NAVLE Nervous

Equine Seizures Study Guide

📅 March 28, 2026 ⏱ 25 min read

Seizures in horses are relatively uncommon compared to other species but represent a critical neurological emergency.

Overview and Clinical Importance

Seizures in horses are relatively uncommon compared to other species but represent a critical neurological emergency. They are defined as transient, paroxysmal disturbances of brain function caused by excessive neuronal discharge, manifesting as alterations in consciousness, motor activity, sensory function, or behavior.

Adult horses have a HIGH seizure threshold, making seizures relatively rare. In contrast, foals have a LOW seizure threshold, making neonatal seizures the most commonly encountered presentation in equine practice.

High-YieldSeizures are more common in foals than adult horses. Hypoxic-ischemic encephalopathy (HIE/dummy foal syndrome) is the most common cause of seizures in neonatal foals, while trauma and neoplasia are most common in adults.

Seizure Type	Clinical Features	NAVLE Pearls
Focal (Partial)	Affects one body region; facial twitching, limb paddling, circling; usually brief (seconds)	Can progress to generalized; suggests focal brain lesion
Generalized Tonic-Clonic	Most common type; recumbency with rigid extension (tonic) then paddling (clonic); LOC, autonomic signs	Duration 5-60 seconds; post-ictal blindness, depression, ataxia
Status Epilepticus	Continuous seizure greater than 5 min or multiple seizures without recovery	EMERGENCY - permanent brain damage; uncommon in horses

Classification of Equine Seizures

Classification by Seizure Type

Seizures are classified based on the extent of brain involvement and clinical manifestations:

Etiological Classification

NAVLE TipCryptogenic epilepsy accounts for approximately 55% of equine seizure cases - most horses with seizures will NOT have an identifiable underlying cause despite thorough workup.

Category	Definition	Examples
Reactive	Normal brain responding to systemic/metabolic insult	Hypoglycemia, hepatic encephalopathy, electrolyte imbalances, toxins
Symptomatic	Seizures due to identifiable structural brain disease	Trauma, neoplasia, encephalitis, abscess, HIE
Cryptogenic	Presumed underlying cause but not identified; MOST COMMON (55%)	Suspected but undetectable lesion
Idiopathic (True Epilepsy)	Recurrent seizures with no identifiable cause; presumed genetic	JIE in Arabian foals - ONLY well-characterized epilepsy in large animals

Etiology of Equine Seizures

Intracranial vs. Extracranial Causes

Intracranial Causes

Viral Encephalitis: EEE, WEE, WNV, EHV-1, Rabies
Bacterial: Brain abscess, meningitis (Streptococcus equi, Actinobacillus)
Parasitic: Halicephalobus gingivalis, Sarcocystis neurona (EPM)
Trauma: Most common cause of acquired epilepsy in adults; seizures may begin weeks after injury
Neoplasia: Pituitary adenoma, cholesteatoma, lymphoma, melanoma (gray horses)

Extracranial Causes

Hepatic Encephalopathy: Pyrrolizidine alkaloid toxicosis (Senecio, Crotalaria)
Electrolyte Imbalances: Hypocalcemia (lactation tetany), hypomagnesemia
Hypoglycemia: Especially in neonatal foals and septic patients
Toxins: Lead, organophosphates, metaldehyde, yellow star thistle

Viral Encephalitides - High-Yield Comparison

Age-Specific Causes

Disease	Vector	Mortality	Key Signs	Prevention
EEE	Culiseta melanura	80-95%	Rapid progression, fever, depression, head pressing	Vaccination (core)
WEE	Culex tarsalis	20-40%	Similar to EEE, less severe; Western US	Vaccination (core)
WNV	Culex spp.	22-44%	Muscle fasciculations, hyperesthesia, ataxia	Vaccination (core)
Rabies	Animal bite	100%	Variable; behavioral changes, paralysis	Vaccination (core)

Hypoxic-Ischemic Encephalopathy (HIE)

Neonatal Encephalopathy (NE), commonly known as 'Dummy Foal Syndrome', is the most common cause of seizures in neonatal foals. Other synonyms include 'barker foal,' 'wanderer foal,' and 'convulsive foal syndrome.'

Pathophysiology

HIE results from impaired oxygen delivery to the brain during the perinatal period:

Placentitis or premature placental separation
Prolonged or difficult delivery (dystocia)
Red bag delivery (chorioallantois delivered first)
Umbilical cord compression

Clinical Signs

Loss of suckle reflex (earliest sign)
Loss of affinity for the mare
Aimless wandering, head pressing
Abnormal vocalizations ('barking')
Seizures - tonic-clonic activity, opisthotonos
Transient blindness (common post-ictal sign)

Treatment of HIE

Seizure control: Diazepam 0.1-0.4 mg/kg IV; phenobarbital if refractory
Intranasal oxygen: 5-10 L/min
IV fluids: Correct hypoglycemia and electrolyte abnormalities
DMSO: 0.5-1 g/kg IV diluted to less than 20% - reduces cerebral edema
Madigan Squeeze Technique: Novel treatment simulating birth canal pressure
Anti-ulcer prophylaxis: Omeprazole or sucralfate

High-YieldPrognosis for HIE is FAVORABLE - approximately 80% of foals survive with appropriate supportive care. Key indicators: ability to stand and suckle within 4 days, absence of septicemia.

Neonatal Foals (less than 30 days)	Adult Horses
Most Common: HIE (Dummy Foal Syndrome), Septicemia/meningitis, Hypoglycemia, Electrolyte imbalances, JIE (Arabian foals)	Most Common: Trauma (head injury), Neoplasia, Viral encephalitis (EEE, WEE, WNV), Hepatic encephalopathy, Toxins

Juvenile Idiopathic Epilepsy (JIE)

Juvenile Idiopathic Epilepsy (JIE) is the ONLY well-characterized epileptic syndrome in large animals. It occurs almost exclusively in Egyptian Arabian foals and is believed to be genetically inherited.

Clinical Features

Age of onset: 2 days to 6 months
Seizure type: Generalized tonic-clonic with staring, loss of consciousness
Post-ictal signs: Transient blindness (most common)
Interictal exam: NORMAL - foals completely normal between seizures
Diagnostics: EEG shows epileptiform activity in central/parietal regions
Prognosis: EXCELLENT - seizures cease by 12-18 months

Condition	Key Differentiating Features	Diagnosis
HYPP	Quarter Horse-related breeds; muscle fasciculations; consciousness PRESERVED; third eyelid prolapse	Genetic testing; elevated K+ during episode
Tetanus	Generalized muscle rigidity; saw-horse stance; third eyelid prolapse; consciousness PRESERVED	Clinical signs; wound history; vaccination status
Botulism	Progressive FLACCID paralysis; dysphagia, weak tongue; round bale feeding	Clinical signs; mouse bioassay
Narcolepsy	Sudden muscle atonia; triggered by stimulation; rapid recovery; no post-ictal phase	Clinical observation; video
Syncope	Brief LOC; exercise-associated; rapid full recovery; cardiac arrhythmia	ECG; Holter; cardiac ultrasound

Differential Diagnosis

Test	Key Parameters	Significance
CBC	Leukocytosis, neutrophilia	Infection, inflammation
Chemistry	Glucose, Ca, Mg, Na, K, liver enzymes	Metabolic causes, organ dysfunction
Hepatic Panel	GGT, SDH, bile acids, ammonia	Hepatic encephalopathy
CSF Analysis	Protein, cytology, xanthochromia	Encephalitis, EHV-1, hemorrhage

Diagnostic Workup

Initial Assessment

History: Vaccination status, recent trauma, toxin exposure, diet, travel
Physical exam: Fever, head wounds, evidence of liver disease
Neurologic exam: Mental status, cranial nerves, gait, postural reactions

Laboratory Evaluation

Advanced Diagnostics

EEG: Non-invasive; identifies seizure focus; gold standard for JIE diagnosis
CT/MRI: Detects structural lesions (neoplasia, abscess, trauma)
Serology: EEE/WEE/WNV IgM titers, EPM testing, EHV-1 PCR
Liver Biopsy: Confirms PA toxicosis (megalocytosis, biliary hyperplasia, bridging fibrosis)

NAVLE TipPA toxicosis triad on liver biopsy: megalocytosis + biliary hyperplasia + bridging fibrosis. Pathognomonic for pyrrolizidine alkaloid toxicity from Senecio (ragwort) or Crotalaria.

Drug	Dose	Route	Use	Notes
Diazepam	0.01-0.4 mg/kg	IV	Emergency	First-line; short duration (15-30 min)
Phenobarbital	2-10 mg/kg	IV, PO	Refractory; maintenance	Hepatic metabolism; monitor levels
K+ Bromide	20-40 mg/kg/day	PO	Adjunctive	Long half-life; no hepatic metabolism

Treatment

Emergency Seizure Management

Safety first: Protect horse and handlers; remove hazards
Diazepam: 0.01-0.4 mg/kg IV (FIRST-LINE) - rapid onset
Midazolam: 0.04-0.1 mg/kg IV or IM - alternative
Phenobarbital: 2-10 mg/kg IV slowly if benzodiazepines fail

Anticonvulsant Medications

Supportive Care

DMSO: 0.5-1 g/kg IV (diluted) - reduces cerebral edema
Mannitol: 0.25-2 g/kg IV over 20-30 min - osmotic diuretic
Treat underlying cause: Antimicrobials for infection, lactulose for hepatic encephalopathy

Condition	Prognosis	Key Factors
HIE (Dummy Foal)	Good (80% survival)	Stands/suckles within 4 days; no sepsis
JIE (Arabian foals)	Excellent (self-limiting)	Seizures cease by 12-18 months
EEE	Poor (80-95% mortality)	Survivors often have residual deficits
Hepatic Encephalopathy	Poor to Grave	Chronic PA toxicosis irreversible

Prognosis

Prevention

Vaccination: Core vaccines (EEE, WEE, WNV, Rabies, Tetanus) per AAEP guidelines
Mosquito control: Eliminate standing water, use fans, apply repellents
Foaling management: Proper supervision to minimize dystocia
Environmental safety: Adequate ceiling height, remove toxic plants

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