Helen P. Morrison

Bio: Helen P. Morrison is an academic researcher. The author has contributed to research in topics: Intervertebral disk & Neutral spine. The author has an hindex of 2, co-authored 2 publications receiving 798 citations.

Mechanical Initiation of Intervertebral Disc Degeneration

Abstract: volves gross structural disruption as well as cell-mediated changes in matrix composition, but there is little evidence concerning which comes first. Comparatively minor damage to a vertebral body is known to decompress the adjacent discs, and this may adversely affect both structure and cell function in the disc. Methods. In this study, 38 cadaveric lumbar motion segments (mean age, 51 years) were subjected to complex mechanical loading to simulate typical activities in vivo while the distribution of compressive stress in the disc matrix was measured using a pressure transducer mounted in a needle 1.3 mm in diameter. “Stress profiles” were repeated after a controlled compressive overload injury had reduced motion segment height by approximately 1%. Moderate repetitive loading, appropriate for the simulation of light manual labor, then was applied to the damaged specimens for approximately 4 hours, and stress profilometry was repeated a third time. Discs then were sectioned and photographed. Results. Endplate damage reduced pressure in the adjacent nucleus pulposus by 25% 6 27% and generated peaks of compressive stress in the anulus, usually posteriorly to the nucleus. Discs 50 to 70 years of age were affected the most. Repetitive loading further decompressed the nucleus and intensified stress concentrations in the anulus, especially in simulated lordotic postures. Sagittal plane sections of 15 of the discs showed an inwardly collapsing anulus in 9 discs, extreme outward bulging of the anulus in 11 discs, and complete radial fissures in 2 discs, 1 of which allowed posterior migration of nucleus pulposus. Comparisons with the results from tissue culture experiments indicated that the observed changes in matrix compressive stress would inhibit disc cell metabolism throughout the disc, and could lead to progressive deterioration of the matrix. Conclusions. Minor damage to a vertebral body end

Effects of backward bending on lumbar intervertebral discs. Relevance to physical therapy treatments for low back pain.

Abstract: Study design Mechanical testing of cadaveric motion segments. Objectives To test the hypothesis that backward bending of the lumbar spine can reduce compressive stresses within lumbar intervertebral discs. Summary of background data Lumbar extension affects the distribution of compressive stress inside normal cadaveric discs, but little is known about its effect on mechanically disrupted and degenerated discs. Methods Nineteen lumbar motion segments (mean donor age, 48 years) were subjected to complex mechanical loading to simulate the following postures: moderate lumbar flexion, 2 degrees of extension, 4 degrees of extension, and the neutral position (no bending). The distribution of compressive stress within the disc matrix was measured in each posture by pulling a miniature pressure transducer along the midsagittal diameter of the disc. Stress profiles were repeated after a mechanical treatment that was intended to simulate severe disc degeneration in vivo. Results The "degeneration" treatment reduced pressure in the nucleus pulposus and generated stress concentrations within the anulus, in a manner similar to that found in severely degenerated discs in vivo. When all discs were considered together, 2 degrees of extension increased the maximum compressive stress within the posterior anulus by an average of 16%, compared with the neutral posture. The size of localized stress peaks within the posterior anulus was increased by 43% (P = 0.02). In 4 degrees of extension, changes observed between 0 degree and 2 degrees were usually exaggerated. In contrast, moderate flexion tended to equalize the distribution of compressive stress. In 7 of the 19 discs, 2 degrees of lumbar extension decreased maximum compressive stress in the posterior anulus relative to the neutral posture by up to 40%. Linear regression showed that lumbar extension tended to reduce stresses in the posterior anulus in those discs that exhibited the lowest compressive stresses in the neutral posture (P = 0.003; R2 = 41%). Conclusions The posterior anulus can be stress shielded by the neural arch in extended postures, but the effect is variable. This may explain why extension exercises can relieve low back pain in some patients.

What is intervertebral disc degeneration, and what causes it?

Abstract: and Introduction Abstract Study Design: Review and reinterpretation of existing literature. Objective: To suggest how intervertebral disc degeneration might be distinguished from the physiologic processes of growth, aging, healing, and adaptive remodeling. Summary of Background Data: The research literature concerning disc degeneration is particularly diverse, and there are no accepted definitions to guide biomedical research, or medicolegal practice. Definitions: The process of disc degeneration is an aberrant, cell-mediated response to progressive structural failure. A degenerate disc is one with structural failure combined with accelerated or advanced signs of aging. Early degenerative changes should refer to accelerated age-related changes in a structurally intact disc. Degenerative disc disease should be applied to a degenerate disc that is also painful. Justification: Structural defects such as endplate fracture, radial fissures, and herniation are easily detected, unambiguous markers of impaired disc function. They are not inevitable with age and are more closely related to pain than any other feature of aging discs. Structural failure is irreversible because adult discs have limited healing potential. It also progresses by physical and biologic mechanisms, and, therefore, is a suitable marker for a degenerative process. Biologic progression occurs because structural failure uncouples the local mechanical environment of disc cells from the overall loading of the disc, so that disc cell responses can be inappropriate or aberrant. Animal models confirm that cell-mediated changes always follow structural failure caused by trauma. This definition of disc degeneration simplifies the issue of causality: excessive mechanical loading disrupts a disc's structure and precipitates a cascade of cell-mediated responses, leading to further disruption. Underlying causes of disc degeneration include genetic inheritance, age, inadequate metabolite transport, and loading history, all of which can weaken discs to such an extent that structural failure occurs during the activities of daily living. The other closely related definitions help to distinguish between degenerate and injured discs, and between discs that are and are not painful.

Role of cytokines in intervertebral disc degeneration: pain and disc content.

Abstract: Degeneration of the intervertebral discs (IVDs) is a major contributor to back, neck and radicular pain. IVD degeneration is characterized by increases in levels of the proinflammatory cytokines TNF, IL-1α, IL-1β, IL-6 and IL-17 secreted by the IVD cells; these cytokines promote extracellular matrix degradation, chemokine production and changes in IVD cell phenotype. The resulting imbalance in catabolic and anabolic responses leads to the degeneration of IVD tissues, as well as disc herniation and radicular pain. The release of chemokines from degenerating discs promotes the infiltration and activation of immune cells, further amplifying the inflammatory cascade. Leukocyte migration into the IVD is accompanied by the appearance of microvasculature tissue and nerve fibres. Furthermore, neurogenic factors, generated by both disc and immune cells, induce expression of pain-associated cation channels in the dorsal root ganglion. Depolarization of these ion channels is likely to promote discogenic and radicular pain, and reinforce the cytokine-mediated degenerative cascade. Taken together, an enhanced understanding of the contribution of cytokines and immune cells to these catabolic, angiogenic and nociceptive processes could provide new targets for the treatment of symptomatic disc disease. In this Review, the role of key inflammatory cytokines during each of the individual phases of degenerative disc disease, as well as the outcomes of major clinical studies aimed at blocking cytokine function, are discussed.

Prevalence and pattern of lumbar magnetic resonance imaging changes in a population study of one thousand forty-three individuals.

Abstract: Study design A cross-sectional population study of magnetic resonance imaging (MRI) changes. OBJECTIVE.: To examine the pattern and prevalence of lumbar spine MRI changes within a southern Chinese population and their relationship with back pain. Summary of background data Previous studies on MRI changes and back pain have used populations of asymptomatic individuals or patients presenting with back pain and sciatica. Thus, the prevalence and pattern of intervertebral disc degeneration within the population is not known. Methods Lumbar spine MRIs were obtained in 1043 volunteers between 18 to 55 years of age. MRI changes including disc degeneration, herniation, anular tears (HIZ), and Schmorl's nodes were noted by 2 independent observers. Differences were settled by consensus. Disc degeneration was graded using Schneiderman's classification, and a total score (DDD score) was calculated by the summation of the Schneiderman's score for each lumbar level. A K-mean clustering program was used to group individuals into different patterns of degeneration. Results Forty percent of individuals under 30 years of age had lumbar intervertebral disc degeneration (LDD), the prevalence of LDD increasing progressively to over 90% by 50 to 55 years of age. There was a positive correlation between the DDD score and low back pain. L5-S1 and L4-L5 were the most commonly affected levels. Apart from the usual patterns of degeneration, some uncommon patterns of degeneration were identified, comprising of subjects with skip level lesions (intervening normal levels) and isolated upper or mid lumbar degeneration. Conclusion LDD is common, and its incidence increases with age. In a population setting, there is a significant association of LDD on MRI with back pain.

Biomechanics of back pain

Abstract: This paper offers a mechanistic account of back pain which attempts to incorporate all of the most important recent advances in spinal research. Anatomical and pain-provocation studies show that severe and chronic back pain most often originates in the lumbar intervertebral discs, the apophyseal joints, and the sacroiliac joints. Psychosocial factors influence many aspects of back pain behaviour but they are not important determinants of who will experience back pain in the first place. Back pain is closely (but not invariably) associated with structural pathology such as intervertebral disc prolapse and endplate fractures, although age-related biochemical changes such as those revealed by a 'dark disc' on MRI have little clinical relevance. All features of structural pathology (including disc prolapse) can be re-created in cadaveric specimens by severe or repetitive mechanical loading, with a combination of bending and compression being particularly harmful to the spine. Structural disruption alters the mechanical environment of disc cells in a manner that leads to cell-mediated degenerative changes, and animal experiments confirm that surgical disruption of a disc is followed by widespread disc degeneration. Some people are more vulnerable to spinal degeneration than others, largely because of their genetic inheritance. Age-related biochemical changes and loading history can also affect tissue vulnerability. Finally the concept of 'functional pathology' is introduced, according to which, back pain can arise because postural habits generate painful stress concentrations within innervated tissues, even though the stresses are not high enough to cause physical disruption.