Wobbler Syndrome and the thoroughbred

By Celia M. Marr



Wobbler syndrome, or spinal ataxia, affects around 2% of young Thoroughbreds. In Europe, the most common cause relates to narrowing of the cervical vertebral canal in combination with malformation of the cervical vertebrae. Narrowing in medical terminology is “stenosis,” and “myelopathy” implies pathology of the nervous tissue, hence the other name often used for this condition is cervical vertebral stenotic myelopathy (CVSM).




Wobbler syndrome was the topic of this summer’s Gerald Leigh Memorial Lectures, an event held at Palace House, Newmarket. Gerald Leigh was a very successful owner/breeder, and these annual lectures, now in their second year, honor Mr. Leigh's passion for the Thoroughbred and its health and welfare. The lectures are attended by vets, breeders and trainers, and this year because of the importance and impact of wobbler syndrome on Thoroughbred health, several individuals involved in Thoroughbred insurance were also able to participate.




Dr. Steve Reed, of Rood and Riddle Equine Hospital, Kentucky and international leader in the field of equine neurology gave an overview of wobbler syndrome. Affected horses are ataxic, which means that they have lost the unconscious mechanisms that control their limb position and movement. Young horses with CVSM will generally present for acute onset of ataxia or gait abnormalities, however, mild ataxia and clumsiness may often go unnoticed. Trainers often report affected horses are growing rapidly, well-fed, and large for their age. It is common for riders to describe an ataxic horse as weak or clumsy. Sometimes, a horse that has been training normally will suddenly become profoundly affected, losing coordination and walking as though they were drunk, or in the most severe cases stumbling and falling. Neurological deficits are present in all four limbs, and are usually, but not always more noticeable in the hindlimbs than the forelimbs. In horses with significant degenerative joint disease, lateral compression of the spinal cord may lead to asymmetry of the clinical signs.

When the horse is standing still, it may adopt an abnormal wide-based stance or have abnormal limb placement, and delayed positioning reflexes. At the walk, the CVSM horse’s forelimbs and hindlimbs may not be moving on the same track, and there can be exaggerated movement of the hindlimbs when the horse is circled. Detailed physical examination may reveal abrasions around the heels and inner aspect of the forelimbs due to interference and short, squared hooves due to toe-dragging. Many young horses affected with CVSM have concurrent signs of developmental orthopedic disease such as physitis or physeal enlargement of the long bones, joint effusion secondary to osteochondrosis, and flexural limb deformities.

Radiography is generally the first tool which is used to diagnose CVSM. Lateral radiographs of the cervical vertebrae, obtained in the standing horse, reveal some or all of five characteristic bony malformations of the cervical vertebrae: (1) “flare” of the caudal vertebral epiphysis of the vertebral body, (2) abnormal ossification of the articular processes, (3) malalignment between adjacent vertebrae, (4) extension of the dorsal laminae, and (5) degenerative joint disease of the articular processes. Radiographs are also measured to document the ratio between the spinal canal and the adjacent bones and identify sites where the spinal canal is narrowed.

Dr. Reed also highlighted myelography as the currently most definitive tool to confirm diagnosis of focal spinal cord compression and to identify the location and number of lesions. The experts presenting at the Gerald Leigh Memorial Lectures agreed that myelography is essential if surgical treatment is pursued. However, an important difference between the U.S. and Europe was highlighted by Prof. Richard Piercy of the Royal Veterinary College, University of London. In Europe, protozoal infection is very rare, whereas in U.S., equine protozoal myeloencephalitis can cause similar clinical signs to CVSM. Protozoal myeloencephalitis is diagnosed by laboratory testing of the cerebral spinal fluid, but there is also a need to rule out CVSM. Therefore, spinal fluid analysis and myelography tends to be performed more often in the U.S. Prof. Piercy pointed out that in the absence of this condition, vets in Europe are often more confident to reach a definitive diagnosis of CVSM based on clinical signs and standing lateral radiographs.

Figure 4

Dr. Reed went on to discuss medical therapy in horses with CVSM, which is aimed at reducing cell swelling and edema formation with subsequent reduction of the compression on the spinal cord. In the immediate period following an acute onset of neurologic disease, anti-inflammatory therapy is important. Thereafter, depending on the type of CVSM and the age of the horse, different therapeutic options exist. A diet that is aimed at reducing protein and carbohydrate intake and, thus, reducing growth will allow the vertebral canal to “catch up”. The three most important nutritional factors appear to be excessive dietary digestible energy, excessive dietary phosphorus, and dietary copper deficiency. However, it is important that restricted diets are carefully managed with professional supervision. Dietary supplementation with vitamin E/selenium is also recommended. In adult horses, the options for medical therapy are restricted to stabilizing a horse with acute neurological deterioration and injecting the articular joints in an attempt to reduce soft tissue swelling and stabilize or prevent further bony proliferation.

The aim of surgical treatment is to stop the repetitive trauma to the spinal cord, which is caused by narrowing of the vertebral canal, and thereby, to allow the inflammation in and around the spinal cord to resolve. Surgical treatment of CVSM is controversial, mainly due to concerns regarding safety of the horse after surgery and potential heritability of the disease. Ventral interbody fusion through the use of a stainless steel “basket” is currently the most commonly used surgery for CVSM. The prognosis of horses following surgical treatment depends on the age of the horse, the grade of neurological deficits that were present prior to surgery, the time the horse has demonstrated neurologic disease for, the number of compressed sites, the severity of the lesions, and the post-operative complications encountered. Following surgery, an improvement of 1-2 out of 5 grades is expected, although some affected horses improve more than 3 grades.

Whether horses are treated medically, surgically or not treated (i.e., just turned out), the response and the prognosis depend on the age of the horse, the severity of the neurological deficits, the duration of neurological signs, and what level of performance is expected from the horse. Without treatment the prognosis in all types of CVSM is poor, as there is continued damage to the cervical spinal cord with an increasing chance of severe cord damage.

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Ulcer medication: are the products different?

By Celia M. Marr

Stomach Ulcers Are Not All the Same

Racehorse trainers and their vets first began to be aware of stomach ulcers over 20 years ago. The reasons why we became aware of ulcers are related to technological advances, which produced endoscopes long enough to get into the equine stomach. At that time, scopes were typically about eight feet long and were most effective in examining the upper area of the stomach, which is called the squamous portion. Once this technology became available, it was quickly appreciated that it is very common for racehorses to have ulcers in the squamous portion of the stomach.

Figure 1

The equine stomach has two main areas: the squamous portion and the glandular portion. The stomach sits more or less in the middle of the horse, immediately behind the diaphragm and in front of and above the large colon. Imagine the stomach as a large balloon with the esophagus—the gullet—entering halfway up the front side and slightly to the left of the balloon-shaped stomach and the exit point also coming out the front side but slightly lower and to the right side. The tissue around the exit—the pylorus—and the lower one-third, the glandular portion, has a completely different lining to the top two-thirds, the squamous portion.

The stomach produces acid to start the digestive process. Ulceration of the squamous portion is caused by this acid. Like the human esophagus, the lining of the squamous portion has very limited defenses against acid.  But, the acid is actually produced in the lower, glandular portion. The position of the stomach is between the diaphragm, which moves backwards as the horse breathes in and the heavy large intestine which tends to push forwards as the horse moves. During exercise, liquid acid produced at the bottom of the stomach is squeezed upwards onto the vulnerable squamous lining. It makes sense then that the medications used to treat squamous ulcers are aimed at blocking acid production.

Lesions in the glandular portion of the stomach are less common than squamous ulcers. The acid-producing glandular portion has natural defenses against acid damage including a layer of mucus and local production of buffering compounds. At this point, we actually know relatively little about the causes of glandular disease, but it is becoming increasingly obvious that disease in the glandular portion is very different from squamous disease. Often, it is more difficult to treat.

Figure 2

Stomach ulcers can cause a wide range of clinical signs. Some horses seem relatively unaffected by fairly severe ulcers, but other horses will often been off their feed, lose weight, and have poor coat quality. Some will show signs of abdominal discomfort, particularly shortly after eating. Other horses may be irritable—they can grind their teeth or they may resent being girthed. Additional signs of pain include an anxious facial expression, with ears back and clenching of the jaw and facial muscles and a tendency to stand with their head carried a little low.




Assessing Ulcers

Ulcers can only be diagnosed with endoscopy. A grading system has been established for squamous ulcers, which is useful in making an initial assessment and in documenting response to treatment.

Grade 0 = normal intact squamous lining

Grade 1 = mild patches of reddening

Grade 2 = small single or multiple ulcers

Grade 3 = large single or multiple ulcers

Grade 4 = extensive, often merging with areas of deep ulceration

Although it is used for research purposes, this grading system does not translate very well to glandular ulcers where typically, lesions are described in terms of their severity (mild, moderate or severe), distribution (focal, multifocal or diffuse), thickness (flat, depressed, raised or nodular) and appearance (reddening, hemorrhagic or fibrinosuppurative). Fibrinosuppurative suggests that inflammatory cells or pus has formed in the area. Focal reddening can be quite common in the absence of any clinical signs. Nodular and fibrinosuppurative lesions may be more difficult to treat than flat or reddened lesions. Where the significance of lesions is questionable, it can be helpful to treat the ulcers and repeat the endoscopic examination to determine whether the clinical signs resolve along with the ulcers.

Medications for Squamous Ulcers

Because of the prevalence and importance of gastric ulcers, Equine Veterinary Journal publishes numerous research articles seeking to optimize treatment. The most commonly used drug for treatment of squamous ulcers is omeprazole. A key feature of products for horses is that the drug must be buffered in order to reach the small intestine, from where it is absorbed into the bloodstream in order to be effective. Until recently only one brand was available, but there are now several preparations on the market and researchers have been seeking to show whether new medicines are as effective as the original brand. There is limited information comparing the new products, and this information is essential to determine whether the new, and often cheaper, products should be used. A team of researchers formed from Charles Sturt University in Australia and Louisiana State University has compared two omeprazole products given orally. A study reported by Dr. Raidal and her colleagues, showed that not only were plasma concentrations of omeprazole similar with both products, but importantly, the research also showed that gastric pH was similar with both products, and both products reduced summed squamous ulcer scores. Both the products tested in this trial are available in Australia and, although products on the market in other regions have been shown to achieve similar plasma concentrations and it is therefore reasonable to assume that they will be beneficial, as yet, not all of them have been tested to show whether products are equally effective in reducing ulcer scores in large-scale clinical trials. Trainers should discuss this issue with their vets when deciding which specific ulcer product they plan to use in their horses.

Avoiding drugs altogether and replacing this with a natural remedy is appealing. There is a plethora of nutraceuticals around and anecdotally, horse owners believe they may be effective. One such option is aloe vera that has antioxidant, anti-inflammatory and mucus stimulatory effects, which might be beneficial in a horse’s stomach. Another research group from Australia, this time based in Adelaide, has looked at the effectiveness of aloe vera in treating squamous ulcers and found that, although 56% of horses treated with aloe vera improved and 17% resolved after 28 days, this is compared to 85% improvement and 75% resolution in horses given omeprazole. Therefore, Dr. Bush and her colleagues from Adelaide concluded treatment with aloe vera was inferior to treatment with omeprazole.

Medications for Glandular Ulcers….

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Osteochondrosis - genetic causes and early diagnosis

By Celia M. Marr

Osteochondrosis (OC) is a common lesion in young horses affecting the growing cartilage of the articular/epiphyseal complex of predisposed joints at specific predilection sites. In the young Thoroughbred, it commonly affects the stifles, hocks and fetlocks. As this condition has such important impact on soundness across many horse breeds, it is commonly discussed in Equine Veterinary Journal. Four recent articles covered causes of the disease, its genetic aspects, and a new and very practical approach to early diagnosis through ultrasound screening programs on stud farms.

OC is a disease of joint cartilage. Cartilage covers the ends of bones in joints, and healthy cartilage is central to unrestricted joint movement. With OC, abnormal cartilage can be thickened, collapsed, or progress to cartilage flaps or osteochondral fragments separated from the subchondral bone leading to osteochondrosis dissecans (OCD). OC and OCD can be regarded as a spectrum rather than two discrete conditions.

Certain joints are prone to OC and OCD, and there is some variation between breeds on which joints have the highest prevalence. In Australian Thoroughbreds, 10% of yearlings had stifle OC, 8% had fetlock OC, and 6% had hock OC. The prevalence data may seem very high, but Thoroughbred breeders may take some comfort in learning that similar, and indeed slightly higher prevalences, are reported in the warmblood breeds, Standardbreds, and Scandinavian and French trotters. Heavy horse breeds have the highest prevalences.

In an article discussing progress in OC/OCD research, Professor Rene Van Weeren concludes that the clinical relevance of OC is man made.  In feral horses, where there is no human influence on mating pairings, OC does occur but at much lower prevalence than in horse breeds selected for sports or racing. Similarly, in pony breeds where factors other than speed and size are desirable characteristics, OC is also rare. These facts suggest that sports and racehorse breeders have inadvertently introduced a trait for OC along with other desired traits. There is a strong link between height and OC, suggesting that one of the desired traits with unintended consequences is height. This is of particular relevance in sports horses: the Dutch warmblood has become taller at a rate of approximately 1 mm per year over the past decades, which might not seem much but it is still an inch in 25 years. Van Weeren points out that if the two-hands tall Eohippus or Hyracotherium and the browsing forest-dweller with which equine evolution started some 65 millions of years ago had evolved at this speed, the average horse would now have stood a staggering 40 miles at the withers.

Drs. Naccache, Metzger and Distal, based at the Institute for Animal Breeding and Genetics in Hannover, Germany, have worked extensively on heritability and the genetic aspects of OC in horses. Their work has shown that there is not one single gene involved. In fact, genes located on not less than 20 of the 33 chromosomes of the horse are relevant to OC.

These researchers use whole genome scanning—otherwise known as genome-wide association studies, or GWAS. This approach has only been possible since the equine genome was mapped. GWAS look at the entire genetic map to detect differences between subjects with and without a particular trait or disease. Millions of genetic variants can be read at the same time to identify genetic variants that are associated with the disease of interest. Based on the number of genetic markers already found in warmblood OC, it is unlikely that a simple single-gene test will prove to be useful for screening young Thoroughbreds for OC.

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Stress Fractures - Are they linked to track surfaces?

Stress Fractures - Are they linked to track surfaces?

Stress fractures not only lead to training interruptions but if they are not identified early and managed appropriately they can be associated with subsequent catastrophic fractures. Stress fractures of the humerus, tibia, ilium and cannon bone (aka third metacarpal bone or McIII) are most common. Stress fractures are a late stage on a pathway of stress-related bone injury.  

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Equine lameness - can it be measured?

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THIS ARTICLE FIRST APPEARED IN - NORTH AMERICAN TRAINER - ISSUE 29

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