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PubMed1998

Protection of mouse photoreceptors by survival factors in retinal degenerations.

PURPOSE: To examine the protective effect of a number of survival factors on degenerating photoreceptors in mutant mice with naturally occurring inherited retinal degenerations, including retinal degeneration (rd/rd), retinal degeneration slow (rds/rds), nervous (nr/nr), and Purkinje cell degeneration (pcd/pcd), in three different forms of mutant rhodopsin transgenic mice and in light damage in albino mice. METHODS: Various survival factors were injected intravitreally into one eye of mice at or soon after the beginning of photoreceptor degeneration, with the opposite eye serving as the control, and the eyes were examined histologically at later ages. The survival factors included brain-derived neurotrophic factor (BDNF), neurotrophin-3, neurotrophin-4, ciliary neurotrophic factor (CNTF), Axokine (a mutein of CNTF), leukemia inhibitory factor, basic fibroblast growth factor, and nerve growth factor and insulin-like growth factor II, either alone or in various combinations. RESULTS: Photoreceptor degeneration was slowed in rd/rd and nr/nr mutant mice and in Q344ter mutant rhodopsin mice by certain forms of CNTF; the degeneration in Q344ter mice was slowed by Axokine and by leukemia inhibitory factor; and the degeneration in a few nr/nr mice was slowed by BDNF. The other agents were ineffective in these mice, and none of the agents were effective in the other mutants and other mutant rhodopsin transgenic mice. However, light damage experiments that compared agent effectiveness in albino mice versus rats suggested a significant delivery problem with the very small mouse eye, thereby making the interpretation of negative findings equivocal in mutant mice. Basic fibroblast growth factor failed to protect the mouse retina from the damaging effects of constant light, whereas it showed a strong protective effect in the rat, indicating an important species difference. CONCLUSIONS: The slowing of degeneration in the rd/rd and Q344ter mutant mice demonstrated that intraocularly injected survival factors can protect photoreceptors from degenerating in animal models with the same or similar genetic defects as those in human inherited retinal degenerations.

Animals↗
PubMed1983

Projections of nucleus caudalis and spinal cord to brainstem and diencephalon in the hedgehog (Erinaceus europaeus and Paraechinus aethiopicus): a degeneration study.

In the light of hypotheses related to the evolution of pain-carrying systems in mammals, terminal projection fields in brainstem and diencephalon of efferents of nucleus caudalis (NC) of the spinal trigeminal complex and spinal cord were determined in hedgehog by using Nauta-Gygax and Fink-Heimer silver techniques for degeneration. Unilateral NC lesions resulted in medullary degeneration in the ventral portion of NC contralaterally and bilaterally in cuneate nucleus (CU) and reticular formation. Pontine degeneration was noted ipsilaterally in medial (PBM) and lateral (PBL) parabrachial, facial motor (VII), and interpolar, oral, and main sensory trigeminal nuclei; degeneration in reticular formation was bilateral. Midbrain degeneration was seen bilaterally in caudal superior colliculus (SC), inferior colliculus (IC), periaqueductal gray, and tegmentum. In thalamus, projections to ventroposterior nucleus (VP) were contralateral and concentrated in a crescent extending along the lateral one-third-to-one-half and ventral border of the nucleus. Bilateral degeneration fields were noted in a dorsomedial sector of the "ventral nuclear field," posterior complex (PO), and mediodorsal nucleus (MD), the degeneration always heavier contralaterally in these nuclei. Sparse degeneration was noted in the medial most portions of the medial geniculate nuclei bordering PO and VP. In rostral diencephalon, bilateral degeneration was traced from the inferior thalamic peduncle to the lateral hypothalamic area (LH). Unilateral spinal cord lesions made between C7 and T1 vertebrae resulted in medullary degeneration in NC contralaterally, ipsilaterally in CU and lateral cuneate nucleus, and bilaterally in gracile nucleus, inferior olivary complex, and reticular formation. Pontine degeneration was limited to ipsilateral PBL and bilaterally to VII. Midbrain degeneration was found bilaterally in IC, SC, nucleus sagulum, and tegmentum; a minor projection was noted in interpeduncular nucleus. In thalamus, projections were confined to ipsilateral PO and zona incerta. In rostral diencephalon bilateral fields were noted in LH. NC terminations in PO and VP parallel results of research in hedgehogs on thalamic projections of the dorsal column nuclei (Jane and Schroeder, '71), and particularly the location in VP of most cells responsive to stimulation of the face (Erickson et al., '67). This suggests that somatic input from NC, some of which may be pain-specific, reaches thalamic areas, a portion of whose neurons are characterized as polymodal and at least partially convergent for somatotopy. These results are consistent with the thesis that specific sensory thalamic nuclei evolved from a diffuse sensory region. Response properties of neurons in the dorsomedial portion of the ventral nuclear field, an area which are also received NC efferents, are not known. Last, NC projections to MD and LH implicate the role of "limbic" aspects of nociception.

Animals↗
PubMed1989

Degeneration patterns in the chicken central nervous system induced by ingestion of the organophosphorus delayed neurotoxin tri-ortho-tolyl phosphate. A silver impregnation study.

Exposure to certain organophosphorus compounds results in a neurological condition known as organophosphorus-induced delayed neurotoxicity (OPIDN). OPIDN is characterized clinically by an initial post-exposure delay period of 8-14 days after which signs of progressively developing ataxia and paralysis of the hindlimbs are observed. Although several studies have reported the presence of degeneration induced by organophosphorus delayed neurotoxins in specific central nervous system (CNS) structures, none have systematically examined CNS changes seen in the most frequently studied animal model for OPIDN--the domestic fowl. In the present study, we assessed the location and extent of anterograde degeneration in the chicken CNS following exposure to tri-o-tolyl phosphate (TOTP). All birds were dosed with 500 mg TOTP/kg body weight and killed after post-exposure periods of 1, 2, 3, or 4 weeks. The brains and spinal cords were processed with Fink-Heimer and Nissl stains. In the spinal cord, axon degeneration was noted in the fasciculus gracilis at cervical levels two weeks after exposure to TOTP. At 3 weeks, degeneration was also present in the cervical part of the dorsal spinocerebellar tract, in the lumbar part of the medial pontine-spinal tract, and in lamina VII in the lumbar ventral horn. In the medulla, moderate amounts of terminal and preterminal degeneration appeared at two weeks in the lateral vestibular, gracile, external cuneate, and lateral cervical nuclei. Lesser amounts of degeneration were noted in the solitary, inferior olivary, and raphae nuclei, in the medial, descending and lateral vestibular nuclei, and in the lateral paragigantocellular, gigantocellular, and lateral reticular nuclei. Fiber degeneration was also present in the medullary portions of the dorsal and ventral spinocerebellar tracts and spinal lemniscus. In the cerebellum, moderate amounts of terminal degeneration appeared in the deep cerebellar nuclei at one week while moderate mossy fiber degeneration was first noted in the granular layers of cerebellar folia I-V at 3 weeks. These results indicate (1) that, in the CNS, axonal and terminal degeneration resulting from TOTP intoxication appears to be confined to the spinal cord, medulla and cerebellum, (2) that the time of onset of degeneration in different fiber tracts and nuclei ranges from one to three weeks post-exposure, and (3) that the delay in the appearance of clinical signs of OPIDN is consistent with the delayed onset of degeneration in many of the affected CNS fiber systems.

Animals↗
PubMed2006

Oocyte degeneration after intracytoplasmic sperm injection: a multivariate analysis to assess its importance as a laboratory or clinical marker.

OBJECTIVE: Oocyte degeneration has historically been associated with the intracytoplasmic (ICSI) technique. We sought to determine whether oocyte degeneration rates were associated with the technician performing the procedure, the baseline characteristics of the patient, and/or ovarian stimulation variables. We also evaluated whether the degeneration rate could serve as a surrogate marker for implantation potential. DESIGN: Cohort study. SETTING: Academic medical center. PATIENT(S): Couples undergoing ICSI. INTERVENTION(S): Six thousand six hundred fifty-three injected oocytes were analyzed to determine whether the degeneration rate was technician dependent. Two hundred thirty first-entry down-regulated cycles were examined to identify predictors associated with oocyte degeneration. Multivariate analyses were performed using generalized linear model routines. MAIN OUTCOME MEASURE(S): Oocyte degeneration rates and implantation rates. RESULT(S): Neither the ICSI technician nor the stripping technician was associated with the oocyte degeneration rate. However, the day 3 FSH, number of mature oocytes retrieved, and E2 levels on the day of hCG were significant independent predictors of degeneration rate. Physician-adjustable ovarian stimulation variables were not associated with the degeneration rate. The degeneration rate did not appear to be associated with the implantation rate. CONCLUSION(S): These data suggest that oocyte degeneration is not technician or physician dependent. Degeneration is likely a function of the inherent oocyte quality in women who underwent ovarian stimulation. However, the remaining cohort of retrieved oocytes appears to be unaffected by virtue of an uncompromised implantation rate.

Adult↗
PubMed1990

Discs degenerate before facets.

The purpose of this study was to determine the relationship between facet joint osteoarthritis and disc degeneration in subjects in whom both MRI and CT scans had been obtained. The MRI scans were used to determine disc degeneration, the CT scans to determine facet joint osteoarthritis. It was hypothesized that disc degeneration would sometimes occur without the presence of facet joint osteoarthritis, but that facet joint osteoarthritis would only occur in the presence of disc degeneration. Sixty-eight sets of scans were included and 330 discs and 390 facet joints were evaluated. There were 144 degenerated discs and 41 levels with facet osteoarthritis. Disc degeneration without facet osteoarthritis was found at 108 levels, while all but one of 41 levels with facet degeneration also had disc degeneration. That one exception occurred in a patient with advanced Paget's disease. Disc degeneration and facet osteoarthritis both were found to increase with increasing age. There was no difference between women and men. Degeneration at the L4-5 and L5-S1 levels was significantly more prevalent than at the L3-4 levels, while degeneration at the L3-4 level was significantly more common than at the L1-2 and L2-3 levels. We conclude that disc degeneration occurs before facet joint osteoarthritis, which may be secondary to mechanical changes in the loading of the facet joints.

Adolescent↗
PubMed2005

The role of interleukin-1 in the pathogenesis of human intervertebral disc degeneration.

In this study, we investigated the hypotheses that in human intervertebral disc (IVD) degeneration there is local production of the cytokine IL-1, and that this locally produced cytokine can induce the cellular and matrix changes of IVD degeneration. Immunohistochemistry was used to localize five members of the IL-1 family (IL-1alpha, IL-1beta, IL-1Ra (IL-1 receptor antagonist), IL-1RI (IL-1 receptor, type I), and ICE (IL-1beta-converting enzyme)) in non-degenerate and degenerate human IVDs. In addition, cells derived from non-degenerate and degenerate human IVDs were challenged with IL-1 agonists and the response was investigated using real-time PCR for a number of matrix-degrading enzymes, matrix proteins, and members of the IL-1 family. This study has shown that native disc cells from non-degenerate and degenerate discs produced the IL-1 agonists, antagonist, the active receptor, and IL-1beta-converting enzyme. In addition, immunopositivity for these proteins, with the exception of IL-1Ra, increased with severity of degeneration. We have also shown that IL-1 treatment of human IVD cells resulted in increased gene expression for the matrix-degrading enzymes (MMP 3 (matrix metalloproteinase 3), MMP 13 (matrix metalloproteinase 13), and ADAMTS-4 (a disintegrin and metalloproteinase with thrombospondin motifs)) and a decrease in the gene expression for matrix genes (aggrecan, collagen II, collagen I, and SOX6). In conclusion we have shown that IL-1 is produced in the degenerate IVD. It is synthesized by native disc cells, and treatment of human disc cells with IL-1 induces an imbalance between catabolic and anabolic events, responses that represent the changes seen during disc degeneration. Therefore, inhibiting IL-1 could be an important therapeutic target for preventing and reversing disc degeneration.

Adult↗
PubMed1981

The temporo-spatial course of degeneration after cutting cortico-cortical connections in adult rats.

Adult albino rats received callosotomies or lesions in the paracingular cortex. Between 12 h and 3 months after injury the structure and topography of the degeneration products were studied by light- and electron-microscopy. The degeneration process was quantified by television-image analysis applied to sections prepared according to a new technique that stains reliably degenerating terminals and lysosomes (Gallyas et al. 1980). All types of cortico-cortical connections show a multiphasic degeneration process: During a precursor stage a small number of dense bodies and mitochondrial granules are stained. These and the few early degenerating axon terminals are much more diffusely distributed than the large number of terminals that degenerate during the following period. The terminal degeneration shows a biphasic time course. One maximum appears at 2-7 days post operation, which corresponds to the well known direct consequence of axotomy. The second peak at 10-20 days post operation could be caused by transneuronal reorganization of the cortical connectivity. Terminal degeneration always begins along the borders between cortical regions and areas, but it may change its laminar and columnar distribution pattern during the second phase. The degeneration products that are phagocytosed by astrocytes seem to be removed by intracellular transport to their perivascular endfeet. The degeneration process ends with fiber degeneration which, especially in laminae I and VI, may form a separate peak after 20 days or more.

Animals↗
PubMed1990

Transneuronal degeneration in the midbrain central gray following chemical lesions in the ventromedial nucleus: a qualitative and quantitative analysis.

In the preceding experiments with electrolytic lesions of the ventromedial nucleus of the hypothalamus, we showed pre- and postsynaptic degeneration in the midbrain central gray of the rat. The postsynaptic degeneration seen may indicate a transneuronal effect of the ventromedial nucleus on the midbrain central gray. Electrolytic lesions, however, destroy afferent endings and fibers in passage, so that the postsynaptic degeneration seen in the midbrain central gray may be due to retrograde degeneration of midbrain central gray afferents to the ventromedial nucleus or due to degeneration of fibers in passage. In order to distinguish among these possibilities, chemical, i.e. kainic acid and N-methyl aspartate, lesions were made in the ventromedial nucleus and the ultrastructure of the midbrain central gray and cerebral cortex was examined at various intervals following the lesions. Both of these excitotoxins have been shown to destroy neurons, sparing afferent terminals and fibers in passage. Animals receiving kainic acid lesions in the right ventromedial nucleus were allowed to survive for one week, and animals receiving N-methyl aspartate lesions in the right ventromedial nucleus were permitted to survive for four, eight, and 20 days. Midbrain central gray tissue of unlesioned animals served as a control for both kainic acid and N-methyl aspartate lesions. In addition, other control animals received injections of the same amount of N-methyl aspartate in the right parietal cortex and were permitted to survive for four and eight days. For each of the above injection and survival conditions, the left cortex and subdivisions of the midbrain central gray were removed and processed for electron microscopy. Animals receiving ventromedial hypothalamic lesions with both kainic acid and N-methyl aspartate showed signs of pre- and postsynaptic degeneration. A quantitative analysis (General Linear Model Procedure) of degeneration was performed on the cortex and midbrain central gray of animals receiving N-methyl aspartate lesions in the ventromedial nucleus and cortex, and several parameters were measured. Animals receiving ventromedial hypothalamic lesions and surviving for eight and 20 days show significantly higher ratios of degenerating presynaptic elements to total presynaptic elements, degenerating postsynaptic elements to total postsynaptic elements, and degenerating total elements to total elements, in the midbrain central gray than in the cortex. Furthermore, the ratio of degenerating postsynaptic elements to total postsynaptic elements is larger than the other ratios.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

Wlds protection distinguishes axon degeneration following injury from naturally occurring developmental pruning.

Axon pruning by degeneration remodels exuberant axonal connections and is widely required for the development of proper circuitry in the nervous system from insects to mammals. Developmental axon degeneration morphologically resembles injury-induced Wallerian degeneration, suggesting similar underlying mechanisms. As previously reported for mice, we show that Wlds protein substantially delays Wallerian degeneration in flies. Surprisingly, Wlds has no effect on naturally occurring developmental axon degeneration in flies or mice, although it protects against injury-induced degeneration of the same axons at the same developmental age. By contrast, the ubiquitin-proteasome system is intrinsically required for both developmental and injury-induced axon degeneration. We also show that the glial cell surface receptor Draper is required for efficient clearance of axon fragments during developmental axon degeneration, similar to its function in injury-induced degeneration. Thus, mechanistically, naturally occurring developmental axon pruning by degeneration and injury-induced axon degeneration differ significantly in early steps, but may converge onto a common execution pathway.

Animals↗
PubMed2005

[Color Doppler imaging of the retrobulbar circulation in non-exudative and exudative age-related macular degeneration].

PURPOSE: To study ocular perfusion in the ophthalmic artery, central retinal artery, nasal and temporal posterior ciliary : arteries in non-exudative and exudative age-related macular degeneration. MATERIAL AND METHODS: Twenty five subjects with non-exudative age-related macular degeneration were compared to twenty five subjects with exudative age-related macular degeneration and to twenty five age-matched control subjects. Color Doppler imaging measured peak systolic velocity (PSV) and end diastolic velocity (EDV) in the ophthalmic artery, central retinal artery, nasal and temporal posterior ciliary arteries of one eye. The resistivity index (RI) and the pulsatility index (PI) were calculated. RESULTS: There were statistically significant differences between: subjects with non-exudative age-related macular degeneration and subjects with exudative age-related macular degeneration in EDV, RI and PI in the ophthalmic artery and PSV in the temporal posterior ciliary artery, subjects with non-exudative age-related macular degeneration and control subjects in RI in central retinal artery, subjects with non-exudative age-related macular degeneration and control subjects in RI and PI in nasal posterior ciliary artery, subjects with exudative age-related macular degeneration and control subjects in PI in nasal posterior ciliary artery. CONCLUSIONS: The study results showed reduced ocular blood flow in patients with non-exudative age-related macular degeneration compared to patients with exudative age-related macular degeneration and to control subjects. The higher RI in central retinal artery in non-exudative age-related macular degeneration compared to control subjects, suggest there may be a more generalized perfusion abnormality beyond the choroid.

Case-Control Studies↗
PubMed1997

Mutations resulting in transient and localized degeneration in the developing zebrafish brain.

In a large-scale mutagenesis screen in the zebrafish, Danio rerio, we have identified a heterogeneous group of 30 recessive, embryonic lethal mutations characterized by degeneration in the developing central nervous system that is either transient or initially localized to one area of the brain. Transient degeneration is defined as abnormal cell death occurring during a restricted period of development. Following degeneration, the affected structures do not appear to regenerate. In each case degeneration is identified after somitogenesis is complete and is not associated with visually identified patterning defects. These 30 mutations, forming 21 complementation groups, have been classified into four phenotypic groups: group 1, transient degeneration (13 mutations); group 2, spreading degeneration, early onset, in which degeneration is initially confined to the optic tectum but subsequently spreads to other areas of the central nervous system (7 mutations); group 3, late-onset degeneration, initially identified after 4 days (6 mutations); and group 4, degeneration with abnormal pigmentation (4 mutations). Although apoptotic cells are seen in the retina and tectum of all mutants, the distribution, temporal progression, and severity of degeneration vary between mutations. Several mutations also show pleiotropic effects, with degeneration involving extraneural structures including the pharyngeal arches and pectoral fins. We discuss some of the pathways important for cell survival in the nervous system and suggest that these mutations will provide entry points for identifying genes that affect the survival of restricted neural populations.

Animals↗
PubMed2005

Validity and interobserver agreement of a new radiographic grading system for intervertebral disc degeneration: Part I. Lumbar spine.

Many different radiographic grading systems for disc degeneration are described in literature. However, only a few of them are tested for interobserver agreement and none for validity. Furthermore, most of them are based on a subjective terminology. The aim of this study, therefore, is to combine these systems to a new one in which all subjective terms are replaced by more objective ones and to test this new system for validity and interobserver agreement. Since lumbar and cervical discs need to be graded differently, this study was divided into the present Part I for the lumbar and a Part II for the cervical spine. The new radiographic grading system covers the three variables "Height Loss", "Osteophyte Formation" and "Diffuse Sclerosis". On lateral and postero-anterior radiographs, each of these three variables first has to be graded individually. Then, the "Overall Degree of Degeneration" is assigned on a four-point scale from 0 (no degeneration) to 3 (severe degeneration). For validation, the radiographic degrees of degeneration of 44 lumbar discs were compared to the respective macroscopic ones, which were defined as "real" degrees of degeneration. The agreement between observers with different levels of experience was determined using the radiographs of 84 lumbar discs. Agreement was quantified using quadratic weighted Kappa coefficients (Kappa) with 95% confidence limits (95% CL). The validation of the new radiographic grading system revealed a substantial agreement between the radiographic and the "real" macroscopic overall degree of degeneration (Kappa=0.714, 95% CL: 0.587-0.841). The radiographic grades, however, tended to be slightly lower than the "real" ones. The interobserver agreement was substantial for all the three variables and for the overall degree of degeneration (Kappa=0.787, 95% CL: 0.702-0.872). However, the inexperienced observer tended to assign slightly lower degrees of degeneration than the experienced one. In conclusion, we believe that the new radiographic grading system is an almost objective, valid and reliable tool to quantify the degree of degeneration of individual lumbar intervertebral discs. However, the user should always remember that the "real" degree of degeneration tends to be underestimated and that slight differences between the ratings of observers with different levels of experience have to be expected.

Adult↗
PubMed2006

Validity and interobserver agreement of a new radiographic grading system for intervertebral disc degeneration: Part II. Cervical spine.

A new radiographic grading system for a more objective assessment of lumbar intervertebral disc degeneration has been described and tested in Part I of this study. The aim of the present Part II of the study was to adapt this system to the cervical spine, and to test it for validity and interobserver agreement. Some modifications of the grading system described in Part I were necessary to make it applicable to the cervical spine. Its basic structure, however, stayed untouched. The three variables "Height Loss", "Osteophyte Formation" and "Diffuse Sclerosis" first have to be graded individually. Then, the "Overall Degree of Degeneration" is assigned on a four-point scale from 0 (no degeneration) to 3 (severe degeneration). For validation, the radiographic degrees of degeneration of 28 cervical discs were compared to the respective macroscopic ones, which were defined as "real" degrees of degeneration. The interobserver agreement was determined between one experienced and one unexperienced observer using the radiographs of 57 cervical discs. Quadratic weighted Kappa coefficients (kappa) with 95% confidence limits (95% CL) were used for statistical evaluation. The validation of the new version of the radiographic grading system showed a moderate agreement with the "real", macroscopic overall degree of degeneration (kappa=0.599, 95% CL 0.421-0.786). In 64% of all discs the "real" overall degree of degeneration was underestimated but never overestimated. This underestimation, however, was much less pronounced and the Kappa coefficients were significantly higher for the three variables: Height Loss, Osteophyte Formation, and Diffuse Sclerosis separately. The agreement between the radiographic ratings of the experienced and the unexperienced observer was substantial for the overall degree of degeneration (kappa=0.688, 95% CL 0.580-0.796), almost perfect for the variable, Height Loss, moderate for Osteophyte Formation and fair for Diffuse Sclerosis. In conclusion, we believe that the new version of the radiographic grading system is a sufficiently valid and reliable tool to quantify the degree of degeneration of individual cervical intervertebral discs. In comparison to the version for the lumbar spine described in Part I, however, a slightly higher tendency to underestimate the "real" overall degree of degeneration and somewhat higher interobserver differences have to be expected.

Aged↗
PubMedDate not supplied

Effects of aging and spinal degeneration on mechanical properties of lumbar supraspinous and interspinous ligaments.

BACKGROUND CONTEXT: The effects of aging and spinal degeneration on the mechanical properties of spinal ligaments are still unknown, although there have been several studies demonstrating those of normal spinal ligaments. PURPOSE: To investigate the mechanical properties of the human posterior spinal ligaments in human lumbar spine, and their relation to age and spinal degeneration parameters. STUDY DESIGN/SETTING: Destructive uniaxial tensile tests were performed on the human supraspinous and interspinous ligaments at L4-5 level. Their mechanical properties were compared with age and spinal degeneration using several imaging modalities. PATIENT SAMPLE: Twenty-four patients with lumbar degenerative diseases on whom posterior surgeries were performed, with the age ranging from 18 to 85 years. OUTCOME MEASURES: The ultimate load and elastic stiffness as structural properties, the degree of disc degeneration, range of segmental motion, the disc height, disc space narrowing ratio and degree of facet degeneration as the parameters of spinal degeneration. METHODS: Twenty-four supraspinous and interspinous ligaments at the L4-5 level were obtained from posterior surgeries of patients with lumbar degenerative disease. The mechanical tests of bone-ligament-bone complexes were performed in a uniaxial tensile fashion with a specially designed clamp device. The ultimate load and elastic stiffness were calculated as structural properties. The degree of disc degeneration, range of segmental motion, the disc height, disc space narrowing ratio and degree of facet degeneration were examined by using radiographs, computed tomography and magnetic resonance imaging. RESULTS: The average and SD value of ultimate load, elastic stiffness, tensile strength and elastic modulus were 203+/-102.9 N, 60.6+/-36.7 N/mm, 1.2+/-0.6 Mpa and 3.3+/-2.1 Mpa, respectively. A significant negative correlation was found between age and tensile strength (p= 0.02). The specimens with facet degeneration showed lower values in tensile strength and elastic modulus than those without facet degeneration (p<0.04). However, no correlation was found between disc-related parameters and tensile strength. CONCLUSIONS: The mechanical strength of human lumbar posterior spinal ligaments decreases with age and facet degeneration, particularly in the ligament substance.

Adolescent↗
PubMed1995

Degeneration and aging affect the tensile behavior of human lumbar anulus fibrosus.

STUDY DESIGN: Samples of human lumbar (L3-L4) anulus fibrosus from four different anatomic sites (anterior outer, posterolateral inner), ranging from normal to severely degenerate, were studied in uniaxial tension and measured for water content. OBJECTIVES: To evaluate the effects of aging and degeneration on the tensile properties and hydration of the anulus fibrosus in a site-specific manner. The relationship between hydration and parameters of the tensile behavior were investigated. SUMMARY OF BACKGROUND DATA: Degeneration and aging have been shown to be related to dramatic changes in the composition and structure of the anulus fibrosus. The associated changes in the tensile, compressive, and shear properties of the anulus fibrosus have not been documented. Numerical studies using finite element models have attempted to simulate the degenerative process by incorporating estimated mechanical properties meant to represent the degenerate anulus fibrosus. Their results present findings that suggest that altered material properties of the anulus fibrosus affect the mechanics of the entire intervertebral disc. METHODS: Samples of human lumbar anulus fibrosus were classified by grade of degeneration based on a morphologic grading scheme. Multiple layer anulus specimens from four sites in the disc were tested in uniaxial tension under quasistatic conditions in a physiologic saline bath. The tensile modules, Poisson's ratio, failure stress and strain, the strain energy density to failure, and the corresponding hydration were determined for each sample. RESULTS: The Poisson's ratio, failure stress, and strain energy density of the anulus fibrosus were found to be affected significantly by degeneration, with some evidence of a sensitivity of the tensile modulus to grade of degeneration. All material properties were found to exhibit a significant and greater dependence on site within the disc than on degenerative grade. Weak correlations between aging and the Poisson's ratio and strain energy density were observed. Water content of anulus fibrosus tissue was not affected by degeneration or aging, although correlations with tensile properties were observed. CONCLUSIONS: The dramatic changes in morphology, composition, and structure that occur in anulus fibrosus with aging and degeneration are accompanied by specific variations in the tensile properties, which were generally small in magnitude. Position of the anulus fibrosus within the intervertebral disc, particularly in the radial direction, appeared to be the most important variable affecting anulus fibrosus tensile properties. This dependence on position did not change with either aging or degeneration. Results from the present study may be useful in future finite element models to assess how altered material properties of the anulus fibrosus during degeneration and aging may affect the mechanics of the entire intervertebral disc.

Adolescent↗
PubMed2003

A cross-sectional study correlating degeneration of the cervical spine with disability and pain in United kingdom patients.

STUDY DESIGN: A prospective cross-sectional study was conducted. OBJECTIVE: To determine the relation between degeneration of all the joints in the cervical spine, and to identify the effects of litigation on pain and disability levels in trauma and nontrauma patients. SUMMARY OF BACKGROUND DATA: The link between spinal degeneration and patient symptoms remains controversial. Two recent similar studies present conflicting results concerning the association between spinal degeneration and symptomatology. These two studies, performed in different countries, did not consider the impact of impending litigation on self-reported pain and disability levels. The role of the uncovertebral and facet articulations has hitherto not been investigated. METHODS: Radiographic and questionnaire data from 180 consecutive patients with neck pain were collected. Neck pain severity was measured using two time-dependent scales. All patients completed the Neck Disability Index (NDI) and questions about chronicity, etiology, and associated litigation. The radiographs were evaluated for the number of levels of degeneration and the severity of degeneration in the discs as well as the uncovertebral and facet articulations. RESULTS: In this study, 71 patients (40.57%) reported neck pain as a result of injury. However, only 5.1% had associated litigation. There was no statistically significant difference in pain severity or disability levels between the patients with and those without cervical degeneration. According to the findings, the number of levels of cervical degeneration and the severity of degeneration in the discs, facets, and uncovertebral joints are not related to the levels of pain and disability. Patients reporting neck pain caused by injury had a tendency (P = 0.055) to more pain during the preceding week and significantly more disability (P < 0.001). Significant differences included pain intensity (P < 0.025), reading (P < 0.001), headaches (P < 0.025), ability to drive (P < 0.01), and concentration (P < 0.01). Women reported significantly more pain (P < 0.01) and disability (P < 0.001) than men, but did not have more degeneration in any of the joints. CONCLUSIONS: In patients with neck pain, there is no difference in reported pain and disability levels between those with and those without evidence of cervical spine degeneration. Patients whose neck pain is the result of trauma report significantly more pain and disability than nontrauma patients. This is not because of more spinal degeneration or overriding litigation issues.

Activities of Daily Living↗
PubMed2005

A slowly progressive and reproducible animal model of intervertebral disc degeneration characterized by MRI, X-ray, and histology.

STUDY DESIGN: The progression of intervertebral disc degeneration following anterolateral "stab" of adult rabbit lumbar discs by 16-gauge hypodermic needle to a limited (5-mm) depth was studied for up to 24 weeks using magnetic resonance imaging, radiograph, and histologic outcome measures. OBJECTIVES: To develop a slowly progressive, reproducible rabbit model of intervertebral disc degeneration suitable for studying pathogenesis and pathophysiology of intervertebral disc degeneration and testing safety and efficacy of novel approaches to the treatment of intervertebral disc degeneration (e.g., growth factors, gene therapy, cell therapy, and tissue engineering). SUMMARY OF BACKGROUND DATA: Numerous animal models of intervertebral disc degeneration have been proposed in the literature, each with attendant advantages and disadvantages. The classic "stab model," involving full-thickness stab of anterior anulus fibrosus of adult rabbit lumbar discs by a number 11 scalpel blade, appears to produce changes in certain biochemical and histologic outcome measures that are similar to changes seen in human intervertebral disc degeneration. However, the immediate herniation of nucleus pulposus on full-thickness stab renders this model less suitable for 1) studying effects of less precipitous changes in nucleus pulposus and anulus fibrosus that may be important in the onset and progression of intervertebral disc degeneration and 2) testing novel therapeutic approaches that target the processes of early intervertebral disc degeneration. METHODS: The L2-L3, L3-L4, and L4-L5 lumbar intervertebral discs of 18 skeletally mature female New Zealand White rabbits were stabbed by 16-gauge hypodermic needle to a depth of 5 mm in the left anterolateral anulus fibrosus. Serial magnetic resonance imaging scans of the stabbed discs and intact L1-L2 and L5-L6 control discs were performed at 3, 6, 12, and 24 weeks post surgery and compared with preoperative magnetic resonance images. Supplemental radiograph and histologic analyses were performed. RESULTS: The stabbed discs exhibited a progressive decrease in "magnetic resonance imaging index" (the product of nucleus pulposus area and signal intensity from T2-weighted midsagittal plane images) starting at 3 weeks post stab and continuing through 24 weeks, with no evidence of spontaneous recovery or reversal of magnetic resonance imaging changes. Radiograph findings included early osteophyte formation by 6 weeks post stab and extensive, bridging osteophytes by 24 weeks. Histologic analysis revealed progressive loss of notochordal cells from the nucleus pulposus, filling of the nucleus pulposus space with fibrocartilage, and derangement of anulus fibrosus. CONCLUSIONS: Stabbing the anterolateral anulus fibrosus of adult rabbit lumbar discs with a 16-gauge hypodermic needle to a limited (5-mm) depth results in a number of slowly progressive and reproducible magnetic resonance imaging, radiograph, and histologic changes over 24 weeks that show a similarity to changes seen in human intervertebral disc degeneration. This model would appear suitable for studying pathogenesis and pathophysiology of intervertebral disc degeneration and testing safety and efficacy of novel treatments of intervertebral disc degeneration.

Animals↗
PubMed2004

Adjacent segment degeneration in the lumbar spine.

BACKGROUND: A primary concern after posterior lumbar spine arthrodesis is the potential for adjacent segment degeneration cephalad or caudad to the fusion segment. There is controversy regarding the subsequent degeneration of adjacent segments, and we are aware of no long-term studies that have analyzed both cephalad and caudad degeneration following posterior arthrodesis. A retrospective investigation was performed to determine the rates of degeneration and survival of the motion segments adjacent to the site of a posterior lumbar fusion. METHODS: Two hundred and fifteen patients who had undergone posterior lumbar arthrodesis were included in this study. The study group included 126 female patients and eighty-nine male patients. The average duration of follow-up was 6.7 years. Radiographs were analyzed with regard to arthritic degeneration at the adjacent levels both preoperatively and at the time of the last follow-up visit. Disc spaces were graded on a 4-point arthritic degeneration scale. Correlation analysis was used to determine the contribution of independent variables to the rate of degeneration. Survivorship analysis was performed to describe the degeneration of the adjacent motion segments. RESULTS: Fifty-nine (27.4%) of the 215 patients had evidence of degeneration at the adjacent levels and elected to have an additional decompression (fifteen patients) or arthrodesis (forty-four patients). Kaplan-Meier analysis predicted a disease-free survival rate of 83.5% (95% confidence interval, 77.5% to 89.5%) at five years and of 63.9% (95% confidence interval, 54.0% to 73.8%) at ten years after the index operation. Although there was a trend toward progression of the arthritic grade at the adjacent disc levels, there was no significant correlation, with the numbers available, between the preoperative arthritic grade and the need for additional surgery. CONCLUSIONS: The rate of symptomatic degeneration at an adjacent segment warranting either decompression or arthrodesis was predicted to be 16.5% at five years and 36.1% at ten years. There appeared to be no correlation with the length of fusion or the preoperative arthritic degeneration of the adjacent segment.

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