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One of the earliest accounts of wobbler syndrome was written more than 80 years ago by staff members in the Department of Veterinary Science at the University of Kentucky. They described 47 cases in central Kentucky between 1937 and 1939. Cases occurred particularly among Thoroughbreds and Saddlebreds, breeds which have long necks. Foals around the time of weaning developed a lack of coordination in the hindlimbs, which progressed to include the forelimbs, eventually causing the animal to stumble and fall. Well-grown weanling and yearling colts seemed particularly prone, with three colts affected to every one filly. As a result of necropsy studies, it was suggested the condition was related to abnormalities of the vertebrae of the neck, which caused damage to the spinal cord.

These observations were confirmed some 20 years later by Dr. James Rooney, also from the University of Kentucky, who identified more precisely the sites and nature of the lesions in the cervical vertebrae. Rooney suggested the overgrowth of the articular processes on which vertebrae move upon each other causes distortion and narrowing of the spinal canal and results in pressure and damage to the cord. The most frequent sites of lesions are between cervical vertebrae C3 and C7, although the presence of lesions does not always result in clinical signs of wobbler syndrome. When the neck is flexed, the lesions may cause pressure to be exerted on the spinal cord.

Clinical signs associated with wobblers may be related to other causes including trauma, parasitic infection of the spinal cord, and infection with equine rhinopneumonitis virus. The prognosis depends on differentiating between possible causes to establish an accurate diagnosis. Wobblers, otherwise known as horses suffering from cervical vertebral malformation (CVM), are identified by taking X-rays of the neck region. To do this, the horse must receive a general anesthetic so that a technique known as myelography can be performed. This involves the injection into the spinal canal of a contrast fluid so that the space between the cord and the surrounding bony mass of the vertebra can be readily visualized. Narrowing of this space due to lesions of CVM can then be located. The procedure involves some risks and should only be undertaken by those who are experienced with the technique and its interpretation.

Two types of lesions have been identified. The first typically affects horses from 4 to 12 months of age and occurs most frequently between vertebrae C3 and C4, and C4 and C5. It causes pinching of the cord only when the neck is flexed. The second affects horses between 12 and 36 months of age and occurs between vertebrae C5 and C6, and C6 and C7. Compression of the spinal cord is not relieved or exacerbated by flexion or extension in this region. Injury to the cord results from pressure which interferes with blood flow, causing damage to the cells comprising the cord. It is this injury which results in signs of incoordination, with severity related to the extent and site of damage.

In the young horse destined to become a wobbler, the problem begins when cartilage maturation is defective and interferes with bone formation in the vertebra. The blood supply becomes inadequate, surrounding tissue dies, and chronic joint lesions develop between the cervical vertebrae. What triggers these pathological changes at this critical growing period is still a matter of considerable debate. The initial suggestion that wobbler syndrome was an inherited condition linked to certain families has not been proven, although genetic influence has not been eliminated. By breeding two wobbler parents, it has not been possible to increase the incidence of wobblers in their offspring. It was noted, however, that the incidence of other bone deformities was increased.

It is interesting to compare the development of similar bone lesions, including spinal deformities, in other species, particularly in poultry and pigs, both of which have been subjected to intensive genetic selection and high planes of nutrition to improve growth rate and feed conversion. It is apparent that within these populations, genetic selection has contributed to an overall increase in skeletal problems. A similar situation may well have evolved in the Thoroughbred, with the current commercial incentive to produce a well-grown but nevertheless skeletally immature yearling in time for the summer and autumn sales. The increased level of feed intake occurs at a time when the skeleton is still not capable of bearing increased muscle mass, nor is it able to respond to the strains and pressures imposed upon it. As a consequence, lesions of osteochondrosis may develop, causing CVM.

The prognosis for a wobbler has always been poor because of the progressive nature of the condition. However, an increasing number of wobblers are being treated surgically, with reports that clinical improvement does occur in some cases. There is still considerable concern as to whether such animals should be allowed to participate in athletic competition. An alternative but less dramatic approach is to try to eliminate factors which might promote the wobbler condition, primarily by reducing the level of dietary energy intake in the young horse.

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