There are two pastern disorders
that are often confused until one actually has seen the “extreme” type.
In addition, there are cases of retained cartilage and the unequal or asynchronous
growth of the two bones in the lower forearm, but these are not included
in the subject of this section. I constantly see variable expressions of
pasterns changed by growth plate disturbances, with some dogs having a valgus
(turned out) deformity of only one carpus, some with little turning out,
many with both feet pointing "east-west". Some dogs have bilateral,
others unilateral involvement; in many the flexion is greater in one pastern
than the other. In most dogs with simply weak pasterns, and probably in
every case of true luxation, both pasterns are equally affected. In some
dogs, a knuckling-over may present, though perhaps this is either a modification
or a slightly different disorder.
The German Shepherd Dog Club of America sponsored a survey in the 1980s
because the situation in the American variety or bloodlines of the German
Shepherd Dog got so bad regarding frank luxation as well as “down” pasterns
from any cause. Several of those surveyed were on vitamin-mineral supplements,
others not; no connection with diet was seen at the time, though the survey
later raised a number of questions about nutrition’s effect on afflicted dogs.
Hyperextension or subluxation/luxation of the pasterns is seen as a flat-footed
condition wherein the dog actually walks on the palmar surface of its wrists
in the most extreme manifestation of this disorder. Some dogs will be partly
(subluxated) or mostly/fully (luxated) “down on their pasterns”, and it
has been my experience that if conditions are not changed, either disorder
will get worse or at least not improve spontaneously as the dog matures.
The older American "parent club" finally officially recognized pastern
problems existed (although it did not fully separate the two right away)
and permitted the circulation of a questionnaire via its official journal
and handouts. However, no real program to stop the breeding of those dogs
producing much of this disorder has to date been enacted by the GSDCA. Only
the nutritional aspect (environmental effect on genes) has been explored
so far. A breeder in St. Louis named Helen “Scootie” Sherlock did a good
job of soliciting testimonials and case histories, but many of the conclusions,
either stated or implied, were fallacious. That is, they lacked adequate,
convincing, logical connection between premises and conclusions. Further,
as the answers were based on testimonial anecdotal response to questions,
they and the tentative conclusions and suggestions must not be construed
to be anything resembling scientific inquiry. For example, many unrelated
data were mentioned that had no relationship to the etiology, course, or
improvement of the disorders except perhaps solely in the minds of the respondents
and readers.
In the normal dog, slope of pasterns varies from the very upright in the
Terriers to only slightly less perpendicular in the Rottweiler to about
22° in the correct German Shepherd Dog (despite the pictures in the
U.S. ads with 35-45° or worse). The proposed reason for some slope in
the trotting and galloping breeds is to cushion the impact of landing on
the front limbs and prevent shock to the joints and fatigue. Excess slope
makes a trotting dog look as if it were wearing socks too long for its feet,
slapping its weak paws onto the ground with a very visible and almost audible
effect. Yet many a professional handler, judge, and supposedly experienced
breeder have been surprised to see it only after having it pointed out and
explained. One source8 claimed that the "normal" standing angle of the canine
carpal joint (average of breeds) is from 2° to 10°, but don’t equate
that with “mean or median”, since that seems too steep to be an average in
my view, and I’ve judged many thousands of dogs of several hundreds of breeds.
GSD owners may resent their breed not being included in the category of "normal",
although in America that may be hard to defend in regard to other characteristics,
orthopaedic or not.
Years ago, the noted Whippet fancier and Greyhound researcher Lou Pegram
worked for Purina and had a chance to see the effect of kennel surfaces
on the weakening and/or strengthening of pasterns. He told me that if you
do not get the affected puppy (in his definition, one with "weak" pasterns,
not full blown carpal subluxation) onto a variety of surfaces by age four
months, there was no chance of correcting the problem — it would stay the
same or get worse. Alexander & Early 8 gave credence to the effect of
smooth surfaces dogs were raised on, which Pegram had discovered years earlier.
Mild cases in their study were "managed" by giving the dog’s free access
to both gravel and grass, as the majority of affected dogs previously had
been reared on concrete or in small pens.
In the GSD, line breeding and neglect in selecting genes are behind probably
all cases of excessively sloping, non luxated pasterns that I have seen
— and they are legion! I have seen the disorder-of-neglect in GSD’s regardless
of surface, and very early, so I believe this weakness — common in the U.S.
and becoming a slight problem in Europe now — is primarily a genetic problem
that is more easily brought out (expressed by environmental forces) in some
breeds than in others. In other words, heritability may vary between breeds.
I doubt that the weak pasterns so pervasive in the American Shepherd (GSD)
has the same root as the severe condition of carpal luxation, because I
have seen the latter arise spontaneously in the Malamute, Lab, Sheltie,
Rottweiler, Wolfhound, and others — breeds that are not neglected in respect
to pasterns the way the GSD was and is in North American (AKC-CKC) lines.
There probably are differences between breeds when it comes to cause, or
at least heritability index. Shar-Peis, Dobes, Danes, and others may have
a different etiology than does the German Shepherd Dog. Or it may be simply
that we are talking about two different disorders. There are various degrees
of extension (greater slope) but in the worst cases, the affected dog walks
on what would be analogous to the human palm. The movement appears like
a seal walking on its flippers; another description is "sloppy, floppy padding".
These dogs remind me of circus clowns with grossly exaggerated shoes, or
of children with socks longer than their feet and flopping as they run. Occasionally,
in the GSD, anyway, pastern luxation (sometimes known as carpal subluxation
syndrome) is accompanied by hyperflexion of the hocks. Since so many over-angulated
American GSD’s are “hock-walkers”, this latter condition may easily go unnoticed
and taken as typical.
Carpal subluxation has been produced experimentally in Beagles by altering
the calcium/magnesium/phosphorus levels and ratios in the diet. 556 In her
report revealing this, Dr. Robin Woodley says that mild to moderate cases
have responded to magnesium supplementation if carefully monitored, and
that the condition has been seen in pups fed "many different types of rations,
from low protein, cheap kibble to premium kibbles to high-protein, home
cooked meals." By the way, that is more evidence of genetic cause. Woodley
has been a member of the GSDCA’s Internal Defects Committee, which has implicated
high energy, high-protein foods in the expression, though not the cause,
of carpal subluxation, with certain brands being more often listed on their
questionnaire returns. Woodley also raises the question of the role of trypsin,
an intestinal/pancreatic enzyme useful in hydrolyzing protein and thought
to be deficient in the German Shepherd Dog. Trypsin is needed to digest soy
protein, and since GSD’s possibly have an intolerance to soy and also are
susceptible to toxic gut syndrome, Woodley proposed that the survey include
questions that might uncover a link between these disorders. Both the weak
pasterns and the disorder known as carpal subluxation/luxation are basically
genetic, as are almost all other problems.
Several breeds have been seen to have the carpal luxation or subluxation
syndromes, although the GSD may be the most often seen, perhaps due to its
population (though in the U.S. more Labs are registered). An e-mail correspondent
has told me that she has heard from people whose mixed breeds, Dachshunds,
Rottweilers, Springer Spaniels, Bloodhounds, and others have had the same
flat-foot condition. While judging in the land of the midnight sun (Alaska)
in the mid80s, I was shown an example of a Malamute — a full, classical
case, but this individual seemed to have a genetic combination of that carpal
luxation and pleiotropic dwarfism associated with anaemia.
Alexander & Early found (although in a very small, statistically insignificant
number of 7 breeds and 12 cases) that Dobes and Danes were most affected
8 incredibly, only one GSD was in that study! Pups in this study were mostly
10-16 weeks old, but I have seen the problem easily identifiable by the
time pups were walking for a very few weeks.
In some German Shepherd Dogs having carpal subluxation, and which were
in the initial GSDCA tabulations, hyperflexion of the hock was also seen
(the dog stands or walks flat on its "hock" like a sitting jackrabbit).
There are two reasons I discount any relationship: one is that no other breeds
so far have shown the two conditions to coexist, and the other is that GSD
breeders in North America have unfortunately and concurrently selected for
extreme rear angulation and have produced a nation of hock-walkers, independently
of most other characteristics except for generally loose ligaments. The
concurrence of carpal subluxation is coincidental, not causal — American
GSD breeders have been negligent in two separate areas at once. Full carpal
luxation is a separate genetic defect from the much more common GSD subluxation/weakness
that shows itself as excessive slope of the pasterns.
Treatments involving splinting have been tried but are not satisfactory
in most cases. Some have tried a Mason’s metasplint to keep the joint somewhat
upright while soft tissue responded to exercise. One should be careful about
believing everything that is said, although there does seem to be some good
to be had with a nutritional approach. The e-mailing woman mentioned earlier
unfortunately took the GSDCA survey responses and Ms. Sherlock’s article
as gospel and has been preaching the use of a wide range of remedies: She
“changed her dog’s feed to Science Diet Lamb and Rice, supplements of Vitamin
C and E, gelatine tablets, Selenium tablets, Prozyme, glucosamine, and chondroitin.
And although not a dietician or veterinary professional says, “Please before
you follow this regimen please contact me first. The dosage for each dog
will be different depending on how bad they are in the pasterns!” Well meaning,
but it’s potentially dangerous for people to quote from survey responses
the same way one might from a scientific study.
The interesting and surprising thing that I learned from recent reports
is that improvement to the point of resuming normalcy is possible with manipulation
of the nutritional intake of the dog. While much of the survey response
had nothing to do with the disorder, a recurring theme and the most likely
approach to use in improving both the weak pastern and the true subluxated
joint, is the lowering of protein level in the diet. Less calcium and phosphorus
(though in the same recommended ratio) also may be beneficial. Conclusions
of the GSDCA survey that might have currency include the elimination or considerable
reduction of such additives to a commercial food as meats, eggs, yoghurt,
milk, and cottage cheese, which are all high in protein, and some rich in
phosphorus and calcium. If your affected dog is eating an otherwise acceptable
ration, you can change the protein/carbohydrate ratio by substituting some
of the meal with “buttered noodles” or other pasta. Poor thyroid function
may play a part, although that may be coincidental. Since it is usually
reported to be familial (CSS appears in dogs closely related to each other
more often than random occurrence would account for), the wise breeder will
avoid the lines in which it appears. Nutritional remedies may merely be
masking a hereditary problem.
