Lameness: Muscle and Nerve Problems Articles

• Tying-Up
• Vitamin E and Equine Motor Neuron Disease

by Stephanie Valberg !VM Ph!

I just bought a Thoroughbred filly which was in race training, but retired
without running because of recurrent bouts of “tying-up.” She had been
turned out for six months before I got her, and neer showed any problems
while on the farm. !hat can you tell me about this disease"
Tying-up is a syndrome or description of a horse with muscle damage that has many different
causes. It proaly is one of the most misunderstood and contro!ersial
syndromes in the athletic horse. "ince there are se!eral causes# some of which appear to e
inherited# there is no single cure. Typical signs of tying-up include a horse which ecomes stiff#
sweats# and is reluctant to mo!e. $esearchers ha!e learned a great deal aout tying-up%or
e&ertional rhadomyolysis%in recent years. Unfortunately# the information has shown that some
of the most common eliefs aout tying-up ha!e een pro!en wrong y scientific study. Thus#
what was considered y some early researchers to e a prolem that had one asic cause# e.g.
lactic acid# is actually a road-scale syndrome that will require continued research on a !ariety of
fronts efore e!ery aspect is understood.
In other words# tying-up is not one disease# ut se!eral different diseases that ha!e similar signs
and different causes. Therefore# the management of a Thoroughred that suffers from tying-up
would differ from the management of a 'uarter (orse that is tying-up# would differ from the
management of a ac)yard pleasure horse that has the same symptoms.
"ome horses are healthy athletes that tie-up sporadically li)ely due to e&ercise in e&cess of their
training le!el# electrolyte depletion# or dietary imalances. They respond well to rest# a gradual
return to a graduated training regime# and alancing the diet. *ther horses will suffer from chronic
episodes of tying-up that can e deilitating. *ur research suggests that there might e se!eral
inherited reasons for chronic tying-up.
+ertain lines of Thoroughreds seem more susceptile to one form of tying-up that has a asis in
anormal regulation of muscle contraction. Muscle contractions are initiated y propagation of
electrical impulses along the outer cell memrane and along memranous connections e&tending
into the cell# which then stimulate the release of calcium from intracellular memranous storage
sites. Muscle rela&ation requires energy-dependent pumping of calcium ac) into storage sites.
*ur research indicates that a common cause of tying-up in Thoroughreds is an inherited
anormality in the way calcium is regulated y memrane systems in the s)eletal muscle. The
narrow genetic origin of Thoroughreds and the common lineage of the pedigrees of horses with
tying-up would support the possiility of an inherited trait. The disease might lie dormant unless
specific factors trigger the calcium regulatory system to malfunction. Triggering e!ents include
stress# e&citement# lameness# high grain diets# and e&ercise at suma&imal speeds.
,oung fillies are most commonly affected and usually are the most ner!ous and high strung.
-re!ention of further episodes of tying-up in susceptile horses should include standardi.ed daily
routines and an en!ironment that stress and e&citement. The diet should e ad/usted
to include a alanced !itamin and mineral supplement# high-quality hay# and a minimum of
carohydrates 0such as grain and sweet feed1. 2eeding less than fi!e pounds of sweet feed and
adding additional calories in the form of fat decrease muscle damage with e&ercise. Daily
e&ercise is essential# either in the form of turnout# longing# or riding.
3nother form of tying-up that affects 'uarter (orses and related reeds# as well as warmloods
and draft reeds# is polysaccharide storage myopathy 0-""M1. 4ith this disorder# horses ha!e an
increased sensiti!ity to insulin resulting in increased storage of sugar 0glycogen1 in the muscle.
This imalance in sugar storage and accumulated precursors apparently distur energy
metaolism# and affected horses de!elop muscle cramping with light e&ercise. 3ffected horses
are often calm# sedate horses that tie-up after a lay-up# especially when fed grain.
Treatment of polysaccharide storage myopathy in!ol!es supplying them with an alternati!e
source of energy rather than sugar. Eliminating grain and sweet feed completely and feeding fats
such as rice ran lood sugar and decreases sugar storage in muscle. It is essential
that horses with -""M e turned out as much as possile and e&ercised often# e!en if only for 56
minutes e!ery day. (orses with mild to moderate clinical signs might e ale to return to full
athletic performance with careful dietary and management changes# which include regular daily
e&ercise without e&tended periods of inacti!ity.
7reeding 'uarter (orses with polysaccharide storage myopathy has resulted in offspring with the
same disorder. More research is needed in this area.
If your horse ties up# here are suggestions of what to do8 51 "top e&ercising the horse and mo!e it
to a o& stall. Do not force the horse to wal). 91 +all your !eterinarian. :1 7lan)et the horse if the
weather is cool. ;1 Determine if the horse is dehydrated due to e&cessi!e sweating. <1 -ro!ide
fluids with small# frequent sips of water to hot horses# and pro!ide free access to water once the
horse has cooled out. =1 $elie!e an&iety and pain. Drugs such as aceproma.ine might e
prescried y your !eterinarian. >1 $emo!e grain and feed? pro!ide only hay until signs suside.
@1 "mall paddoc) turnout is good once the horse wal)s freely# usually in 59-9; hours. If the
prolem recurs# ha!e the horse e!aluated for a specific cause of recurrent e&ertional
Stephanie Valberg, DVM, PhD, of the University of Minnesota is a leading researcher on the
subject of tying-up. She will present her research findings at the !P convention in early
)eywords8 tying-up# pssm# polysaccharide storage myopathy.
posted8 =A5=A9669. Bast updated8 9A9>A966:.

Vitamin " and "#uine Motor Neuron !isease
by $arold $int% Ph! MS

Thomas C. Di!ers# DVM# Dipl. 3+VIM# 3+VE++# reported at the +ornell at "aratoga "ymposium
on Equine (ealth +are that many of the questions aout equine motor neuron disease 0EMND1
ha!e een answered. EMND was first reported in 5DD6 y the late Cohn +ummings# DVM# -hD. It
is an acquired neurodegenerati!e disease of adult horses that is similar to amyotrophic lateral
sclerosis 0Bou EehrigFs disease1 in humans. Di!ers said the clinical signs in horses !ary
according to the form of the disease.
Subacute &orm
(orses de!elop acute onset of tremling# fasciculations 0rief# spontaneous muscle contractions1#
lying down more than normal# frequent shifting of weight in the rear legs# and anormal sweating.
(ead carriage might e anormally low. 3ppetite and gait usually are not noticealy affected. The
owner might mention that the horseshad een losing weight 0loss of muscle mass1 for one month
prior to the tremling.
'hronic &orm
The tremling and fasciculations suside and the horse ut with !arying degrees of
muscle atrophy. In some cases# the atrophy is so se!ere that the horse loo)s emaciated. In other
cases# there is noticeale impro!ement in muscle mass andAor fat deposition. The tail head
frequently is in an anormally high resting position.
Subclinical &orm
$esearch has pro!en that horses maintained on prolonged low !itamin E diets might ha!e
suclinical 0underlying1 disease. This could ha!e significant implications since affected horses
would# un)nowingly to the rider or owner# ha!e decreased strength. Di!ers and his colleagues
ha!e demonstrated that the damage to the neurons is caused y an o&idati!e disorder. They also
ha!e shown that all horses with EMND ha!e a low plasma concentration of !itamin E.
"ince the relationship of !itamin E to EMND has een disco!ered# the incidence of EMND has
greatly decreased.
'ause And Treatment
Vitamin E can e a !ery effecti!e antio&idant. That is# it is well )nown to protect against o&idati!e
damage. 3ll affected horses had a history of eing off pasture for an e&tended period of time.
-asture is an e&cellent source of !itamin E# ut the !itamin E content of hay can e deficient
ecause of losses of !itamin E during har!est and storage.
The disease was produced e&perimentally at +ornell in 56 horses which for more than a year
were fed a diet containing a low concentration of !itamin E. The research clearly showed that the
lac) of dietary !itamin E is a primary factor in the de!elopment of EMND. The studies were
supported y the Morris 3nimal 2oundation and the 3myotrophic Bateral "clerosis 3ssociation.
Treatment of affected animals with !itamin E can lead to some impro!ement# ut complete
reco!ery is unli)ely. "tudies supported y the Morris 3nimal 2oundation are underway at +ornell
to further define the role of !itamin E as a treatment.
Prevention (s )ey
The disease can e pre!ented y access to pasture. Di!ers recommended that all horses without
access to green forage for more than a year e routinely tested for plasma !itamin E# then
supplemented with !itamin E if needed.
GIf this were a standard policy# most# if not all cases of EMND could e pre!ented#G Di!ers stated.
GIf only the human disease were this simple.G
#arold #int$, PhD, MS, is delivering the %ran& '. Milne State of the rt (ecture on )utrition at this
year*s convention of the "erican ssociation of !+uine Practitioners. #e*s a professor of ni"al
)utrition at ,ornell and a new "e"ber of The (orse !ditorial dvisory -oard.
.he horse has long been considered livestoc& in the United States and throughout the world.
.his does not prevent individuals fro" enjoying their horses as co"panion ani"als. .hat is their
privilege, just as it is the right of others to continue to care for the" as livestoc&. ,hanging the
legal definition of horses to co"panion ani"als under state law, however, could adversely affect
horse owners and breeders and not necessarily better protect horses. #orse owners and others
should be "indful of this when considering various state initiatives.
American Association o* "#uine Practitioners
+,-. (ron /or0s Pi0e
Le1ington )2 +,.33
45,56 788-,3+-
posted8 =A5=A9669. Bast updated8 =A5=A9669.

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