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At least 19 recordsLinked to original sources
PubMed1986

Delayed swayback in goat kids, a study of 23 cases.

The results of a retrospective study of 23 goat kids with delayed swayback are reported. Principal clinical signs were ataxia, loss of postural control, spasticity of the hindlimbs, and muscular weakness, often progressing to permanent recumbency. Denervation of skeletal muscles was demonstrated by electromyography in 2 kids. Three kids slowly recovered during hospitalisation. Histopathological changes were characterized by degeneration of selected neuronal populations with their processes within the central and the peripheral nervous system. Affected systems included upper motor neuron, vestibular, general proprioceptive, and lower motor neuron pathways, with additional involvement of the cerebellar cortex in some animals. Our findings, including limited ultrastructural observations, support the notion that the neuraxon rather than the myelin sheath is the prime target of disease in delayed swayback. The available copper values of affected kids and their unaffected herd mates were significantly lower than those of random control goats, which provides further support for a role of copper deficiency in the aetiology of this disease in the goat.

Animals↗
PubMed1978

California goats with a disease resembling enzootic ataxia or swayback.

In a retrospective study typical signs and lesions of enzootic ataxia or swayback were found in 16 young dairy goats from eight widely scattered herds in California. In addition to the constant appearance of chromatolytic neurons in brainstem and spinal cord, and myelin deficiency in certain tracts of the cord, cerebellar hypoplasia was found frequently. Liver copper was subnormal in six of nine kids tested. The disease is viewed as a developmental defect in which failure of neuronal perikaryon metabolism leads to distal axonopathy with secondary demyelination.

Animals↗
PubMed1990

Copper deficiency and posterior paralysis (Shalal) in small ruminants in the Sultanate of Oman.

A posterior ataxia or paralysis in goats and sheep is a syndrome known as Shalal within the Sultanate of Oman. An investigation was carried out into the etiology of the syndrome. Samples of blood and tissues were obtained from normal and Shalal-affected goats and sheep. Samples of feed were collected from the affected areas of the Sultanate. Chemical analyses of samples showed that affected animals suffered from severe copper deficiency in spite of sufficient copper contents in feed. However, concentrations of sulphur and iron in the feed were high. It was concluded that the Shalal syndrome in Oman is the condition generally known as swayback or enzootic ataxia caused by conditioned copper deficiency. The deficiency is probably due to copper-sulphur and copper-iron interactions in the rumen, enhanced by feeding of fresh roughage containing rumen degradable proteins.

Animal Feed↗
PubMed1989

Animal models of amyotrophic lateral sclerosis and the spinal muscular atrophies.

The causes of human amyotrophic lateral sclerosis (ALS) and the spinal muscular atrophies (SMA) are, almost without exception, unknown. This ignorance has stimulated the search for animal models to obtain insight into the etiology, pathogenesis and biochemical mechanisms underlying the human disorders. None of the 38 animal models, described in this review, provides an exact animal copy of a specific human motor neuron disease. Most of the models reproduce certain structural or physiological aspects of their human counterparts. The various experimental models can be classified according to the pathogenetic mechanism involved and according to the structural changes observed. Models based on experimentally induced disease, include heavy metals and trace elements (lead intoxication in guinea pigs, rabbits, rats, cats and primates; mercury intoxication in rats; aluminium intoxication in rabbits; swayback in goat kids; calcium and magnesium deficient rabbits and primates and calcium deficient cynomolgus monkeys), toxins (IDPN, vincristine, vinblastine, podophyllotoxin, colchicine, maytansine, maytanprine, L-BMAA, lectins, adriamycin), nutritional factors (ascorbic acid deficient guinea pigs), virus infection (spongiform polioencephalomyelitis, attenuated poliovirus, lactate dehydrogenase-elevating virus), and immunological factors (immunization with motor neurons). Hereditary models comprise hereditary canine spinal muscular atrophy, hereditary neurogenic amyotrophy in the pointer dog, Stockard paralysis, Swedish Lapland dog paralysis, "wobbler" mouse, "shaker" calf, and hereditary spinal muscular atrophy in zebra foals, crossbred rabbits,

Amyotrophic Lateral Sclerosis↗
PubMed1992

Deficiency of copper can cause neuronal degeneration.

The aim of this article is to emphasize the important role that copper plays in the function of nerve cells. We are reporting preliminary data which suggest that the swelling of axons which we produce in rats by iminodipropionitrile, IDPN, is due to its chelating action on copper, and how conversely supplementation with copper abolishes both symptoms and lesions. The copper values we obtained by atomic absorption spectrophotometry of the spinal cord and brain from the animals fully support this contention. In comparing these results with the diseases that are known to be due to copper deficiency, namely Menkes disease in man, swayback in lambs and several neurological mutant mice, we find not only similar axonal swellings, but also amelioration of symptoms and lesions by early administration of copper. Considering the main forms in which copper is present, we discuss the cuproproteins, i.e. ceruloplasmin and metallothionein, and their role in transport and delivery of copper to various organs. Further, the many cuproenzymes i.e. superoxide dismutase, tryptophan-2,3-dioxygenase, lysine oxidase, cytochrome oxidase, monoamine oxidases, tyrosinase, dopamine-beta-hydroxylase and d-amino levulinate dehydratase are noted for their roles in the nervous system. Finally, we suggest that neuronal copper deficiency should be more fully investigated as a possible etiological factor in the more common neurodegenerative diseases, such as Alzheimer's disease and amyotrophic lateral sclerosis, ALS.

Animals↗
PubMedDate not supplied

Prevalence of trunk abnormalities in eleven-year-old schoolchildren in Rotterdam, The Netherlands.

The prevalence of trunk abnormalities was studied in 4,915 children aged 11 years (2,528 boys, 2,387 girls); 33% of the children were of non-Dutch origin. The following measurements were recorded: height, weight, signs of puberty, and menarche. Trunk abnormality was assessed in the erect child (asymmetry of shoulders, waistline, imbalance of the trunk, scoliosis, lordosis, kyphosis, swayback, and flexibility) and by the forward bending test (rib hump or lumbar prominence, persistence of scoliosis, kyphosis, deviant lateral aspect); 85.9% of boys and 81.3% of girls were symmetric, and abnormal forward bending test was noted in 7.1% of boys and 10.6% of girls. In non-Dutch girls, trunk abnormalities were more prevalent.

Anthropometry↗
PubMed1988

Copper heptonate for the treatment of hypocupraemia in sheep.

Trials were carried out to compare the efficacy of copper heptonate with other available therapeutic products. On nine farms with a copper deficiency problem, over 2000 ewes were treated in mid-pregnancy. All the treatments increased whole blood copper levels and plasma caeruloplasmin (ferroxidase) activity in ewes, and protected their lambs from swayback. The lambs from ewes treated with copper heptonate and copper oxide needles had significantly higher blood copper levels than lambs from untreated control ewes. Treatment with copper heptonate was shown to have a therapeutic index of at least 5 in Swaledale ewes of normal copper status. In two groups of Welsh mountain sheep from different backgrounds, both with normal blood copper levels before treatment, the therapeutic indices were 3 to 5.

Animals↗
PubMed1991

Footwear and posture. Compensatory strategies for heel height.

The belief that wearing high-heeled shoes increases lumbar lordosis is firmly ingrained in clinical folklore. Proponents of negative heel footwear argue that because high positive heels increase the lumbar lordosis, negative heels will decrease the lumbar lordosis. Quantitative documentation of the assumption regarding high heels is not to be found in the literature, although sporadic attempts to prove this assumption have been made throughout the 20th Century. Although other effects, such as decreased gait speed and step length, and increased knee flexion at heel strike have been found in more than one study, no increase in lumbar lordosis has been found. Where an actual decrease in lordosis has been found, authors tend to explain it away as inconsistent with what every clinician feels that he or she has observed. We felt it appropriate, then, to conduct both a static and a dynamic study to assess the effects of heel height on lumbar spine and lower limb joint kinematics in the sagittal plane, as well as other strategies to compensate for heel height. The results indicate that the greatest compensation is at the ankle and knee. Where a significant effect occurred in the lumbar spine (males, dynamic study), high heels decreased the lumbar lordosis, i.e., resulted in less swayback rather than more.

Adolescent↗