Small Ruminant Neurology Made Simple: PEM for NAVLE<sup>®</sup> Prep
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Small Ruminant Neurology Made Simple: PEM for NAVLE® Prep

by Elizabeth Brock, DVM, MS

Polioencephalomalacia (PEM) is a neurologic disease of small ruminants that is very likely to be on the NAVLE®. The pattern of disease is unmistakable once you know it, and early treatment can turn a critical case around in hours. Because PEM is typically a clinical diagnosis made in the field, and it progresses rapidly, the ability to recognize and treat it on sight is essential for both exam success and clinical practice.

Early Recognition is Crucial 

PEM typically results from thiamine deficiency or excessive dietary sulfur, both of which disrupt normal cerebral energy pathways. It can also be triggered by lead toxicosis and water deprivation/sodium toxicosis.

PEM affects any aged animal, but younger animals are more susceptible. These animals often present suddenly with central neurologic signs: stargazing/dorsomedial strabismus, cortical blindness, dull mentation, staggering, or recumbency.

Untreated PEM can progress to seizures, coma, and death. Fortunately, when caught early, thiamine therapy can reverse most signs, highlighting the necessity of quick recognition. Thiamine reverses clinical signs by restoring cerebral carbohydrate metabolism, and early treatment significantly improves prognosis.

Focus on the Big Three Clinical Clues

PEM is a pattern-recognition disease. The three most distinguishing diagnostic clues include: 

1. Dorsomedial Strabismus (“Stargazing”)

This sign is considered pathognomonic and worthy of immediate action. The eyes deviate upward and inward as if the animal is trying to look at the stars.

2. Opisthotonos

The animal extends the neck dorsally while recumbent, which is a sign of severe cortical dysfunction.

3. Cortical Blindness

Animals navigate poorly, bump into objects, and remain unresponsive to visual stimuli (e.g., menace response) despite intact pupillary light reflexes.

Triage for PEM

PEM is primarily a clinical diagnosis. On the NAVLE® and in field settings, advanced diagnostics are not necessary (and post-mortem is the only definitive diagnostic). Instead:

  • Identify the classic neurologic pattern
  • Rule out a few key differentials, when necessary
  • Give thiamine immediately and note response

Differentials worth considering include tetanus (rigid limbs, sawhorse stance), listeriosis (asymmetric cranial nerve deficits, circling), hypocalcemia in dairy cattle, and scrapie in sheep. When the animal(s) presents with bilateral symmetric brain signs and dorsomedial strabismus, PEM is a clear diagnosis.

Treatment Habits That Improve Prognosis

Aggressive thiamine therapy is the cornerstone, but supportive management strengthens outcomes.

Start IV, Then Transition to IM/SQ 

Begin treatment with slow administration of IV thiamine for rapid effect. Transition to IM or SQ for several days.

Maintain Hydration and Nutrition

Recumbent animals may require fluid therapy, nutritional support, and protection from pressure sores from recumbency.

Reduce Environmental Stress

Minimize handling stress and provide a quiet environment while neurologic function recovers.

Monitor for Recovery Benchmarks

Blindness is the final sign to resolve. Improvement often occurs within hours, but delayed treatment leads to permanent deficits or death. If clinical signs look like polio, but animal does not respond to thiamine treatment as expected, test water and feed for sulfur content.

Fast Recognition Saves the Brain

PEM is one of the most time-sensitive neurologic diseases in small ruminants. Early thiamine treatment can restore normal function and prevent irreversible cortical damage. The key is rapid recognition of its unmistakable pattern: dorsomedial strabismus, cortical blindness, and opisthotonos.

Understanding this disease prepares you for both exam questions and real-world emergencies where swift, decisive care changes everything.

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