WOBBLER SYNDROME

by Fred Lanting

 

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. However, no term is more used, more succinct, more descriptive, or even perhaps more accurate 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 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.

 

  Return Home

 

Copyright 2001 Fred Lanting, Canine Consulting.  Mr.GSD@juno.com.  All rights reserved.  Used with permission.  Please view his site Real GSD. 

 

NOTE:  A well-respected AKC and Schaferhund Verein judge, Mr. Lanting has judged in more than a dozen countries, including the prestigious FCI Asian Show hosted by Japan Kennel Club, the Scottish Kennel Club, a Greyhound specialty in England, and more.  National Specialties: 1994 GSD Club of America National; 1991 Tibetan Mastiff National; 1990 Shiba National; Fila Brasileiro Nationals (several times), Dogo Argentino National, Pyrenean Shepherd National.  Numerous Chinese Shar Pei and Australian Shepherd specialties; regional Anatolian Shepherd specialty. Numerous GSD, Rottweiler, & Boxer specialties worldwide.  He is also the author of several ‘must read’ books, including THE TOTAL GERMAN SHEPHERD DOG, CANINE HIP DYSPLASIA, CANINE ORTHOPEDIC PROBLEMS.  A former professional all-breed handler in the US and Canada, he has lectured in over fifteen countries on Gait-and-Structure (Analytical Approach), Canine Orthopedic Disorders, and other topics, as well as being a  Sr. Conf. Judges Ass’n (SCJA) Institute instructor. WV Canine College instructor & member, advisory board.  His full Curriculum Vitae is very impressive and we are grateful to him for sharing that knowledge on this site.