Description
There is a disorder (it may actually be two) in the
canine similar to the “wobbles” in thoroughbred horses. Much has been
written on this, with various descriptions such as cervical vertebral
instability (CVI), cervical spondylopathy, stenosis of the cervical
vertebral canal, and even the mouthful, caudal cervical vertebral
malformation- malarticulation. It was once referred to (incorrectly) as
spondylolisthesis. Scientists do not like the vagueness associated with
the word, but no term is more used, more succinct, more descriptive, or
even perhaps more accurate to the general animal-owning public than
“wobbler syndrome”. In the horse, about 12% of this syndrome can be blamed
on osteochondrosis and here, too, there may be some parallels with the
dog.
That we may be dealing with two very similar disorders or two variations
of a disorder is indicated by the differences seen in early studies on
Doberman Pinschers and Basset Hounds and later work with Great Danes. The
earlier work pointed at instability, subluxation of the vertebrae, and a
tendency for one of the vertebral bodies (the actual bone segments of the
spine, not including the material between) to lose bone, ride up onto the
one in front of it, and thus compress the spinal cord from the bottom.
This would be a little like a car with an angled bumper running into
another car ahead of it, its front bumper sliding up and over the rear
bumper of the other vehicle and smashing into its trunk and taillights,
although in slow motion. Mostly large breeds have been involved such as
those named above plus Saints, Old English Sheepdogs, and Rhodesian
Ridgebacks, though infrequently in smaller breeds, also.
Stenosis is a squeezing or partial closing of a tubular structure such as
an artery, heart arch, or, as in this context, the spinal canal (where the
spinal cord runs through the vertebrae). It is congenital (found at
birth), developmental (gets worse), and degenerative (has destructive
effects) in man and probably so in dogs as well. Stenosis has been seen in
the cervical and lumbar vertebral canal and the intervertebral foramina
(spaces between the vertebrae), and may be “silent” not giving rise to
complaint, in many individuals unless accompanied by other factors such as
protrusion of a disk, spinal instability, or movement such as the extreme
flexion or extension of the neck or other part of the spine.
Most of the lesions in early studies were between the sixth and seventh
cervical (neck) vertebrae, which are designated C6 and C7. It has been
thought that there was an inherited malformation of these spinal segments
(vertebrae) with possibly a simple recessive trait but more recent
evidence indicates more genes are involved in ways that are somewhat more
complex. We know a little more about osteochondrosis and the etiology of
osteophyte formation now.
Clinical Signs
At the point of greatest cord compression, the damaged
ascending sensory neurons (those nerve cell carrying electrical impulses
to the brain) begin to die. Their myelin sheaths deteriorate, and
confusing impulses cross over from one axon to another, in effect making
the brain and cord “think” they are coming from someplace else, and thus
the return messages to contract certain muscle fibers may be sent to some
of the wrong places. This gives rise to much of the missteps and poor
movement. Many of the axons (main conductors) also die, and loss of
sensation results.
Simultaneously, descending motor neurons are affected the same way, so
fewer of them function from that part back to the muscles. Therefore, the
dog may seem not to know where its limbs are, drags its toes in a manner
similar to those with GSD myelopathy or stands on the top surface of one
of its rear paws, has poor coordination especially in the pelvic limbs,
may stand wide and, if the thoracic limbs are affected, may have a
prancing gait. In severe cases, the dog falls down easily and has a hard
time getting up on its feet. The syndrome affects both sides of the body
equally.
The descriptive terms “ataxia” and “spastic paresis” in this disorder
refer to weakness and partial paralysis with uncoordinated motion, and
these are seen principally in the rear. When cervical spinal cord damage
is further toward the head, the forelimbs and even perhaps the diaphragm
may be involved, but in canine Wobblers, the lesion is usually found in
the caudal (rearmost) vertebral spaces such as C6-7, rarely C5-6, although
in Basset Hounds the same or a similar syndrome is associated with the
cord pinching occurring around C2-3. Wherever it exists, it may cause an
abducted (limbs move away from each other) and sometimes a fast-beat gait
with stumbling especially when turning. The ataxia, of course, is due to
the damage to the ascending neurons and the jerky movement and paresis to
damage to the descending neurons, both at the point of cord compression.
Cause
It was discovered very early in man and described in
the dog by 1967 that vertebral canal stenosis is a cause of spinal cord
compression and these researchers considered deformation of the vertebral
bodies to be the cause of that stenosis. Others have looked at this and
similar problems in a variety of breeds.
About the same time as the above work and a little later, another cause of
spinal canal stenosis was proposed: a deformation of the vertebral arches
(that part of the segments covering the canal), as well as the disks, the
processes, and articulations in the joints between the bone segments.
Other things happening at the same time and possibly contributing to
stenosis or associated with it otherwise include hypertrophy (overgrowth
or thickening) of the flavum ligament or of the dorsal longitudinal
ligament or of the dorsal annulus. Simple poor alignment and
malarticulation have also been blamed or implicated. Another cause of
compression of the cord is the CVI (cervical vertebral instability)
mentioned earlier, and identified by various names such as
spondylolisthesis and vertebral subluxation.
In the earlier work on CVI, instability was the diagnosis when greater
flexion between two vertebrae than “normal” was evident. When we speak of
flexion, we mean the bending of joints so that the limb or extremity is
“folded” toward the centerline of the torso, while extension is a
straightening-out away from the rest of the body. In speaking of the neck,
flexion is the bending of the head downward toward the sternum, and
extension is the bending up as if stretching to reach over the back. How
valid is the diagnosis of neck instability as “shown” in flexion, was
brought into question in 1977 by Wright who found the abnormal angulation
(one bone starting to slip or ride up on another) in many dogs who had no
clinical signs of cervical spinal problems. It had been standard practice
to bend the neck down fully and see if there were any irregularities or
subluxation on the radiograph. These pictures were compared to the neck in
a neutral position (same as it would be carried in standing). These
pictures were almost invariably taken in a lateral view (from the “side”,
with the dog in lateral recumbency), although some people showed how
useful a ventrodorsal view could be in demonstrating lateral compression
of the cord.
In 1982 Olsson, Stavenborn, and Hoppe in Sweden studied Great Danes and
found that the ones with wobbler syndrome had radiographically
demonstrable lesions only when the neck was in extension, which ran
counter to the experiences previously reported. They did not find any CVI
or vertebral body deformation, except for a slight deformation in the
vertebrae of one dog, and guessed at a number of possible reasons. Their
work was only with Great Danes, and previous studies had also included
Bassets and Dobes, so perhaps there is a different genetic pathway for
some breeds than for others. The syndrome in Danes occurs mostly in young
dogs and in Dobes they occur mainly in older dogs. The 1982 Swedish study
involved “wobbler” dogs from 4½ to 24 months. Both plain radiographs and
some made after the injection of a dye for myelography were studied, with
the necks in all positions. The euthanized dogs’ spinal systems were then
studied for comparison.
Even normal Danes have relatively smaller ventrodorsal height to the
spinal canal, and larger prominent intervertebral joints compared to many
other breeds. When they looked at a dog without wobbler signs and
increased C3-4 flexion as seen on a regular film, the myelogram did not
indicate any pinching of the cord, even though it looked as if the bone
could have done so. The wobbler dogs with increased flexion between two
vertebrae showed no pinching, either. The picture that came out of this
work in Sweden is that compression of the cord is most severe when the
neck is extended. It also appeared that the compression and stenosis took
place at the cranial end of the vertebral canal, where the height was less
and the “roof” was pushed down onto the cord when the neck was lifted
(extended). This is probably why many wobblers will hold their heads down,
by the way, but that is not the best diagnostic sign. Often, Danes with
wobbler syndrome have an abnormal vertebral arch (between the “neckbones”)
that is plump and longer, and frequently it is seen in association with
deformed and asymmetrical articular processes. Many also have considerable
osteophytic deposits that may contribute to further compression.
Compression was more dynamic than static, meaning other forces combined
with the malformation to produce the compression, such as disk protrusion
and even the normal movement of the head and neck. Possibly the most
important finding of this research, beyond the hint of breed and genetic
differences, is that cord pinching might not be demonstrated in wobblers
unless myelography is used in conjunction with radiography and pictures
are taken with the neck in different positions.
The breeder/owner can make a tentative diagnosis based on symptoms before
taking the dog in for myelograms. However, you want to remember that there
are other problems, and you should differentiate between them. Part of
that diagnostic guess may be influenced by what breed you have, as Wobbler
is more likely in Dobes while myelopathy is more common in GSDs, for
example. If the dog has no pain, but the unstable gait described, it is
very possibly wobbler syndrome. If pain and hypersensitivity are present,
your dog may instead have cervical disk protrusion syndrome. The pain
probably comes more from the secondary inflammation that results when the
disk’s nucleus pulposus tissue extrudes into the epidural space in the
canal and calcifies with this “hardened cement-like” material acting much
the way osteophytes do in irritating and abrading the surrounding soft
tissues. In the wobbler, inflammation is not much of a problem if at all.
In the important 1974 work at Cornell on Great Danes, joint problems, and
nutrition, evidence indicated that vertebral body deformation is a
manifestation of osteochondrosis brought on by rapid growth and
overnutrition. Olsson and colleagues commented that some of the changes
seen in the cartilage between the vertebrae have similarities to
osteochondritic changes seen in other joints, and implies that
high-energy, high-calorie “rich” diets may, in certain dogs and breeds
genetically predisposed to these disorders, bring on the osteochondrosis
responsible for the stenotic myelopathy (pinching and disease of the
spinal cord) seen in animals.
Other environmental factors may worsen a congenital or hereditary problem.
It has been theorized that the very heavy head of a thoroughbred horse, a
Great Dane, or a Basset Hound put great stress on certain vertebrae during
early growth, but there are too many questions to give much credence to
that. Dobes certainly do not have heavy heads, and different vertebrae are
involved in different breeds. Separate genes and locations may be involved
in Bassets compared to other breeds. A cooperative pedigree and clinical
study program between breeders and some veterinary school teams could
provide more accuracy in detection and improve some breeds of dogs through
prevention of disease.
Treatment of Wobbler Syndrome
Earlier treatments have included fusion of adjacent
vertebrae with bone grafts and bone cements, or simply the use of
anti-inflammatory drugs, but improvements were needed. A technique
developed at the U. of TN in 1983 calls for drilling a slot between the
two segments and filling the gap with about ½ to 1-inch of bone cut from
the pelvis. What makes it different is the use of stainless alloy rods
with hooked ends attached to other vertebrae, and a threaded section with
nuts that can be tightened to adjust tension. About 75% of the dogs
treated this way at the U. of Florida vet school regain at least partial
use of their legs, a much better prognosis than has previously been had.
Fewer dogs now face euthanasia.
ATLANTO-AXIAL SUBLUXATION
This is another spinal cord problem with much
similarity to Wobbler Syndrome. Indeed, it may be only a matter of
location on the spine, determined by breed differences, that causes this
to be considered a different disorder. The first two neck vertebrae are
called, respectively, the Atlantis and the Axis. The articulation between
the skull and the Atlantis has been referred to as the “no” joint, while
the Atlanto-axial articulation is the “yes” joint, which is all the
description anyone needs to understand the range of motion there. (I can
see you nodding and turning right now!) In illustrations and journalistic
shorthand, these vertebrae will often be referred to as C1 and C2.
Most common in toy and miniature breeds, this disorder appears without
initialization by trauma; typically the affected pup between 3 and 10
months age has rather sudden pain or a very stiff carriage of the neck,
and increased discomfort when the head and neck are manipulated.
Histologic and radiographic examinations reveal similarities to necrosis
seen in some other bone disorders, and the wearing away of bone that
encourages the axis to ride up and into the canal ahead of it, the
vertebral body putting pressure on the ventral surface of the cord. There
is a projection on the axis called the dens, resembling the prow of a
boat, which is normally attached to the atlas by a ligament between the
tip of the dens and the floor of the spinal canal in the atlas, and is
also attached to the rear of the skull by ligaments running through the
atlas. In the case of congenital absence of the dens, this internal
support between the axis and the bones ahead of it is also missing,
tending to let the axis tilt upward in front, eventually tearing another
ligament which holds the tops of C1 and C2 close together.
Because this subluxation is an abnormal flexion of the two vertebrae, it
is partially alleviated only while the dog holds its head up and its neck
somewhat extended. If the cord is sufficiently pinched, short stride,
pain, paresis, paraplegia, quadriplegia, and complete paralysis may be the
successively worse signs. The reason all four limbs are often affected,
whereas just the rear is affected in Wobbler Syndrome or GSD myelopathy,
is that the cord is compressed closer to the brain, ahead of the branching
out of nerves to the rest of the body.
Treatment has included fusing of these two vertebrae, wiring the dorsal
arches together so they cannot move up and down in relation to each other,
or even stabilization with plates and/or screws.
CES (Cauda Equina Syndrome)
This is another type of stenosis (usually), and is the subject of another
article by the author.
_____________________________________________
Fred Lanting, Union Grove, AL, USA - is
the author of “Canine Hip Dysplasia” and “The Total German Shepherd Dog”,
and lectures and judges worldwide. His e-mail is
Mr.GSD@Juno.com Contact him to
schedule seminars in your area.