3 Neurologic Equine Diseases to Know

These difficult-to-diagnose conditions can undermine a horse’s balance and coordination.

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3 Neurologic Equine Diseases to Know
A vet demonstrates a foot-placing test to assess rate of replacement in a neurologic horse. | Photo: Stephanie L. Church

Neurologic diseases can be deceiving, presenting as subtly as an extremely mild lameness or as plainly as a suddenly staggering, dogsitting, or recumbent (down and unable to get up) horse. And while a large number of conditions can cause neurologic signs in horses, some are much more likely to than others. Our experts report the following as three conditions all horse owners need to be aware of:

  • Equine protozoal myeloencephalitis (EPM) – Inflammation of the spinal cord and brain caused by protozoa (single-celled parasites);
  • Equine herpesvirus myeloencephalopathy (EHM) – A disease affecting the brain and spinal cord as a result of equine herpesvirus-1 (EHV-1) infection; and
  • Wobbler syndrome (cervical vertebral compressive myelopathy, CVCM) – Compression of the spinal cord in the cervical, or neck, region by the vertebrae and associated soft tissues.

Here’s an in-depth look at what we know about these conditions. Call your veterinarian immediately if you think your horse might be neurologic. Such horses lack balance and coordination, making them unpredictable to ride and handle.

Equine Protozoal Myeloencephalitis

Two distinct protozoa cause EPM: Sarcocystis neurona and Neospora hughesi. Most of what we know about EPM involves S. neurona. Opossums, which are definitive hosts for EPM, ingest muscle of S. neurona-infected intermediate hosts (cats, skunks, raccoons, and armadillos) and, in turn, shed sporocysts in their feces. Horses consume food and water contaminated by these feces and are considered accidental or aberrant hosts because S. neurona’s natural life cycle does not involve them. Next, the parasites spread throughout the horse’s body.

“We believe the parasite can be found in muscle and perhaps other tissues in horses but is then cleared by the horse’s immune response,” explains Martin Furr, DVM, MA Ed, PhD, Dipl. ACVIM, head of the Department of Physiological Sciences at Oklahoma State University College of Veterinary Medicine, in Stillwater. “The parasite does not ‘target’ the nervous system but, rather, appears to be an accidental infection which the horse then cannot clear from the nervous system as it does in other tissues.”

“To the best of my knowledge, the definitive and intermediate hosts are still not known for N. hughesi, but we believe that the parasite migrates to the CNS (central nervous system) the same way as S. neurona,” says Amy Johnson, DVM, Dipl. ACVIM, section chief of internal medicine and ophthalmology at the University of Pennsylvania School of Veterinary Medicine, in Kennett Square.

Our lack of knowledge pertaining to N. hughesi could, at least in part, be because it causes infection far less commonly than S. neurona. Up to 89% of U.S. horses have antibodies against S. neurona, depending on location. Studies show only about 3-10% of horses, and possibly up to 34%, have antibodies against N. hughesi (James et al., 2017).

The presence of S. neurona or N. hughesi antibodies in a horse’s blood, however, doesn’t necessarily mean the horse is actively infected and suffers from EPM. Instead, antibodies simply reveal a horse has been exposed to them at some point. Only a small number of exposed horses develop neurologic disease; most fight off the parasite without showing signs.

“Both parasites cause similar neurologic deficits because they both cause similar types of damage to the brain and spinal cord,” says Johnson, though the signs are highly variable.

“Because the migratory path of the parasites through the horse’s body to the brain and spinal cord appears random, we typically see multifocal or asymmetric signs, with one side of the body more affected than the other,” Johnson explains.

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“There are lots of horses with evidence of exposure to the protozoa (i.e., antibodies) but no signs of neurologic disease,” says Johnson. “I also have lots of examples within my neurologic caseload of horses that have positive serology (antibodies) but no lesions or organisms found within their CNS on postmortem examination.”

An industrywide perception is that stress levels dictate which horses develop signs of EPM and which don’t. Examples of such stressors include transport, heavy exercise/intense competition, injury, surgery, and foaling. Johnson, however, thinks horse-specific factors might be more important than environmental ones.

“My personal feeling is that the host’s immune system is probably the most important factor, with parasite load and environmental stressors acting like modifying factors,” she says. “In other words, there are probably some horses that will likely never get EPM no matter how frequently they are naturally exposed. There might be some horses that are likely to get EPM if they are exposed. And then there is probably a group of horses in the middle that has a lesser tendency to develop EPM, but if the situation is right—such as high parasite load or environmental stressors—might develop EPM.”

Furr concurs, adding, “The role of stress in the development of EPM is unclear and complex. Some studies show that activities perceived as stressful were associated with disease; however, laboratory studies intended to mimic those conditions do not consistently show the same results. One possible interpretation is that the laboratories have not appropriately ‘mimicked’ naturally occurring disease.”


No test can definitively diagnose EPM in live horses. Instead, the gold standard diagnostic test is postmortem identification of the parasites in the CNS.

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“Still, this is rarely achieved,” says Furr. “It is very difficult to find the parasites— it’s like looking for a needle in a haystack.”

Instead, veterinarians consider inflammation around blood vessels called perivascular cuffing adequate for postmortem diagnosis.

To diagnose EPM in a live horse, says Johnson, the vet must see clinical signs of CNS disease and exclude all other diseases, and immunologic testing must confirm S. neurona or N. hughesi exposure.

“We now believe that the best way to diagnose EPM is evaluation of CSF (cerebrospinal fluid) for antibodies and then comparing the results to the amount of antibody in the bloodstream,” says Furr. “A serum/CSF ratio of < 100 is highly accurate in the diagnosis of EPM when paired with the other diagnostic criteria.”


Vets can choose from one of three approved EPM treatments. Scientists have shown these are all about 60% effective. This means horses’ neurologic score improved by at least one grade on a five-point scale or their CSF converted to negative status on test results.

From an athletic standpoint, what does this mean? Johnson cites historic data suggesting 60% of affected horses improved, but only 15-20% returned to normal function.

“These numbers might be higher now because diagnostic testing is more accurate and some of the treatment failures early on were probably due to misdiagnosis,” Johnson explains.

Says Furr, “If the horse has a solid diagnosis of EPM and is treated appropriately, there is a good chance he will return to usable soundness. But, the degree of severity and duration of the disorder likely have a significant effect on outcome.”

Learn more about this complex disease and its treatment at TheHorse.com/EPM.

Equine Herpes Myeloencephalopathy

Equine herpesvirus-1, despite wide- spread vaccination, continues to cause respiratory infection, abortion, and neurologic disease. It spreads primarily via respiratory secretions, direct contact between horses, or fomites (brushes, feed buckets, tack, etc.). Importantly, horses previously infected with EHV-1 do not fully clear the virus. Instead, it lies dormant and resurges during times of stress.

“These latently infected horses don’t usually become clinically ill again,” says Furr. “Instead, they just shed the virus in their nasal secretions and cause infection in naive (not previously exposed) in-contact horses.”

Essentially, the virus gets from the respiratory tract to the CNS by accessing the lymph nodes and bloodstream. From there it infects endothelial cells lining blood vessels in the CNS.

“Swelling in the endothelial cells compromises blood supply to the nervous tissue,” says Furr. “There is also inflammation that causes nerve cell dysfunction.”

This microdamage typically results in ataxia (incoordination) of all four limbs, with the hind limbs usually weaker than the forelimbs. Fecal retention, decreased anal tone, and urine dribbling often occur. Horses might also assume an unnatural “dog sitting” position.

In the most severe cases involving the brain and brainstem, horses are depressed and have a head tilt, cranial nerve deficits (e.g., drooping face and lip), and more. Many of these horses become recumbent and must be euthanized, but Furr says few horses are affected this severely.


In theory, diagnosing EHM requires specific testing at specific times during the disease course. Fever is typically the first clinical sign, and the vet should take swabs of nasal secretions within five days of onset. Other classic signs are urinary incontinence and symmetrical ataxia without muscle wasting. The virus spreads through the blood (the viremic phase) from Days 4 to 10 after infection. Due to this overlap in timing, vets should collect swabs and blood for polymerase chain reaction (PCR) testing.

“In reality, the veterinarian and owner likely do not know when the exposure happened or when the fever started,” Furr says. “Testing should be performed as soon as the fever or clinical signs appear.”

He also recommends CSF analysis, “especially if there is any doubt that something is going on other than EHM.”

Furr says if the horse displays classic clinical signs, he might not need a CSF analysis until swab and blood results return. “In my experience, however, a significant number of EHM horses do not present so clear-cut in the early stages of infection,” he adds. “A full work-up is therefore often needed for most neurologic horses, including CSF tapping.”

Scientists previously found that an EHV-1 virus strain with a single mutation (the D752 genotype) causes most EHM cases. Still, the “wildtype” virus (N752 genotype) causes up to one-quarter of all EHM cases, meaning factors other than viral genome increase EHM risk. Scientists suggest circulating virus numbers are higher and neurologic signs worse with the D752 or neuropathic strain. However, Furr says authors on a recent study (Pusterla et al., 2020) showed the strains cause a similar degree of ataxia, while horses with the neuropathic form are more likely to experience incontinence.

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As with EPM, not all horses with EHV- 1 circulating in the bloodstream develop EHM and neurologic disease.

“The rate of clinical disease varies a good bit among outbreaks and probably depends on the patient population, stress factors, virulence or ‘strength’ of the infecting virus, and immunologic status of the horse,” says Furr.

Overall, the incidence of EHM associated with confirmed EHV-1 infection is low. But older horses do appear particularly susceptible to disease.


Supportive care involving hydration, nutrition, physical support (using a sling), rectal evacuation of feces, and emptying the bladder is the only treatment. Vets might also administer non-steroidal anti-inflammatory drugs (NSAIDs) and antivirals.

In mild cases horses have a fair to good chance of recovering and returning to athletic performance, typically showing improvements five to seven days after peak clinical disease severity. Recumbent horses usually do not recover fully, and mortality rates of these severely affected horses vary from 5% to 40%.

Vaccination does not appear to protect against the neurologic forms of the virus, says Furr. So, even fully vaccinated horses can become neurologic from either strain. The vaccine does protect against other manifestations of EHV-1, including abortion, and veterinarians are encouraged to follow American Association of Equine Practitioners vaccination guidelines.

Wobbler Syndrome (CVCM)

Cervical spinal cord compression can cause ataxia that severely limits a horse’s performance and can make him unsafe to ride or handle. It occurs in older horses with stenosis—narrowing of the space in which the spinal cord lies—most often as a result of osteoarthritis (OA) of the cervical joints. However, it most commonly affects young horses. How the stenosis and compression occur in younger animals remains unclear, but researchers say it’s likely related to developmental orthopedic disease and rapid growth rates.


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Horses with CVCM exhibit symmetric ataxia as well as muscle weak-ness and an abnormal and spastic gait.

These signs occur in all four limbs but are often more noticeable in the hind limbs.

Vets suspecting CVCM begin their diagnostic quest by taking radiographs of the standing horse’s neck vertebrae.

“We use these X rays to measure the space for the spinal cord,” says Melinda (Mindy) Story, DVM, Dipl. ACVS, ACVSMR, a clinician at the Colorado State University (CSU) Veterinary Teaching Hospital, in Fort Collins. “If the canal is too narrow, then the cord can become compressed, and we see the subsequent neurologic deficits.”

Yvette Nout-Lomas, DVM, PhD, Dipl. ACVIM, ACVECC, associate professor of internal medicine at CSU, adds, “We determine a ratio of the canal width compared to the vertebral body height.

The goal is to determine whether we think the canal is wide enough to accommodate the spinal cord. The radiographs just give us an impression as to what the chance is that the horse has a too-narrow canal. Additional testing—a myelogram (X ray under general anesthesia after injecting a contrast agent around the spinal cord)—is needed to confirm our suspicion and determine the actual site(s) of compression.”


Once vets locate the compression, management options are limited. Diet changes might help growing horses younger than 2. Feeding them a low-protein and -carbohydrate diet balanced in vitamins and minerals can allow the diameter of the vertebral canal to en- large and “catch up” to the horse’s overall growth, says Nout-Lomas. Vets might also administer NSAIDs or corticosteroids to address inflammation.

Traditionally, vets recommended confining affected young horses to stalls, but Nout-Lomas suggests exercise and strength training are more beneficial to overall return to function.

“In young horses, surgical stabilization of affected vertebral bodies can lead to noticeable improvement in about 70% of horses operated,” she says. “Depending on the horse, sites affected, and neurologic status, these horses can be excellent surgical candidates due to their young age.”

Adult horses can be candidates for conservative medical therapy, which includes injecting articular facet joints with corticosteroids and/or a polysaccharide such as hyaluronic acid, or surgery. Vets might reach for regenerative therapies such as platelet-rich plasma or autologous conditioned serum if they’re concerned about corticosteroid use, such as in horses at increased risk of laminitis, Story says.

“In addition, shock wave and integrative therapies such as acupuncture, TENS, PEMF, and manual therapies may help with pain management,” she says.

Regardless of the horse’s age, the goal of surgery is to stabilize, or fuse, the joint causing spinal cord compression.

“Once the joint is stabilized and there is no movement anymore, over time, soft tissue and bony remodeling occurs,” Nout-Lomas says. “Because there is no movement, similar to when you break a bone and lose muscle mass from not moving, over time there is also resorption of bone. The ultimate goal is that there will be more space available to accommodate the spinal cord. Furthermore, we then expect to obtain some level of spinal cord regeneration and rewiring and are depending on the recovery and plasticity potential of the spinal cord.”

Vets should check horses’ stability regularly; not all patients respond to treatment, making them unsuitable for riding.

“About 60-70% of horses improve in function after surgery, but not all of these horses return to performance,” Nout- Lomas says. “A lot depends on age of the horse, how long it has been neurologic for, and severity of neurologic signs.”

Take-Home Message

Diagnosing equine neurologic conditions is complicated and constrained by the inherent limitations of testing.

A major concern is rider and handler safety, Story says. Veterinary reevaluation frequently during recovery will be the best way to determine whether the horse can recover sufficiently to be ridden safely or needs to transition to retirement.


Written by:

Stacey Oke, MSc, DVM, is a practicing veterinarian and freelance medical writer and editor. She is interested in both large and small animals, as well as complementary and alternative medicine. Since 2005, she’s worked as a research consultant for nutritional supplement companies, assisted physicians and veterinarians in publishing research articles and textbooks, and written for a number of educational magazines and websites.

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