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Canine Hip Dysplasia
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Hip dysplasia, or HD, is a medical term that describes a malformation
of the femur head and/or
the socket of the hip where the femur head rests, that leads to debilitating arthritis
of the hip joint. As
a result of this malformation, the bones are in contact with each other causing
them to rub together, which eventually leads to arthritis. Depending
on the severity of dysplasia, outward signs can range from nothing at all,
to severe pain. The only way to conclusively diagnose HD is through X-rays.
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THE
PET HEALTH LIBRARY
By Wendy C. Brooks, DVM, DipABVP
Educational Director, VeterinaryPartner.com
http://www.veterinarypartner.com
Canine
Hip Dysplasia
Hip dysplasia
is a common condition of large breed dogs and many dog owners
have heard of it but the fact is that anyone owning a large breed
dog or considering a large breed dog as a pet should become familiar
with this condition. The larger the dog, the more likely the development
of this problem becomes, particularly as the dog ages. The following
is a review of this disease. If you have additional questions, please
send them through the Ask A Vet feature on the home page.
So What is Hip Dysplasia?
The term dysplasia
means abnormal growth, thus hip dysplasia means abnormal growth
or development of the hips. Hip dysplasia occurs during the growing
phase of a puppy, usually a large breed puppy, and essentially
refers to a poor fit of the ball and socket nature of the hip.
The normal hip consists of the femoral head (which is round like
a ball and connects the femur to the pelvis), the acetabulum (the
socket of the pelvis), and the fibrous joint capsule and lubricating
fluid that make up the joint. The bones (femoral head and acetabulum)
are coated with smooth cartilage so that motion is nearly frictionless
and the bones glide smoothly across each other’s surface.
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The
femoral head (the ball in the ball and socket joint) is outlined
in yellow. The acetabulum (the socket in the ball and socket
joint) is outlined in red. The femoral head ball is designed to
fit inside the acetabulum socket.
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For
more detail on the structures of the normal joint (see Normal
Joints)
When
a dog has hip dysplasia, the ball and socket do not fit smoothly.
The socket is flattened and the ball is not held tightly in place,
thus allowing for some slipping. This makes for an unstable joint
and the body’s attempts to stabilize the joint only end up yielding
arthritis.
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normal hip - femoral head fits snugly
inside acetabulum
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early stage hip dysplasia - note space
between femoral head and acetabulum
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If this Disease Starts in
Puppy hood Why are Most Affected Dogs Elderly?
Actually, there are two sets
of patients typically affected by hip dysplasia. The first group
is the adolescent dog, typically 6 to 18 months of age. The radiograph
on the right shows the hips of such a patient. This dog has hip
dysplasia but has not yet developed arthritis. Note the shallow
hip sockets. This dog was brought to the vet’s office for signs of
discomfort. Radiographs were taken and hip dysplasia was discovered.
Many dogs with similar radiographs will not be in pain and thus
will not end up coming to the vet for an evaluation. These dogs
show up as elderly dogs, after they have been walking on their poorly
formed hips for many years. After many years, bony build up along
the margins of the socket, mineralization of the joint capsule, cartilage
wear, and inflammatory change in the joint (i.e., degenerative arthritis)
has become painful and now the dog comes to the vet for an evaluation.
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bad hip dysplasia
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Why Do Some Dogs Have Pain
at a Young Age While Others Don't Have Pain Until They're Old?
Obviously
different individuals may have different degrees of dysplasia.
A dog’s weight makes a difference (a lighter dog can tolerate
a more abnormal hip joint). The muscle mass supporting the joint
is greater in a younger dog and helps reduce the stress directly on
the bones. Still, some dogs have truly shocking radiographs and virtually
no symptoms while others show relative subtle changes and are very
uncomfortable. We don’t know why there isn’t a better correlation
between radiographs and actual pain.
How Can an Owner Tell if
their Dog is Having Discomfort?
Do
not expect a dog with dysplasia (or any other chronically painful
condition for that matter) to cry or whine in pain. Instead discomfort
is shown with reduced activity, difficulty rising or lying down or
going up stairs. A characteristic swivel of the hips is seen from
behind and classically stairs are taken in a bunny hop fashion.
What Causes Hip Dysplasia?
The primary cause of hip dysplasia
is genetic but inheritance of this trait is not as simple as
a dominance/recessive relationship like we study in high school biology.
Normal dogs can breed and yield dysplastic offspring as the condition
may skip generations. Until a test based on the actual DNA can
be developed, the best we can do to prevent this disease is to breed
only dogs with normal hips (a challenge since often dogs are not
apparently dysplastic until they have already started a breeding career.)
Nutritional
factors are also important in the development of hip dysplasia.
For example, it has been popular to try to nutritionally “push”
a large breed puppy to grow faster or larger by providing extra protein,
more calcium, or even just extra food. Practices such as these have
been disastrous, leading to bones and muscle growing at different rates
and creating assorted joint diseases of which hip dysplasia is one.
One study showed that when puppies of hip dysplasia prone breeds were
allowed to free feed, two thirds went on to develop hip dysplasia while
only one third developed hip dysplasia when the same diet was fed in meals.
Another study showed German Shepherds were nearly twice as likely to develop
hip dysplasia if their adult weights were above average. Studies such
as these have led to the development of puppy foods designed for large
breed puppies, where the optimal nutritional plane is lower than for small
breed puppies.
How Can I Find out if My
Dog has Hip Dysplasia?
There
are two reasons to pursue testing: to explain a dog’s discomfort/rear
weakness or to screen a dog for breeding purposes. If a dog is
not going to be bred and is not in any apparent discomfort, there
may be no benefit to looking at the conformation of the bones in
a radiograph except possibly to look back at a future time to get
a sense for progression of bony changes.
The
first step in diagnosis is an examination. Your veterinarian
will likely extend the dog’s hind leg backward to check for pain.
(Hip dysplasia causes pain on hip extension.) The dog may be
asked to walk around to demonstrate the possible hip swivel.
Another test involves having the dog lie on its back with a
hind leg perpendicular to the body. As the
leg is moved away from perpendicular to the body, a dysplastic
hip will generate a pop as the femoral head slips to the center
of the acetabulum. This pop, which can be felt if one’s hand
is resting on the hip during the exercise, is called an Ortolani
sign. You may hear this term used as hip dysplasia is discussed.
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in
a dog suffering hip dysplasia, femoral head has moved away
from acetabulum
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Ortalani
sign: an audible pop is heard as the femoral head slips back
to the center of the acetabulum
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To find out for sure about dysplasia, radiographs
are necessary and this generally involves some sort of sedation
to minimize the patient’s discomfort as their hips are properly
positioned for the picture. Sedation also helps the veterinary
team control the dog’s position better so they can minimize the number
of radiographs needed in order to get one good diagnostic view. The
classical view is called a VD pelvic view where the dog is held on
its back with its legs straight out. This shows the seating of the
two femoral heads as well as any bony changes indicating arthritis.
This is the view required by the Orthopedic Foundation for Animals for
registration.
What is OFA Registration?
When purchasing a puppy, particularly one of
a larger breed, often the parents will be listed as “OFA Good”
or “OFA Excellent.” What this means is that the breeder has had the
hips of the dog’s parents certified by the Orthopedic Foundation
for Animals. The OFA is an organization with a goal of reducing the
incidence of hip dysplasia (though now it is also possible to obtain
certification for elbows, thyroid function, and other issues). The idea
here is that a dog for breeding can have radiographs taken at age 24
months. The radiographs are sent to the OFA for review by several independent
radiologists where they are graded. Hips that are rated as good or
excellent receive a registration number. Offspring of OFA-certified
parents would be less likely to develop dysplasia themselves, however,
it is important to realize that a dog with excellent hips at age 2 may
not have such excellent hips at age 5, 7, or 10. OFA certification
is no guarantee that a dog will not develop hip dysplasia symptoms in
the future and does not guarantee that the offspring will not develop
hip dysplasia.
What is PennHip Registration?
Many
people with potential breeding dogs do not 
want to have to wait two years for OFA registration.
The University of Pennsylvania Hip Improvement Plan, developed
by Dr. Gail Smith, allows for another way to predict if a dog will
develop hip dysplasia. For PennHip certification, the veterinarian
taking the radiographs must receive special training and special equipment
is necessary. The pet is anesthetized and two radiographs are taken:
one with the femoral heads compressed (pushed into the acetabula as
far as they will go) and one with the femoral heads distracted (pulled
out of the acetabula as far as they will go). A measurement called
a distraction index is calculated from these radiographs, the
idea being that a tighter fitting hip (one allowing less distraction)
is less likely to develop dysplasia. Each dog breed has a different range
of distraction indices that are considered acceptable. Puppies can be
certified as young as 16 weeks of age with this system.
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view
in distraction
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view
in compression
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Is Surgery the Best Treatment for Hip Dysplasia?
There
are many surgical options for hip dysplasia and it is important
to understand which patients benefit from which surgery. Some
surgical procedures are controversial and some are not. All will
entail a recovery period as well as expense. Often both hips need
not be treated surgically; treating one hip is often enough to yield
good results. Hip surgery is expensive, usually $2000 to $3000 in the
Los Angeles area. If you are considering surgery for your dog, these
are the procedures to know about:
•
Triple Pelvic Osteotomy
This
surgery is appropriate for young (age 8-18 months) dogs with
dysplasia but without degenerative arthritis changes. This means
that there is a window of opportunity for this surgery and if the dog
develops arthritis or becomes too old, it will be too late for this
surgery to be performed. In this surgery the ill-fitting acetabulum
is essentially sawed free of the rest of the pelvis, re-positioned for
a tighter fit on the femoral head, and then plated back into place.
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Three cuts are made to free the
acetabulum from the pelvis
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Many
times surgery on one hip leads to positive changes in the other
hip so that surgery on the second hip is not necessary. Alternatively
it is possible to do the TPO on both hips if it seems clear that ultimately
both will need surgical correction. This is a surgery that requires
a board certified surgeon or a surgeon with extensive orthopedic
experience. After care involves a good 3 to 4 months of exercise restriction.
No leashed walks are allowed for 2 months except to go outside for
elimination.
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Femoral Head/Neck Ostectomy
This
surgery is commonly referred to as the “FHO” and is best used
for smaller dogs (50 lbs or less) or very active dogs. Here, the
femoral head is cut off and removed, allowing the joint to heal as
a false joint (just a
capsule connecting the two bones but no actual
bone to bone contact. If the dog is not carrying too much weight,
a false joint is strong enough. If the dog is very active, a false
joint will form quickly. The pet typically does not want to use
the leg for the first 2 weeks but should at least be partially using
the leg after 4 to 6 weeks. The leg should be used nearly normally
after a couple of months. Many veterinarians are well experienced
with this surgery and often a specialist is not needed. This surgery is
typically substantially less expensive than the other procedures.
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femoral head before FHO
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femoral head cut off after FHO
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Total Hip Replacement
This
procedure is for dogs with established degenerative hip changes.
For these dogs, the best choice may be to simply replace the hip
(or hips) with a prosthetic hip. This procedure may sound radical
but it has been commonly performed for nearly 20 years in dogs with
great success. This is a highly invasive procedure, obviously, and
infection must be avoided at all costs (no skin disease can be present
in the skin over the hips, extra precautions for sterility are used).
In other words, when complications occur they have potential to be disastrous.
Complications have about a 10% incidence. Expect about 3 months of exercise
restriction after this procedure. Usually only one hip receives surgery
at a time. Often only one replacement is needed and the pet does well enough
not to need surgery on the other side.
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x-ray
of a bilateral (both hips) total hip replacement
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•
DARthroplasty
“DAR”
stands for dorsal acetabular rim. In this procedure, bone grafts
taken from other areas of the pelvis are used to build a longer
rim on the acetabulum so that the femoral head will have a deeper
socket in which to fit. This procedure is best done in dogs that are
too old for triple pelvic osteotomy or have just started developing
degenerative arthritis. This is a fairly new procedure in the hip
dysplasia arena and thus somewhat controversial. Long term success
(i.e., how patients do when they are old) is not really known as the
procedure has not been performed long enough to collect results from
a large number of patients. A specialist is needed for this surgery.
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Juvenile Pubic Symphysiodesis
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This
surgery is performed on young puppies before age 5 months, so
it is generally done as a preventive procedure before it is known
if the puppy will indeed have dysplastic hips. The pubic symphysis
is the cartilage seem connecting the right side of the pelvis to the
left side. As an individual matures, this cartilage converts to
bone and the two halves of the pelvis fuse permanently. This surgery
prematurely seals the symphysis, which in turn results in rotation
of the developing hip sockets into a more normal alignment. While studies
show promise, because this procedure is done on puppies who do not
yet actually have hip dysplasia, it is hard to evaluate success.
What Non-Surgical Treatment is Available?
Non-surgical
treatment of hip dysplasia is essentially the same as non-surgical
treatment for any other type of arthritis. There are nutritional
supplements to help repair cartilage, pain medications, and anti-inflammatory
medications. Physical therapy and massage are also important and
helpful in non-surgical joint therapy. For details see Medications
for Degenerative Arthritis.
Date
Published: 2/21/2005 10:50:00 AM
Copyright 2005 - 2007 by
the Veterinary Information Network, Inc. All rights reserved.
This work was originally published
by Veterinary Information
Network, Inc. (VIN) and is republished with
VIN's permission.
*************************
Hip
Dysplasia latest News
A research study funded by
Morris Animal Foundation with grants from The Seeing Eye, Inc.
and the Golden Retriever Club of America has raised quite a few eyebrows.
The data, presented at the 27th Veterinary Orthopaedic Society
meeting, held in France in 2000, concerned Golden Retrievers radiographed
for signs of hip joint laxity. Average age was 11 months. Three views
were made; including the traditional hip-extended one used by OFA
and almost every control registry in the world, and the PennHIP distraction
and compression views that more accurately reveal joint looseness.
In the hip-extended view, the measure
of observable laxity was made using the Norberg Angle (NA),
and in the view with the femoral heads levered out from the
sockets as far as they will go, the measure used is the distraction
Index (DI) developed by PennHIP for early and accurate detection
of that most important HD risk factor. The study was to determine
heritability estimates for the different types of hip scores in this
breed. Heritability is a ratio that refers to how much effect "selection
pressure" (choices of breeding partners, mostly) has on genetic progress;
it is expressed by a number between zero and one (0 - 1). The higher
the number, the faster one can make progress (in reducing HD, for
example). These heritability numbers vary considerably from one diagnostic
technique to another.
The heritability estimate of the subjective
hip-extended scoring method was 0.22 and this was not statistically
different from zero (0). Remember, when we use the word "statistically"
we are talking about a specific mathematical science, not the
very loose use of such words by the general public. The heritability
estimate for the only objective part of the hip-extended view (NA)
was 0.46, a big improvement. Both it and the 0.64 heritability
estimate of the DI method are statistically significant.
Conclusions: Using DI, genetic
change (progress in your hip improvement program) will occur
40% faster than you would expect using the NA, and a whopping 290%
faster than by using the OFA-type hip-extended subjective method.
Further calculations and comparisons showed that the square roots
of these heritability estimates are important: the subjective hip-extended
figure here is 0.47, which means that if you use just that knowledge
to choose breeding partners, you have no more chance of making a
lucky decision (improvement in hips) than if you had just flipped a
coin. The DI square root of 0.8 is twice as high, and your odds of making
a wise move armed with such knowledge are vastly improved. When you
factor in the relatively new and until now obscured calculation of Breeding
Value or Zuchtwert, you can get even more accuracy and faster progress.
The Seeing Eye has been using BV for years, and the largest breed club
in the world, the SV (GSD’s) has begun publishing ZW numbers for all
breeding dogs, active or potential. I think when the more sensible leaders
of the Golden club see these data and conclusions, they will want to
implement a BV-ZW system as well as encourage PennHIP DI use by breeders.
copyright Fred Lanting,
may be forwarded only with permission of author:
Fred
Lanting is one of only two SV conformation judges in North
& Central America, and has judged the breed in more than
a dozen countries beyond that. His most recent international assignments
have included Peru (See USA’s Nov-Dec 1999 issue), India and Pakistan,
Edmonton, Jamaica, and Chile. He annually offers a tour of parts
of Germany and sometimes neighbouring countries for the days before,
during, and after the Sieger Show (BSZS), with visits to working-line
kennels and clubs as well as show aspects of the breed. He believes
in trying to live up to the name of his book, “The TOTAL GSD”.
Fred Lanting, Canine Consulting Lectures & Seminars
on Orthopaedic Disorders, Gait-&-Structure, Etc.
*****************************************
Gait & Structure (Analytical
Approach)
Fred
Lanting, Canine Consulting. Mr.GSD@hiwaay.net
Seminars: Canine HD & Other
Orthopedic Disorders;
GSD myelopathy - GSD myelopathy,
also known as DM for Degenerative (chronic and progressive)
Myelopathy (spinal cord disease), is the first disorder that
comes to mind when German Shepherd Dogs and spinal lesions are
spoken of together. Almost peculiar to Shepherds, the first symptoms
are usually seen at about six to eight years of age and have a
duration of five to twenty four months, a bit longer if aggressive
measures are taken. Initially, the dog does not seem to realize
what position his rear legs are in; soon he will begin to drag his
toenails and the top part of his paws, and may tremble as if palsied.
Eventually, he will be unable to get up on all four legs, and by this
time most owners will have decided upon euthanasia. Symptoms and histological
changes are very similar to those in multiple sclerosis (MS).
First described as a specific, separate
disease in 1973, GSD myelopathy has been around a long time,
but previously not as well understood or distinguished from other
pathologies. It gets its common name from the fact that German
Shepherd Dogs are found relatively often, compared to much more uncommonly
in a few other large breeds. As a matter of fact, the peculiar
syndrome seen in our breed is also seen only (though rarely) in
the Belgian Shepherd and the Old English Sheepdog, and Dr. R. M.
Clemmons, neurology professor at University of Florida's veterinary
school, feels what is seen in other breeds may well be a different disorder.
Those other degenerative myelopathies are probably not caused by the
same immune-system-related deficiency as we have in the GSD.
Diagnosis is by the process of elimination,
since regular neurological tests aren't definitive, except
for the presence of a brain fluid protein in the lumbar area
of the cord. Your best bet would be to consult an experienced breeder
who's been through it with his own dog or dogs, and use the local
vet for confirmation and medication. He will see what you have:
the dog atrophies in the haunches and croup. Autopsy will not
help you or your dog, but would find the obvious demyelination (loss
of the insulating sheath) of the spinal cord, destruction of some
large axons (nerve cells leading from the cord to smaller branch nerves),
and abnormal cells (or certain cells in abnormal locations).
Similar signs may be seen in the brain's white matter, and plasma cell
infiltrates in the kidneys and intestines give further evidence of the
immune system failure at the root of this disease.
Since GSD myelopathy is so similar to
multiple sclerosis, perhaps it would be worth trying the nutritional
approaches used by some who treat that human disorder. Wheat
germ oil contains octocosanol, a fatty or waxy high molecular
weight alcohol also given to patients with encephalitis and
cerebral palsy, and also contains linoleic acid (as do several vegetable
oils). But one fatty acid, docosahexanoic acid, is not at all
abundant in normal diets, yet seems to be the first one depleted
from the nerves' myelin sheaths in such disorders as MS. In many
diets for MS patients, foods such as sardines and mackerel are emphasized,
because they are among the very few foods that can supply this compound.
Of course, vitamin B complex high in inositol, B6, B12, and choline
is also highly recommended as an adjunct to vitamin E for nerve muscle
disorders.
Since only a percentage of patients with
MS or DM respond satisfactorily to a vitamin only approach,
the concomitant use of drugs and exercise should always be
prescribed. As of this writing, there were three FDA-approved
drugs for MS that not only help manage symptoms but also appear
to "impact disease course" in relapsing MS, according to the National
Multiple Sclerosis Society. They are Copaxone (Teva Marion),
Avonex (Biogen), and Zanaflex (Athena Neuro sciences). Your vet
would have to decide whether or not he wanted to "go off-label",
since these have not (yet?) been approved for dogs.
For several years, there was no generally
accepted treatment, but as breeders became aware of the benefits
of high vitamin E dosages, the veterinary profession began
to see its efficacy and the relation to the immune system.
When I first encountered it, I got an extra one or two years useful
life out of one of my dogs by giving him 800 units (IU) a day,
plus vitamin C for its synergistic effect. Years later it
was discovered that 2000 IU of vitamin E daily, 500 mg of vitamin
C twice a day, and a high strength vitamin B complex twice a day is
the best dosage. Vitamin E is an important nutrient with a number
of physiologic and pharmacological effects. As an antioxidant it
helps reduce oxidation of fats and increases the production of HDL
cholesterol. At higher doses it decreases production of prostaglandins
and has anti-inflammatory action There is no known side effects
to vitamin E at levels less than 4000-6000 IU per day (except in
cats, where levels above 100 IU/day can create hepatolipidosis.
In DM, low serum and tissue concentrations of vitamin E have been observed.
I recommend that vitamin E be given to all German Shepherd dogs.
For GSD's less than 2 years of age, give 400 IU of vitamin E daily.
For older GSD's, give 800 IU of vitamin E daily. If your dog develops
DM, then the dose of vitamin E should be increased to 2000 IU daily.
Dr. Clemmons recommends the vitamin E be dropped temporarily to about
100 IU if the dog has to be given aspirin for any reason during the
treatment, and recommends that daily DEC (diethylcarbamazine) replace
the monthly heartworm medications ivermectin (Heartgard, Heartgard
Plus, Ivomec) and Interceptor because these increase immune responsiveness;
also use the DEC in place of styrid caracide or Filaribits. Personally,
I would simply stop all use of heartworm medication, because the dog
with DM isn't going to last as long as it takes for a case of heartworm
to become life threatening anyway. Flea control should be limited to
Precor™ for the house, and carbamates or pyrethrin/pyrethrum on the
dog.
Chemical-pharmacological treatment has
largely been via the use of aminocaproic acid, something
my friend Wayne Riser (founder of OFA) told me about many years
ago. More recently, acetylcysteine three times a day has found
acceptance. It now appears the best treatment is a combination
of all three approaches, along with exercise. Alternate day
dosage with a steroid such as prednisone, plus acetylcysteine, added
to the aminocaproic acid and vitamin formula, is enough to keep
the dog owner very busy and tied to the home, but it offers the
best chance at reducing progression, thus prolonging life considerably
more than in the past. The drugs should be given in liquid form,
mixed with a palatable solution such as chicken broth. There
are generic varieties available. Medication helps up to 80% of afflicted
dogs, especially if started early.Hydergine, a prescription drug
derived from ergot fungus is being researched, since it seems to
promote nerve regeneration. For dogs with advanced DM, Dr. Clemmons
suggests trying 5 mg three times a day for at least three months.
I mentioned exercise, and this is the
third of the four part fight against the disease. Every other
day, the dog should be given at least 30 minutes of aerobic
activity such as vigorous walking or swimming; if you start late,
build up to the strenuous level gradually; if your dog can't do the
most, do less, but make it regular and stretch the limits where you
can. The alternating days of relaxation are important for repair and
renewal. If the dog acts sore, give him the analgesic prescribed by
your vet (after he has "read up" on the interactions of medications in
regard to GSD myelopathy. The fourth part is stress reduction. The
vitamin C, that anti stress vitamin, is there for a good reason,
but take steps to avoid stressful situations, including surgery; if
the dog needs surgery, make sure he gets the acetylcysteine as
well.
Dogs with GSD myelopathy often develop
lick granulomas, which are ulcerations or (if you are lucky)
callous like reactions of the skin to extremely frequent licking,
sometimes chewing, at the location of a supposed itch. It is probably
a case of the limb feeling as if it has "fallen asleep",
to put it into terms familiar to human experience. The tingling
sensation caused by incomplete and erroneous signals by the nerves
serving that place is much like the irritation caused by an ant bite,
or hairs out of place, or anything in between. In trying to
lick it away, the dog actually softens and wears away the hair and skin.
The best I could do for my dog was prick the vitamin E capsule, squeeze
out a little for topical application to the granuloma, pop the rest
into his mouth, and then give him some distraction such as go for a
walk. These ulcers on the feet or elsewhere don't easily respond, but
the battle must be waged if the dog's life and comfort are to be prolonged.
The approach to treatment of GSD Myelopathy
that is proposed by Dr. Clemmons is called "integrative treatment".
It combines conventional pharmaceutical treatment with "alternative
medicine" or "supportive therapy". Paraphrasing some of his
comments might be helpful here. Conventional drug therapy (medicines)
has been of little lasting help to patients with DM. However,
the combination of exercise, vitamins and certain drugs have delayed
the progression of DM in many dogs. Treatment has been directed
at suppression of symptoms, and since the cause of this autoimmune
disease is not known, little has been done in the way of finding
out how to prevent it. There are possibly genetic, environmental and
toxic factors involved. Saying that Degenerative Myelopathy is an
autoimmune disease means the animal's immune system attacks its own
cells; in this case, the central nervous system. The myelin insulation
sheath around the nerves and axons (fibres) is gradually destroyed.
It's worst in the thoraco-lumbar area of the spinal cord, but can also
affect the brain stem and other nerve tissue.
Integrative or supportive treatment of
German Shepherd Dog Myelopathy as promoted at the University
of Florida vet school suggests the use of dietary alternatives
and supplements to combat the immune system, and are derived
from an approach to treating Multiple Sclerosis. You probably know
at least one person with MS, and can recognize the similarity in
symptoms. Besides the vitamins E and C, the drugs, and the exercise
mentioned above, avoidance of toxins such as is found in pesticides and
lawn chemicals, and perhaps in some processed foods, is possibly helpful.
If you cannot manage "home cooking" with its involved recipes, supplement
dog food that is as natural as possible with recommended aids. Soybean
curd (tofu) protein contains flavonoids; raw garlic (action is lost
when is cooked or dried) is anti-bacterial and anti fungal, and may benefit
the dog by reducing immune challenge. Ginger is also anti-inflammatory
and with garlic, can replace aspirin and other NSAIDs. Adding soy concentrate,
soy lecithin, and beta-carotene and other vitamins to commercial food
is recommended. Use "stress formula" B-complex containing 100 mg
of most of the B vitamin components; or use yeast as a good source of
these B-complex vitamins, trace minerals, and some protein. It is relatively
inexpensive; try half a tablespoon mixed in each meal. If your dog gets
flatulence, use a discount or mail order vitamin B complex pill instead.
Antioxidants vitamins E and C are synergistic;
i.e., they work together better than they do separately.
While dogs produce vitamin C, those with DM may need more than
they can manufacture. In excess, it also can cause flatulence.
I normally recommend not supplementing with vitamin C for longer
than a month or two at a time, but in the case of a permanent,
chronic disorder like DM, it's better to continue usage. Tolerance
in the intestines may be for as much as 3000 mg per day, but up to
1000 mg twice a day should be enough unless it causes diarrhoea. Selenium
also is synergistic, helping vitamin E to be more effective. It can
be toxic if given at more than 200 µg (micrograms) of selenium
per day. I take 200 µg whenever I feel I'm not getting much
western grain (good source of selenium) in my daily diet, and I weigh
twice as much as my largest German Shepherd Dog.
Clemmons says that "Omega-3 fatty acids
such as EPA (eicosapentanoic acid) and DHA (docosahexanoic
acid) are the constituents of fish oils that act as anti-inflammatory
agents and may be worth trying if your dog has an autoimmune disorder
or arthritis." Fortunate is the owner who can give an afflicted
dog a couple of cooked sardines or a small piece of salmon as a daily,
natural source of such fatty acids. A 1000-mg fish oil capsule, tablespoon
of ground flax seeds, or flaxseed or wheat germ oil supplement can
do about the same thing. If you are really "into" the health food store
shopping, 500 mg twice a day of GLA (gammalinolenic acid), a fatty
acid found in evening primrose and black currant oils is an alternative
anti-inflammatory without the side effects of most anti-inflammatory
drugs. All of the above should be considered as optional adjuncts
to conventional treatment with the drugs, vitamins, and exercise,
not replacements for them.
Cauda equina syndrome, giant axonal neuropathy,
and tumours may also mimic DM. Many cases of spinal and related
nerve damage are due to sudden trauma, but some can result
from encroachment of bone or tumours into the space occupied
by the cord. Since nervous tissue does not regenerate, such conditions
result in partial or complete paralysis. Symptoms similar to myelopathy
may be brought on by a nerve cell degeneration normally associated
with age. However, with the latter disorder the rapidly progressive
nature of GSD myelopathy is not seen. Neoplasms also cause the dog
to display symptoms similar to those of GSD myelopathy. These
tumours on the spinal cord, neuroepitheliomas, have a special
predilection for German Shepherd Dogs from six months to maturity
at three years of age.
copyright Fred Lanting, may be forwarded only
with permission of author:
Fred Lanting, Canine Consulting.
mailto:Mr.GSD@hiwaay.net
Seminars: Canine HD & Other
Orthopedic Disorders
Fred's latest book "The Total German Shepherd
Dog"
**************************************
The following article was written in response
to an article claiming that the cause of HD within our breed
lay in diet. Read original article here
Cause of HD — A Summary
There will always be those
who rebel against evidence, and pick a seeming exception on which
to build a contrarians theory. It’s like the cults that take a verse
of the Bible, misinterpret or mistranslate it, and build a whole
religion on it. They balance an Egyptian pyramid upside down on
its pointed head. Eventually such a structure will fall.
The bane of the scientist has always been
the multitude of anecdotal reports that, like mushrooms,
pop up suddenly and unexpectedly in the dark. One such report
(without scientific controls) from Norway in the early 1990s argued
that in five breeds, but not two others, HD was more likely to show
up in puppies that grew up in the fall and winter. As in other amateur
observations, questions were raised regarding exercise and sunlight
(vitamin D) among other differences. In fact, most attempts to pin
the blame of HD onto environment involve diet and exercise. While
we must not reject out of hand all anecdotal claims, we must also place
our bets on the repeatable, controlled studies, if we want to gain
true knowledge. People have blamed the brand of dog food, the footing
puppies were raised on, and other things for the appearance of dysplasia
in puppies that they have sold, with or without guarantees and/or stipulations.
There is no scientific basis for these excuses people use in order to
not make good on defective “products”.
On the other hand, there is plenty of
support for the fact that “over nutrition” and more rapid
growth are responsible for the genetically pre-disposed dog
to develop worse and earlier HD than might be the case if on a restricted
diet. My new revision of the HD book will deal with this in detail.
While some have claimed that exercise is needed to maintain a
“deep acetabulum”, there is likewise no controlled study to back up
this concept. It is “common wisdom” that hip-extended radiographs
seem to show less laxity in young dogs that have been kept lean and
frequently exercised, such as in training for schutzhund and police
work, than found in dogs living a more relaxed life, but stress radiography
shows every case of laxity. Muscle tone can have some positive effect
on the tightness of the joint capsule, as long as regular exercise
is maintained. It has no effect, however, on the genes, so a dog that
has been “lean and mean” until its skeleton had fully ossified, is
just as dangerous to breed to as is his litter mate who has reclined
on a couch most of his growing up life.
GENES, NUTRITION, AND DENIAL
At the end of Year 2000, an article appeared
in the underground media, primarily Internet and e-mail discussion
groups, called “The Error of the Millennium in Veterinary
Medicine”, a sequel to a “compendium” pamphlet called “The
Thirty Years’ War”. The reason it was there but was refused by
all legitimate journals and magazines was that its premise was
so preposterous. It reminded me of the inflammatory claim of the same
decade that the Nazi Holocaust never happened. Of course, history
is full of examples of error that promenade as fact, and discoveries
that are suppressed for long years until someone else proves their
validity. For one, an Australian researcher named Barry Marshall
stated that stomach ulcers were caused by bacteria, and even proved
it by swallowing the microbes, developing ulcers, and curing them
with antibiotics. Yet the textbooks for years continued to give the
“risk factors” as smoking, alcohol, stress, and genes. We now know that
TB and peptic ulcers are infectious disorders, as the November 27, 2000
issue of News week stated, in its review of “Plague Time”. In that new
book, Amherst biologist Paul Ewald put forth the equally revolutionary
concept that parasitic germs are the cause of many forms of Alzheimer’s,
heart disease, cancer, mental illness, etc.
But the exception does not become the
rule. A lot of error can be cloaked in a very little truth,
and if viewers want to see only the flashy ornamentation, then
that’s all they will see. The authors of the current heresy that
HD is not genetic, but is caused by nutrition, make at least as
many false claims as did the purveyor of ascorbate as a preventative
and cure for dysplasia. While doing so, they hypothesize (or fabricate,
really) a monstrous conspiracy drama in which the villains are “the
dog breeding associations in the United States, United Kingdom,
France, and Germany [that] developed X-ray systems”. They claim
that attempts to eliminate HD through selective breeding “proved
fruitless” for three decades, and they make the illogical conclusion
that this is the reason the incidence “persists at around 60-65%”.
Quoting themselves in their book, a vet named Torel and a journalist
named Kammerer make amazing far-out statements such as “breeding
programs… cannot hope to bring about any fundamental improvements
…because CHD is not heritable and existing dog food… is in fact the
original cause of CHD.”
How ridiculous this is, can quickly become
clear by asking yourself why the dogs I and countless others
have bred selectively for good hips are not ruined in spite
of lavish helpings or restricted diets (doesn’t matter). Why do
Greyhounds not get HD, when they eat the same rations that Clumber
Spaniels do? Why are some of us who use selective breeding successful,
while those who do not, have multiple failures, and yet we all feed
basically the same commercial preparations?
The conspiracy theory includes accusations
that the national all-breed club in Germany colluded with
the veterinary association and the Association of Publishers
and Booksellers to have the Torel-Kammerer book banned by the “biased
and prejudicially influenced” courts, and were supported by “behind
the scenes manipulation among the judges”. The VDH, the vet association,
and leading publishers are accused of “fraud, unfair competition
(?) and corruption with active and passive bribery.” The Zuchtwert
(breed value) system headed by Prof. Beuing is called “a piece of profitable
charlatanism”. The diatribe that goes on for pages would take too
many additional pages to debunk, but the work has more holes than a
Swiss cheese factory.
SUMMARY
The base cause of HD and other orthopaedic
diseases is a collection of enough genes that act together
to bring on the condition and the signs. Since it is extremely
expensive and difficult to find specific genes, even in this day
of genome mapping, it is more convenient, when speaking of the “causes”,
etiology, or pathogenesis (they all mean much the same thing), to
focus on the secondary causes. These may include development of a
deep or shallow acetabulum, weak musculature and ligaments, speed
of growth of bones vs. muscles, synovial fluid aberrations, and other
features which might be identified early, but remember that all these
have their own “bad genes”. No matter how much research into the role of
those factors you support, you must still practice good genetics if you
wish to make progress in your own kennel or breed
Dr. Lust of Cornell, for example, says
flat out “Canine hip dysplasia is a hereditary disease”. All
of the best work of hundreds of dedicated scientists in a score
of countries is summed up in that simple, concise statement of
truth. Unadorned, forceful, and direct, this says it all.
copyright Fred Lanting, may
be forwarded only with permission of author:
Fred
Lanting, author of the book on HD and worldwide lecturer on
the subject, is working on a greatly expanded version of the book.
Fred Lanting's latest book:“The Total
German Shepherd Dog”
************************************************
Dealing
With Wrong Ideas about Hip Dysplasia
Fred Lanting
Background
Friends and fellow dog fanciers: I was
asked to comment on some accusations and remarks re HD that
have been on chat lists. First, so you understand where I am
coming from, you should know a little history of my involvement
in dogs, veterinary science, and hip dysplasia in particular. I
got my first purebred dog in 1937, bred my first litter in 1945, got
my first GSD in 1947, started handling and more extensive breeding in
1966, gave up all-breed pro handling to become a judge in 1979, am
one of only two in North & Central America licensed by the SV
(world parent club for the GSD), and I lecture and judge around the
world. I have done so in some 20 countries, lately several countries
per year. Among other books, I wrote The Total GSD and Canine Hip Dysplasia.
I received early encouragement and support in my research and study
in orthopaedic problems from the founder of the OFA, Dr. Wayne Riser
of the U. of PA (Penn). Although I was accepted to that university's
vet school around 1958, I could not attend because of financial and family
reasons. I continued my studies in science instead, and added to my earlier
B.S. in Organic Chemistry with graduate work in chemistry and physics.
I approach all serious matters with the open and inquiring, analytical
mindset of a true scientist.
Having constructed that frame, I will
now fill in more of the picture. Vet schools, breeders associations,
and other groups across the globe do not invite me to speak and
judge without good reason. Nor do I write this from an antagonistic
point of view. It is strictly because of my dedication to the
philosophical science of logic and to the physical sciences that
I feel compelled to rebut statements that run contrary to those principles.
I do so in a completely impartial manner, and from the historical
perspective mentioned above. Quotes from Internet remarks by one Mr.
N., for example, should not go uncorrected. I have corresponded
with him before and it is my impression that he does not read the veterinary
literature with comprehension, or he has some personal bone to
pick with Penn, or else he has some unreasonable attachment to
or bias toward OFA. I use his initial instead of a name because
his attitude and misunderstanding are near-clones of those found in
a few others. However, with enough time, patience, and scientific
evidence, most of such anti-progress naysayers are eventually converted
by the facts and deductive reasoning. I hate to mix personalities
with science, but this situation has been a source of ir 
condition can have on the dog and what
can be done about it. Because Hip Dysplasia
in dogs is a complex topic, it requires extensive consideration
in order to have a good understanding of its nature. Cats
do suffer from Hip Dysplasia, too, but it is seen less frequently in
cats. 
period on slippery surfaces such as newspapers
will be prone to hip difficulties. That is not to say
that smooth concrete, wood or newspaper surfaces cause dysplasia,
just that they can make a bad situation worse. Better
surfaces for newborn pups would be blankets or towels... something
they can get a better grip on.
that the shape it changes to is abnormal.
