EQUINE SHIVERS
Clinical Aspects of Myasthenia ('Shivers") in Horses
CLINICAL ASPECTS OF MYASTHENIA (‘SHIVERS’) IN HORSES


Copyright 2011 by Brenda Bishop, VMD
All rights reserved.
No part of this publication may be reproduced, stored in a retrieval system or transmitted, in
any form or by any means, without prior written permission of the author.


Abstract

Shivers is a hind leg unsoundness (a spasmodic condition affecting the thigh muscles of the
horse) that has been documented as early as the 1800’s primarily in certain draft horse breeds
and draft crosses.  Despite this historical record, many twenty-first century veterinarians fail to
recognize and diagnose Shivers; at best, a peculiar lameness is noticed for which there is no
treatment coupled with the expectation of no improvement and a gradual steady decline in the
horse’s usefulness.  This in-depth look at Shivers abandons the conventional classification of
‘lameness’ and attempts to characterize and appreciate a broader definitive context, namely that
of underlying autoimmune disease.  Taking into consideration the clinical aspects of three stress-
related immune mediated disorders (Myasthenia Gravis(MG), Lambert-Eaton Myasthenic
Syndrome (LEMS) and Fibromyalgia Syndrome (FMS)), Shivers is redefined as a component of
two autoimmune states traditionally labeled MG and LEMS in humans and as a potential
development in horses with equine FMS.  On the basis of this new approach to a centuries old
problem, useful and effective nutritional treatment protocols are reported.

The average age of onset for Shivers is 2 to 4 years or older, and the vast majority of affected
horses are male (geldings or stallions).  Shivers is somewhat unique in that it manifests
sporadically and only while standing and (eventually) at the walk, most obviously when walking in
the backward direction.  The blacksmith will frequently comment that the affected horse has
unusual difficulty holding one or both hind legs up; the affected hind leg will be held
spasmodically in a hyper-flexed position for several seconds before being placed on the ground.  
Careful observation will reveal fluttering eyelids and ears and possibly a raised tail at the same
time.  Stress in any of its various forms will exacerbate the problem; for example, work in excess
of the horse’s fitness level, extreme summer or winter weather, traveling long distances, etc.  
There are many historical accounts of horses developing Shivers after a long train journey.  
Stress and Shivers are such intertwined partners it is hard to tell how, when or where one stops
and the other begins.  As the body’s immune system is pushed beyond its capacity to function in
a healthy manner, the system goes into overdrive, a serious imbalance is created and the
possibility of an autoimmune state arises.



The Myasthenia Gravis (MG) Horse


When comparing multiple Shivers horses with each other it becomes abundantly clear that
several clinical entities exist.  If an effective treatment approach is to be formulated the
management team (caretaker, veterinarian, blacksmith, body worker, nutritionist, etc.) should be
informed with rudimentary knowledge of what goes on at the cellular level.  Within the
autoimmune category (an overly stressed immune system attacks some of its own body proteins
producing antibodies), Shivers reflects a disease of neurotransmission, specifically at the
neuromuscular junction (NMJ).  At the NMJ, the neurotransmitter acetylcholine is released from
small nerve endings, flooding the synapse between nerve endings and muscle receptors.  When
a sufficient number of acetylcholine molecules can attach to muscle receptors, there is an electric
discharge of the normal membrane potential and the muscle fiber contracts.  If many or most of
these receptors are already occupied by antibodies, neuromuscular transmission is blocked.  
This blockade is happening at the end of the chain of transmission, a condition referred to as
Myasthenia Gravis (MG).  In MG not enough acetylcholine molecules find receptors to trigger
normal muscle contraction.  The muscle endures a delayed irregular seizure type contraction
which is uncomfortable (not to mention frightening) for the horse and potentially dangerous for
any human standing near the affected body part.  MG in horses, dogs and cats is usually
localized to the point of being organ specific and even tissue specific.  For example, German
shepherd dogs with MG will display an enlarged esophagus and difficulty swallowing.  Horses
with MG will primarily have painful muscle spasms and cramping in their inner thigh muscles,
historically called Shivers.  Deficits caused by acetylcholine receptor antibodies, skeletal muscle
weakness, cramping within the inner thigh muscles and occasional sweating at rest characterize
what could be called the ‘post-synaptic myasthenic horse’.  

Current day symptomatic treatment of MG in humans, dogs and cats is based on knowledge of
the synaptic transmission of motor impulses at the NMJ by acetylcholine.  Conventional handling
of MG uses drugs which inhibit cholinesterase and which therefore serve to promote an
acetylcholine rich environment at the NMJ.  Examples of such pharmaceuticals are: neostigmine,
pyridostigmine, potassium chloride and DMSO.  All are impractical for treating a large animal
such as a horse.  Both neostigmine and pyridostigmine, agents of transient action, have some
limited value; for example, when a blacksmith appointment is looming and the horse needs to be
symptom free for a specific window of time on a specific day.  In this case a dose of 1800
milligrams pyridostigmine orally in the morning feed (using 60 milligram tablets) followed by a
dose of 10 milligrams neostigmine intramuscularly no less than three hours prior to the
appointment helps the horse dramatically (as well as all concerned) but this approach is
temporary and requires coordination and timing.  

The medical community agrees that MG frequently starts during or after a prolonged period of
intense stress, for example, emotional stress, malnutrition, chemical exposure, food sensitivity
and so on.  When prisoners of war in Singapore during World War II developed MG malnutrition
was suspected.  After introducing a vitamin rich diet, these patients were restored to more or less
permanent remission.  Following the war Europe experienced a virtual epidemic of MG.  When a
highly nutritious diet was used, similar improvement was reported.  Nutrients generally accepted
as stress-protective include all the B vitamins, magnesium, manganese, copper, zinc, and
vitamins C and E.  They are some of the many vitamins and minerals involved in energy
production and neurotransmitter production.  

Vitamin B1 alone is exceedingly useful; it is key for acetylcholine synthesis, it helps acetylcholine
bind to receptors and it enhances the effects of acetylcholine.  Vitamin B2 plays a role in tissue
respiration.  Vitamin B3 helps nerve cells make serotonin, an important neurotransmitter.  
Vitamin B6 also plays an essential part in neurotransmitter synthesis.  Vitamin B12 is a
requirement for the synthesis of choline, a building block for acetylcholine.  Magnesium activates
many enzymes; it is energizing at moderate levels but at higher levels it acts as a muscle
relaxant.  Manganese has a role in acetylcholine synthesis.  Copper is interesting in that women
require more than men; many horse owners believe mares require more copper than geldings
and stallions.  Zinc reinforces the immune system.  Vitamin C alone has as much if not more
value than vitamin B1; in addition to promoting healthy muscle contraction and metabolism and
helping with neurotransmitter synthesis, it has (drum roll please) mild anticholinesterase activity.  
A deficiency in Vitamin E, important in energy metabolism in muscles, leads to elevated muscle
protein breakdown as in MG.  According to several published reports, human MG patients have
been successfully treated with megadoses of vitamins B1, C and E.

As of the 1930’s some doctors were prescribing vitamin supplements in megadoses; in 1967 the
term Orthomolecular Medicine was contributed by Linus Pauling in order to convey the concept
“the right molecules in the right amounts”.  One of the early originators of Orthomolecular
Medicine was a 1936 graduate of Duke University School of Medicine, Frederic Klenner.  Using
vitamin C in conjunction with other nutrients to fight a number of illnesses, among them MG, he
was influenced by earlier work that linked nerve degeneration with multiple nutritional
deficiencies.  Eventually he developed a protocol for MG (and multiple sclerosis), described in his
paper, “Response of Peripheral and Central Nerve Pathology to Mega-Doses of the Vitamin B-
Complex and Other Metabolites”.  This same protocol can be extrapolated for use in horses with
extraordinary positive results.  For the average one thousand pound post-synaptic myasthenic
horse on a healthy diet the following nutrients can be added to the total daily ration:

10,000 IU Vitamin E              24 grams Vitamin B1                            2 grams Vitamin B2
1.5 grams Vitamin B3            9 grams Vitamin B6                             175 grams Vitamin C
50 grams Choline                  3 grams Magnesium                            300 milligrams Zinc        

Additionally, 10,000 micrograms (mcg) Vitamin B12 (for example 2cc of 5,000mcg/cc B12) can be
given intramuscularly 2 to 3 times weekly.  Loose manure from megadoses of Vitamin C is not a
problem because MG horses have a tendency toward constipation to start with and Ascorbic Acid
with wild Rose Hips (rich in bio-flavonoids) can be fed using time release 1500 milligram tablets
blended into hay cubes pre-soaked in water.  Injectable vitamins are impractical on a daily basis
and come with the added unnecessary risk of allergic reactions (anaphylactic shock).

In conjunction with megavitamin therapy, there are a variety of herbs suitable for use in horses
with MG that are useful for restoring and maintaining a healthy immune system.  For restoration
the combination known as Essiac Blend can be top dressed on the grain or added to soaked
fiber (beet pulp, hay cubes, hay pellets, hay stretcher, wheat bran, etc.).  It is comprised of
Burdock (a strong liver purifying and hormone balancing herb), Sheep Sorrel (a diuretic), Slippery
Elm (for all inflamed surfaces), Rhubarb Root (a mild laxative), and Talisman.  For immune
system maintenance in a horse with MG, all of the following are of benefit: Horseradish Root
powder, Broccoli powder, Parsley Leaf powder, Red Clover blossoms powder, Wheat Grass
powder, Cat’s Claw and Astragalus.  Astragalus is an adaptogen; it is respected as probably the
most important of all herbal deep immune tonics.

The MG horse will fare better if the caretaker remembers that MG has a tendency to reappear in
stressful situations, especially if the diet is unsuitable.  Usually the condition gets worse as the
day progresses.  Any planned activity that amounts to a stress should be scheduled early in the
day, such as transport, shoeing or trimming.  Denial of pasture access and heavy exercise are
both known to drop the bottom out of even a healthy horse’s circulating vitamin C levels.  Aside
from the main objective of stress reduction, pro-active immune support is helpful; one option is
once a month dosing with Colloidal Silver (60 milliliters of a 500 parts per million colloidal
suspension orally or intravenously).  All vaccination and deworming programs should be re-
examined.  Research has shown that even routine vaccination exacerbates active MG in other
species.  Repetitive vaccination amounts to an immunologic challenge to the horse’s already
compromised system.  Many over the counter deworming products contain ivermectin, a GABA
(inhibitory neurotransmitter) agonist.  Antibiotics belonging to the class Aminoglycosides are
likely to cause problems if used systemically, as they can cause neuromuscular blockade;
examples from this group are Gentamycin, Tobramycin, Amikacin, Kanamycin, Streptomycin and
Neomycin.  Slightly less risky are the Quinolone antibiotics (Ciprofloxacin), the Macrolide
antibiotics (Erythromycin, Azithromycin) and the Tetracyclines.  Immunosuppressive steroids
should be reserved for those horses that have lived with Shivers for years; they have a place in
critical situations but should be set aside once the patient is stabilized and made reasonably
comfortable.  


The Lambert-Eaton Myasthenic Syndrome (LEMS) Horse


With an understanding of Shivers as a problem of neurotransmission at the NMJ it becomes
possible to differentiate a second clinical entity that could be called the ‘pre-synaptic myasthenic
horse’.  When release of the neurotransmitter acetylcholine from the nerve endings into the
synaptic gap is reduced due to antibodies against a membrane protein of those nerve cells (the
active zone of the pre-synaptic membrane), the consequence is interruption of
neurotransmission and eventually the typical myasthenic syndrome.  In MG the autoimmune
process happens at the post-synaptic location, at the acetylcholine receptor sites of the muscle
cells.  When the autoimmune process takes place at the pre-synaptic nerve terminal the disorder
is labeled (in humans) Lambert-Eaton Myasthenic Syndrome (LEMS).  Interestingly the affected
human body parts are primarily the proximal muscles of the lower limbs (thigh and pelvis)
resulting in an abnormal gait.  Most patients are between 50 and 70 years old; LEMS is twice as
common in men as in women, the same ratio found in horses with Shivers.  A striking
component of LEMS is ‘anti-cholinergic syndrome’.  The LEMS horse likewise displays a
multitude of symptoms that would be expected in the presence of acetylcholine insufficiency.  
Whether the absolute quantity of acetylcholine is sufficient or not should not hinder our
comprehension of what the outside of the horse is telling us.   A thorough assessment for clues
will enable the observer to correctly conclude whether a Shivers horse is pre-synaptic or post-
synaptic.  (The post-synaptic horse is generally quite normal except for hind leg muscle
cramping.)

In light of current research on LEMS in humans, the specific findings in a ‘pre-synaptic
myasthenic horse’ are exactly as one might expect: any and all parts of the autonomic nervous
system are dysfunctional to one degree or another.  Those bodily functions that happen
automatically in a normal horse are now deficient.  Everyday caretakers have the responsibility of
noticing all these peculiarities which veterinarians can easily miss.  Even if everyone else misses
the diagnosis, the blacksmith will recognize the horse’s primary discomfort when attempting to
trim one or both hind feet.  Over a long period (years) the horse will eventually demonstrate
categorically that he has a number of other symptoms.  The pre-synaptic horse prefers to dunk
his grain and/or hay in a water bucket.  Why?  Because he has a dry mouth (inadequate
salivation).  Naturally he has a predilection for choking on dry foodstuffs.  He tends to take a long
time to eat for the same reason.  His eyes are also dry due to reduced lacrimation (tear fluid
production).  His manure piles are scant.  Why?  He is chronically constipated.  He periodically
hyperventilates at rest, suggestive of a Chronic Obstructive Pulmonary Disease (COPD) horse.  
Why?  He has pulmonary muscle fatigue which contributes to patchy sweating.  He has a
shortened stride going up and/or down hills.  Why?  Overall muscle tone is weak, especially in
the hind legs.  Delayed tendon reflexes ultimately lead to marked distension of the flexor tendon
sheaths above the hind fetlocks.  Even the muscles of the upper eyelids might be drooping.  
Dehydration should be monitored when the horse experiences excessive sweating at rest; a hot
humid day can trigger excessive stress for a body already at war with itself.  The history might
include food allergies and ‘sweet itch’ dermatitis in summer; different autoimmune problems
tend to cluster.

One wonders what goes on at the cellular level to initiate such a host of LEMS-like issues in
these horses.  The primary disorder in LEMS is reduced release of acetylcholine from the nerve
endings into the synaptic gap.  The body makes antibodies against a membrane protein of the
nerve cells; this type of membrane (the voltage gated calcium channel) is affected by several
classes of neurotransmitters called neuromodulators.  Neuromodulation is a relatively new
concept.  It can be thought of as ‘neurotransmitters on assignment’, floating around in the
cerebrospinal fluid, influencing (modulating) the overall activity of the brain.  Some
neurotransmitters are considered to be neuromodulators, for example, serotonin and histamine.  
Serotonin is famous for promoting feelings of well-being.  It is found predominantly in the
intestinal tract of humans and animals.  A smaller amount that is synthesized in the central
nervous system has various functions: regulation of mood, appetite, sleep, muscle contraction,
memory and learning.  In humans stress in the form of poor diet and/or lack of sleep ultimately
leads to serotonin deficiency (along with clinical depression according to most researchers).  
Nutrients that foster serotonin synthesis and thereby plug the drain are: vitamins B3, B6, C and E,
biotin, folic acid, methionine, copper, iron, magnesium, manganese and zinc.  These nutrients
can be termed serotonin boosters; certainly most of them also have value as anti-stress
nutrients.  An amplified potential for positive changes that can be jump started by using certain
nutrients in certain amounts and ratios (and in the same respect by using megavitamin therapy)
is implied by the concept of neuromodulation.   

Approximately two-thirds of all Shivers horses are male.  Male horses have the sex hormone
testosterone.  Testosterone antagonizes serotonin.  Female horses have the sex hormones
estrogen and progesterone.  Progesterone is the best friend serotonin ever had; it is a selective
re-uptake inhibitor and an inhibitor of serotonin breakdown all in one.  Perhaps female horses
have a built-in protection mechanism against developing Shivers in the form of their circulating
estrogen and progesterone levels.  In fact, progesterone DOES have a well documented
neuroprotective effect, so much so that it is given to humans with massive brain trauma in those
cases so extreme that no other options are viable.  The pre-synaptic Shivers horse can use all
the neuroprotection it can get.  (The problem is on the nerve cell side of the NMJ which is taking
orders from the central nervous system which ultimately involves the brain.)  Oral
supplementation with a 0.22% solution of synthetic progesterone , at a dose of 0.02 milligrams
per pound of body weight once daily will dramatically reverse all the symptoms displayed by a pre-
synaptic Shivers horse (of either sex) within 2 to 3 days.  How is this possible?  Progesterone
boosts serotonin levels which does much more than just make the horse feel peaceful.  Among
other things, serotonin has a direct effect on muscle contraction, it modulates skeletal muscle
oxygenation and it plays a role in sleep cycles. (Typically myasthenic syndromes get worse as the
day goes along).  But most impressively serotonin acts as a neuromodulator.  Neuromodulators
by definition influence both the release of neurotransmitter from the pre-synaptic nerve cell and
the post-synaptic cell’s response to the neurotransmitter, altering in a complementary way both
the input and the input-output relationship.  

Over the last several decades it has become acceptable veterinary practice to provide different
preparations of estrogen and/or progesterone to horses of both sexes for purposes ranging from
mood alteration (the lunatic stallion or the grumpy mare) to helping maintain muscle tone (‘loose
stifles’, weak back muscles) to attention deficit.  (More conservative over the counter oral
supplements promoted as ‘calming’ usually contain some combination of magnesium, vitamin
B1, tryptophan (a precursor of serotonin) and a wide range of herbs: chaste berry (vitex), skullcap,
chamomile, vervain, milk thistle, meadowsweet, passion flower or raspberry leaf.)  How can
administration of a hormone, progesterone, by boosting serotonin, a neurotransmitter, not just
make a moody horse feel better but thoroughly over-ride anti-cholinergic syndrome in the pre-
synaptic Shivers horse?  Serotonin must be operating in the role of neuromodulator.  This
premise can be substantiated when the hormone progesterone (with its ascribed inherent
capacity for neuroprotection) is eliminated from the treatment plan completely.  By substituting a
combination of all serotonin’s next best friends into the same pre-synaptic Shivers horse the
same all encompassing improvement is achieved.  As expected, by virtue of the fact that they are
friends as opposed to best friends they take an extra day or two to get the job done.  Appropriate
daily supplementation for a one thousand pound pre-synaptic horse would be the following
serotonin boosters:

20 grams tryptophan          1500 milligrams vitamin B3                600 milligrams vitamin B6
12 milligrams folic acid      3 grams methionine                            1 gram magnesium
6 grams vitamin C               65 milligrams copper                           275 milligrams zinc
250 milligrams manganese                4000 IU vitamin E

balanced with vitamin B1 (2 grams), vitamin B2 (500 milligrams) and choline (2 grams) along
with serotonin allies chromium (2 milligrams) and Ginko Biloba (500 milligrams). This formula
works quickly (within 3 to 4 days) and efficiently for the pre-synaptic horse.  It produces mild to
moderate improvement in the post-synaptic horse.

For the pre-synaptic Shivers horse supplementation with serotonin boosters amounts to a fairly
sophisticated yet simple to administer horse friendly approach.  Unfortunately for the patient
those bothersome in-laws, the autoantibodies, are not leaving anytime soon.  
Immunosuppressive drugs like steroids and azathioprine can force their eviction within about six
weeks but the total body will suffer collateral damage in the interim.  A better treatment approach
could be more accurately thought of as ‘enhanced neuromodulation’.  Mechanisms for healing
already contained within the system are maximized while simultaneously a healthier immune
system is enabled and enhanced.  Long term considerations might include herbal additives and
joint supplements.  Of all the herbs that are used for mood disorders in horses, chaste berry
(also known as vitex) is arguably the most useful; it balances estrogen and progesterone in
females and counteracts testosterone (not a friend of serotonin) in males.  It is thought to have
the added benefit of delaying the onset of Cushing’s syndrome, another stress related scenario,
in older horses.  Oral or injectable glucosamine is a good pain relief strategy for the post-synaptic
horse that competes on a regular basis as well as for the average pre-synaptic horse.  Without
question the most helpful management practice for any Shivers horse is 24 hour turn-out, with
constant grazing available.  For horses and humans alike exposure to sunlight is a requirement
of serotonin.  Humans are not the only species to suffer from seasonal affective disorder (SAD).



The Fibromyalgia Syndrome (FMS) Horse

Fibromyalgia in horses is in most instances a diagnosis by exclusion.  The afflicted horse is not
‘right’, nothing has been found to improve the horse, and specific symptoms are easily mistaken
for behavioral bad habits.  A thorough history becomes particularly useful ideally when it covers a
span of years.  Watching a FMS horse deteriorate is like watching grass grow.  In almost every
case there is an account of some (often forgotten) traumatic emotional or physical event prior to
the onset of symptoms.  The classic example is the gelding that had a ‘difficult castration’.  
Performance horses that spend much of their lives in transit or in dusty stalls are prime
candidates.  Many times the history includes an episode of prolonged treatment with antibiotics
and/or steroids; the one infectious scenario that is not usually considered or easily documented
but is almost always present is an underlying chronic systemic low-grade fungal infection.  
Fungal infections in horses can be external, internal or both, acute or chronic, and more frequent
at certain times of the year, typically late summer and fall.  In every case they are opportunistic by
nature; like rare orchids that require certain growing conditions, they thrive in environments
characterized by darkness, dampness, warm temperatures and low oxygen.  Examples of the
many acute (sudden onset) fungal diseases occasionally seen in horses are moldy corn
poisoning, Australian stringhalt, fescue toxicity and certain foal pneumonias.  In cases of chronic
(slow onset) fungal disease, when the possibility of a fungal component is targeted and
appropriate measures are instituted, the bulk of the FMS horse’s problems melt away within a
few weeks.  These problems fall into five general categories: cranial nerve deficits,
microcirculatory deficits, generalized chronic fatigue, endocrine imbalances and immune
mediated sequelae.  Due to the common denominator of stress, a complex immune mediated
cascade of events can set the stage for a specific autoimmune problem like Shivers to eventually
make its appearance.  

Typical of ‘flight or fright’ animals, horses react to stress with a natural reflex posture that can be
seen from afar.  They switch from the relaxed back, head down grazing stance to a hollow backed
high headed one.  Wild horses, dependent on their ability to forage steadily and still get moving
quickly, alternate between these two frames continuously.  Domestic horses that are healthy and
stress free have little need for the flight stance.  Nevertheless, they respond to stress in the same
predictable manner.  Just look at a horse while racing, walking on sharp rocks or responding to a
drastic change in environment.  Horses with FMS are perpetually hollow through their toplines;
they can no longer carry any muscle mass over their backs due to skeletal muscle
deconditioning.  Similarly, deconditioning of pulmonary (lung) muscle amounts to loss of
compliance (ability to expand and contract) at the level of the alveoli, where oxygen exchange
occurs, producing bouts of asthma or COPD (heaves).  Breathing becomes hard work.  Cardiac
muscle weakness leads to mitral valve prolapse in humans and to aortic regurgitation in horses,
i.e., a loud diastolic murmur with or without left ventricular enlargement.  Chronic fatigue quite
naturally ensues.

Horses with FMS seldom have dapples (branches of the capillary tree of arterial oxygen rich
blood supply) because they have microcirculation deficits and poor oxygenation of tissues
farthest from the heart.  Low oxygen levels in the feet can result in persistent thrush around the
frog, white line disease and poor quality hoof growth.  Total body soreness might include the
soles of the feet and hypersensitivity to touch (grooming tools, insects) anywhere on the upper
body.  Myofacial pain will be manifested according to which cranial nerves are involved.  TMJ
(temporomandibular joint) and masseter muscle (facial nerve) pain can turn eating into a long
distance marathon.  Hypersensitivity to certain wavelengths of light (optic nerve neuritis) or sound
(auditory nerve neuritis) can result in head shaking or explosive behavior.  Loss of equilibrium
(vestibular nerve neuritis) eventually leads to stumbling, falling down, problems moving on
uneven ground and problems standing up in a moving horse trailer.  Not surprisingly some
individuals start cribbing (a compulsive habit which affords the horse some relief in the form of
endorphin release).   

To say that hormones and neurotransmitters enjoy a close relationship is a gross
understatement; the details of their interactions are varied and complex.  Reflecting different
endocrine imbalances, FMS horses can exhibit extremely high or low estrogen, progesterone or
testosterone levels, excessive sweating or anhidrosis, and/or insomnia: sleep disturbances
which contribute to chronic fatigue.  Chronic depression, mood swings or sudden kicking
episodes which have a biochemical basis will slowly escalate.  Horses that display a shifting leg
lameness (lame in one leg this week and lame in a different leg next week) from front to back
and/or from side to side are nearly always FMS horses.  Small animal veterinarians dealing with
a shifting leg lameness will quickly suspect underlying infection; equine veterinarians are
cautiously reluctant in this regard.  (Immune mediated disorders are more commonly diagnosed
and treated in small animals than in horses.)

Immune mediated neuritis in the FMS horse manifests most dramatically in the head area
(cranial nerve involvement) and the hind legs (stringhalt, another hind leg lameness).  Stringhalt
is defined as intermittent upward fixation of the patella and usually has its origins in trauma to the
nerves supplying the lower cervical and upper thoracic portion of the horse’s nervous system.  It
can be observed at any of the forward gaits and is much more common in FMS than Shivers.  By
the time either condition appears veterinary intervention is critical.  The following protocol is user
friendly, horse friendly and effective: a double dose of fenbendazole daily (4.6 milligrams per
pound) for 5 consecutive days followed by a once daily dose of ketoconazole tablets in the feed (2
milligrams per pound) for 15 days.  Ketoconazole, a 200 milligram time release tablet, is quite
palatable and can be added directly to the grain without any extra steps for the caretaker.  
Fenbendazole in this instance is used to rejuvenate the lining of the gastrointestinal tract.  It strips
off the top layer of non-functioning cells in the large intestine, it has an escharotic (drying) effect
on any ulcers, it elevates the white blood cell count, it stimulates the immune system and it kills
off any overgrowth of Candida in the lower gut.  Conveniently it also deworms the horse
simultaneously.  Ketoconazole kills most garden variety fungal species so efficiently that an ultra
conservative dose is sufficient.  It has the added beneficial side effect of lowering the horse’s
serum cortisol, the stress hormone associated with Cushing’s syndrome.  With serum cortisol
back within normal levels healing can proceed naturally and unimpeded.  Stringhalt in these
horses will gradually resolve but a follow-up treatment regimen of the appropriate nutrients in the
right amounts will be necessary for the FMS horse displaying Shivers.

All the same aforementioned long term goals of stress reduction and stress management apply
to the MG horse, the LEMS horse and the FMS horse.  Shivers can be effectively handled with
common sense nutritional support, custom tailored to the particular myasthenic syndrome at
hand, either pre-synaptic or post-synaptic.  Once the immune system is returned to a normal
state of affairs, it is important to appreciate the potential for relapse if care is not taken to
safeguard the horse’s health.  In the particular case of a draft horse or draft horse cross, a
genetic pre-disposition to developing Shivers cannot be ruled out.  Consequently it behooves any
prospective new owner to question the breeder about the occurrence of Shivers in any known
family members as part of the preliminary information gathering process. Any consulting
veterinarians might be asked to contribute their personal opinions about the subject horse’s
ability to back up and move the hindquarters over while standing quietly; this exercise is easily
incorporated into the standard pre-purchase evaluation for overall soundness.  

This work honors those teachers who have gone before us and continue to light the way: Joseph
Haines, DVM, Frederick Klenner, MD, Frank Palka, DVM, Walter Pruitt, Ray LeRoy and the horses
Piedmont Pete, Brave Illusion and Percy Vere.




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