Neurology is Not a Euphemism for Necropsy

When faced with a horse exhibiting neurologic disease, the importance of a thorough physical exam and diagnostic testing cannot be emphasized enough. Stephen Reed, DVM, Dipl. ACVIM, of Rood & Riddle Equine Hospital in Lexington, Ky., described selected equine neurologic diseases during his presentation of the prestigious Milne Lecture at the 2008 American Association of Equine Practitioners Convention, held Dec. 6-10 in San Diego, Calif.

A review of selected neurological diseases affecting horses

Some elements of the exam include evaluating proprioception (the horse's awareness of where his feet are in space), gait changes, the presence of unusual gaits, and identifying the neuroanatomical location of an abnormality. He explained that proprioceptive deficits are the first signs of compressive lesions in the spinal cord, while deep pain sensation is the last function lost.

While a horse's history is important, Reed's relies on a full exam. He begins with evaluating the horse's behavior and mental status, and examining the head and cranial nerves. Then he moves systematically along the body and limbs toward the tail, and finally assesses gait. The type of response is important--whether it be a deficiency, a "discharge," such as a stereotypic (continuous, repetitive, and serving no purpose) behavior, seizure, or spasm; or a "release," such as an exaggerated, weak, or ataxic (incoordinated) response. Gait evaluation is a critical part of the exam. All findings should be recorded, signs characterized, and attempts made to localize the lesion to help determine the cause.

The first condition Reed discussed is cervical vertebral stenotic myopathy (CVM), also known as wobbler syndrome. (Stenosis implies a narrowing of the vertebral canal.) This can be a developmental problem in young light-breed horses, or it can be an acquired problem in older horses (over 10 years) from osteoarthritis of the neck vertebral articular process joints (facets). Elongation of the dorsal laminae (the bony plates that form the roof of the vertebral canal) into the intervertebral space (between the vertebrae) can cause stenosis, requiring surgical correction. Compression in a wobbler most commonly occurs between cervical vertebrae 6 and 7 (C6-C7).

Osteochondrosis dissecans (OCD)of the facets is a common developmental cause of wobbler syndrome, and growth plate abnormalities (vertebral epiphysitis) can also narrow the canal. The vertebral column is sensitive to dietary imbalances, particularly of copper, which influences vertebral development, or excess energy, which causes rapid skeletal growth. This rapid growth influences vertebral development and the propensity for OCD. Often, wobbler syndrome changes in the axial skeleton occur in conjunction with developmental orthopedic disease in the limbs. Reed noted that conservative treatment of diet (protein and energy) and exercise restrictions might prove successful for young wobbler horses.

Malalignment of vertebrae can also cause CVM, especially at C2-C3. Such malalignment is unusual, but it tends to be associated with the fixed, high arch of head and neck seen in Saddlebreds or some Warmbloods.

Reed described the tenets of the approach used by Barrie Grant, DVM, MS, Dipl. ACVS, a veterinarian in Bonsall, Calif., known for his CVM treatment methods:

  • Keep the horse alive and treat the underlying cause when possible, as this might result in an amazing recovery.
  • Take an aggressive approach to achieving an accurate diagnosis, using spinal taps and myelograms (which involve injecting a contrast agent, which is a solution that shows up on X rays, into the spinal canal to reveal any compressive lesions of the spinal cord) as necessary.
  • Standing cervical (neck) radiographs can be performed; pay careful attention to vertebral anatomy and measurements.
  • A mildly ataxic horse might perform okay, and a horse that is lame might perform okay, but a horse that is both ataxic and lame neither can perform, nor is he safe to ride.

Sheared heels can be a general sign of ataxia, but typically a horse with wobbler syndrome has symmetric ataxia, weakness, or spasticity, most notably in the rear limbs. Toe dragging, stumbling, and outward excursion of the rear limbs are also typical signs. It is important to recognize that other musculoskeletal diseases can make a horse look ataxic, such as bilateral suspensory ligament desmitis or bilateral stifle OCD. It is possible for a horse to have several coexisting conditions.

A mildly ataxic horse might perform okay, and a horse that is lame might perform okay, but a horse that is both ataxic and lame neither can perform, nor is he safe to ride.

Reed stressed the importance of addressing the situation early, as residual damage to neuromuscular tissue might not be resolved. He noted that patience is essential, and you should allow at least 18-24 months to realize the outcome with treatment. Physical therapy during rehabilitation improves the outcome. The intended use of the horse is important to consider when attempting treatment, and all measures should be taken to conduct follow-up exams to help ensure rider and horse safety.

Genetic influences of wobbler syndrome are still under investigation. Research has shown breeding wobbler horses to other wobbler horses resulted in an increase in limb OCD occurrence, but this effort never reproduced a wobbler. This disease can affect horses of all ages, but if the horse is older than 10 years, he likely has an acquired ostearthritic problem. Breed distribution of wobbler-affected horses is as follows: 37% Thoroughbred, 25% Warmblood, 16% Quarter Horse, 21% other (including a fair number of Tennessee Walkers), and 1% pony.


The next topic Reed discussed is equine protozoal myeloencephalitis (EPM), which is viewed as a serious parasitic disease with neurologic consequences. The opossum, identified as the definitive host, eats the flesh of an intermediate host (skunk, armadillo, sea otter, or domestic cat) that has encysted stages of the protozoan parasite Sarcocystis neurona. Then the opossum excretes parasitic oocysts in its feces, which are inadvertently eaten by horses in contaminated feed or pasture. Opossums tend to be opportunistic feeders, especially on forest edges. If separate sources of water are available for horses and wildlife so horses drink separately from opossums, there is lessened chance of infection.

Horse ingestion of contaminated feces might result in parasitic development in the horse's central nervous system (CNS), leading to asymmetric ataxia with muscular atrophy. Horses might be exposed to S. neurona, but they might not necessarily develop clinical disease. Therefore, blood testing is fraught with false positives.

A positive response in the CSF (cerebral spinal fluid) indicates that S. neurona entered the CNS and evoked an immune response; however, any blood contamination of the CSF tap can produce false positive results. False negatives are rare on blood or CSF, but they have been observed in the first seven to 10 days post-infection. The most important consideration is to rule out all other possible causes of ataxia.

With treatment, a horse is 50 times more likely to survive if there is notable improvement in clinical signs. Prevention is important and most effective and involves keeping wild animals away from horses, removing carcasses of intermediate hosts, keeping definitive hosts (opossums) away from horse feed and water sources, and by decreasing risk factors of stress and transport as much as possible.

Neurologic EHV-1

The final neurologic disease discussed by Reed is that of equine herpesvirus-1 (EHV-1), which can cause respiratory disease (rhinopneumonitis), abortion, severe neonatal disease, and it uncommonly takes a neurologic form that is acute and progressive. EHV-4 also can cause neurologic disease.

EHV-1 can be a mutated or nonmutated strain that induces symmetric ataxia with ascending (starting at the rear and moving forward) paralysis beginning with urinary incontinence, poor tail and anal tone, and incoordination in the rear limbs. The virus attacks the blood vascular supply of nerves. An affected horse might also show facial nerve signs, head tilt, and nystagmus (involuntary, rapid eye movement), as well as dementia and other cerebral signs.

The 2003 EHV-1 neurologic outbreak in Ohio demonstrated the rampant communicability of this disease. Of 137 horses in a barn, 117 had fever, and 46 of those showed neurologic signs, 14 of which died. Fever, cough, and nasal discharge preceded ataxia or recumbency by about five days. All horses had been previously immunized with rhinopneumonitis vaccines, which afforded no protection. Reed said the virus multiplies rapidly once the horse is exposed, thus increasing its contagion level.

The EHV-1 mutated strain also magnified the degree of virulence for longer. In 132 Thoroughbred broodmares, George Allen, PhD, found that while 46% harbored the wild-type strain, 8% harbored the mutant EHV-1 strain in their submandibular lymph nodes; the mutant strain comprised 18% of the total latent viral reservoir (the horses that weren't showing signs of illness). This high proportion of neurologic herpesvirus necessitates implementing measures to control its spread.

Veterinarians have learned from neurologic EHV-1 outbreaks that they must enforce diligent biosecurity measures in suspected outbreaks to limit the numbers of horses exposed. Horses older than 15 years of age and especially older than 20 seemed to be at the highest risk of infection; these are horses with less competent cell-mediated immunity. Stress plays a huge role in onset of clinical signs.

Reed believes that future goals for managing neurologic disease in horses should be to decrease mortality and improve outcomes. This would be best achieved by developing improved diagnostic tools to facilitate early diagnosis and treatment along with providing the ability to identify unknown disorders.

About the Author

Nancy S. Loving, DVM

Nancy S. Loving, DVM, owns Loving Equine Clinic in Boulder, Colorado, and has a special interest in managing the care of sport horses. Her book, All Horse Systems Go, is a comprehensive veterinary care and conditioning resource in full color that covers all facets of horse care. She has also authored the books Go the Distance as a resource for endurance horse owners, Conformation and Performance, and First Aid for Horse and Rider in addition to many veterinary articles for both horse owner and professional audiences.

Stay on top of the most recent Horse Health news with FREE weekly newsletters from Learn More