SINDROME de WOBBLER

Cervical Vertebral Malformation Complex:

Wobbler’s disease occurs in young and old animals. In young animals, it appears to be secondary to inherited malformation and mis-articulation of the cervical vertebrae which is accentuated by high protein diets. In older animals, it appears to be secondary to chronic degenerative disc disease. Although other large breeds can be affected, it is said to be a disease of young Great Danes and old Doberman Pinchers. When a Doberman Pincher presents with signs of rear leg ataxia with “root signature” in the forelegs, there is a high probability that the dog has Wobbler’s disease.
The onset of clinical signs can be acute or slow and insidious. There is evidence of ataxia in all four limbs with the pelvic limbs being more affected. There will be both conscious and unconscious proprioceptive dysfunction with a wide-based stance in the rear legs.
The forelegs may show a stiff and stilted gait with atrophy or fasciculations of the deltoideus, biceps and infra- and supraspinatus muscles. There is usually some degree of neck pain on palpation and neck manipulations. One sign of this is a reluctance to hop medially with the forelegs.
The diagnosis can be suspicioned on survey radiographs of the neck, looking for narrowed IVD spaces and sclerosis of the demi-facets.
CSF analysis is usually within normal limits, although a small number of cases will show a mild increase in cells (4-10 cells/:l) and protein (25-35 mg/ml).
EMG can help confirm the location and the denervation of the muscles with fasciculations.
The diagnosis in confirmed on myelography, which shows evidence of IVD protrusion and the presence of ligamentous or bony intrusion into the neural canal. Since CVM represents a dynamic lesion, myelography with mildly flexed and extended views is the diagnostic technique of choice.
It is also important to take a “lazy” lateral view, since stretching the neck can reduce the lesion so as to overlook it. If the lesion is alleviated with flexion and accentuated on extension, the problem is partially due to ligamentous hypertrophy. On the other hand, if flexion and extension do not affect the lesion, it is probably secondary to IVD protrusion. I feel that a single lesion is better than multiple ones.
Further, an IVD protrusion is less problematic than one with ligamentous hypertrophy.
The treatment of CVM is surgery. In cases where surgery is not possible (patient has complications or is elderly), medical management with prednisolone and diazepam may provide temporary relief. However, in the absence of compelling reasons not to perform surgery, surgical decompression is needed.
There are several surgical techniques available to treat Wobbler’s disease including dorsal laminectomy, ventral slot and ventral slot with distraction (by various means).
In cases of multiple lesions, dorsal laminectomy was the method of choice, in the past. Dorsal laminectomy has risks and the success rate is the lowest of methods for correcting CVM. In qualified hands, it is still a good technique. The overall success is around 75% with a 20-25% morbidity and a 5-10% mortality.
Large breeds do not tolerate dorsal laminectomy well. Ventral slot is excellent for IVD protrusion, but increases compression from ligamentous hypertrophy. In simple IVD protrusion, ventral slot has a 90-95% success rate with a 5% morbidity and <1% mortality. The morbidity and mortality increase for ventral slots when ligamentous hypertrophy is present.
When ligamentous hypertrophy is present, ventral slot alone is generally inadequate to correct the problem. A number of techniques have been described to perform a ventral slot and maintain distraction across the IVD space. These methods include various implants from Harrington rods to screws (or pins) and methylmethacrylate. The method we use is a modified “screw and washer” technique. The washer we use is a polypropylene ring made from the end of an endotracheal tube. This is packed with bone graft and the screw stabilizes the implant while fusion takes place. In this method, the “slot” is performed by discectomy without removing the endplates. It is my belief that fusion is the goal of CVM surgery and this is best done in distraction.
Another popular method (which I do not believe provides adequate fusion) is to inject methylmethacrylate between the vertebrae at the ventral slot site. This can be used as a salvage procedure.
Following surgery, the patient should be kept quite for 30 days and supported with a neck brace and bandage. After the first month, the activity level is gradually returned to normal. Depending upon the severity of the initial damage, most patients will improve, reaching 80% of their recovery in the first 3 months. There is a potential for the “domino” effect, whereby the IVD on either side of the surgery site will develop problems in 6 months to 2 years following the initial correction. I find that this is more often when the beginnings of CVM were present in the beginning. We now are much more aggressive than in the past, fixing multiple lesions from the start.