• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Equine motor neuron disease: findings in 28 horses and proposal of a pathophysiological mechanism for the disease.

作者信息

Divers T J, Mohammed H O, Cummings J F, Valentine B A, De Lahunta A, Jackson C A, Summers B A

机构信息

Department of Clinical Sciences, New York State College of Veterinary Medicine, Cornell University, Ithaca 14853-6401.

出版信息

Equine Vet J. 1994 Sep;26(5):409-15. doi: 10.1111/j.2042-3306.1994.tb04411.x.

DOI:10.1111/j.2042-3306.1994.tb04411.x
PMID:7988544
Abstract

Over a three and one-half year period, 28 adult horses were diagnosed with equine motor neuron disease (EMND). The most commonly identified environmental risk factors for a horse having EMND were absence of grazing for more than a year and provision of poor quality hay. Quarter Horses were 5.4 times more at risk than other breeds but this was thought to be an epiphenomenon related to the frequency of Quarter Horses at boarding stables. Weight loss, excessive recumbency and/or trembling were the first signs noted. Other clinical diagnostic signs included: constant shifting of the weight in the rear limbs, abnormally low head carriage and muscle fasciculations. Excellent to ravenous appetites were present in all cases and marked coprophagia in some cases. Abnormally high serum concentration of muscle-derived enzymes was the only consistent serum chemistry abnormality found. Abnormal glucose absorption, increased cerebrospinal fluid total protein and intrathecal production of IgG were identified in a number of cases. Euthanasia was performed on 5 horses within 4 days of hospital admission, because of inability to stand or respiratory distress, and on 18 horses after the diagnosis had been completed. Five affected horses were maintained for observational purposes for periods of 9 months to over 2 years after the onset of clinical signs. They were given access to pasture and 2 were given supplemental vitamin E as the only therapy. Marked clinical improvement occurred in the 4 more acutely affected horses. Pathological findings, preference of type 1 muscle fibre atrophy and lipopigment accumulation within the capillary endothelium of the spinal cord of all cases, supported the hypothesis of EMND being an oxidative disease.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

相似文献

1
Equine motor neuron disease: findings in 28 horses and proposal of a pathophysiological mechanism for the disease.
Equine Vet J. 1994 Sep;26(5):409-15. doi: 10.1111/j.2042-3306.1994.tb04411.x.
2
Horses on pasture may be affected by equine motor neuron disease.在牧场放牧的马匹可能会患上马运动神经元疾病。
Equine Vet J. 2006 Jan;38(1):47-51. doi: 10.2746/042516406775374207.
3
Intrinsic, management, and nutritional factors associated with equine motor neuron disease.与马运动神经元病相关的内在、管理和营养因素。
J Am Vet Med Assoc. 1997 Nov 15;211(10):1261-7.
4
Vitamin E deficiency and risk of equine motor neuron disease.维生素E缺乏与马运动神经元病风险
Acta Vet Scand. 2007 Jul 2;49(1):17. doi: 10.1186/1751-0147-49-17.
5
Association between plasma vitamin E concentration and the risk of equine motor neuron disease.
Vet J. 1997 Nov;154(3):203-13. doi: 10.1016/s1090-0233(97)80021-4.
6
[Equine motor neuron disease: a review based on a case report].[马运动神经元病:基于一例病例报告的综述]
Tijdschr Diergeneeskd. 2001 Jun 1;126(11):376-80.
7
Evaluation of the risk of motor neuron disease in horses fed a diet low in vitamin E and high in copper and iron.对喂食低维生素E、高铜和高铁日粮的马匹患运动神经元疾病风险的评估。
Am J Vet Res. 2006 Jan;67(1):120-6. doi: 10.2460/ajvr.67.1.120.
8
Incidence and risk factors of equine motor neuron disease: an ambidirectional study.
Neuroepidemiology. 1995;14(2):54-64. doi: 10.1159/000109779.
9
Eosinophilic Enteritis in Horses with Motor Neuron Disease.患有运动神经元疾病马匹的嗜酸性粒细胞性肠炎
J Vet Intern Med. 2016 May;30(3):873-9. doi: 10.1111/jvim.13944. Epub 2016 Mar 26.
10
Risk factors associated with equine motor neuron disease: a possible model for human MND.
Neurology. 1993 May;43(5):966-71. doi: 10.1212/wnl.43.5.966.

引用本文的文献

1
Review of the Foundational Knowledge Required for Assessing Horse Welfare.评估马匹福利所需基础知识综述。
Animals (Basel). 2022 Dec 1;12(23):3385. doi: 10.3390/ani12233385.
2
Postmortem diagnoses of spinal ataxia in 316 horses in California.加利福尼亚州 316 匹马的脊髓共济失调死后诊断。
J Am Vet Med Assoc. 2021 Jun 15;258(12):1386-1393. doi: 10.2460/javma.258.12.1386.
3
Neuromyotonia in a horse.一匹马的神经性肌强直。
J Vet Intern Med. 2019 Jan;33(1):287-291. doi: 10.1111/jvim.15353. Epub 2018 Dec 3.
4
Equine motor neuron disease in 2 horses from Saskatchewan.来自萨斯喀彻温省的两匹马患马运动神经元病。
Can Vet J. 2016 Jul;57(7):771-6.
5
Eosinophilic Enteritis in Horses with Motor Neuron Disease.患有运动神经元疾病马匹的嗜酸性粒细胞性肠炎
J Vet Intern Med. 2016 May;30(3):873-9. doi: 10.1111/jvim.13944. Epub 2016 Mar 26.
6
Immunological aspects in amyotrophic lateral sclerosis.肌萎缩侧索硬化症的免疫学方面。
Transl Stroke Res. 2012 Sep;3(3):331-40. doi: 10.1007/s12975-012-0177-6. Epub 2012 May 3.
7
Differential expression of TAR DNA-binding protein (TDP-43) in the central nervous system of horses afflicted with equine motor neuron disease (EMND): a preliminary study of a potential pathologic marker.马运动神经元病(EMND)中枢神经系统中 TAR DNA 结合蛋白(TDP-43)的差异表达:潜在病理标志物的初步研究。
Vet Res Commun. 2012 Dec;36(4):221-6. doi: 10.1007/s11259-012-9533-y. Epub 2012 Aug 24.
8
The role of dietary antioxidant insufficiency on the permeability of the blood-brain barrier.饮食中抗氧化剂不足对血脑屏障通透性的作用。
J Neuropathol Exp Neurol. 2008 Dec;67(12):1187-93. doi: 10.1097/NEN.0b013e31818f8f51.
9
Vitamin E deficiency and risk of equine motor neuron disease.维生素E缺乏与马运动神经元病风险
Acta Vet Scand. 2007 Jul 2;49(1):17. doi: 10.1186/1751-0147-49-17.
10
Endothelial lipopigment as an indicator of alpha-tocopherol deficiency in two equine neurodegenerative diseases.
Acta Neuropathol. 1995;90(3):266-72. doi: 10.1007/BF00296510.