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Basics ⬇

Basics

Definition

  • Epilepsy-recurrence of seizures from primary brain origin.
  • Genetic epilepsy-epilepsy with no observable underlying brain lesion or other neurologic signs or symptoms.
  • Structural epilepsy-seizures are the result of identifiable structural brain lesions.
  • Epilepsy of unknown cause-structural epilepsy is suspected but a lesion cannot be demonstrated.
  • Cluster seizures-> 1 seizure/24 hours.
  • Status epilepticus-continuous seizure activity or seizures repeated at brief intervals without complete recovery between seizures.
  • Status epilepticus can be convulsive or nonconvulsive.
  • Seizures are classified as focal (limited to one hemisphere), generalized (involve both hemispheres), and focal with secondary generalization.

Pathophysiology

  • Any thalamocortical disturbance may lead to seizure activity.
  • Not all cortical regions have equal propensity to seize; from the most to the least likely to cause seizures-temporal, frontal, parietal, and occipital lobes.
  • As more seizures occur, the tendency for neuronal damage and propensity for more seizures or SE increases; this kindling effect does not occur in all cortical regions.
  • The clinical appearance of a seizure is related to the location of the neuronal hyperactivity.

Signalment

  • Dogs of any breed, age, or sex.
  • SE-overrepresentation of German shepherd dog, English foxhound, Pug, teacup poodle, Boston terrier, Lakeland terrier.

Mean Age and Range

SE-4.2–5 years (0.15–15 years)

Signs

General Comments

  • Prodrome-hours to days prior to the seizure; no EEG changes.
  • Aura-short period (seconds) prior to generalization of a seizure where the dog seeks help, looks lost, frightened or has a glazed look. Focal seizure. If it precedes the tonic-clonic generalized seizure, the seizure has a focal onset.
  • Ictus-may start with an aura and progress to GS; lateral recumbence with bilateral symmetrical tonic-clonic contractions of limb muscles; often with autonomic signs, e.g., salivation, urination, defecation.
  • GS-may be mild, the animal remaining sternal or even standing during the event; may be long-lasting, 20 minutes or more. Convulsive or nonconvulsive.
  • Post-ictal phase-disorientation, confusion, aimless pacing, blindness, polydipsia, polyphagia.
  • A seizure lasts < 2 minutes.
  • Most seizures occur when dog is resting or sleeping.

Historical Findings

  • Confirm that seizure has occurred.
  • Seizure pattern (age at onset of seizure, seizure type and frequency)-most important factor in establishing list of possible causes.
  • Metabolic diseases usually cause generalized seizures.
  • Asymmetric neurologic signs before, during, or after the seizure suggest structural brain lesion.
  • Presence of behavioral changes in the days/ weeks preceding seizure onset indicates structural brain disease.

Neurologic Examination Findings

  • Mental status, menace responses, responses to nasal septum stimulation, and proprioceptive positioning-neurologic tests that evaluate the cerebral cortex. Asymmetry indicates structural brain lesion contralateral to deficits.
  • Compensated SE, first 30 minutes-salivation, hyperthermia, tachycardia, arrhythmia, increased blood pressure.
  • Decompensated SE-difficulty breathing, weak pulse, low blood pressure, poor capillary refill.

Causes

Extracranial

  • Metabolic-electrolyte disturbances, hypoglycemia (insulinoma); hypocalcemia; acute renal failure; hepatic encephalopathy.
  • Toxicities-metaldehyde, pyrethrins/pyrethroids, lead, hexachlorophene, chlorinated hydrocarbons, organophosphates, bromethalin, mycotoxins, macademia nut, theobromine (chocolate), 5-fluorouracil.

Intracranial

  • Degenerative-encephalopathy.
  • Malformations-cortical dysplasia.
  • Genetic epilepsy.
  • Metabolic-cell storage diseases.
  • Neoplasia-primary (meningioma, gliomas); secondary (metastatic).
  • Inflammatory infectious-viral (e.g., canine distemper); fungal; protozoal (Neospora, Toxoplasma); rickettsial (ehrlichiosis, Rocky Mountain spotted fever).
  • Inflammatory non-infectious-meningoencephalomyelitis of unknown origin, eosinophilic meningoencephalomyelitis; breed-related encephalitis (pug, Maltese, Yorkshire terriers, etc).
  • Trauma.
  • Vascular-cerebrovacular accident.
  • Epilepsy of unknown cause-post-encephalitic glial scar.

Diagnosis ⬆ ⬇

Diagnosis

Differential Diagnosis

  • Syncope-body is limp, rapid recovery with no abnormal behavior; occurs at exercise, cough, excitement.
  • Insulinoma-seizures occur at exercise, excitement.
  • Obsessive-compulsive behaviors or stereotypes-complex and goal-directed behaviors; behavior can be stopped.
  • Seizurogenic toxins-progression from whole body tremor to SE and death if left untreated.
  • Metabolic encephalopathy-seizures unusual and accompanied with obtunded mental state and abnormal behavior; no lateralizing signs.
  • Structural brain disease likely-if acute onset of > 2 GS within first week of onset, acute onset of focal seizures with gradual progression to GS, or presence of interictal neurologic deficits including behavioral changes.
  • Genetic epilepsy-differentiated on age, breed, and seizure pattern; progressive onset of GS with/without aura.
  • Cervical pain/spasms-may be mistaken for focal seizures.
  • Head bobbing or idiopathic head tremor-dog remains active; can eat, drink, walk.

CBC/Biochemistry/Urinalysis

  • Infectious CNS diseases-may reflect multisystem involvement.
  • Hypoglycemia-small/toy breeds during SE; insulinoma.
  • Hepatic and renal dysfunction-advanced SE.
  • Urinalysis-rule out myoglobinuria.

Other Laboratory Tests

  • Blood gases-metabolic acidosis frequent with SE. Respiratory acidosis needs immediate treatment.
  • Coagulation profile-DIC in advanced SE.
  • Bile acids-suspected hepatic encephalopathy.
  • Fasting blood glucose and amended insulin:glucose ratio-dogs > 5 years with occasional seizures during exercise.
  • Serology (infectious diseases)-as suggested by systemic signs and laboratory abnormalities.
  • Toxicity screen-cholinesterase levels.

Imaging

  • Thoracic radiographs and abdominal ultrasound-to identify metastatic or systemic illness, or lung pathology from SE.
  • MRI-best to define location, extent, and nature of lesion.

Diagnostic Procedures

ECG-arrhythmias can occur in SE due to myocardial damage. CSF-if intracranial structural cause is suspected; CSF and serum titers and PCR for diagnosing infectious diseases. EEG-to document ongoing seizure activity once physical manifestations have ceased.

Treatment ⬆ ⬇

Treatment

Appropriate Health Care

  • Outpatient-isolated seizures in an otherwise healthy dog.
  • Inpatient-cluster seizures and SE.

Nursing and Supportive Care

  • SE and cluster-seizures-constant supervision.
  • Ensure airway patency. May need to be suctioned due to excessive salivation.
  • Administer 100% oxygen via non-rebreathing mask.
  • Cool down if hyperthermia.
  • Install IV line for drug and fluid administration.
  • Draw blood for rapid measurement of blood gases, glucose, calcium, renal and hepatic function, and AED levels if pertinent.
  • Monitor urine output with indwelling urinary catheter.

Client Education

  • Treat cluster of GS and GSE early-the more seizures in a given time, and the more drugs for seizure control, time for recovery, and cost for treatment.
  • Antiepileptic treatment in structural epilepsy may not help until the primary cause is addressed.
  • Client to keep a seizure calendar noting date, time, severity, and length of seizures to objectively evaluate response to treatment.
  • Outline an in-home treatment emergency plan for cluster-seizures.

Medications ⬆ ⬇

Medications

Drug(s) Of Choice

Seizure type and frequency determine the therapeutic approach. Important to seek and treat primary cause.

Convulsive Cluster Seizures or Status Epilepticus

Diazepam

  • Administer 0.5–1 mg/kg IV bolus; repeat 5 minutes later if gross motor activity has not subsided; follow with CRI of 0.5–1 mg/kg/h added to hourly maintenance fluids in an in-line burette or through syringe pump.
  • Rectal-only where IV access cannot be obtained; may diminish or stop gross motor seizure activity to allow IV catheter placement.
  • Refractoriness may rapidly develop, necessitating the addition of phenobarbital CRI.

Phenobarbital

  • Add if seizures persist after second diazepam bolus or during diazepam CRI; administer CRI phenobarbital (2–6 mg/dog/h added to diazepam infusion) if patient already treated with PB, or loading dose if patient naïve to PB.
  • Loading dose-12–24 mg/kg given as boluses of 4 mg/kg IV, 20 minutes apart until desired effect is reached, to a maximum of 24 mg/kg. Optimal therapeutic range: 100–120 µmol/L (23–28 mg/L).
  • If patient already on PB, obtain serum level prior to initiating PB CRI. IV bolus 2–6 mg/kg can be administered once while waiting results if serum levels believed inadequate.
  • Once seizures have been controlled for 4–6 hours, gradually wean the patient off CRI over as many hours.
  • Start/resume oral maintenance AED using PB and/or other GS AED as soon as patient can swallow.

Other

  • If seizures continue, propofol at 1–2 mg/kg IV slowly over 60 sec, followed with CRI at 0.1–0.6 mg/kg/min to effect; monitor anesthetized patient with EEG to evaluate treatment response.
  • Ketamine is also used occasionally at 5 mg/kg IV bolus followed with CRI at 5 mg/kg/h.
  • Dexamethasone-0.2 mg/kg q24h for 1–3 days; reduce cerebral edema.
  • Dexamethasone-for acute treatment of cerebral edema secondary to severe inflammatory CNS disease, even if infectious.

Acute Focal Status Epilepticus

  • Often harbors brain lesion.
  • Diazepam and PB CRI-effective for focal and GS.
  • Frequently difficult to reach seizure control.
  • Instances of chronic nonconvulsive generalized or focal SE-owner unaware it is occurring (e.g., senile encephalopathy); if seizures remain focal and patient's quality of life not significantly altered, no treatment necessary. Long-term antiepileptic treatment if necessary-PB (3–5 mg/kg q12h PO), levetiracetam (20 mg/kg q8h PO), or zonisamide (5 mg/kg q12h PO).

Contraindications

  • Potassium bromide-do not use to treat SE; too long half-life; loading dose not recommended.
  • Aminophylline, theophylline-CNS excitement; may cause seizure.
  • Steroids-alter CSF parameters; avoid if considering CSF analysis.

Precautions

  • Phenobarbital-liver disease, lower dose; monitor levels closely; for SE, add cautiously to diazepam because the drugs potentiate each other, cardiac/respiratory depression may ensue.
  • Steroids-contraindicated in infectious diseases, but one dose of dexamethasone (0.2 mg/kg IV) may decrease brain edema when impending brain herniation or life-threatening edema is suspected.

Possible Interactions

  • Cimetidine, ranitidine, and chloramphenicol-interfere with PB metabolism; may lead to PB toxic level.
  • Phenobarbital decreases zonisamide serum levels. Dosage recommended when drugs are used simultaneously-10 mg/kg q12h.
  • If levetiracetam used concomitantly with PB-measure serum levels (humans 10–40 µg/mL).

Alternative Drug(s)

Levetiracetam-20–60 mg/kg IV; use upper end dosage if patient already on oral phenobarbital. Good alternative in liver disease or portosystemic shunts, as the drug is not metabolized in the liver. Use with caution in patients with renal disease.

Follow-Up ⬆ ⬇

Follow-Up

Patient Monitoring

  • Inpatients-constant supervision for seizure monitoring.
  • Eyelid or lip twitching in a heavily sedated patient is sign of ongoing seizure activity.
  • Monitor heart rate, respiratory rate, oxygenation/ventilation, body temperature, blood pressure, urine production, neurologic examination.
  • EEG monitoring for ongoing seizure activity.
  • Patient may need 7–10 days before returning to normal after SE.

Possible Complications

  • Phenobarbital-hepatotoxicity after long-term treatment with serum levels >140 µmol/L (> 33 µg/L); acute neutropenia (rare) in the first few weeks of use requires permanent withdrawal.
  • Paradoxical hyperexcitability.
  • Permanent neurologic deficits (e.g., blindness, abnormal behavior, cerebellar signs) may follow severe SE.
  • GSE may lead to hyperthermia, acid-base and electrolyte imbalances, pulmonary edema, cardiovascular collapse and death.

Expected Course and Prognosis

  • Genetic epilepsy or epilepsy of unknown cause represents a large proportion of dogs with GSE or cluster-seizures. In-home emergency measure using diazepam rectal/nasal should be provided.
  • Dogs with encephalitis and GSE-poor outcome.
  • Structural epileptic dogs recovered from primary disease (e.g., Ehrlichia canis)-slowly (over months) wean patient off AEDs after 6 months seizure-free; if seizures recur, reinstate AED.

Miscellaneous ⬆

Miscellaneous

Age-Related Factors

  • The immature brain has a higher propensity to seize.
  • Genetic epilepsy-6 months–5 years; often epilepsy refractory when onset at < 2 years.
  • Phenobarbital-higher dose needed in puppies (< 5 months) to reach therapeutic range.

Abbreviations

  • AED = antiepileptic drug
  • CNS = central nervous system
  • CRI = constant rate infusion
  • CSF = cerebrospinal fluid
  • CVA = cerebrovacular accident
  • DIC = disseminated intravascular coagulation
  • ECG = electrocardiogram
  • EEG = electroencephalogram
  • GS = generalized seizure
  • GSE = generalized status epilepticus
  • KBr = potassium bromide
  • MRI = magnetic resonance imaging
  • PB = phenobarbital
  • PCR = polymerase chain reaction
  • SE = status epilepticus

Author Joane M. Parent

Consulting Editor Joane M. Parent

Client Education Handout Available Online