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Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • Abnormal movement or loss of consciousness associated with abnormal electrical activity of the brain
  • Partial seizures involve a focal area of the cerebral cortex. Partial seizure with secondary generalization occurs when partial seizures progress and spread throughout the cerebral cortex
  • Complex partial seizures are partial seizures in which consciousness is impaired
  • Generalized seizures involve the entire cerebral cortex, and result in generalized tonic–clonic activity and loss of consciousness
  • Status epilepticus is rare, but appears as multiple generalized seizures in succession

Pathophysiology!!navigator!!

  • Mechanisms of abnormal electrical activity in the brain include increased excitatory neurotransmitters and decreased inhibitory neurotransmitters
  • Electrolyte abnormalities can cause abnormal electrical activity, leading to seizures. Hypoglycemia is a rare cause of seizures in foals
  • NE is the most common cause of seizures in neonatal foals. It is proposed that periods of asphyxia may be associated with cerebral edema and necrosis. Hypoxia leads to a breakdown of cerebral energy metabolism, alterations in neurotransmitter metabolism (particularly glutamate), increase in cytosolic calcium concentration, and alterations in cerebral blood flow, leading to neuronal cell death. Alterations in neurosteroid metabolism may also represent a cause of NE distinct from perinatal asphyxia

Systems Affected!!navigator!!

Nervous

Genetics!!navigator!!

  • Idiopathic epilepsy affects Arabians. A genetic link is suspected
  • Lavender foal syndrome also affects primarily Egyptian Arabians—autosomal recessive; a genetic test is available
  • Persistent hyperammonemia in Morgan foals—suspected inherited disorder

Geographic Distribution!!navigator!!

Locoweed is most commonly found in western USA, but is an uncommon cause of seizures in foals.

Signalment!!navigator!!

Breed Predilections

  • Idiopathic epilepsy in the Arabian breed
  • Persistent seizures in Egyptian Arabian foals affected by lavender foal syndrome
  • Hyperammonemia in weanling Morgan foals

Mean Age and Range

  • Usually <2 days of age
  • Foals with bacterial meningitis and systemic sepsis are generally <2 weeks of age
  • Seizures secondary to congenital abnormalities usually occur within the first few days of birth
  • Seizures secondary to intestinal hyperammonemia in Morgan foals occur shortly after weaning

Predominant Sex

None

Signs!!navigator!!

General Comments

Generalized seizures are the most common form of seizure in foals, although partial and complex partial seizures may be seen. Status epilepticus is uncommon.

Historical Findings

A history of dystocia, placental insufficiency or placentitis, and maternal illness should raise the suspicion of NE as a cause of seizures.

Physical Examination Findings

  • Partial seizures can appear as facial twitches, rapid eye movements, or compulsive chewing or suckling
  • Generalized seizures result in tonic–clonic muscle contractions. Paddling of the limbs, jaw movements, extensor rigidity, and opisthotonos are common. Depression is seen after the seizure (postictal)
  • Foals with HE or kernicterus will be icteric
  • Signs of sepsis with seizure activity are suggestive of bacterial meningitis
  • Abrasions and corneal ulcers may indicate a previous seizure

Causes!!navigator!!

Neonatal Encephalopathy

  • Dystocia
  • Premature placental separation
  • Maternal illness (colic, endotoxemia)

Congenital Neurologic Abnormalities

  • Hydrocephalus
  • Hydranencephaly
  • Idiopathic epilepsy of Arabians

Traumatic

Brain trauma

Metabolic

  • Electrolyte abnormalities—hyponatremia, hyperkalemia, hypocalcemia, hypomagnesemia, hypo- or hyperosmolality
  • Hypoglycemia
  • HE
  • Intestinal hyperammonemia
  • Kernicterus (secondary to neonatal isoerythrolysis)

Infectious

  • Septicemia
  • Bacterial meningitis
  • Cerebral abscesses
  • Viral meningitis (equine herpes virus 1)
  • Severe pneumonia (hypoxia)

Toxic

  • Moldy corn
  • Locoweed
  • Organophosphates
  • Strychnine
  • Metaldehyde
  • Moxidectin

Risk Factors!!navigator!!

  • Dystocia, placental insufficiency, and maternal illness are associated with NE
  • Failure of transfer of passive immunity, poor environmental hygiene, and early infections are associated with sepsis, which can lead to septic meningitis

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Septicemia—depression and weakness; seizures with septic meningitis
  • Colic/pain—paddling/flailing may be seen, but the tonic–clonic contractions typical of seizures are not seen and mentation is generally normal
  • Hyperkalemic periodic paralysis—muscle fasciculations and prolapsed nictitating membrane are typical but do not progress to tonic–clonic movements or loss of consciousness. Occurs in Quarter Horses and crosses
  • Syncope secondary to cardiac abnormalities
  • Narcolepsy—uncontrollable loss of muscle tone with gradual lowering of the head and collapse
  • Tetanus—muscular rigidity may appear similar to seizure activity, but contractions are progressive and not “tonic–clonic” as with seizures. Usually occurs in foals >7 days

CBC/Biochemistry/Urinalysis!!navigator!!

Dependent on the underlying cause.

Other Laboratory Tests!!navigator!!

  • Check IgG
  • Blood culture to confirm septicemia in cases of septic meningitis
  • Plasma ammonia concentrations if HE or intestinal hyperammonemia are suspected

Imaging!!navigator!!

  • Skull radiographs to rule out fracture
  • MRI or CT of brain/skull to rule out skull fracture, subdural hematoma, intracranial abscess, and cerebral edema

Other Diagnostic Procedures!!navigator!!

  • Cerebrospinal fluid analysis—increased protein and white blood cell count can be indicative of meningitis. Increase in red blood cells may indicate trauma or disruption of the blood–brain barrier
  • Electroencephalography can document abnormal electrical activity from the cerebral cortex

Pathologic Findings!!navigator!!

Postmortem examination of the brain may reveal edema, necrosis, or abscessation.

Treatment ⬆ ⬇

Outline

TREATMENT

Aims!!navigator!!

  • Control and prevent seizure activity
  • Prevent or decrease hypoxic–ischemic damage
  • Antimicrobial coverage

Appropriate Health Care!!navigator!!

Any foal with signs of seizure activity should have further evaluation to address any underlying cause. Initial treatment and monitoring require emergency inpatient intensive care management.

Nursing Care!!navigator!!

  • Soft bedding to prevent pressure sores or decubital ulcers in foals that are recumbent and paddling
  • Eyes should be lubricated with artificial tears and examined for self-trauma/corneal ulcers
  • Plasma should be given IV if serum IgG is <800 mg/dL
  • Hypotension will lead to decreased cerebral perfusion and possible worsening of neurologic function. IV fluids and pressors may be needed to maintain perfusion
  • If hypoglycemia is the suspected cause, dextrose should be administered immediately and blood glucose levels should be monitored closely
  • Respiratory function should be monitored, and oxygen supplementation and ventilation started, if needed. Elevated PaCO2 can worsen cerebral edema

Activity!!navigator!!

Foals may need to be restrained to prevent trauma during seizure activity.

Diet!!navigator!!

  • Normal mentation, suckle reflex, and swallowing reflex should be confirmed before nursing from the mare is permitted. If the foal is unable to nurse but is able to sit sternally it may be fed via nasogastric feeding tube
  • If the foal is minimally responsive or if intestinal function is uncertain, parenteral nutrition should be instituted

Client Education!!navigator!!

Owners should be informed of the possible genetic link in those conditions (see Genetics).

Surgical Considerations!!navigator!!

Craniotomy for abscess drainage has been described in horses.

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

For Seizure Control

  • Diazepam—0.1–0.4 mg/kg IV
  • Midazolam—0.04–0.1 mg/kg IV or IM, or constant rate infusion of 1–3 mg/h in a 50 kg foal for recurrent seizures
  • Phenobarbital—2–10 mg/kg IV (maintenance 2–10 mg/kg PO every 12 h). Start with the lowest dosage and increase until desired effect is achieved. Phenobarbital has a long half-life in foals and therefore increases in dosing should be done with caution
  • Phenytoin—1–5 mg/kg IV or PO

Antimicrobial Coverage

  • Trimethoprim–sulfa—20–30 mg/kg PO every 12 h
  • Cefotaxime (40 mg/kg IV every 6 h) or ceftazidime (50 mg/kg IV every 6 h)
  • For septicemia without meningitis, penicillin (22 000 IU/kg IV every 6 h) and amikacin (25 mg/kg IV every 24 h)

Prevent Further Neurologic Damage

  • Magnesium sulfate—50 mg/kg/h as a 1% solution for 1 h, then decrease to maintenance dose of 25 mg/kg/h
  • DMSO—0.5–1.0 g/kg as a 10% solution IV every 12 h
  • Mannitol—0.25–1.0 g/kg as a 20% solution IV, up to every 12 h to decrease cerebral edema
  • Corticosteroids—dexamethasone 0.05–0.2 mg/kg IV every 12–24 h or methylprednisolone sodium succinate 1–2.5 mg/kg IV within 4 h of trauma. Use of corticosteroids is controversial
  • Thiamine and antioxidants have also been used without evidence of effect

Contraindications!!navigator!!

  • Acepromazine—may lower the seizure threshold
  • Xylazine—may increase intracranial pressure and decrease cerebral blood flow, causing further cerebral hypoxia
  • Corticosteroids—high doses are contraindicated with septicemia

Precautions!!navigator!!

  • Higher or repeated doses of phenobarbital can cause hypotension, hypothermia, and decreased respiratory drive
  • Mannitol should not be used if intracranial bleeding is suspected
  • The use of corticosteroids with cerebral inflammation or trauma is controversial, and steroids should be used with caution if underlying septicemia is suspected
  • Ketamine—increases intracranial pressure, which may exacerbate seizures, although may be beneficial in targeting NMDA receptors

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

24 h monitoring to detect further seizure activity and to prevent self-trauma.

Possible Complications!!navigator!!

  • Head trauma during seizures
  • Pressure sores
  • Corneal ulceration

Expected Course and Prognosis!!navigator!!

  • Survival of foals with uncomplicated NE is 80%, and long-term neurologic deficits are rare. Athletic performance is not typically affected. Concurrent septicemia will decrease prognosis
  • Foals with head trauma have variable prognosis, dependent on the severity and extent of injury
  • Foals with septic meningitis have a guarded to poor prognosis
  • Foals with lavender foal syndrome have a grave prognosis. Arabian foals with idiopathic juvenile epilepsy generally outgrow the seizure activity by 12 months of age

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

  • Neonatal encephalopathy
  • Septicemia

Synonyms!!navigator!!

  • Epilepsy
  • Convulsions

Abbreviations!!navigator!!

  • CT = computed tomography
  • DMSO = dimethylsulfoxide
  • HE = hepatoencephalopathy
  • Ig = immunoglobulin G
  • MRI = magnetic resonance imaging
  • NE = neonatal encephalopathy
  • NMDA = N-methyl-d-aspartate
  • PaCO2 = partial pressure of carbon dioxide in arterial blood

Suggested Reading ⬆ ⬇

MacKay RJ. Neurologic disorders of neonatal foals. Vet Clin North Am Equine Pract 2005;21:387–406.

Wilkins PA. How to use midazolam to control equine neonatal seizures. Proc Am Assoc Equine Pract 2005;51:279–280.

Author(s) ⬆ ⬇

Author: Laura K. Dunbar

Consulting Editor: Margaret C. Mudge

Acknowledgment: The author acknowledges the prior contribution of Margaret C. Mudge.

Additional Further Reading ⬆

Click here for Additional Further Reading