NAVLE · ⏱ 5 min read · 📅 Apr 6, 2026 · by NAVLE Exam Prep Team · 👁 0

NAVLE Neurology: Neurolocalization, IVDD, Seizures, and Cross-Species Conditions

Neuro questions on the NAVLE typically require two steps: localize the lesion, then match it to a diagnosis. Get the UMN/LMN distinction and the localization chart memorized—everything else flows from there.

Neurolocalization: UMN vs LMN

UMN Signs (lesion above LMN pool)

  • Spastic, stiff gait
  • Hyperreflexia (exaggerated reflexes)
  • Normal or increased muscle tone
  • Crossed extensor reflex present
  • Muscle atrophy: slow disuse (weeks)

LMN Signs (lesion at or below LMN pool)

  • Flaccid, weak gait
  • Hyporeflexia or areflexia
  • Decreased or absent muscle tone
  • No crossed extensor reflex
  • Rapid neurogenic muscle atrophy (days)
Lesion LocationForelimbsHindlimbs
C1–C5UMNUMN (tetraparesis, spastic)
C6–T2LMNUMN
T3–L3NormalUMN (paraparesis, spastic)
L4–S2NormalLMN (flaccid, hyporeflexia)
Sacral (S1–S3)NormalLMN bladder/anal sphincter (incontinence)
NAVLE PearlSchiff-Sherrington phenomenon: severe thoracolumbar lesion (T3–L3) causes forelimb extensor rigidity. This is NOT forelimb involvement—it is a release phenomenon from inhibitory lumbar interneurons. The forelimbs have normal strength and reflexes. It looks scary but does NOT worsen the prognosis.

Canine IVDD

Hansen Type I: Chondrodystrophic breeds (Dachshund #1, Beagle, Pekingese, Shih Tzu); nucleus pulposus extrusion; acute onset; any age. Hansen Type II: Large non-chondrodystrophic breeds; annulus fibrosus protrusion; chronic progressive; older dogs.

IVDD grading: Grade 1 (pain only) → Grade 5 (paralysis, absent deep pain). Deep pain is the most important prognostic indicator. Present = >90% recovery with surgery. Absent >48 hours = guarded prognosis (<50% with surgery). Treatment: Grade 1–2 = strict cage rest 4–6 weeks; Grade 3–5 = surgery within 24–48 hours improves outcomes significantly.

Wobbler Syndrome (Cervical Spondylomyelopathy)

Two populations: Great Danes (young, bony malformation C3–C5) and Dobermans (middle-aged/old, disc-ligament instability C5–C7). Classic presentation: hindlimb worse than forelimb, progressive ataxia ("wobbler" gait). Diagnosis: MRI or CT myelogram for definitive. Treatment: surgical decompression or medical management.

Seizure Management

Acute seizure (status epilepticus or cluster): diazepam 0.5 mg/kg IV (repeat ×2); if refractory → phenobarbital loading or propofol CRI. Maintenance: phenobarbital (therapeutic range 20–40 μg/mL; causes ALP elevation without true hepatotoxicity at therapeutic levels) or potassium bromide (adjunct, especially in dogs with hepatic concerns).

Cross-Species Neurological Conditions

Bovine PEM (Polioencephalomalacia): Thiamine deficiency; high-grain or high-sulfur diet; cortical necrosis → blindness, opisthotonus, circling, seizures. Treatment: thiamine IV (10–20 mg/kg), dramatic response if treated early. CSF: normal or mildly elevated protein, no pleocytosis.

Bovine Listeriosis: Listeria monocytogenes from silage; brainstem signs (CN V, VII, IX–XII); circling toward lesion side; treatment: high-dose penicillin G.

Equine EPM: Sarcocystis neurona; opossum is definitive host, horse is dead-end host; asymmetric ataxia and weakness; diagnosis: serum or CSF titers (SAG 2,4/3 IFAT); treatment: ponazuril (diclazuril alternative).

Equine Tetanus: Clostridium tetani; horse is MOST susceptible species; spastic paralysis, third eyelid prolapse, lockjaw, sawhorse stance; treatment: penicillin G, tetanus antitoxin, muscle relaxants (diazepam, guaifenesin).

Classic NAVLE TrapBovine PEM treatment: thiamine IV, not dexamethasone and not penicillin. The response is dramatic if treated early—a calf with cortical blindness, opisthotonus, and high-grain diet that improves rapidly with thiamine is classic PEM. Listeriosis (penicillin) has brainstem signs (cranial nerve deficits), not cortical signs.

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