p < 0.05), and decreased lateral bending from 8.0 ± 2.1 to 4.5 ± 1.1° (p < 0.05). Coupled lateral bending decreased from 0.62 ± 0.16 to 0.39 ± 0.15° for each degree of axial rotation (p < 0.05). Flexion-extension stiffness of the reconstructed segment with the prosthesis in the middle position did not deviate significantly from intact controls, whereas the lateral bending and axial rotation stiffness values were significantly larger than intact. Implanting the prosthesis in the posterior position as compared to the middle position did not significantly affect the ROM, motion coupling, or stiffness of the reconstructed segment; however, the COR location better approximated intact controls with the prosthesis midline located within ± 1 mm of the disc-space midline. Overall, the kinematic response after reconstruction with the compressible, six-degree-of-freedom prosthesis within ± 1 mm of the disc-space midline approximated the intact response in flexion-extension. Clinical studies are needed to understand and interpret the effects of limited restoration of lateral bending and axial rotation motions and motion coupling on clinical outcome.

Restoration of spinal alignment and disk mechanics following polyetheretherketone wafer kyphoplasty with StaXx FX.

BACKGROUND AND PURPOSE: EPFs sustained during VCFs degrade the disk's ability to develop IDP under load. This inability to develop pressure in combination with residual kyphotic deformity increases the risk for adjacent vertebral fractures. We tested the hypothesis that StaXx FX reduces kyphosis and endplate deformity following vertebral compression fracture, restoring disk mechanics. MATERIALS AND METHODS: Eight thoracolumbar, 5-vertebrae segments were tested. A void was selectively created in the middle vertebra. The specimens were compressed until EPF and to a grade I-II VCF. PEEK wafer kyphoplasty was then performed. The specimens were then tested in flexion-extension (±6 Nm) under 400-N preload intact, after EPF, VCF, and kyphoplasty. Endplate deformity, kyphosis, and IDP adjacent to the fractured body were measured. RESULTS: Vertebral body height at the point of maximal endplate deformity decreased after EPF and VCF and was partially corrected after StaXx FX, remaining less than intact (P = .047). Anterior vertebral height decreased after VCF (P = .002) and was partially restored with StaXx FX, remaining less than intact (P = .015). Vertebral kyphosis increased after VCF (P < .001) and reduced after StaXx FX, remaining greater than intact (P = .03). EPF reduced IDP in the affected disk in compression-flexion loading (P < .001), which was restored after StaXx FX (P = 1.0). IDP in the unaffected disk did not change during testing (P > .3). CONCLUSIONS: StaXx FX reduced endplate deformity and kyphosis, and significantly increased anterior height following VCF. Although height and kyphosis were not fully corrected, the disk's ability to pressurize under load was restored.

Healing of partial flap necrosis in ankle disarticulation amputation by débridement and continued weight-bearing.

Five patients with partial tissue loss of the weight-bearing surface of the heel pad following ankle disarticulation were treated with residual-limb debridement and continued end-weight-bearing using a total-contact cast. The patients, ranging in age from 53 to 76 years, had insulin-requiring diabetes and insensate heel pads and were low-demand, limited-activity, community walkers before amputation surgery. Each underwent amputation surgery as a consequence of peripheral vascular disease. All patients progressed to complete wound healing over 3 to 6 months and were able to return to their previous ambulatory level using a prosthesis. At a minimum 2-year follow-up, no patient experienced further residual-limb complications. Partial loss of the weight-bearing heel pad in ankle disarticulation amputation does not preclude successful return to independent ambulation using a standard ankle disarticulation prosthesis. Weight-bearing ambulation need not be avoided during healing.

The biomechanical effect of postoperative hypolordosis in instrumented lumbar fusion on instrumented and adjacent spinal segments.

STUDY DESIGN: Change in lumbar lordosis was measured in patients that had undergone posterolateral lumbar fusions using transpedicular instrumentation. The biomechanical effects of postoperative lumbar malalignment were measured in cadaveric specimens. OBJECTIVES: To determine the extent of postoperative lumbar sagittal malalignment caused by an intraoperative kneeling position with 90 degrees of hip and knee flexion, and to assess its effect on the mechanical loading of the instrumented and adjacent segments. SUMMARY OF BACKGROUND DATA: The importance of maintaining the baseline lumbar lordosis after surgery has been stressed in the literature. However, there are few objective data to evaluate whether postoperative hypolordosis in the instrumented segments can increase the likelihood of junctional breakdown. METHODS: Segmental lordosis was measured on preoperative standing, intraoperative prone, and postoperative standing radiographs. In human cadaveric spines, a lordosis loss of up to 8 degrees was created across L4-S1 using calibrated transpedicular devices. Specimens were tested in extension and under axial loading in the upright posture. RESULTS: In patients who underwent L4-S1 fusions, the lordosis within the fusion decreased by 10 degrees intraoperatively and after surgery. Postoperative lordosis in the proximal (L2-L3 and L3-L4) segments increased by 2 degrees each, as compared with the preoperative measures. Hypolordosis in the instrumented segments increased the load across the posterior transpedicular devices, the posterior shear force, and the lamina strain at the adjacent level. CONCLUSIONS: Hypolordosis in the instrumented segments caused increased loading of the posterior column of the adjacent segments. These biomechanical effects may explain the degenerative changes at the junctional level that have been observed as long-term consequences of lumbar fusion.

Load-carrying capacity of the human cervical spine in compression is increased under a follower load.

STUDY DESIGN: An experimental approach was used to test human cadaveric cervical spine specimens. OBJECTIVE: To assess the response of the cervical spine to a compressive follower load applied along a path that approximates the tangent to the curve of the cervical spine. SUMMARY OF BACKGROUND DATA: The compressive load on the human cervical spine is estimated to range from 120 to 1200 N during activities of daily living. Ex vivo experiments show it buckles at approximately 10 N. Differences between the estimated in vivo loads and the ex vivo load-carrying capacity have not been satisfactorily explained. METHODS: A new experimental technique was developed for applying a compressive follower load of physiologic magnitudes up to 250 N. The experimental technique applied loads that minimized the internal shear forces and bending moments, loading the specimen in nearly pure compression. RESULTS: A compressive vertical load applied in the neutral and forward-flexed postures caused large changes in cervical lordosis at small load magnitudes. The specimen collapsed in extension or flexion at a load of less than 40 N. In sharp contrast, the cervical spine supported a load of up to 250 N without damage or instability in both the sagittal and frontal planes when the load path was tangential to the spinal curve. The cervical spine was significantly less flexible under a compressive follower load compared with the hypermobility demonstrated under a compressive vertical load (P < 0.05). CONCLUSION: The load-carrying capacity of the ligamentous cervical spine sharply increased under a compressive follower load. This experiment explains how a whole cervical spine can be lordotic and yet withstand the large compressive loads estimated in vivo without damage or instability.

Animal models of spinal cord contusion injuries.

BACKGROUND AND PURPOSE: Traumatic spinal cord injury causes initial mechanical disruption of tissue, leading to a complex secondary sequence of pathophysiologic changes and neurologic impairment. These sequelae depend on the impact force delivered to the spinal cord at the time of injury. Successful clinical evaluation of the efficacy of any therapeutic regimen depends on the reliability and reproducibility of an experimental animal model. We describe a trauma device and the biomechanical parameters required to induce severe or moderate spinal cord contusion injury in cats and rats. METHODS: Recovery after injury was determined by behavioral, electrophysiologic, and histologic evaluations. RESULTS: Behavioral and electrophysiologic tests after injury clearly identified the experimental groups. A stable severe paraplegic state (defined as 6 months for cats and 8 weeks for rats), without evidence of behavioral or electrophysiologic recovery, was induced by a 65-Newton (N) load for cats and a 35-N load for rats. Moderate spinal cord contusion injury, from which cats and rats partially recovered after approximately 3 months and 4 weeks, respectively, was induced by a 45- and 25-N load, respectively. CONCLUSION: Use of these injury conditions provides reliable animal models for studies designed to evaluate potential therapeutic regimens for spinal cord injury.

A follower load increases the load-carrying capacity of the lumbar spine in compression.

STUDY DESIGN: An experimental approach was used to test human cadaveric spine specimens. OBJECTIVE: To assess the response of the whole lumbar spine to a compressive follower load whose path approximates the tangent to the curve of the lumbar spine. SUMMARY OF BACKGROUND DATA: Compression on the lumbar spine is 1000 N for standing and walking and is higher during lifting. Ex vivo experiments show it buckles at 80-100 N. Differences between maximum ex vivo and in vivo loads have not been satisfactorily explained. METHODS: A new experimental technique was developed for applying a compressive follower load of physiologic magnitudes up to 1200 N. The experimental technique applied loads that minimized the internal shear forces and bending moments, made the resultant internal force compressive, and caused the load path to approximate the tangent to the curve of the lumbar spine. RESULTS: A compressive vertical load applied in the neutral lordotic and forward-flexed postures caused large changes in lumbar lordosis at small load magnitudes. The specimen approached its extension or flexion limits at a vertical load of 100 N. In sharp contrast, the lumbar spine supported a load of up to 1200 N without damage or instability when the load path was tangent to the spinal curve. CONCLUSIONS: Until this study, an experimental technique for applying compressive loads of in vivo magnitudes to the whole lumbar spine was unavailable. The load-carrying capacity of the lumbar spine sharply increased under a compressive follower load, as long as the load path remained within a small range around the centers of rotation of the lumbar segments. The follower load path provides an explanation of how the whole lumbar spine can be lordotic and yet resist large compressive loads. This study may have implications for determining the role of trunk muscles in stabilizing the lumbar spine.

Human growth hormone transgene expression increases the biomechanical structural properties of mouse vertebrae.

STUDY DESIGN: Caudal vertebrae were obtained from male and female mice from two transgenic lines expressing an erythroid-specific human growth hormone transgene construct, and gender-matched, age-matched, non-transgenic control mice. OBJECTIVE: To characterize the effect of human growth hormone transgene expression on the biomechanical structural properties of caudal vertebrae in compression. SUMMARY OF BACKGROUND DATA: An increase in trabecular and cortical bone deposition caused by erythroid-specific human growth hormone transgene expression was demonstrated previously. METHODS: Compression tests were performed on individual caudal vertebrae (Ca4, Ca5, Ca6) obtained from male and female mice from two transgenic lines (TG420 and TG450) and nontransgenic control mice. Two age groups were evaluated: 12 weeks old and 6 months old. The data were used to obtain axial stiffness, maximum load, and energy to failure. RESULTS: Vertebrae from male TG420 transgenic mice produced significantly larger values for maximum load, energy to failure, and axial stiffness at both 12 weeks and 6 months in comparison with their age-matched non-transgenic male controls. Vertebrae from female TG420 transgenic mice produced similar responses at 6 months. Vertebrae from male TG450 transgenic mice showed significant increases in maximum load and energy to failure at 6 months. In general, the biomechanical properties of vertebrae were significantly larger in the 6-month age group than in the 12-week age group, and this increase was significantly greater in the transgenic mice than in the gender-matched control mice during the same time span. This process was also influenced by transgenic genotype and gender. CONCLUSIONS: Erythroid-specific production of human growth hormone in transgenic mice resulted in significant increases in biomechanical properties of their caudal vertebrae in compression. The changes in the biomechanical properties were influenced by genotype, age, and gender.

Walking pattern of midfoot and ankle disarticulation amputees.

Measurements of the vertical component of ground reaction force (ORF) and dynamic center of pressure (COP) were recorded for five subjects with midfoot level amputations and six with Syme's ankle disarticulation amputations. All of the subjects underwent amputation surgery as a consequence of peripheral vascular disease and diabetes. GRF measurement was accomplished with the F-Scan system (Tekscan, Boston, MA). Each group exhibited a consistent, reproducible pattern of gait. Subjects with Syme's ankle disarticulation initiated initial loading response, i.e., heel strike, with a concentration of GRF in the center of the anatomic heel. COP progressed along the midline to the center of the anatomic forefoot, where GRF was concentrated at push-off. Midfoot amputees initiated loading at the lateral-posterior heel. COP progressed medially to the midline, where it progressed distally to the level of the distal residual limb (proximal metatarsal metaphyses). It then shifted medially under the base of the first metatarsal, where a small concentration of GRF occurred at push-off, similar to the normal foot. These findings explain the decreased magnitude of propulsion seen in midfoot level amputees and may explain the seemingly paradoxical increased metabolic cost of walking observed in midfoot amputees as compared with Syme's ankle disarticulation amputees.

The role of the interosseous membrane and triangular fibrocartilage complex in forearm stability.

This study investigated the relative roles of the interosseous membrane (IOM) and triangular fibrocartilage complex (TFCC) in the transmission of force from the hand to the humerus. Our findings suggest a spectrum of forearm destabilizing injuries. The intact radius abutting the capitellum provides the primary restraint to proximal migration of the radius. After radial head excision, up to 7 mm of proximal radial migration can occur under axial compression. If the TFCC or the IOM alone is disrupted, little alteration in load or displacement is evident. When both the midportion of the IOM and TFCC are incompetent, however, further proximal radial migration occurs, the radial stump abuts the humerus, and load is shifted back to the radial column. These data suggest that the central portion of the IOM is the crucial structural subdivision within the IOM acting as a restraint to proximal radial migration. The TFCC also resists proximal radial migration and participates in load transfer. We propose that clinical migration of the radius under an axial load greater than 7 mm implies disruption of both the midportion of the IOM and TFCC.