Understanding Wobbler Syndrome

Wobbler syndrome is associated with cervical stenotic myelopathy (CSM), a malformation of the vertebrae or a narrowing of the spinal canal that compresses the spinal cord, damaging nerves and affecting proprioception.  Clinical signs include gait abnormalities signified by a loss of balance, loss of coordination (ataxia), weakness, and in some cases, paresis or paralysis.

Other scientific names for the disease include cervical vertebral malformation, cervical vertebral compressive myelopathy, cervical vertebral stenotic myelopathy, and cervical vertebral stenosis.

CSM is primarily classified as a developmental or orthopedic disease and typically occurs in young horses between the ages of 4 months and 4 years of age, with a mean age of 2 for diagnosis and distinct peaks of diagnosis coinciding with periods of rapid skeletal growth around 6 months and 1.5 years of age. The prevalence of the disease in young horses is due to increased susceptibility to growth abnormalities and trauma until their skeletons fully mature and all of their growth plates close. The vertebral processes are the last part of the skeleton to mature, at between 3 and approximately 5 years of age.  CSM also affects older horses as a secondary effect of arthritis.

Causes & Pathogenesis

The causes of CSM are multifactorial and may include one or a combination of the following, a high carbohydrate diet to promote faster than normal growth rates, nutritional imbalances leading to copper deficiencies and excessive dietary zinc, instability of the vertebral column, physical trauma, osteochondrosis and osteosclerosis due to the abnormal maturation of bone and cartilage, genetics, and arthritis.

There are two theories of pathogenesis, the developmental theory and the biomechanical theory. The developmental theory proposes that cervical vertebral malformations occur in response to an underlying bone disorder that affects cartilage formation and maturation. Whereas the biomechanical theory proposes that cervical static stenosis, narrowing of the cervical canal between C5 and C7, is the result of force and mechanical stress on the cervical column which causes structural changes in the vertebrae. Mechanical stresses include strain or physical trauma from injuries, such as when a young horse is restrained with a halter and tied up for the first time, or is cast in a stall, vibration, and oscillation of the neck.

Young horses diagnosed with CSM between the ages of 4 to 18 months typically have lesions between the C3 and C5 vertebrae which compress on the spinal cord when the neck is flexed, known as dynamic compression, or cervical vertebral instability caused by abnormal movement of the cervical vertebrae. Whereas, horses between 1 to 4 years of age are more likely have a narrowing of the cervical canal, which causes static compression to occur regardless of the position of the neck due to the abnormal formation and shape of the vertebrae. In some cases, narrowing of the spinal canal may be more extensive, extending from C3 to C7. In older horses static compression and narrowing of the cervical canal is most likely the result of chronic trauma to the neck or arthritis in the cervical vertebrae.

Breed & Genetic Predisposition

While it has been reported in a variety of breeds, there is a higher incidence of the disease in rapidly growing horses, Thoroughbreds, Warmbloods, Quarter Horses, and Tennessee Walking Horses, with males being affected more frequently than females. However, there is still considerable debate regarding genetic predisposition, see Prevention below. The reasons for the gender predisposition are thought to be related to the different effects of testosterone and estrogen on growth rates. Affected horses, generally, tend to be larger males with longer necks compared to age-matched horses in control groups.

Clinical Signs & Diagnostics

Clinical signs associated with CSM include mild to progressive ataxia (loss of coordination) most often observed in the hind limbs, weakness, and in some cases paresis or paralysis. Ataxia is generally more prevalent in the hind limbs than the forelimbs because the nerves that are connected to the hindlimbs are located along the outside of the cervical area of the spinal cord and are easily damaged by any compression or trauma of the cervical spine, whereas the nerves connected to the forelimbs are located deeper within the spinal cord and thus better protected.

There is a series of preliminary tests that can be performed, preferably with a veterinarian present for safety reasons, to confirm the presence of ataxia and impaired neurological function indicative of Wobbler syndrome. These include 1) turning the horse in a small circle – a horse with CSM will swing rear legs out while turning; 2) walking the horse backwards – wobblers will have trouble backing up, hopping with the rear legs rather than in the normal two-beat fashion; 3) while one person is walking the horse forward, another person will pull the horse to one side by the tail – a wobbler will have an impaired sense of proprioception and will easily be pulled over without being able to correct its position; 4) if the horse does not exhibit any resistance to having its tail lifted, this is a good indication of nerve damage along the spinal cord.

Following a complete neurological exam, advanced diagnostics will be used to determine the specific cause of the gait abnormality and confirm whether or not cervical damage has occurred. It is also necessary to rule out other diseases that can cause ataxia, including equine protozoal myeloencephalitis, West Nile, equine herpes virus, and rabies. A definitive diagnosis depends on radiographs of the cervical vertebrae to measure the diameter of the spinal canal and, if stenosis is indicated, a myelogram will also be performed to determine the presence and extent of spinal cord compression.

Treatment & Potential Complications

Initial treatment with anti-inflammatories and corticosteroids may help minimize acute inflammation but will not have any significant long-term benefit.  Osmotic diuretics may be more effective at decreasing swelling of the nerve tissue and relieving intracranial pressure, but this too is a temporary measure.  In young horses, if caught early enough, dietary adjustments and a reduced level of exercise for an extended period of time may be an adequate level of intervention and the horse may grow out of the problem. In some mature horses, depending on the degree of ataxia, the location of compression and number of vertebrae involved, surgical fusion may be performed. The most common surgical intervention involves placing a titanium basket around the affected vertebrae to promote fusion and relieve compression on the spinal cord.  

In many cases, CSM is performance-limiting even after surgery. While Crabbe indicates approximately 70% of horses treated surgically will experience some degree of improvement, only about 50% are likely to be able to perform in athletic disciplines. Even following improvements from vertebral fusion surgery, horses may still have residual neurological problems, including mild ataxia and should be considered unsafe to ride.


Orthopedic development of the disease may be preventable through balanced nutrition for both mare and foal to promote natural growth rates. Horse pairings that have previously produced foals with wobblers should not be bred again, as there may be a genetic predisposition. However, it has been reported that breeding trials between stallions and mares confirmed to have CSM did not produce any foals with Wobbler syndrome. More research is needed regarding the role of genetics in the development of the disease.  Preventative measures for the mature horse were not indicated in the literature.

Owner Impact

Horses with Wobbler syndrome pose a danger to themselves and others.  Severe ataxia can increase chances of traumatic self-injury and casting, and the horses may also be difficult to safely handle and/or ride. These cases have significant financial impact related to diagnostic and treatment expenses, as well as a significant emotional impact, as owners must make a decision between treatment and euthanasia. For humane reasons, it is common for horses affected by CSM to be euthanized, particularly in more advanced or severe cases, for the safety of both horse and human.


Bennett, D. (2008). “Timing and Rate of Skeletal Maturation in Horses, With Comments on Starting Young Horses and the State of the Industry.” Equine Studies Institute. Retrieved from http://www.equinestudies.org/ranger_2008/ranger_piece_2008_pdf1.pdf

Camargo, F. C. & J. Janes (2010). “Wobbler Syndrome in Horses.” University of Kentucky College of Agriculture ID-182. Retrieved from http://www2.ca.uky.edu/agcomm/pubs/id/id182/id182.pdf

Church, S.L. (2016). “Wobbler Syndrome: What’s Going on With the Neck Vertebrae?” The Horse Feb 10, 2016. Retrieved from http://www.thehorse.com/articles/37087/wobbler-syndrome-whats-going-on-with-the-neck-vertebrae

Crabbe, B. (2007). The Comprehensive Guide to Equine Veterinary Medicine. New York, NY: Sterling Publishing Co.

Finno, C. (undated). “Major Causes of Spinal Ataxia in the Horse.” University of Minnesota Horse Extension. Retrieved from http://www.extension.umn.edu/agriculture/horse/health/major-causes-of-spinal-ataxia-in-the-horse/index.html

Foreman, J.H. (2016). “Some Important Diseases of the Equine Neurological System.” University of Illinois College of Veterinary Medicine. Retrieved from http://vetmed.illinois.edu/search-results/?wpq=wobbler%20horse

Grant, B. (undated). “Equine Wobbler Syndrome.” Retrieved from http://www.equinewobblers.com/index.html

Janes, J. (2015). “Wobbler Syndrome: What We Know and Where We’re Headed.” The Horse Jul 1, 2015. Retrieved from http://www.thehorse.com/articles/36020/wobbler-syndrome-what-we-know-and-where-were-headed

Janes, J.G., Garrett, K.S., McQuerry, K.J., Waddell, S., Voor, M.J., Reed, S.M., Williams, N.M. & J.N. MacLeod. (2015). “Cervical Vertebral Lesions in Equine Stenotic Myelopathy.” Veterinary Pathology (2015) 52 (5) p. 919-927

Larson, E. (2011). “Wobbler Syndrome in Horses: An Overview.” The Horse Aug 6, 2011. Retrieved from http://www.thehorse.com/articles/27750/wobbler-syndrome-in-horses-an-overview

Levine, J.M., Ngheim, P.P., Levine, G.H., & N.D. Cohen. (2008). “Associations of sex, breed, and age with cervical vertebral compressive myelopathy in horses: 811 cases (1974-2007).” Journal of the American Veterinary Medical Association 233(9) p.1453-1458

Oswald, J., Love, S., Parkin, T.D.H., & K.J. Hughes. (2010). “Prevalence of cervical stenotic myelopathy in a population of thoroughbred horses.” Veterinary Record (2010) 166, p.82-83

Slater, J. D. & E.J. Knowles. (2012). Ch. 14: “Medical nursing.” In K.M. Coumbe (Ed.), Equine Veterinary Nursing. P.246-285 John Wiley & Sons Incorporated


Breed Profile: Paso Fino

The Smoothest riding horse in the world!

This video of a Paso Fino foal was making the rounds several months ago, right around the time I had to choose a breed to profile for an assignment in my Equine Industry course. Naturally, I had to learn more.

Origin: Puerto Rico

Aptitudes: riding horse

Population Status: common

Origins of the breed

A show and pleasure horse with Spanish heritage, Los Caballos de Paso Fino, the horses with the fine walk, were bred from the Andalusians, Spanish Barbs, and the now extinct Spanish Jennets that were introduced to the Caribbean Islands by the conquistadors beginning in 1493. It is believed that the first generations of Paso Fino-like horses were the offspring of Spanish Jennet mares and Andalusian stallions, inheriting the unique gait of the Jennet, which was possibly inherited from a very rare, small horse from Northern Spain, the Asturian, and the brio (energy and spirit) of the Andalusian.

It is very likely that the Spanish Jennet and Andalusian offspring were taken to the Dominican Republic (Santo Domingo at the time of Columbus’ second voyage) and used as foundation stock to populate the expanding territory throughout the Caribbean as it was conquered. Over time, these Paso Fino-like horses became refined through selective breeding of Spanish Jennets, Andalusians and Barbs, resulting in a hardy horse with a smooth gait. Innate to the Paso Fino, the gait is unique to the breed and cannot be learned by other horses.

In the early days of the breed, a number of different Paso Fino lines developed, most notably in Puerto Rico and Colombia, and to a lesser extent in Cuba and Peru, each with subtle variations in appearance but all with the lateral four-beat gait. This gait was a highly valued characteristic of the horse because long journeys on horseback were common at the time, and the horse’s smooth gait eased some of the physical strain for the rider.

From the 16th century up until at least WWII, the Paso Fino was solely known within the Caribbean and Latin America, where it was in high demand from hacienda and plantation owners due to its tireless work nature. It was not introduced to North America until it was imported from Puerto Rico in the mid-1940s. Two decades later, many more Paso Fino horses began to be imported from Colombia as well, and the American Paso Fino was born – bred from the best of the Puerto Rican and Colombian bloodlines.

Puerto Rican v. Colombian v. American: the subtle variations

Due to different breeding specifications and the fact that they developed independently of one another, the Colombian Paso Finos and the Puerto Rican Paso Finos are technically considered to be two different breeds. One obvious distinction is that the Colombian Paso Finos developed an additional gait called the trocha, an unevenly timed diagonal four-beat gait. Bred primarily from  Colombian and Puerto Rican Paso Finos, the American Paso Fino can also have traces of Peruvian Paso Fino blood and may perform the trocha in addition to the traditional gaits.

Use by humans

A highly athletic, sure-footed, versatile and gentle breed, the Paso Fino is used in a range of disciplines, including trail riding, endurance, drill team, dressage, gaming and Western disciplines. The natural smoothness and versatility of the gaits make it ideal for riders who have had back and knee injuries.

Physical description

The Paso Fino is a small horse most commonly reaching 13.3 to 14.2 hands at the withers, although the American Paso Fino tends to be larger and is often up to 15 to 16 hands tall. They have long, luxurious manes and tails and can be registered in any equine colour and may have white markings. The conformation of the Paso Fino can be described as graceful and elegant. It has a slightly convex or straight profile with an alert and intelligent face and large, expressive eyes carried high on a gracefully arched neck. The back is strong and muscular and when in motion, the tail is carried away from the body.

Well-proportioned and strong, the Paso Fino is powerful without extreme muscling. Its durable hooves are rarely shod and its legs are well-defined, with long forearms and shorter cannon bones.


The natural gait of the Paso Fino is a smooth, rhythmic ambling gait, a four-beat rhythm with the footfall pattern of a walk in which the horse can reach speeds comparable to or exceeding the pace of a trot without the typical aerial phase of the traditional faster gaits. This unique gait can be performed at three speeds, known as the Classic Fino, the Paso Corto, and the Paso Largo. The first of these, the Classic Fino is a gait with full collection and a slow forward speed, characterized by extremely rapid footfall with very short steps and extension. The Paso Corto is performed at a moderate speed with a moderate degree of collection and medium extension and stride. The Paso Largo has a longer extension and stride with moderate to minimal collection, and is the fastest speed of the gait.

Additional notes or facts

The Spanish Jennet was thought to have been a type of horse rather than a distinct breed, a term used to describe the assorted Iberian horses arriving in the Americas. Although they did become more uniform through selective breeding and geographic isolation during the Middle Ages. There is no clear record of when the Spanish Jennet became extinct.

In recent years, a new Spanish Jennet has been created and registered through the Spanish Jennet Horse Society. Direct descendants of the Paso Fino, the new Spanish Jennet is essentially a patterned Paso Fino. The pinto patterned Pintado must have 100% Paso Fino heritage, and the leopard patterned Atrigado must have at least 50% purebred Paso Fino or Peruvian Paso blood.

Associations/clubs/breed registries

  1. Central Canada Paso Fino Horse Association http://www.centralcanadapfha.com
  2. Forest Gait Farm http://www.pasofino.ca/about-paso-finos
  3. Paso Fino Horse Association http://www.pfha.org/the-breed
  4. Paso Fino Association Europe http://www.pfae.org/index.php/en
  5. Pure Puerto Rican Paso Fino Federation of America http://pprpffa.org/index.html
  6. The Spanish Jennet Horse Society http://www.spanishjennethorses.org


Central Canada Paso Fino Horse Association http://www.centralcanadapfha.com/

Equine Avenue: The Gateway for Horses and Their People – Spanish Jennet http://www.spanishjennethorses.org/registry.html

Forest Gait Farm http://www.pasofino.ca/about-paso-finos/

Hendricks, Bonnie L. 1995. International Encyclopedia of Horse Breeds. University of Oklahoma Press

Paso Fino Horse Association http://www.pfha.org/the-breed

Paso Fino Association Europe http://www.pfae.org/index.php/en/the-breed

Promerova, M. et al. 2014. “Worldwide frequency distribution of the ‘Gait keeper’ mutation in the DMRT3 gene.” Stichting International Foundation for Animal Genetics 45 (2014) 274-282 http://www.ucm.es/data/cont/docs/345-2014-10-07-gait_keeper_mutation.pdf

Pure Puerto Rican Paso Fino Federation of America http://pprpffa.org/index.html