Spinal ataxia in horses (Proceedings)


Differential diagnoses for spinal ataxia in horses includes: cervical vertebral stenotic myelopathy (CVSM), equine protozoal myelitis (EPM), trauma, congenital abnormalities, equine degenerative myelopathy (EDM), and equine herpes virus-1.

Differential diagnoses for spinal ataxia in horses includes: cervical vertebral stenotic myelopathy (CVSM), equine protozoal myelitis (EPM), trauma, congenital abnormalities, equine degenerative myelopathy (EDM), and equine herpes virus-1. This lecture will present each differential by a case by case basis, and then summarize.

Cervical vertebral stenotic myelopathy:

Signalment: two age groups.

Young horses: Have spinal cord compression as a result of developmental abnormalities of the cervical vertebral column. Young horses are usually well feed and fast growing. Typical age at presentation is 1-2 years (but maybe older or younger).

Older horses: May present with ataxia or predominately neck pain due to osteoarthritis of the articular facets of the vertebrae.

Clinical signs:

Young horses: Onset of ataxia maybe insidious or more acute. Symmetric ataxia, paresis, dysmetria and spasticity in all 4 limbs. Hindlimbs usually 1 grade worse than front. No cranial nerve signs. Usually no significant neck pain.

Older horses: Usually ataxia is symmetric (with hindlimbs more severely affected). In some horses may notice asymmetry of ataxia due to lateral compression of the spinal cord due to degenerative joint disease of the articular process. Neck pain (on palpation) is usually present, and maybe the most important clinical finding. Horses may actually present for a front limb lameness due to compression of a nerve root. Other clinical signs may include focal muscle atrophy, focal sweating, or palpable bony abnormalities of the articular processes.

Neuroanatomic location: Cervical Vertebrae with a focal distribution.


Standing cervical vertebral radiographs may be very helpful in certain cases. However, there are cases that will have normal cervical radiographs and a myelogram is helpful.

Abnormalities include: 1) flare of the caudal vertebral epiphysis (more common in young horses) 2) abnormal ossification of the articular processes (young horses); 3) malalignment between adjacent vertebrae (more common in young horses) 4) extension of the dorsal laminae (young and old horses) and 5) degenerative joint disease of the articular processes (more common in older horses and at C5-C6 and C6-C7).

Further assessment: measurement of the cervical vertebral sagittal ratios: an assessment of the width of the spinal canal width. Must be lateral.

Myleography is required to confirm diagnosis of a focal spinal cord compression, and is necessary if surgical treatment is a consideration.

Treatment options:

Medical treatment: Medical treatment aimed at reducing swelling and edema with anti-inflammatory medications and rest.

Young horses less than one year of age: "pace diet"- restricts exercise, reduce diet to 80% of NRC. Make sure that trace minerals are balanced (such as copper and zinc)

Adult horses: intra-articular injection of the facets with steroids will reduce inflammation, and improve pain. Done via ultrasound guidance.

Equine Protozoal Myelitis:

Signalment: any age

Clinical signs:

The clinical signs are highly variable. Asymmetric ataxia is the most common. Other clinical signs include asymmetric muscle atrophy, and occasionally cranial nerve disease. Cerebral disease (such as seizures) is very rarely reported. EPM can range in severity, from a mild gait abnormality to recumbency.

Neuroanatomic location:

Can vary. Classical descriptions include a multifocal distribution, which often includes spinal cord and brainstem (cranial nerve disease). However, it can present as a cervical vertebrae and with a focal distribution.


The clinical diagnosis remains a challenge. Diagnosis of EPM should include two facts: 1) the horse has clinical signs of neurological disease and 2) clinicians should rule out as many other diseases resulting in similar clinical signs.

There must be signs of neurological disease that are consistent with EPM. This can be difficult in horses with mild gait abnormalities (lameness versus mild spinal ataxia)

Ruling out other potential causes of EPM. The most common example would include horses with spinal ataxia, localized to the cervical vertebrae. Cervical vertebral radiographs are indicated in these horses.

Other diagnostics include:

Cytology of spinal fluid: which is usually normal in horses with EPM (but maybe helpful in ruling other diseases out)?

Immunodiagnostic testing: It was originally believed that the presence of S. neurona specific antibodies in the CSF indicated the presence of an active infection, due to the blood brain barrier. The sensitivity of specificity of the tests range from 68-100%. Clinical experience has proven this not to be the case. There are many reports of antibody in the CSF of clinically normal horses. This may occur due to iatrogenic blood contamination. Antibodies within plasma can cross through an intact blood-brain barrier and into the CSF. Therefore it is important to make sure that other neurologic diseases are ruled out before trying to interpret a positive test on CSF. There are several labs that offer immunodiagnostic testing for EPM.

Testing options


Ponazuril (Marquis, Bayer Animal): 5 mg/kg PO q 24 hours for 28 days. Recommend re-evaluation at end of treatment to determine if further treatment is necessary (many cases it is). Very safe.

Nitazoxanide (NTZ, Navigator, Idexx Pharmaceuticals): Toxicity problems are reported (diarrhea, depression and laminitis). The manufacturer recommends a reduced dose, and slowly increasing the disease over the final 21 days.

Sulfadiazine and pyrimethamine combination (ReBalance, Phoenix Scientific): duration of treatment ranges from 3-6 months.

Combination: some veterinarians have used a combination of Marquis and ReBalance.

Prognosis: 60-80% of horses will at least improve 1-2 grades. Anecdotal reports- that up to 20% will completely recover. Relapse is reported.

Equine degenerative myelopathy:


Usually young horses (< 2 years). There maybe a genetic basis. History can include lack of green grass.

Clinical signs:

insidious to acute onset of ataxia. Ataxia ranges from symmetric to hind limbs being more severely affected. No cranial nerve abnormalities or muscle atrophy is reported.

Neuroanatomic Location: cervical vertebrae, focal


No antemortem test. Vitamin E concentrations are low in some horses (less than 1.5 ug/ml


None. Early in course of disease vitamin E supplementation may improve clinical signs (6,000 IU/day) for at least 1-3 years.

Congenital abnormalities of the spinal cord

Occipito-atalanto-axial Malformation (OAAM): is the most common. There are a number of variations of this disease, but the basic abnormality involves fusion of the atlas and the occiput and hypoplasia of the atlas and dens. .


Can present as a foal at birth, or occasionally present later. OAAM occurs in all breeds of horses, but is familial in Arabian horses

Clinical signs:

Varying degrees of ataxia to recumbency. Horses can be affected at birth or develop clinical signs later in life. Horses may have an abnormal head and neck carriage. In some cases- can hear a "click" when head is moved.

Neuroanatomic Location: cervical vertebrae, focal

Diagnosis: radiographs

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