Major Causes of Spinal Ataxia in the Horse
The 4 major causes of spinal ataxia in the horse are:
- Cervical vertebral compressive myelopathy (i.e. “Wobblers” disease)
- Equine Protozoal Myeloencepahalitis (EPM)
- Neuroaxonal Dystrophy/Equine Degenerative Myeloencephalopathy (NAD/EDM)
Infection with equine herpes virus type-1 (equine herpes myeloencephalopathy) can cause clinical signs that resemble these conditions, but the onset is usually acute (fast) and other clinical signs (fever, urine dribbling) and history (recent travel to an event) will help your veterinarian determine if EHV-1 should be considered in your horse. West Nile Virus (WNV) is also a cause for sensory ataxia in the horse and highly accurate diagnostic tests are available to test for WNV. Additionally, vaccination programs have greatly reduced the incidence of WNV.
Cervical vertebral compressive myelopathy (CVCM) is also known by the names: cervical vertebral stenotic myelopathy, cervical vertebral malformation and malarticulation (CVM), spinal ataxia, cervical stenotic myelopathy, and “wobbler’s” syndrome. It is one of the most common causes of neurologic disease in horses worldwide. There are two types of CVCM:
Type I CVCM is a developmental disease, caused by problems during development of the vertebrae or spinal canal. Type I CVCM results in a dynamic instability of the vertebral canal. This means that, when the horse flexes or extends his neck, the bony column of the vertebrae will compress the spinal cord. When the spinal cord is compressed, certain tracts are damaged and this will result in a sensory ataxia with or without weakness.
Type I CVCM typically affects young, rapidly growing horses and is most common in Thoroughbreds, Tennessee Walking Horses, Warmbloods and Quarter horses.
Type II CVCM occurs more commonly in older horses (≥8 years old) and results from arthritis within the joints of the neck vertebrae. This often results in a static compression of the spinal cord (the cord is compressed all the time, not only during flexion and extension)
Clinical signs of Type I and Type II CVCM include a sensory ataxia and signs of upper motor neuron weakness (spasticity). To diagnosis CVCM, a veterinarian will typically start with x-rays of the neck. These x-rays are done with your horse standing under sedation. It is very important to obtain high quality x-rays of all neck vertebrae. This usually involves bringing your horse to a facility that has a large x-ray unit powerful enough to shoot through the region of the fifth through seventh cervical vertebrae. This region contains a lot of muscle and quality x-rays are often impossible to take in the field with a portable x-ray machine.
Although veterinarians are not able to visualize the cervical spinal cord on the x-rays since it is soft tissue, they can visualize the canal that it runs through and all of the surrounding bony structures. The cervical x-rays may reveal the following:
- Highly suggestive abnormalities consistent with Type I or Type II CVCM. These would include malalignment of the cervical vertebrae at a particular joint, evidence of a severely narrowed spinal canal, or severe arthritis of the neck joints.
- Suggestive abnormalities. The use of ratio measurements is employed when analyzing these cervical x-rays and you may discover that your horse has ratio measurements that are “suggestive” of compression. These ratios provide a likelihood that your horse’s abnormalities are due to CVCM, but it is not definitive. If a horse appears to have a region of the canal that is narrowed and/or has some evidence of arthritis of the neck joints, your horse MAY have CVCM.
- Normal neck x-rays. Although this makes CVCM more unlikely, it does not, unfortunately, rule it out completely. The reasons for this are because sometimes the compression is dynamic, when the neck is flexed, and we are only seeing the spinal canal in the horse's natural stance. Additionally, we can only take lateral (from the side) x-rays in a standing horse so asymmetric compression (i.e. the right is compressed but the left is not) can be missed.
The next step that may be recommended is a myelogram. A myelogram involves placing your horse under general anesthesia and injecting a contrast agent into the space that surrounds the spinal cord. X-rays are then taken with your horse's neck in a neutral, flexed and extended position. When examining the x-rays, the contrast will outline the spinal cord and veterinarians can determine if there is any evidence of compression. Results of the myelogram may tell you the following:
- Highly suggestive/definitive evidence of Type I or Type II CVCM.
- No evidence of compression. At this stage, CVCM is highly unlikely. However, it is important to note that an asymmetric compression could still be missed. Many Universities are now working to obtain dorsoventral views to reduce the chance of missing asymmetric compressions.
If available, a CT (computed tomography) using contrast can accurately diagnose the location and severity of compressive lesions in cases of CVCM; however, most units are unable to image adult equine cervical vertebrae at this time.
Equine Protozoal Myeloencepahalitis (EPM) is one of the 4 major causes of spinal ataxia in the horse.
EPM is caused by protozoan parasites. There are two types of protozoa that can cause EPM in the horse, Sarcocystis neurona and Neospora hughesi. EPM is most commonly caused by S. neurona (>90% of cases). The definitive host for S. neurona is the opossum and horses become infected from ingesting feed that has been contaminated with feces from opossums. The chances of your horse becoming infected with EPM due to S. neurona depend on a variety of factors:
- Geographic region of the country: in areas with more opossums, your horse has a greater chance of becoming infected
- Immune system of your horse: immune-compromised horses may be more susceptible to acquiring EPM
Additionally, your horse's age and breed (Thoroughbred and Warmbloods are more likely than Quarter horses) may play a role in determining his susceptibility.
Clinical signs of EPM vary widely. Most horses with EPM show signs very similar to horses with sensory ataxia. Horses with EPM may demonstrate asymmetric abnormalities. For example, the right hind leg may be more severely affected that the left hind leg. This asymmetry is uncommon for other diseases and therefore, this finding may help the veterinarian prioritize diagnostic testing.
There are many tests available to try and diagnose EPM but none of them are perfect. The reason for this is that these tests rely upon antibodies to S. neurona or N. hughesi. None of the available tests actually test for the parasite. Therefore, a “positive” blood test in your horse means either your horse is infected with EPM or your horse was exposed to EPM at some point in their life and now has antibodies.
How do veterinarians tell the difference? The only way to reliably know for sure is to use those same antibody tests in the cerebrospinal fluid (CSF). The CSF is the fluid that surrounds the spinal cord and brain. This fluid is separated from blood by a blood-brain barrier. The purpose of the barrier is to not allow large proteins and other substances into the CSF, thereby protecting the brain and spinal cord from potential toxins. Antibodies are too big to fit across an intact blood-brain barrier. Therefore, if a horse was simply exposed to either S. neurona or N. hughesi, they shouldn't have any antibodies in the CSF. If, however, the horse is infected with EPM, the parasites live in the brain and spinal cord and therefore, the horse will produce antibodies in these tissues, which will leak out into the CSF and test positive.
Therefore, the next step in testing for EPM is to have a spinal tap performed on the horse. This procedure is generally done under standing sedation and a small amount of fluid is collected the region surrounding the lumbosacral spinal cord.
One caveat to the lumbosacral CSF tap is that there may be some blood that leaks into the needle site as the veterinarian is collecting the CSF. To obtain CSF from an adult horse, the needle is inserted about 4 to 5 inches into the muscle, which may result in some blood contamination. Once CSF is collected, a veterinarian can determine how many red blood cells are present in the sample and if it is necessary to be concerned about a “false positive ” due to blood contamination.
An alternative to the lumbosacral tap and possible blood contamination is to have an atlanto-occipital tap performed on the horse. This collection procedure involves injectable anesthesia as it cannot be done safely in a standing horse. The CSF is collected from the site behind the ears, which is only 1.5 to 2 inches into the muscle and thereby minimizes blood contamination. This collection site is not routinely used because it requires anesthesia and carries more risk to the horse.
Since EPM testing is not always straightforward, many owners may elect to try a course of treatment for EPM based on a positive blood test. The problem with this approach is that the course of treatment is very expensive (averages $800/month and at least 2-3 months of treatment should be provided) and, the horse can “relapses” after discontinuation of the drug. The importance of obtaining an accurate diagnosis as cannot be overemphasized. Owners will end up saving money in the long-run if they follow the recommended diagnostic course from the start.
Neuroaxonal Dystrophy/Equine Degenerative Myeloencephalopathy (NAD/EDM) is a neurologic disease that typically affects young (<3 years old) horses of various breeds. Males and females appear to be equally affected. NAD/EDM appears to be an inherited condition and often the disease is observed on breeding farms or occurs within siblings or half-siblings. There is also strong evidence that dietary vitamin E, especially in utero and during the first year of life, plays an important role in the development of NAD/EDM. Current evidence suggests that horses may be genetically “at risk” to develop NAD/EDM and then, if they are in a vitamin-E deficient state in utero and during the first few months of life, the disease becomes apparent.
Clinical signs include a symmetric sensory ataxia with upper motor neuron weakness (identical to ones observed for CVCM).
At this time, there is no genetic test available for NAD/EDM. It is recommended to test your horse's blood for vitamin E levels. A low vitamin E level is suggestive that your horse may have NAD/EDM but a normal/high vitamin E level does not rule the disease out, especially considering the fact that many horses aren't examined until they are over 1 year of age and the deficiency may have occurred earlier in their lives.
The University of Minnesota is currently doing research on this condition. Please contact Dr. Finno at firstname.lastname@example.org if you think your horse is affected.
Trauma to the neck or another region of the spine may result in a sensory ataxia with or without weakness that resembles EPM and other neurologic diseases. Cervical x-rays and/or a myelogram may be needed to confirm a neck fracture. In foals, fractures of the thoracic spine may occur and these may be detected on a physical examination and confirmed with x-rays. Many cases of trauma that do not displace the position of the vertebrae may be treated successfully with anti-inflammatories, rest and time.