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Basics ⬇

Basics

Definition

  • Epilepsy-recurrence of seizures from primary brain origin.
  • Genetic epilepsy-syndrome that is only epilepsy, with no demonstrable underlying brain lesion or other neurologic signs; the genetic origin must be proven through family studies, gene isolation or other specific forms of evidence (ILAE). Rare in cats.
  • Structural epilepsy-syndrome in which the epileptic seizures are the result of identifiable structural brain lesions; frequent in cats.
  • Epilepsy of unknown cause-structural epilepsy suspected but a lesion cannot be demonstrated; frequent in cats.
  • Cluster seizures-> 1 seizure/24 hours.
  • Status epilepticus-continuous seizure activity, or seizures repeated at brief intervals without complete recovery between seizures. Can be nonconvulsive.
  • Convulsive SE-life-threatening medical emergency.

Pathophysiology

  • Paroxysmal disorganization of one or several brain functions originating from the thalamocortex. Any thalamocortical disturbance or disease process may lead to seizure activity.
  • Not all cortical regions have the same 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 the seizure is directly related to the location of the neuronal hyperactivity. If the electrical abnormality remains regional, the seizure is focal. If there is recruitment of both hemispheres, the seizure is generalized.
  • The great majority of seizures and SE in cats are secondary to structural brain lesions.

Systems Affected

Nervous

Incidence/Prevalence

Unknown

Geographic Distribution

Worldwide

Signalment

Cats of any breed, age, or sex

Signs

General Comments

  • Nonconvulsive generalized seizures-frequent in cats; movements of facial musculature predominate, such as bilateral twitches of eyelids, whiskers and ears, salivation, lip smacking; may be associated with whole body trembling/shaking, piloerection, dilated pupils. Nonconvulsive SE frequent in cats.
  • Focal seizure-when limited to one hemisphere; frantic running and colliding with objects (aura), unilateral facial twitches or eyelid blinks, unilateral limb motions or head/neck turning to one side. Focal seizures often generalize.
  • Generalized convulsive seizures-bilateral symmetrical tonic-clonic contractions of limb muscles and dorsiflexion of the head, often associated with autonomic signs such as salivation, urination, defecation. At time of admission, the gross motor activity may have stopped, but there may still be twitching of the lids and body/limb jerks.
  • Mutilation frequent-biting of tongue, nail avulsion.

Historical Findings

  • Confirm that seizure activity has indeed occurred.
  • Pattern of seizures (age at seizure onset, type and frequency of seizures)-most important factor in listing the possible causes.
  • Metabolic diseases may cause GS.
  • With most seizurogenic toxins, there is a crescendo of hyperexcitability, shaking, trembling, with ultimately GS and death.
  • Asymmetry in the signs (eyelid twitches, limb movements primarily on one side, circling) before, during or after the seizure suggests focal cortical lesion.
  • Overdose of insulin, post-renal transplant, bilateral thyroidectomy lead to GS shortly after the fact.
  • Presence of abnormal behavior in the days/ weeks preceding the seizure activity indicates structural brain disease.
  • Presence of concomitant gastrointestinal, respiratory, or other systemic signs indicates multisystem disease.

Physical Examination Findings

  • If chorioretinitis present, look for infectious diseases.
  • Dark red mucous membranes suggest polycythemia vera.

Neurologic Examination Findings

  • Mental status, menace responses, responses to nasal septum stimulation, and proprioceptive positioning are neurologic tests that evaluate the cerebral cortex. Asymmetry indicates structural brain lesion on the contralateral side of the deficits.
  • In most cases of structural epilepsy, neurologic deficits are present at presentation.

Causes

Extracranial

Metabolic-hypoglycemia from insulin overdose, hypocalcemia from bilateral thyroidectomy, severe hyperthyroidism, hypertension secondary to renal transplant, hepatic encephalopathy, uraemia, polycythemia vera, severe hypertriglyceridemia.

Toxins; Intracranial

  • Anatomic-congenital malformation.
  • Metabolic-cell storage disease (e.g., neuronal ceroid-lipofuscinosis reported in one cat with myoclonus and seizure activity).
  • Neoplastic-meningioma, astrocytoma, lymphoma.
  • Inflammatory infectious-viral non-FIP, FIP, toxoplasmosis, cryptococcosis.
  • Toxicity-organochlorines, pyrethrins, and pyrethroids; seizures usually observed at end stage; chlorambucil in lymphoma treatment.
  • Vascular-polycythemia vera secondary to hyperviscosity, feline ischemic encephalopathy secondary to Cuterebra larva.
  • Trauma has not been linked to seizures in cats.

Risk Factors

  • Any forebrain lesion
  • Diabetes mellitus
  • Treatment with chlorambucil
  • Renal failure

Diagnosis ⬆ ⬇

Diagnosis

Differential Diagnosis

  • Sleep disorders-the cat does not wake up, or has a normal waking behavior following the episode.
  • Syncope-the body is limp with a rapid recovery phase, with no abnormal behavior.
  • When seizures are preceded by 2–3 weeks of vague transient systemic illness (decreased appetite, GI signs) in an otherwise healthy cat-viral non-FIP encephalitis or epilepsy of unknown cause.
  • When seizures are preceded by systemic signs that persist (>3 weeks)-FIP, cryptococcosis.
  • Insidious abnormal behavior with/without circling in a cat > 10 years old presented for seizure activity suggests meningioma.
  • Cats with hepatic encephalopathy drool excessively.
  • Cats with polycythemia vera have GI signs and dark mucous membranes.

CBC/Biochemistry/Urinalysis

  • Extracranial metabolic causes are diagnosed on history, physical examination, and blood test results.
  • High PCV (> 60%) in polycythemia vera.
  • Low blood glucose in insulin overdose.
  • Low calcium in bilateral post-thyroidectomy.
  • High BUN and creatinine with low specific gravity in acute renal failure.
  • Creatine kinase-mild to markedly elevated in cats with SE, even nonconvulsive; with or without myoglobulinuria; indicates muscle necrosis.

Other Laboratory Tests

  • Serologic testing-FIV, FeLV titers often non-contributory to diagnosis; FIP and Toxoplasma gondii titers non-reliable by themselves.
  • Bile acid testing-in cats with suspected hepatic encephalopathy.

Imaging

  • Thoracic radiographs and abdominal ultrasound-if infectious disease suspected; to evaluate lung pathology if SE; to look for neoplasia if tumor suspected.
  • MRI-best to define location, extent, and nature of lesion.

Diagnostic Procedures

CSF-sensitive to detect structural disease; unspecific in itself to reach diagnosis except when organism is seen (e.g., cryptococcosis).

Pathologic Findings

  • Findings reflect etiology.
  • It is unknown if hippocampal necrosis is a cause or the consequence of seizures.
  • Small lesions may be easily missed in cats diagnosed with epilepsy of unknown cause.

Treatment ⬆ ⬇

Treatment

Appropriate Health Care

  • Outpatient-isolated recurrent seizures in an otherwise healthy cat.
  • Inpatient-cluster seizures and SE. Isolated recurrent seizures in an ill cat.

Nursing and Supportive Care

  • Constant supervision.
  • Install IV line for drug and fluid administration.
  • Draw blood for rapid measurement of blood gases, glucose, calcium, and antiepileptic drug levels if pertinent.
  • Cool if hyperthermia.

Client Education

Antiepileptic treatment in structural epilepsy may not help until the primary cause is addressed. Seizures can be difficult to stop in cases of SE, especially with nonconvulsive status.

Surgical Considerations

Craniotomy-tumor excision with meningioma or other accessible mass.

Medications ⬆ ⬇

Medications

Drug(s) Of Choice

Seizure type and frequency determine therapeutic approach.

Isolated Recurrent Generalized Seizures

  • First line-phenobarbital 7.5–15 mg/cat q12h; optimal therapeutic serum levels 100–130 µmol/L (23–30 µg/L).
  • Second line-gabapentin 3–8 mg/cat q8–12h.
  • Levetiracetam-20 mg/kg q8h (serum levels humans 10–40 µg/mL).
  • Initiate gradually to avoid overt sedation.

Convulsive Cluster and Status Epilepticus

  • Treat cluster and GSE early-the more seizures in a given time, and the more drugs for seizure control, time for recovery, and cost for treatment.
  • No ongoing seizure activity at presentation and patient naïve to the drug-phenobarbital IV bolus 10 mg/kg to a maximum of 60 mg/cat over 15 minutes, continued with phenobarbital maintenance dosage PO 12 hours later.
  • Ongoing seizure activity at presentation-diazepam IV bolus 0.5–1 mg/kg, continuing with CRI at 0.25–0.5 mg/cat/h in an in-line burette using a fluid pump; IV bolus of diazepam can be repeated 5 minutes after the first bolus if gross seizure activity persists; in this case, add phenobarbital to CRI at 4 mg/cat/hour.
  • Start oral phenobarbital at maintenance dose as soon as patient can swallow.
  • After 6 hours seizures-free, wean CRI gradually over 4–6 hours.

Persistent Seizures

Sub-anesthetic doses of IV propofol (1–3.5 mg/kg) bolus and 0.01–0.25 mg/kg/minute CRI titrated to effect.

Non-antiepileptic Drug Treatment

  • Dexamethasone 0.25 mg/kg IV q24h for 1–3 days, to improve edema secondary to SE and treat the primary cause if systemic infectious disease is not suspected; dexamethasone alters CSF results.
  • Thiamin-5–50 mg/cat in any cat presented with acute neurologic signs, including seizures.

Contraindications

  • Do not use KBr in cats; side effects include life-threatening respiratory disease.
  • Avoid giving aminophylline, theophylline, ketamine, and fentanyl to epileptic cats.

Precautions

  • Prolonged use of propofol (> 24 hours) may cause Heinz body anemia in cats.
  • Cats on CRI of antiepileptic drug(s) are often overtly sedated; cardiovascular and respiratory depression may occur; close monitoring necessary; lubricate eyes, express bladder manually, correct hypothermia.
  • Close monitoring necessary to observe if mild ongoing seizure activity persists.

Possible Interactions

N/A

Alternative Drug(s)

  • Zonisamide-5–10 mg/kg PO q24h (serum levels humans 15–45 µg/mL).
  • Diazepam-0.5–2.0 mg/kg/day PO divided q12h.

Follow-Up ⬆ ⬇

Follow-Up

Patient Monitoring

  • CBC, biochemistry, urinalysis prior to initiating AED.
  • Phenobarbital-induced hepatotoxicity is not a problem in the cat.
  • CK to evaluate muscular necrosis and indirectly subtle ongoing seizure activity in cats presented in SE.
  • Measure phenobarbital serum level 2 weeks after initiation; correct dosage accordingly; it is difficult to titrate phenobarbital in cats, i.e., a mild increase in dosage often leads to a major increment of the serum levels.
  • CBC and biochemistry-repeat every 6–12 months.
  • If structural epileptic patient has recovered from primary disease and remains seizure-free for 6 months-seizures may recur when drug is weaned off.

Possible Complications

  • SE-seizure control may not be reached despite polypharmacy.
  • Rare hypersensitivity to phenobarbital-thrombocytopenia, neutropenia, pruritus, swollen feet; do CBC 4–6 weeks after onset of phenobarbital.
  • Diazepam rarely may cause acute hepatic necrosis and death.
  • Cardiovascular and respiratory collapse from overdose during SE treatment.

Expected Course and Prognosis

  • Depends on the underlying cause and response to treatment.
  • Cats with epilepsy of unknown cause have good long-term prognosis.
  • Cats can recover despite episode of severe cluster-seizures and GSE.

Miscellaneous ⬆

Miscellaneous

Age-Related Factors

Cats with seizure onset prior to < 1 year of age and diagnosed with epilepsy of unknown cause have guarded prognosis for seizure control.

Abbreviations

  • AED = antiepileptic drug
  • CK = creatine kinase
  • CRI = constant rate infusion
  • CSF = cerebrospinal fluid
  • FeLV = feline leukemia virus
  • FIP = feline infectious peritonitis
  • FIV = feline immunodeficiency virus
  • GI = gastrointestinal
  • GS = generalized seizures
  • GSE = generalized status epilepticus
  • ILAE = International League Against Epilepsy
  • MRI = magnetic resonance imaging
  • PCV = packed cell volume
  • SE = status epilepticus

Suggested Reading

Barnes HL, Chrisman CL, Mariani CL, et al. Clinical signs, underlying cause, and outcome in cats with seizures: 17 cases (1997–2002). J Am Vet Med Assoc 2004, 225:1723–1726.

Pakozdy A, Gruber A, Kneissl K, et al. Complex partial cluster seizures in cats with orofacial involvement. J Feline Med Surg 2011, 13:687–693.

Parent J. Seizures and status epilepticus in cats. In: Veterinary Emergency and Critical Care Manual, 2nd ed. Guelph, Ontario: Lifelearn, 2006, pp. 456–459.

Wahle AM, Brühschwein A, Matiasek K, et al. Clinical characterisation of epilepsy of unknown cause in cats. J Vet Intern Med 2014, 28:182–188.

Author Joane M. Parent

Consulting Editor Joane M. Parent

Client Education Handout Available Online