Aim:To determine if patients with coronal plane deformity in the lumbar spine have a higher grade of lumbar spine subtype compared to controls.Method:This was a retrospective case/control study bas...

Elderly vertebrae frequently develop an "anterior wedge" deformity as a result of fracture and creep mechanisms. Injecting cement into a damaged vertebral body (vertebroplasty) is known to help restore its shape and stiffness. We now hypothesise that vertebroplasty is also effective in reducing subsequent creep deformations. Twenty-eight spine specimens, comprising three complete vertebrae and the intervening discs, were obtained from cadavers aged 67-92 years. Each specimen was subjected to increasingly-severe compressive loading until one of its vertebrae was fractured, and the damaged vertebral body was then treated by vertebroplasty. Before and after fracture, and again after vertebroplasty, each specimen was subjected to a static compressive force of 1kN for 1h while elastic and creep deformations were measured in the anterior, middle and posterior regions of each adjacent vertebral body cortex, using a 2D MacReflex optical tracking system. After fracture, creep in the anterior and central regions of the vertebral body cortex increased from an average 4513 and 885 microstrains, respectively, to 54,107 and 34,378 microstrains (both increases: P<0.001). Elastic strains increased by a comparable amount. Vertebroplasty reduced creep in the anterior and central cortex by 61% (P=0.006) and 66% (P=0.017) respectively. Elastic strains were reduced by less than half this amount. Results suggest that the beneficial effects of vertebroplasty on the vertebral body continue long after the post-operative radiographs. Injected cement not only helps to restore vertebral shape and elastic properties, but also reduces subsequent creep deformation of the damaged vertebra.

Vertebral fracture is the most common type of osteoporotic fracture and is associated with significant health and economic costs. In recent years, patient-specific vertebral body finite element (FE) models based on quantitative computed tomography (QCT) have been developed to investigate vertebral strength. Current models consider the vertebral body alone with loading restricted to pure compression. However, osteoporotic vertebral fractures are often associated with forward bending which concentrates loading on the anterior vertebral body leading to the typical wedge fractures observed in life. The purpose of this study is to compare the vertebral strengths derived from FE models with those measured experimentally under forward bending conditions. Sixteen cadaveric spinal units, each consisting of two vertebrae and an intervertebral disc (IVD), were scanned using clinical QCT. Specimens were then potted in dental cement and loaded on a materials testing machine to generate a wedge fracture. Custom codes developed and validated previously in MATLAB were used to generate FE models with an 8-node voxel mesh: one of the vertebral body alone (”VB”), and another of the vertebral body with posterior elements intact (”VB w/PE”). Artificial padding was generated at the inferior and superior endplates to represent the dental cement and facilitate the simulation of the forward-bending condition. Transverseisotropic linear-elastic material properties were assigned to the vertebra, and the FE model was solved using ANSYS. Vertebral strength was defined in two different ways; i) the load that caused maximum Von Mises strain exceeding a yield strain of 0.78% (VM_ER), and ii) the load that caused maximum Von Mises stress exceeding a yield stress (VM_SR) in contiguous elements that occupied at least 244.14 mm3. Linear regression was used to compare FE- and experiment-derived vertebral strength data. This showed that there was a positive correlation between the strength measured experimentally and the strength derived from both FE models; VM_SR (r2= 0.78 VB, r2= 0.75 VB w/PE), VM_ER (r2= 0.75 VB, r2= 0.68 VB w/PE). The results of this study indicate that a simple vertebral body FE model under forward-bending conditions may be sufficient for the estimation of vertebral strength.

Study Design: Mechanical study on cadaver motion segments. Objective: To determine if high gradients of compressive stress within the intervertebral disc are associated with progressive disc degeneration. Summary of Background Data : Mechanical loading can initiate disc degeneration, but may be unimportant in disease progression because degenerative changes cause the disc to be increasingly “stress-shielded” by the neural arch. However, the most typical feature of advanced disc degeneration (delamination and collapse of the annulus) may not depend on absolute values of compressive stress, but on gradients of compressive stress which act to shear annulus lamellae. Methods: 191 motion segments (T8-9 to L5-S1) were dissected from 42 cadavers aged 19-92 yrs. Each was subjected to approximately 1 kN compression, while intradiscal stresses were measured by pulling a pressure transducer along the disc’s mid-sagittal diameter. “Stress gradients” in the annulus were quantified as the average rate of increase in compressive stress (MPa/mm) between the nucleus and the region of maximum stress in the anterior or posterior annulus. Measurements were repeated before and after creep loading, and in simulated flexed and erect postures. Disc degeneration was assessed macroscopically on a scale of 1 to 4.

The belief that an intervertebral disc must degenerate before it can herniate has clinical and medicolegal significance, but lacks scientific validity. We hypothesised that tissue changes in herniated discs differ from those in discs that degenerate without herniation. Tissues were obtained at surgery from 21 herniated discs and 11 non-herniated discs of similar degeneration as assessed by the Pfirrmann grade. Thin sections were graded histologically, and certain features were quantified using immunofluorescence combined with confocal microscopy and image analysis. Herniated and degenerated tissues were compared separately for each tissue type: nucleus, inner annulus and outer annulus. Herniated tissues showed significantly greater proteoglycan loss (outer annulus), neovascularisation (annulus), innervation (annulus), cellularity/inflammation (annulus) and expression of matrix-degrading enzymes (inner annulus) than degenerated discs. No significant differences were seen in the nucleus tissue from herniated and degenerated discs. Degenerative changes start in the nucleus, so it seems unlikely that advanced degeneration caused herniation in 21 of these 32 discs. On the contrary, specific changes in the annulus can be interpreted as the consequences of herniation, when disruption allows local swelling, proteoglycan loss, and the ingrowth of blood vessels, nerves and inflammatory cells. In conclusion, it should not be assumed that degenerative changes always precede disc herniation. Cite this article: Bone Joint J 2013;95-B:1127-33.

Introduction Discogenic back pain is closely associated with fissures in the annulus fibrosus,1,2 and with ingrowth of nerves and blood vessels.3 We test the hypothesis that annulus fissures encourage such ingrowth. Materials and Methods Three complementary studies were performed. Firstly, 15 cadaveric disks that contained an annulus fissure were subjected to 1 kN compression, while a miniature pressure transducer was pulled through the disk to obtain distributions of matrix compressive stress perpendicular to the fissure axis. Secondly, safranin O staining was used to evaluate focal loss of proteoglycans from within annulus fissures in 25 surgically removed disk samples. A novel image analysis method was used to quantify proteoglycan concentration along a line profile that was perpendicular to the fissure axis. Thirdly, in 21 elderly cadaveric disks, proteoglycan and water concentration were measured biochemically in disrupted regions of annulus containing one or more fissures, and in adjacent intact regions. The second experiment had good spatial resolution but was unable to quantify proteoglycan loss precisely, whereas the third experiment had poor spatial resolution but allowed precise quantification of proteoglycan loss. Results Reductions in compressive stress within annulus fissures averaged 36>46%, and were greater than average at the fissure axis. Stress reductions were greater in degenerated disks, and were inversely related to nucleus pressure (R2 = 0.47, p < 0.005). Safranin O stain intensity indicated that proteoglycan concentration was typically reduced by 40% at a distance of 600 µm from the fissure axis, and the width of the proteoglycan-depleted zone increased with age (R2 = 0.29, p = 0.006) and with general proteoglycan loss (R2 = 0.32, p < 0.005). Disrupted regions of annulus contained 36 to 54% less proteoglycans than adjacent intact regions from the same disks, although water content was reduced only slightly ( p > 0.05). Conclusion Annulus fissures provide a low-pressure microenvironment, especially if there is insufficient fluid pressure in the disk nucleus to tension the annulus and prevent fissures from “opening up.” A disk's collagen network is disrupted within an annulus fissure, and this disruption, combined with low pressure, permits local tissue swelling even though some of the proteoglycans are lost in the process. Blood vessels are attracted into this microenvironment by a combination of low pressure (which is less likely to collapse hollow blood vessels than a high pressure) and by a low concentration of proteoglycans, which are known to inhibit blood vessel4 and nerve5 ingrowth. Finally, nerve ingrowth into annulus fissures is facilitated by the presence of blood vessels, and by the low proteoglycan concentration. In this way, an annulus fissure in a degenerated intervertebral disk comprises a distinct microenvironment that is mechanically and chemically conducive to nerve and blood vessel ingrowth. This can explain the close association between annulus fissures and suspected discogenic back pain. I confirm having declared any potential conflict of interest for all authors listed on this abstract Yes Disclosure of Interest None declared Videman T, Nurminen M. The occurrence of anular tears and their relation to lifetime back pain history: a cadaveric study using barium sulfate discography. Spine 2004;29(23):2668–2676 Peng B, Wu W, Hou S, Li P, Zhang C, Yang Y. The pathogenesis of discogenic low back pain. Journal of Bone and Joint Surgery British Volume 2005;87(1):62–67 Freemont AJ, Peacock TE, Goupille P, Hoyland JA, O'Brien J, Jayson MI. Nerve ingrowth into diseased intervertebral disk in chronic back pain. Lancet. 1997;350(9072):178–1781 Johnson WE, Caterson B, Eisenstein SM, Roberts S. Human intervertebral disk aggrecan inhibits endothelial cell adhesion and cell migration in vitro. Spine 2005;30(10):1139–1147 Johnson WE, Caterson B, Eisenstein SM, Hynds DL, Snow DM, Roberts S. Human intervertebral disk aggrecan inhibits nerve growth in vitro. Arthritis and Rheumatism 2002;46(10):2658–2664

Introduction The “weak link” in the thoracolumbar spine is the vertebral body endplate, which is easily damaged in compression. Vertebral endplate fracture can decompress the adjacent intervertebral disk and allow the annulus to collapse inwards.1 This can lead to disk degeneration in animal models2 and in patients.3 However, population MRI studies indicate that endplate damage is strongly associated with adjacent disk degeneration only in the upper lumbar spine.4 We hypothesize that lower lumbar disks are less affected by endplate fracture. Materials and Methods Mechanical experiments were performed on cadaveric “motion segments” comprising two vertebrae and the intervening disk and ligaments. Each specimen was compressed to failure, until the elastic limit was just exceeded, and measurements of intradiscal (nucleus) pressure were compared before and after failure, at a reference load of 1 kN. Pressure measurements were made with a strain-gauged pressure transducer side-mounted near the tip of a 1.3-mm-diameter catheter. Multiple linear regression (SPSS v16) was used to analyze factors that influence the fall in nucleus pressure. Results A total of 143 specimens aged 19 to 96 years (mean 67 years) were tested, from all spinal levels between T7-8 and L5-S1. Radiographs confirmed the endplate as the site of compressive failure, and damage caused an average specimen height loss of 1.9 mm (STD 0.9 mm). The resulting fall in nucleus pressure averaged 59% (STD 37%), and increased with age and (pre-existing) disk degeneration ( p < 0.001). Apart from specimen height loss, the greatest determinant of nucleus decompression was spinal level, with decompression averaging 70 to 90% in the lower thoracic spine, and falling linearly from T11-12 to just 6% at L5-S1. Spinal level explained 28% of the variance in nucleus decompression ( p < 0.001). Conclusion The relatively small effects observed in lower lumbar disks may be due to the relatively large height and anteroposterior diameter of the nucleus at L4-5 and L5-S1: a larger nucleus volume would lead to a smaller drop in pressure for the same amount of endplate damage. Results suggest that compressive overload may well initiate disk degeneration in the upper lumbar and thoracic spine, explaining the strong relationship between disk degeneration and Schmorl's nodes at these levels.4 At L4-5 and L5-S1, however, another mechanism is likely to be important: these lower lumbar disks are particularly susceptible to radial fissure formation, leading to disk prolapse, in response to high loading in bending.1 The concept of two distinct mechanisms of disc degeneration (‘annulus-driven’ in the lower lumbar spine, and “endplate-driven” at higher spinal levels) may explain why the genetic influence in disk degeneration varies with spinal level.5 I confirm having declared any potential conflict of interest for all authors listed on this abstract Yes Disclosure of Interest None declared Adams MA, Freeman BJ, Morrison HP, Nelson IW, Dolan P. Mechanical initiation of intervertebral disc degeneration. Spine 2000;25(13):1625–1636 Holm S, Holm AK, Ekstrom L, Karladani A, Hansson T. Experimental disc degeneration due to endplate injury. Journal of Spinal Disorder and Techniques 2004;17(1):64–71 Kerttula LI, Serlo WS, Tervonen OA, Paakko EL, Vanharanta HV. Post-traumatic findings of the spine after earlier vertebral fracture in young patients: clinical and MRI study. Spine 2000;25(9):1104–1108 Mok FP, Samartzis D, Karppinen J, Luk KD, Fong DY, Cheung KM. ISSLS prize winner: Prevalence, determinants, and association of Schmorl nodes of the lumbar spine with disc degeneration: a population-based study of 2449 individuals. Spine (Phila Pa 1976) 2010;35(21):1944–1952 Battie MC, Videman T, Levalahti E, Gill K, Kaprio J. Genetic and environmental effects on disc degeneration by phenotype and spinal level: a multivariate twin study. Spine 2008;33(25):2801–2808

Introduction: Vertebral fractures in the elderly are often assumed to be "osteoporotic" and require anti-osteoporosis therapy. However, some of these fractures may represent traumatic injuries to vertebrae that have comparatively normal bone mineral density (BMD). We hypothesize that radiographic appearances can be used to differentiate between "osteoporotic" fractures of vertebrae with low BMD and strength, and "traumatic" fractures of vertebrae with normal BMD and strength.Methods: 73 cadaveric specimens (each comprising two vertebrae with the intervening intervertebral disc and ligaments) were obtained from donors aged 42 to 91 (mean 74) years. Areal BMD was measured in the lateral projection for each vertebral body, using DXA. Each specimen was secured in metal cups containing dental plaster, and compressed to failure at 3 mm/s on a computer-controlled materials testing machine. Mechanical failure was detected by a reduction in the gradient of the load-deformation curve. Compressive deformation for each specimen was limited to 4 mm in order to prevent gross destruction of the vertebra. Radiographs, obtained before and after mechanical loading, were assessed by an experienced radiologist (GJ) who was blinded to BMD and mechanical data. The algorithm-based qualitative method (ABQ) was used to assign each specimen to two possible outcomes: no discernible fracture of either vertebra, or fracture. The latter were further classified into specimens with osteoporotic fracture and those with traumatic fracture, by applying additional criteria for differential diagnosis. The relationship of failure load to BMD was tested using correlation. BMD and failure load for the three diagnostic outcomes were compared using one-way analysis of variance (ANOVA).Results: Failure load was proportional to BMD (R=0.63, p<0.001). "Osteoporotic," "traumatic" and "no discernible" fractures were reported in 16,26 and 31 specimens respectively. "Traumatic" fracture specimens had higher BMD and failed at higher loads than "osteoporotic" fracture specimens (p<0.05).Conclusions: Some vertebral fractures in the elderly may be traumatic rather than osteoporotic in origin. Our radiological criteria help to differentiate between them. (C) 2010 Elsevier Inc. All rights reserved.

Introduction: Cranial endplates of human vertebrae are injured more often than caudal, in both young and elderly spines. We hypothesise that cranial endplates are inherently vulnerable to compressive loading because of structural asymmetries in the vertebrae.Methods: Sixty-two "motion segments" (two vertebrae and the intervening disc and ligaments) were obtained post-mortem from thirty-five human spines (17F/18M, age 48-92 yrs, all spinal levels from T8-9 to L4-5). Specimens were compressed to failure while positioned in 2-6 degrees of flexion, and the resulting damage characterised from radiographs and at dissection. 2 mm-thick slices of 94 vertebral bodies (at least one from each motion segment) were cut in the mid-sagittal plane, and in a para-sagittal plane through the pedicles. Microradiographs of the slices were Subjected to image analysis to determine the thickness of each endplate at 10 locations. Optical density of the endplates and adjacent trabecular bone was also measured. Measurements obtained in cranial and caudal regions, and in mid-sagittal and pedicle slices, were compared using repeated measures ANOVA with age, level and gender included as between-subject factors. Linear regression was used to determine significant predictors of compressive strength (failure stress).Results: Fracture affected the cranial endplate in 55/62 specimens. Cranial endplates were thinner than caudal (p=0.003) by 14% and 11% on average, in mid-sagittal and pedicle slices respectively. Caudal but not cranial endplates were thicket at lower spinal levels (p=0.01). Optical density of trabecular bone adjacent to the endplates was 6% lower cranially than caudally (p=0.004), and the average optical density of trabecular bone in mid-sagittal slices was 10% lower in women than in men (p=0.025). Vertebral yield stress (mean 2.22 MPa, SD 0.77 MPa) was best predicted by the density of trabecular bone underlying the cranial endplate of the mid-sagittal slice of the fractured vertebra (r(2)=0.67, p=0.0006).Conclusions: When vertebrae are compressed naturally by adjacent intervertebral discs, cranial endplates usually fail before caudal endplates because they are thinner and supported by less dense trabecular bone. (C) 2008 Elsevier Inc. All rights reserved.

The management of pelvic sarcoma is challenging and goals of surgery are adequate oncologic local control, maintenance of optimum function with good quality of life.We have evaluated the results of internal hemipelvecotmy including age, type of resection, reconstruction, radiotherapy or chemotherapy. From 2010 to 2016, 23 patients with pelvic bone tumors (13 with Ewing's sarcoma, 9 with Osteosarcoma, 1 with chondrosarcoma) were treated by surgical resection.The mean follow-up was 18 months (0.5–5) years. In 12 patients reconstruction was performed and 11 were without reconstruction. A total of 3 patients (13%) had an infection develop at a mean follow up of 1 month. Surgical debridement’s and antibiotics in three patients led to complete recovery. One patient had sciatic nerve injury.One patient had injury to femoral vein; was treated with femoral vein reconstruction. Two patients (9%) developed a local recurrence and were treated with best supportive treatment. Distal pulmonary metastases were seen in four patients and treated with supportive treatment. Five-year disease-specific survival rates of all patients were 83%. The mean functional MSTS score was 18(14–24).Proper selection of patients, preopertive planning and wide surgical margins with reconstruction provides good functional outcomes following internal hemipelvectomy. The surgical site infection and flap necrosis tend to be minor complication and can be managed leading to optimal outcomes and justifies the need for this complex surgery. The oncological and functional outcome after internal hemipelvectomy suggests that it’s an effective method for treatment of patients with pelvic sarcomas.

Study Design. Cadaveric motion segment experiment.Objective. To show how two physical aspects of disc degeneration (dehydration and endplate disruption) contribute to spinal instability.Summary of Background Data. The origins of spinal instability and its associations with back pain are uncertain. Methods. Twenty-one cadaveric thoracolumbar motion segments aged 48 to 90 years were secured in cups of dental plaster and loaded simultaneously in bending and compression to simulate full flexion, extension, and lateral bending movements. Vertebral movements, recorded using a two-dimensional "MacReflex" motion analysis system, were analyzed to calculate neutral zone (NZ), range of motion (ROM), bending stiffness (BS), horizontal translational movements, and the location of the center of rotation (COR). Intradiscal "stresses" were measured by pulling a miniature pressure transducer through the disc along its midsagittal diameter. All experiments were repeated after each of two treatments, which simulated physical aspects of disc degeneration: creep loading to dehydrate the disc and compressive overload to disrupt the endplate. Results were analyzed using ANOVA and linear regression.Results. Motion segment height was reduced by 1.0 (SD 0.3) mm during creep and by a further 1.7 (0.6) mm after endplate disruption. In flexion and lateral bending, the combined treatments increased NZ and ROM by 89% to 298%, and increased the "instability index" (NZ/ROM) by 43% to 61%. Translational movements increased by 58% to 86%, whereas BS decreased by 42% to 48%. In extension, ROM and NZ were little affected, although the COR moved closer to the apophyseal joints. Measures of instability increased most in lateral bending, and following endplate disruption. Stress concentrations in the posterior anulus fibrosus increased markedly after endplate disruption.Conclusions. Two physical aspects of disc degeneration (dehydration and endplate disruption) cause marked segmental instability. Back pain associated with instability may be attributable to stress concentrations in degenerated discs.

STUDY DESIGN:Cadaver motion segments were used to evaluate the effects of vertebroplasty on spinal loading following vertebral fracture.OBJECTIVES:To determine if vertebroplasty reverses fracture-induced changes in the distribution of compressive stress in cadaver motion segments.SUMMARY OF BACKGROUND DATA:Vertebroplasty involves reinforcement of vertebrae by injection of cement and is now being used increasingly to treat osteoporotic vertebral fractures. However, its effects on spinal load-bearing are largely unknown. We hypothesize that vertebroplasty, following vertebral fracture, helps to equalize stress acting on the intervertebral disc and adjacent vertebral bodies.METHODS:Nineteen cadaver thoracolumbar motion segments (age 64-90 years) were induced to fracture by compressive overload. Specimens were then subjected to vertebroplasty, and subsequently creep loaded for 1 hour at 1.5 kN. The compressive stress acting on the intervertebral disc was measured before and after fracture, after vertebroplasty, and after creep, by pulling a pressure transducer mounted in a 1.3-mm needle across the disc's midsagittal diameter. This information was then used to calculate neural arch load-bearing. At each time point, measurements were also made of compressive stiffness.RESULTS:Vertebral fracture reduced motion segment compressive stiffness, decompressed the adjacent nucleus, increased stress concentrations in the posterior anulus, and increased neural arch load-bearing, all by a significant amount. Vertebroplasty partially, but significantly, reversed all of these fracture-induced changes.CONCLUSIONS:Vertebroplasty reduces stress concentrations in the anulus and neural arch resulting in a more even distribution of compressive stress on the intervertebral disc and adjacent vertebral bodies.

We validate a technique for measuring neural arch load-bearing in cadaveric spines, and use it to test the hypothesis that such load-bearing rises to high levels in old and degenerated spines. Fifty-nine cadaveric lumbar motion segments, aged 19–92 yr, were subjected to compressive creep loading to reduce intervertebral disc water content and height to in vivo levels. The distribution of compressive "stress" within the disc was then measured by pulling a miniature pressure transducer, side-mounted in a 1.3 mm-diameter needle, along its mid-sagittal diameter. During these measurements, the motion segment was subjected to a compressive load of 2 kN, and positioned in 2° of extension to simulate erect standing. Measurements of compressive "stress" were integrated over disc area, and this force subtracted from the applied 2 kN to give the force resisted by the neural arch. An empirical calibration factor was applied to normalise results from each disc to values obtained under conditions when all of the compressive force could be assumed to pass through the disc. Disc degeneration was graded macroscopically on a scale of 1–4. Validation tests showed that calculated values of disc loading were proportional to actual applied load (r2>0.96) and predicted it with errors of 2–8%. Neural arch load-bearing in non-degenerated specimens was generally less than 20%, but averaged 49% for specimens aged over 70 yr. Multiple regression showed that neural arch load bearing (%)=14.4×disc degeneration score+0.46×age−35. These results indicate a substantial shift in vertebral load-bearing with increasing age and degeneration.

Study Design. Mechanical testing of cadaveric lumbar motion segments.Objectives. To test the hypothesis that degenerative changes in the intervertebral discs can influence loading of the anterior vertebral body in a manner that makes it vulnerable to fracture.Summary of Background Data. Measurements of systemic bone loss do not fully explain the patterns of osteoporotic vertebral fractures.Methods. Thirty-three cadaveric lumbar motion segments ( aged 19 - 82 years) were subjected to 2 kN of compressive loading while positioned to simulate habitual erect standing postures and forwards bending. Intradiscal stresses were measured in each posture by pulling a miniature pressure transducer along the midsagittal diameter of the disc. "Stress profiles" were then integrated over area to calculate the force acting on the anterior and posterior halves of the vertebral body. These forces were subtracted from the applied 2 kN to determine the compressive force on the neural arch.Results. In motion segments with nondegenerated discs, < 5% of the compressive force was resisted by the neural arch, and forces on the vertebral body were always distributed evenly, irrespective of posture. However, with severely degenerated discs, neural arch load-bearing increased to 40% in the erect posture, and the compressive force on the vertebral body was concentrated anteriorly in forwards bending, and posteriorly in erect posture.Conclusions. Severe disc degeneration causes the anterior vertebral body to be stress-shielded during the usual erect posture, and yet severely loaded whenever the spine is flexed. This could help to explain why this region is frequently the site of osteoporotic fracture, and why forward bending movements often precipitate the injury.

4 subjects performed repeated eccentric contractions with leg extensors during prolonged downhill walking (−25% gradient) at 6.44 km · h−1 until collapse due to muscle weakness (range of exercise duration 29 to 40 min). During the exercise oxygen uptake rose progressively from ∼45% of the previously determined \(\dot V_{O_{2max} } \) at 10 min to ∼65% at the end of the exercise. Following the exercise there was an immediate, significant, and sustained reduction in maximal voluntary isometric contraction, and short term (anaerobic) power output measured concentrically on an isokinetic ergometer. These reductions in muscle function persisted for 96 hours post exercise, and were reflected by significant reductions in the tension generated at low frequency (20 Hz) relative to higher frequency (50 Hz) percutaneous stimulation of the quadriceps. All four subjects showed an increase in plasma levels of creatine kinase post eccentric exercise. Performing concentric contractions by walking uphill for one hour at a significantly greater metabolic cost failed to induce comparable reductions in muscle function. These results provide evidence for the consequences of prolonged eccentric work upon dynamic function which complements earlier reports of structural, enzymatic, and static function changes.

Study Design. A longitudinal study of spinal position sense in 27 patients with mild ankylosing spondylitis (AS).Objectives. To test the hypothesis that disease progression in AS is associated with deficits in spinal position sense.Summary of Background Data. AS is a progressive disease that frequently leads to deterioration in spinal posture. The cause of postural change is unknown. However, pathologic involvement of spinal entheses that contain proprioceptive afferents suggests that impaired proprioception may play a role. This study investigates whether longitudinal changes in posture and other measures of disease progression are associated with deficits in spinal position sense in patients with mild AS.Methods. Position sense was assessed using an electromagnetic movement analysis system, the 3-Space Fastrak, to determine the absolute error in reproducing flexed and upright spinal postures. Measurements were taken from sensors at T1, T7, L1, and S2 and repeated following a mean time interval of 13.7 months. Assessments of posture, disease activity, and function were also made on both occasions.Results. Patients showed a significant increase in disease activity, and losses in spinal mobility, over time. However, no significant changes in spinal posture or position sense were found. Repositioning errors in flexed postures were less than or equal to 3.50degrees at the first testing session and less than or equal to 3.77degrees at follow-up. Corresponding values for upright postures were less than or equal to 2.71degrees and less than or equal to 2.25degrees, respectively.Conclusions. Spinal position sense appears unaffected by disease progression in patients with mild AS. Longer follow-ups may help determine any association between disease-related postural change and spinal position sense in AS.