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PubMed1995

1995 Volvo Award in clinical sciences. Determinants of lumbar disc degeneration. A study relating lifetime exposures and magnetic resonance imaging findings in identical twins.

STUDY DESIGN: Retrospective cohort. OBJECTIVES: To investigate the effects of lifetime exposure to commonly suspected risk factors on disc degeneration using magnetic resonance imaging, and to estimate the effects of these suspected risk factors relative to age and familial aggregation, reflecting genetic and shared environmental influences. SUMMARY OF BACKGROUND DATA: Structural and biochemical changes associated with disc degeneration are suspected as the underlying conditions of many back-related symptoms. Little is known about the determinants of disc degeneration. METHODS: Based on lifetime discordance in suspected environmental risk factors for disc degeneration, 115 male identical twin pairs were selected. An in-depth interview was conducted of occupational and leisure time physical loading, driving, and smoking. Disc degeneration was evaluated using observational and digital magnetic resonance imaging assessment methods. RESULTS: Heavier lifetime occupational and leisure physical loading was associated with greater disc degeneration in the upper lumbar levels (P = 0.055 - 0.001), whereas sedentary work was associated with lesser degeneration (P = 0.006). These univariate associations did not reach statistical significance in the lower lumbar region. In multivariate analyses of the upper lumbar levels, the mean job code explained 7% of the variability in observational disc degeneration scores; the addition of age explained 16%, and familial aggregation improved the model such that 77% of the variability was explained. In the lower lumbar levels, leisure time physical loading entered the multivariate model, explaining 2% of the variability. Adding age explained 9%, and familial aggregation raised the variability in disc degeneration scores explained to 43%. CONCLUSIONS: The present study findings suggest that disc degeneration may be explained primarily by genetic influences and by unidentified factors, which may include complex, unpredictable interactions. The particular environmental factors studied, which have been among those most widely suspected of accelerating disc degeneration, had very modest effects.

Adult↗
PubMed1995

Spatial and temporal pattern of Purkinje cell degeneration in shaker mutant rats with hereditary cerebellar ataxia.

Temporal-spatial patterns of surviving Purkinje cells were studied quantitatively in a rat mutant (shaker) with differential hereditary cerebellar ataxia and Purkinje cell degeneration. Shaker rat mutants are characterized behaviorally as mild if they are ataxic or as strong if they have ataxia and tremor. Purkinje cells degenerate in both mild and strong shaker mutants, but the temporal and spatial patterns of cell death are strikingly different. In mild shaker mutants, Purkinje cell death is temporally restricted, with 31-46% of the Purkinje cells in lobules I-IX dying by 3 months of age. Very few Purkinje cells degenerate after this age. Purkinje cell death is spatially random. In lobules I-IX, every second, third, or fourth Purkinje cell degenerates. Purkinje cells in lobule X do not degenerate. In strong shaker mutants, Purkinje cell degeneration is temporally protracted and spatially restricted. By 3 months of age, most Purkinje cells in lobules I-VIa, -b, and -d have degenerated. Numerous Purkinje cells in the paravermis of lobules VIIb-VIII have also degenerated. Surviving Purkinje cells in the vermis and lateral hemisphere of lobules VIIb-VIII are aligned in parasagittally oriented stripes or transversely oriented bands. Purkinje cells continue to degenerate in localized areas of the posterior lobe such that, by 18 months of age, surviving Purkinje cells are limited primarily to lobules VIc, VIIa, IXd, and X. Quantitative analysis indicates that none of the Purkinje cells in these lobules degenerate.

Animals↗
PubMed1991

Significance of degenerating endoneurial cells in peripheral neuropathy.

In 42 human sural nerve biopsies degeneration of endoneurial cells was evaluated semiquantitatively at the electronmicroscopic level. These cells were of non-Schwannian origin since they were not surrounded by a basement membrane. Most of the degenerating cells resembled endoneurial fibroblasts: their remaining cytoplasmic processes were quite extensive, not finger-like as in macrophages, and their cytoplasm did not contain conspicuous lysosomes or phagolysosomes that would identify them as degenerating macrophages. Criteria for regarding these cells as degenerating were defects of the cytoplasmic surface membrane with extracellularly situated organelles. The ratio between normal and degenerating endoneurial cells in five different groups of peripheral neuropathies was compared to a group of normal controls. No degenerating endoneurial cells were found in the latter. The largest proportion of degenerating endoneurial cells was noted in patients with panarteritis nodosa (30% of the endoneurial cells evaluated). Between 9% and 18% of the evaluated endoneurial cells were seen degenerating in hereditary motor and sensory neuropathies, in neuropathies associated with IgG or IgM gammopathy, and in chronic demyelinating inflammatory polyradiculoneuropathy. These findings suggest that degeneration of endoneurial cells is a nonspecific sign of peripheral neuropathy occurring in various types of neuropathy, although vasculitis represents the most frequent cause. Thus, degeneration of endoneurial cells can be added to the growing list of changes that possibly indicate an inflammatory disorder, even during the intervening stage when apparent inflammatory cell infiltrates are lacking.

Adult↗
PubMed1979

Further observations on transganglionic degeneration in trigeminal primary sensory neurons.

Transganglionic degeneration has been studied with the Fink-Heimer method in the trigeminal sensory nuclei of adult cats and rats following peripheral nerve transections. Degeneration was observed ipsilaterally as well as contralaterally in all cats, surviving 11-30 days after transection of the infraorbital nerve. In the rats the infraorbital or the auriculotemporal nerve was transected. After transection of the former nerve the first signs of transganglionic degeneration were observed after 7 days postoperative survival and even after 130 days there were still a lot of degenerating structures present. Between 7 and 14 days survival there was a small amount of degeneration in substantia gelatinosa. After transection of the auriculotemporal nerve, degeneration was observed only in the most caudal parts of the trigeminal sensory nuclear complex. Opposite to the situation in the cat, there was no contralateral degeneration in the rat. All degeneration areas were somatotopically organized, both in the cat and in the rat. The results are discussed in relation to a previous study of transganglionic degeneration in the trigeminal sensory nuclear complex by the authors and to anatomical and physiological studies of somatotopic organization in the trigeminal sensory nuclei. They clearly show the value of transganglionic degeneration used as a tool for analysis of central projections of primary sensory neurons.

Age Factors↗
PubMed1994

Pre-degenerated nerve grafts enhance regeneration by shortening the initial delay period.

In the present study we tested how nerve grafts with different pre-degeneration periods (1-28 days) influenced the early regenerative response in the rat sciatic nerve. The sciatic nerve on the right side was crushed and after 1-28 days of pre-degeneration, a 10 mm segment was used as an autologous nerve graft and transposed to a freshly made 10 mm long nerve defect on the left side. The regeneration distance was measured by the sensory pinch test 2-10 days after nerve repair. A newly developed mathematical model was used to calculate regeneration rates and initial delay periods from the measured regeneration distances. Pre-degenerated nerve grafts improved nerve regeneration by decreasing the initial delay period as compared to fresh nerve grafts without affecting the regeneration rate. Only one day of pre-degeneration was sufficient to reduce the initial delay period from 3.6 days to 1.7 days. The maximal effect on the initial delay period was achieved after 3 days of pre-degeneration. The initial delay period at later pre-degeneration intervals (7-14 days) was about 1 day. The effect persisted for at least 28 days of pre-degeneration. The regeneration rate was 1.5 mm/day for fresh nerve grafts and between 1.8-2.1 mm/day for pre-degenerated grafts. The results suggest that the effects of pre-degeneration are not only due to the increased cell proliferation in the graft, but that also trophic and/or inflammatory mechanisms may be of importance. Grafts pre-degenerated by crush may have clinical implications since they are easy to perform if an elective nerve grafting procedure is planned.

Animals↗
PubMed2006

A new model of retinal photoreceptor cell degeneration induced by a chemical hypoxia-mimicking agent, cobalt chloride.

Retinal photoreceptor cell degeneration was induced by cobalt chloride, a chemical hypoxia-mimicking agent in rodents. Time course and dose-response of photoreceptor cell degeneration in mouse retina after intravitreal injection of cobalt chloride were examined by conventional histological analysis by hematoxylin and eosin staining and in situ terminal dUTP-biotin nick end labeling of DNA fragments (TUNEL) method with the use of paraffin-embedded sections. The dose-response of photoreceptor cell degeneration in rat retina was also examined. Photoreceptor cells progressively degenerated with time and under dose-response relationship. The suitable dose of cobalt chloride for the selective photoreceptor cell degeneration in mice is 10-12 nmol intravitreal injection at the volume of 2 microl. The retinal morphology of the mice 2 weeks after the 10-12 nmol intravitreal injection was similar to that of retinal degeneration in the mutant rd mouse. Retinal damage of total retinal layers was induced by an excessive dose of cobalt chloride. The progression of retinal damage after cobalt chloride injection, measured morphologically, was completed at 1 week. However, nuclear DNA fragmentation, mainly detected at outer nuclear layer by TUNEL, peaked at 48 h after 12 nmol cobalt chloride injection. Thus, the selective photoreceptor cell degeneration induced by cobalt chloride follows DNA fragmentation at outer nuclear layer. The photoreceptor cell degeneration is established optionally by cobalt chloride without use of the retinal degeneration mutant animals. Thus, we have described the development of a new model of retinal photoreceptor cell degeneration induced by a chemical hypoxia-mimicking agent.

Animals↗
PubMed2006

Targeted inactivation of synaptic HRG4 (UNC119) causes dysfunction in the distal photoreceptor and slow retinal degeneration, revealing a new function.

HRG4 (UNC119) is a photoreceptor protein predominantly localized to the photoreceptor synapses and to the inner segments to a lesser degree. A heterozygous truncation mutation in HRG4 was found in a patient with late onset cone-rod dystrophy, and a transgenic (TG) mouse expressing the identical mutant protein developed late onset retinal degeneration, confirming the pathogenic potential of HRG4. Recently, the dominant negative pathogenic mechanism in the TG model was shown to involve increased affinity of the truncated mutant HRG4 for its target, ARL2, which leads to a delayed decrease in its downstream target, mitochondrial ANT1, mitochondrial stress, synaptic degeneration, trans-synaptic degeneration, and whole photoreceptor degeneration by apoptosis. In this study, the mouse HRG4 (MRG4) gene was cloned and targeted to construct a knock-out (KO) mouse model of HRG4 in order to study the effects of completely inactivating this protein. The KO model was examined by genomic Southern blotting, Western blotting, immunofluorescence, funduscopy, LM and EM histopathology, ERG, and TUNEL analyses. The KO model developed a slowly progressive retinal degeneration, characterized by mottling in the fundus, mild thinning of the photoreceptor layer, and increase in apoptosis as early as 6 months, dramatic acceleration at approximately 17 months, and virtual obliteration of the photoreceptors by 20 months. When compared to retinal degeneration in the TG model, significant differences existed in the KO consisting of more severe and early photoreceptor death without evidence of early synaptic and trans-synaptic degeneration as seen in the TG, confirmed by LM and EM histopathology, ERG, and Western blotting of synaptic proteins. The results indicated a dysfunction in the KO outside the synapses in the distal end of photoreceptors where MRG4 is also localized. Differences in the phenotypes of retinal degeneration in the KO and TG models reflect a dysfunction in the two opposite ends of photoreceptors, i.e., the distal inner/outer segments and proximal synapses, respectively, indicating a second function of MRG4 in the distal photoreceptor and dual functionality of MRG4. Thus, inactivation of MRG4 by gene targeting resulted in a retinal degeneration phenotype quite different from that previously seen in the TG, attesting to the multiplicity of MRG4 function, in addition to the importance of this protein for normal retinal function. These models will be useful in elucidating the functions of HRG4/MRG4 and the mechanism of slow retinal degeneration.

Adaptor Proteins, Signal Transducing↗
PubMed2003

Snowflake vitreoretinal degeneration: follow-up of the original family.

PURPOSE: The ocular findings, systemic features, and genetic loci distinguishing known genetic causes of vitreoretinal degenerations were studied in the original Snowflake family. DESIGN: Prospective, comparative study and molecular genetic investigation. PARTICIPANTS: Members of the original snowflake vitreoretinal degeneration family. METHODS: Clinical data were collected on 26 family members by history and examination. Thirteen of the 26 total family members underwent prospective examination. Linkage to known vitreoretinal degeneration loci (COL2A1, COL11A1, and the Wagner disease locus) was evaluated with short tandem repeat markers. MAIN OUTCOME MEASURES: Ocular and systemic features of known vitreoretinal degenerations. RESULTS: Six of the 13 prospectively examined subjects had snowflake vitreoretinal degeneration. Corneal guttae (4/5; 80%), early onset cataract (5/6; 83%), fibrillar vitreous degeneration (6/6; 100%), and peripheral retinal abnormalities (5/6; 83%), including minute crystallinelike deposits called snowflakes (4/6; 67%), were common. Retinal detachment was seen in 1 of 6 of these prospectively examined subjects (17%). A total of 14 affected subjects were identified within the family, and in 3 (21%), retinal detachment developed. Orofacial features, early-onset hearing loss, and arthritis typical of Stickler syndrome were absent. Linkage to known vitreoretinal degeneration loci was excluded. CONCLUSIONS: The absence of vitreous gel in the retrolental space and presence of fibrillar vitreous degeneration were consistent with the vitreous structure reported for collagen 11A1 (COL11A1) but not collagen 2A1 (COL2A1) mutations. The absence of systemic features was characteristic of the vitreoretinopathies linked to chromosome 5q13 (Wagner disease and erosive vitreoretinopathy) and mutations in exon 2 of the COL2A1 gene. Snowflakes in the peripheral retina and the absence of nyctalopia, posterior chorioretinal atrophy, and tractional retinal detachment were inconsistent with the chromosome 5q13 vitreoretinopathies. The association of Fuchs' corneal endothelial dystrophy found in this family has not been reported previously in other vitreoretinal degenerations. These findings and the exclusion of known genetic loci suggest snowflake is a distinct vitreoretinal degeneration.

Adult↗
PubMed1990

Phorbol ester induces photoreceptor-specific degeneration in a Drosophila mutant.

In the retinal degeneration B (rdgB) mutant of Drosophila, the major class of photoreceptors degenerate when the fly is raised in the light for several days; raising the fly in the dark largely prevents the degeneration. Thus, the rdgB is a conditional mutant that requires the operation of some stages of the phototransduction cascade to express its characteristic phenotype. We report here experiments that examine the ability of chemical agents to mimic light by causing photoreceptor-specific degeneration in the dark. Application of a specific activator of protein kinase C, phorbol ester, to eyes of rdgB flies led to a degeneration of the photoreceptors that was indistinguishable from that caused by light: both light and phorbol ester-induced degeneration were characterized by (i) selective degeneration of one class of photoreceptors; (ii) a unique pattern of degeneration; and (iii) the appearance of light-induced regenerative spikes at early stages of degeneration. Application of phorbol ester to the eyes of wild-type flies had no effect. We suggest that light or phorbol ester activates a protein kinase C and results in a sustained or excessive phosphorylation of proteins in the rdgB mutant, leading to photoreceptor degeneration. Furthermore, the results are consistent with identification of the rdgB gene product as a phosphoprotein phosphatase that is nonfunctional or absent in the mutant.

Animals↗
PubMed1972

Degeneration of sympathetic nerves in vitro and development of smooth muscle supersensitivity to noradrenaline.

1. The sequence of events involved in degeneration of sympathetic nerve terminals has been studied in vitro in the expansor secundariorum muscle of the chicken.2. The muscle underwent a degeneration contraction due to abrupt release of noradrenaline stores from the nerves about 18 hr after isolation. The tension reached its peak within 6 hr at about 44% of the maximum tension developed to added noradrenaline.3. Responses to nerve stimulation were transiently potentiated by 35% on average just before the onset of the degeneration contraction and then failed abruptly.4. Degeneration release of noradrenaline was Ca(2+)-dependent. Development of the degeneration contraction was delayed by temporary withdrawal of Ca(2+) from the medium and was accelerated by a twofold increase in Ca(2+) concentration when applied at a critical period close to the onset.5. Neither continuous nerve stimulation nor alterations in the length of the nerve stump influenced the course of the degeneration contraction in vitro.6. When the muscle was left in situ after denervation, the degeneration contraction occurred between 2 and 3 days later depending on the length of the distal portion of nerve. Cutting the nerve supply 5 cm closer to the muscle in vivo hastened the loss of transmission and the onset of the degeneration contraction by 24-48 hr.7. Supersensitivity to noradrenaline occurred soon after the degeneration contraction but the full development of a sevenfold supersensitivity to noradrenaline, equivalent to that produced by cocaine, took up to 48 hr. No further increase in sensitivity to noradrenaline could be detected in vitro after chronic denervation in vivo for up to 30 days.8. It is concluded that the degeneration contraction and failure of transmission was precipitated by an abrupt increase in the Ca(2+) permeability of the axon causing discharge of transmitter from vesicles. This was probably the result of depletion of essential factors normally transported somatofugally in the axon at 1-2 mm/hr. The supersensitivity to noradrenaline that develops subsequently appears to be due to a loss of the uptake mechanism of the nerve terminals.

Animals↗
PubMed2001

Evaluation of distal and proximal axonal degeneration in patients with carpal tunnel syndrome.

In patients with carpal tunnel syndrome, varying degrees of demyelination and axonal degeneration occur in the median nerve. Only a few studies have examined axonal degeneration produced at proximal to the lesion. In this study proximal axonal degeneration was evaluated and compared with other parameters. In 40 consecutive CTS patient hands, distal latency (DL), compound muscle action potential amplitude (CMAP) and motor conduction velocity (MCV) were analyzed by conventional motor nerve conduction studies. Intrafascicular compound nerve action potential amplitude (N-CNAP) at the elbow after wrist simulation and its nerve conduction velocity (NCV) between wrist and elbow were also analyzed. The negative correlation of DL with CMAP was statistically significant (r = 0.577, p < 0.001). CMAP was correlated with either MCV (r = 0.537, p < 0.001) or N-CMAP (r = 0.710, p < 0.001). A significant correlation of MCV with NCV (r = 0.517, p < 0.001) was also indicated. There were no any other significant correlation among the parameters. In CTS the degree of demyelination and axonal degeneration influence the prognosis for nerve recovery after decompressive surgery. DL is mainly influenced by demyelination that results in conduction block and slowing at the carpal tunnel. CMAP and N-CNAP indicate the degree of axonal degeneration at distal and proximal to the compression site. As in electrophysiologic evaluation of mononeuropathies, proximal axonal degeneration is best assessed by both stimulation and recording electrode locationing proximal to the lesion. Recording of intrafascicular nerve action potential was a little invasive method, but it provided important informations. The negative correlation between DL and CMAP implies that distal axonal degeneration can occur in proportion to the conduction disturbance. Moreover, N-CNAP had a higher correlation with CMAP. The greater the distal axonal degeneration, the more the proximal axonal degeneration. Conduction velocity represents the velocity of the fastest conduction fiber, not the degree of axonal degeneration.

Action Potentials↗
PubMed2002

Relation between size at birth and risk of age-related macular degeneration.

PURPOSE: To determine whether poor fetal growth, as determined by size at birth, is associated with increased risk of age-related macular degeneration. METHODS: A total of 660 men and women born in Sheffield, United Kingdom, between 1922 and 1930 and whose size at birth was available were traced and invited to take part in the study. Of these, 392 attended for ophthalmic examination. Age-related macular degeneration in these volunteers was determined by the Wisconsin Age-Related Maculopathy Grading System. RESULTS: The mean birth weight of subjects with macular degeneration (early or late) was heavier than that of those without (7.6 lb vs. 7.3 lb, respectively; P = 0.03). After adjustment for age, gender, and risk factors for macular degeneration, a significantly increased risk of macular degeneration was found in subjects with higher birth weight (odds ratio [OR] 1.5, 95% confidence interval [CI] 1.1-2.0 for each SD [1 lb, 5 oz] increase in birth weight). Other parameters describing size at birth showed a weaker relation or no relation with macular degeneration, but one of the measures of fetal proportion (head circumference-to-birth weight ratio) was significantly associated with risk of macular degeneration. Subjects with macular degeneration had a significantly lower head circumference-to-birth weight ratio than did those without (11.2 vs. 12.0 respectively, P = 0.01). CONCLUSIONS: The finding that age-related macular degeneration was associated with increased rather than decreased birth weight was unexpected. Failure of the developing fetus's normal brain-sparing mechanism is a possible explanation for our finding of a lower head circumference-to-birth weight ratio among subjects with macular degeneration.

Aged↗
PubMed2004

Apolipoprotein E epsilon 4 is a determinant for Alzheimer-type pathologic features in tauopathies, synucleinopathies, and frontotemporal degeneration.

OBJECTIVES: To determine if apolipoprotein E epsilon 4 influences the frequency of Alzheimer-type pathologic features in tauopathies, synucleinopathies, and frontotemporal degeneration and to determine if the frequency of Alzheimer-type pathologic features in synucleinopathies is similar to the frequency of such features in tauopathies and frontotemporal degeneration. METHODS: A total of 285 patients with pathologically proven neurodegenerative disorders, including diffuse and transitional Lewy body disease, frontotemporal degeneration, progressive supranuclear palsy, corticobasal degeneration, and multiple system atrophy, with a mean age of 75.1 +/- 9.3 years, were suitable for genetic and pathological analysis. Disorders were grouped as tauopathies (progressive supranuclear palsy and corticobasal degeneration), synucleinopathies (Lewy body disease and multiple system atrophy), and frontotemporal degeneration. Braak neurofibrillary tangle staging and quantitative scores of senile plaques were used to determine the degree of concomitant Alzheimer-type pathologic features in each case, and apolipoprotein E genotype was determined from DNA isolated from frozen brain tissue. The relationship of apolipoprotein E epsilon 4 to Alzheimer-type pathologic features was determined. RESULTS: Across all neurodegenerative disorders, apolipoprotein E epsilon 4 and older age independently predicted the co-occurrence of Alzheimer-type pathologic features (P<.001), whereas female sex had a lesser effect (P = .03). When divided into the 3 subgroups (tauopathies, synucleinopathies, and frontotemporal degeneration), apolipoprotein E epsilon 4 had a similar effect, whereas older age and female sex were less predictive. There was a significant difference between the frequency of Alzheimer-type pathologic features in synucleinopathies and the frequency of such features in tauopathies and frontotemporal degeneration (P<.001 for both). The frequency of apolipoprotein E epsilon 4 allele was not significantly different among the 3 groups. CONCLUSIONS: Apolipoprotein E epsilon 4, independent of older age and sex, contributes to the co-occurrence of Alzheimer-type pathologic features in tauopathies, synucleinopathies, and frontotemporal degeneration, but this does not explain why Alzheimer-type pathologic features are significantly more likely to coexist with synucleinopathies than with either tauopathies or frontotemporal degeneration.

Aged↗
PubMed1977

Degeneration of germ cells in normal, hypophysectomized and hormone treated hypophysectomized rats.

In normal adult rats some germ cells degenerate at several vulnerable steps of spermatogenesis. These are the type A spermatogonia, midpachytene spermatocytes, primary and secondary spermatocytes which degenerate during their respective maturation divisions and step 7 and 19 spermatitids. In the present study, these degenerating cells were examined under the electron microscope, and their frequency was determined in toluidine blue stained semithin sections of testes from normal, hypophysectomized (at 5.5 days after operation) and hypophysectomized rats injected with FSH and LH separately or in combination. With the exception of the step 19 spermatids, the degenerating germ cells underwent necrosis in vacuolated spaces delimited by Sertoli cells. In the case of the affected step 19 spermatids, an apical cytoplasmic process of the Sertoli cell initially ensheathed a long segment of their flagellum, and then each degeneration cell was drawn deep in the seminiferous epithelium where it was phagocytozed by the Sertoli cell. Soon after hypophysectomy the incidence of degenerating mid-pachytene spermatocytes, step 7 and 19 spermatids which are present in stages VII or VIII of the cycle of the seminiferous epithelium, increased significantly. In contrast the number of degenerating primary or secondary spermatocytes during the meiotic divisions seen in stage XIV of the cycle or of any other germinal cell was not significantly modified. While the injection of FSH alone had no influence on the number of degenerating cells in hypophysectomized rats, injections of LH at the two doses administered (0.7 microng or 20 microng) reduced significantly the number of degenerating cells seen in stages VII-VIII of the cycle; combined injections of FSH and LH (20 microng) reduced the number of these degenerating cells to the normal low values. Thus it appeared that the mid-pachytene spermatocytes and the step 7 and 19 spermatids, all present in the adluminal compartment of the seminiferous epithelium in stages VII or VIII of the cycle, were more sensitive to the presence of absence of gonadotropic hormones than the other germ cells present in the seminiferous epithelium.

Animals↗
PubMed1997

Disc degeneration in young patients with isthmic spondylolisthesis treated operatively or conservatively: a long-term follow-up.

The purpose of this long-term follow-up was (1) to investigate disc changes in the olisthetic segment in patients treated conservatively, (2) to compare disc changes above the slipped vertebra in conservatively treated patients with those in operatively treated patients, and (3) to establish possible relations of disc changes to the degree of the slip and to subjective back pain symptoms of the patients. The subjects were 227 patients with isthmic L5 olisthesis diagnosed under 20 years of age (mean 13.8 years) with a mean follow-up of 15.4 (range 5-30) years. Of these, 145 patients had been treated with segmental fusion and 82 had been treated conservatively. At follow-up, standing anteroposterior and lateral radiographs as well as flexion/extension views of the lumbar spine were taken. Disc degeneration was graded semiquantitatively: 0 = normal disc height, 1 = decrease of disc height < 50%, 2 = decrease > or = 50%, and 3 = obliteration of the disc. In the conservatively treated patients degeneration of the olisthetic disc was distributed by grade as follows: O: n = 38, 1: n = 24, 2: n = 14, 3: n = 6. No motion at all was observed in the olisthetic segment in 40 patients (48%) with a mean slip of 30%, segmental motion of 4 degrees-18 degrees was found in 42 patients with a mean slip of 14%. There was a statistically significant association of the degree of slip to the severity of disc degeneration and non-mobility of the segment. Grade 1 degeneration of the L4/5 disc occurred in 25.6% of the conservatively treated patients and in 32% of 48 patients treated with L5-S1 fusion. This correlated with the severity of the slip, but not with pain symptoms or pathologic segmental mobility at the time of follow-up. Out of 84 patients with L4-S1 fusion, in 17% grade 1 degeneration of the L3/4 disc was observed, and 3 out of 13 patients (23%) with L3-S1 fusion had grade 1 degeneration of the disc above the fusion. The disc changes had no correlation with subjective pain symptoms. It is concluded that the natural course of isthmic spondylolisthesis is associated with disc degeneration and spontaneous stabilization of the olisthetic segment. Fusion operations do not significantly increase the rate of disc degeneration in the adjacent disc above the fusion after a mean postoperative follow-up of 13.8 years. No correlation between the number of degenerated discs or the degree of degeneration and subjective low back pain symptoms was found.

Adolescent↗
PubMed2005

Review of existing grading systems for cervical or lumbar disc and facet joint degeneration.

The aim of this literature review was to present and to evaluate all grading systems for cervical and lumbar disc and facet joint degeneration, which are accessible from the MEDLINE database. A MEDLINE search was conducted to select all articles presenting own grading systems for cervical or lumbar disc or facet joint degeneration. To give an overview, these grading systems were listed systematically depending on the spinal region they refer to and the methodology used for grading. All systems were checked for reliability tests and those recommended for use having an interobserver Kappa or Intraclass Correlation Coefficient >0.60 if disc degeneration was graded and >0.40 if facet joint degeneration was graded. MEDLINE search revealed 42 different grading systems. Thirty of these were used to grade lumbar spine degeneration, ten were used to grade cervical spine degeneration and two were used to grade both. Thus, the grading systems for the lumbar spine represented the vast majority of all 42 grading systems. Interobserver reliability tests were found for 12 grading systems. Based on their Kappa or Intraclass Correlation Coefficients nine of these could be recommended for use and three could not. All other systems could neither be recommended nor not be recommended since reliability tests were missing. These systems should therefore first be tested before use. The design of the grading systems varied considerably. Five grading systems were beginning with the lowest degree of degeneration, 37, however, with the normal, not degenerated state. A 5-grade scale was used in six systems, a 4-grade scale in 24, a 3-grade scale in eight and a 2-grade scale in three systems. In 15 cases the normal, not degenerated state was assigned to "grade 0", in another 15 cases, however, this state was assigned to "grade 1". This wide variety in the design of the grading systems makes comparisons difficult and may easily lead to confusion. We would therefore recommend to define certain standards. Our suggestion would be to use a scale of three to five grades, to begin the scale with the not degenerated state and to assign this state to "grade 0".

Cervical Vertebrae↗
PubMed2005

Degeneration and height of cervical discs classified from MRI compared with precise height measurements from radiographs.

STUDY DESIGN: Descriptive study comparing MRI classifications with measurements from radiographs. OBJECTIVES: 1. Define the relationship between MRI classified cervical disc degeneration and objectively measured disc height. 2. Assess the level of inter- and intra-observer errors using MRI in defining cervical disc degeneration. SUMMARY OF BACKGROUND DATA: Cervical spine degeneration has been defined radiologically by loss of disc height, decreased disc and bone marrow signal intensity and disc protrusion/herniation on MRI. The intra- and inter-observer error using MRI in defining cervical degeneration influences data interpretation. Few previous studies have addressed this source of error. The relation and time sequence between cervical disc degeneration classified by MRI and cervical disc height decrease measured from radiographs is unclear. METHODS: The MRI classification of degeneration was based on nucleus signal, prolaps identification and bone marrow signal. Two neuro-radiologists evaluated the MR-images independently in a blinded fashion. The radiographic disc height measurements were done by a new computer-assisted method compensating for image distortion and permitting comparison with normal level-, age- and gender-appropriate disc height. RESULTS/CONCLUSIONS: 1. Progressing disc degeneration classified from MRI is on average significantly associated with a decrease of disc height as measured from radiographs. Within each MRI defined category of degeneration measured disc heights, however, scatter in a wide range. 2. The inter-observer agreement between two neuro-radiologists in both defining degeneration and disc height by MRI was only moderate. Studies addressing questions related to cervical disc degeneration should take this into consideration.

Adult↗
PubMed2002

Control of muscle degeneration following autotomy of a hindleg in the grasshopper, Barytettix humphreysii.

When the grasshopper, Barrytettix humphreysii, sheds a hindlimb during autotomy, certain thoracic muscles degenerate although they are neither directly damaged nor denervated. Muscle degeneration is induced when a leg nerve (N5) that does not innervate the thoracic muscles is severed. Together these results suggest that transneuronal mechanisms influence muscle survival. To further characterize this autotomy-induced process, we studied the degeneration of a thoracic tergotrochanteral muscle (M#133b,c) following autotomy or experimental manipulation in adult animals. Its degeneration is correlated with reduced activity of its neural input and occurs by programmed cell death (PCD). PCD onset is variable between individual muscle fibers, indicating that the trigger of degeneration is fiber specific. Muscle degeneration appears to be triggered by the loss of proprioceptive input from the autotomized limb, since severing of axons from proprioceptive organs, but not exteroceptive chemo- or mechanoreceptors, leads to muscle degeneration. Muscle disuse, neuronal degeneration, or changes in juvenile hormone titer do not appear to play a role in autotomy-induced degeneration. We propose that the loss of proprioceptive input from proximal campaniform sensilla on the tibia deafferents the thoracic muscle motor neurons and leads to a decrease in their activity. Muscle degeneration is ultimately triggered by the loss of normal neural activity.

Journal Article↗