Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Swayback”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1996

Swayback in a blesbok (Damaliscus dorcas phillipsi) and a black wildebeest (Connochaetes gnou).

Ataxia associated with myelopathy and low liver copper concentrations is described in a blesbok (Damaliscus dorcas phillipsi) and black wildebeest (Connochaetes gnou) from the Karoo Nature Reserve, Graaff-Reinet. This syndrome, which occurs in neonatal and delayed forms, has been described in sheep, goats, pigs and domesticated red deer, but reports in other ungulates, including antelope, are very rare and generally unconfirmed by histopathological examination. The 2 animals examined exhibited a typical pattern of Wallerian degeneration in selected tracts of the spinal cord. Many blesbok in the reserve are markedly pale in colour. Fading of the hair is also associated with copper deficiency in ungulates. High lamb mortality occurs as a result of the ataxia and threatens the survival of the blesbok herd in the reserve. Confirmation of low liver copper concentrations in affected animals offers direction towards the solution of the problem.

Animal Nutritional Physiological Phenomena↗
PubMed1998

Swayback warning.

Explore the source record for details and available documents.

Animal Husbandry↗
PubMed2006

Copper deficiency myelopathy (human swayback).

The hematologic manifestations of copper deficiency are well known and include anemia and neutropenia. In the past few years, the neurological manifestations of acquired copper deficiency in humans has been recognized, the most common being a myelopathy presenting with a spastic gait and prominent sensory ataxia. The known causes of acquired copper deficiency include prior gastric surgery, excessive zinc ingestion, and malabsorption; however, often the cause is unclear. Hyperzincemia may be present even in the absence of exogenous zinc ingestion. The clinical features and neuroimaging findings are similar to the subacute combined degeneration seen in patients with vitamin B12 deficiency. Copper and vitamin B12 deficiency may coexist. The neurological syndrome may be present without the hematologic manifestations. Copper supplementation resolves the anemia and neutropenia promptly and completely and may prevent the neurological deterioration. Improvement, when it occurs, is often subjective and preferentially involves sensory symptoms. This article describes patients with copper deficiency myelopathy seen at the Mayo Clinic in Rochester, Minn, and reviews the literature on neurological manifestations of acquired copper deficiency in humans.

Adult↗