📋 At a Glance
⚠️ Neurological Signs Requiring Immediate Veterinary Contact
- Any sudden onset of incoordination, stumbling, or abnormal limb placement
- Hindlimb weakness — particularly if asymmetric (one side worse)
- A horse that falls or cannot rise from a lying position
- Head tilting, circling, or vestibular dysfunction
- Drooping lip, eyelid, or ear — facial nerve paresis
- Difficulty swallowing or abnormal tongue function
- Progressive worsening of any gait abnormality over hours to days
Neurological vs. Orthopedic — The Clinical Distinction
One of the most common diagnostic challenges is distinguishing a neurological gait abnormality from an orthopedic one. Both can produce abnormal movement, reluctance to move, and apparent weakness. Several clinical features help differentiate them.
The key distinguishing feature of neurological gait is ataxia — the horse placing its feet in abnormal positions relative to where they should be, not simply avoiding weight-bearing. An orthopedic lameness produces a horse that moves carefully to protect a painful structure; a neurological problem produces a horse that cannot accurately control where its feet go.
| Feature | Orthopedic Lameness | Neurological Condition |
|---|---|---|
| Primary mechanism | Pain avoidance | Loss of proprioception and/or motor control |
| Limb placement | Careful, protective | Abnormal — wide-based, cross-stepping, stumbling |
| Head elevation effect | May worsen if forelimb | Typically worsens neurological signs — ataxia increases with head elevation |
| Circles | Often worse on circle — consistent pattern | Worse on circle; may 'fall in' or 'drift out'; loses the circle |
| Reversing | Usually manageable | Often very difficult; stumbling, falling backward possible |
| Asymmetry | Consistent limb preference | May be asymmetric (EPM) or symmetric (CVSM) |
| Muscle wasting | Disuse atrophy over time | May be neurogenic atrophy — more rapid, more focal |
| Response to nerve block | Lameness improves with analgesia | Does NOT improve with perineural analgesia |
AAEP Neurological Grading Scale
The AAEP 5-grade neurological grading scale provides a standardized framework for assessing severity and tracking change over time. Knowing this scale allows horse owners to describe what they observe in terms their veterinarian can immediately interpret.
| Grade | Description | What You See | Handler Safety |
|---|---|---|---|
| 0 | Normal | No detectable gait abnormality | Normal |
| 1 | Barely perceptible deficit | Subtle ataxia detectable only with manipulation (head elevation, tight circles, slopes) | Safe |
| 2 | Mild deficit | Ataxia detectable at normal gaits; worse with manipulation | Generally safe; monitor |
| 3 | Moderate deficit | Ataxia prominent at normal gaits; stumbles spontaneously; may fall with manipulation | Caution — do not ride; handler at risk |
| 4 | Severe deficit | Stumbles spontaneously; falls with circling or inclines; near recumbent possible | High risk — significant injury risk to horse and handler |
| 5 | Recumbent | Cannot or will not rise; recumbent | Emergency — human safety concern; do not attempt to force standing |
EPM — Equine Protozoal Myeloencephalitis
EPM is caused by Sarcocystis neurona, a protozoan parasite whose definitive host is the Virginia opossum (Didelphis virginiana). Opossums shed sporocysts in their feces, which can contaminate hay, grain, and water sources accessed by horses. When horses ingest sporocysts, the protozoa can invade the central nervous system and cause focal or multifocal damage — producing the characteristic asymmetric neurological signs.
Diagnosis is complicated by the high background seropositivity in North America — many horses have antibody titers indicating exposure without clinical disease. Definitive diagnosis combines clinical scoring, exclusion of other neurological conditions, serum and ideally CSF antibody testing, and response to treatment. Three FDA-approved antiprotozoal protocols exist (ponazuril, diclazuril, sulfadiazine-pyrimethamine).
EPM — Key Clinical Points
- Asymmetric neurological signs are a hallmark — unlike CVSM which tends to be more symmetric
- Most commonly affects the spinal cord; brainstem involvement produces cranial nerve deficits
- Stress events (transport, competition, illness) may trigger clinical disease in previously exposed horses with latent infection
- Opossum control on the property reduces environmental sporocyst burden
- Grade 1–2 horses treated promptly have significantly better outcomes than Grade 3–4 horses with delayed treatment
Wobbler Syndrome (CVSM)
Cervical Vertebral Stenotic Myelopathy (CVSM) — wobbler syndrome — produces progressive ataxia from spinal cord compression in the neck. Unlike EPM, CVSM signs tend to be symmetric (both sides equally affected) and tend to be more prominent in the hindlimbs, though forelimbs are also affected in significant cases.
CVSM has two forms: a dynamic form in younger horses (instability of cervical vertebral articulations that compresses the cord during flexion) and a static form in older horses (degenerative joint disease producing constant narrowing of the spinal canal). Myelography (contrast study of the spinal cord via CSF injection) is the traditional diagnostic gold standard; CT myelography is increasingly available at referral centers.
EHM — The Neurological Form of EHV-1
Equine Herpesvirus Myeloencephalopathy (EHM) represents the most serious outcome of EHV-1 infection — vascular inflammation in the spinal cord and brain causing ischemic neurological damage. Signs include hindlimb ataxia and weakness, urinary incontinence, and in severe cases, inability to rise.
EHM is reportable to state veterinary authorities in most states and has caused significant outbreaks at equine events. Fever typically precedes neurological signs by 1–2 days — temperature monitoring after exposure to horses from events is the most important early detection tool. Any horse with neurological signs following an EHV fever episode requires immediate veterinary evaluation and isolation.
✅ Responding to Neurological Signs
- Call your veterinarian immediately — neurological disease requires urgent evaluation
- Restrict movement — a horse with significant ataxia is at serious fall and injury risk for horse and handler
- Secure safely — deeply bedded stall, away from fences, water tanks, and other horses
- Video the gait if you can do so safely — documenting the specific pattern is extremely helpful for the vet
- Note recent history — any transport, illness, vaccination, deworming, or new horse contact in prior 3–14 days
- Do not ride or attempt to longe a horse with suspected neurological signs
📋 Neurological Health Discussion Points for Your Vet
- EPM testing protocol — serum vs CSF; which products if treatment is indicated
- EHM biosecurity if multiple horses are affected — possible outbreak protocol with state vet notification
- CVSM workup — myelography or CT myelography at a referral center
- Neurological grade at diagnosis and target grade for treatment success
- Return-to-work criteria after neurological treatment — objective grading, not just 'looks better'
- Opossum exclusion on the property for EPM risk reduction
Questions to Ask Your Veterinarian
- What AAEP neurological grade do you assign today, and what does that mean for prognosis?
- Is EPM or another condition your primary differential, and what testing do you recommend?
- Should we do serum testing, CSF testing, or both?
- If EPM is confirmed, which treatment protocol do you recommend and why?
- At what grade of improvement would you consider this horse safe to resume work?
- Is EHM a concern given this horse's recent history, and should we notify anyone?
