Seizures in Cats (Felis) | Vetlexicon (2024)

• Definition: the term seizure literally means a sudden attack or recurrence of disease and as such the term is non-specific. It is also used to describe an epileptic seizure and is often used interchangeably with the word ‘convulsion’.
• Epileptic seizure:the physical manifestation of paroxysmal transient disturbance of central nervous system function resulting from excessive and/or hypersynchronous abnormal neuronal activity within the cerebral cortex.
• Cause: aseizure should be considered as a sign of forebrain disease rather than a diagnosis. Causes for seizures are therefore numerous but can be broadly grouped into extracranial and intracranial causes.
• Signs: seizures are often associated with autonomic signs such as urination, salivation and defecation.
• Diagnosis: the key to diagnosis of a seizure is by inspection of an episode. Nowadays this can easily be achieved by the owner filming a typical episode.
• Treatment: this centers on treatment of the primary cause when possible as well as the administration of antiepileptic medications as appropriate.
• Prognosis: epileptic seizures have a varying prognosis depending on the primary cause.

Print off the owner factsheet Epileptic seizures and epilepsyEpileptic seizures and epilepsyto give to your client.

Presenting signs

• Involuntary muscle contractions.
• Autonomic signs:
  • Salivation.
  • Urination.
  • Defecation.
• Behavioral signs.

Classification

• Epileptic seizures can be classified into two major categories:
  • Generalized Seizures: these tend to be the most common seizure type in cats. Generalized seizures have no localizing signs and indicate involvement of both cerebral hemispheres.Consciousness/awareness is impaired and motor manifestations are bilateral.
    • Generalized tonic-clonic seizures are the most common form of generalized seizure with its clinical recognition being relatively straightforward. Typically a cat will lose consciousness whilst suddenly falling to the ground and show chomping/chewing, foaming at the mouth, paddling of the legs, and sometimes the passing of urine or stools. They usually last no more than a few minutes.
    • Myoclonic seizures are generalized seizures by definition in that they involve both cerebral hemispheres and involve loss of consciousness. However, they are often so brief in nature that an objective measurement of consciousness is impossible and observation of an episode may pass without any obvious discernible loss of awareness. Myoclonus manifests as a sudden jerk as if the cat has been given an electric shock. Therefore, the keywords in identifying myoclonus are ‘shock-like’ movements. When myoclonus occurs in series, the resulting jerks may be synchronous or moderately asynchronous.
    • Absence seizures are another type of generalized seizure. This is when a cat loses awareness of their surroundings for a transient period of time. Cats will seem to stare vacantly into space and not respond to their name being called. These seizures are very uncommon and are sometimes referred to as petit mal seizures.
  • Partial seizuresPartial seizures: these tend to be more common in cats than in dogs. This type of seizure indicates abnormal neuronal activity in a localized region of the cerebral hemisphere.Any portion of the body can be involved during a focal seizure depending on the region of the brain affected.There are two main forms of partial seizure:
    • Simple partial seizure: unaltered consciousness with asymmetric localised motor signs such as facial twitching, or the clonus of muscle groups of one limb (‘deer-stalking’).
    • Complex partial seizure: these differ from simple partial seizures in that they involve some degree of impaired consciousness/awareness. They include psychom*otor seizures which are ‘behavioral’ seizures involving the limbic system which may present as rage, aggression without provocation, fly-catching, running in circles, floor licking, vocalization, tail chasing, star-gazing etc. Psychom*otor seizures are controversial in the sense that they may represent a form of obsessive compulsive disorder. No evidence exists to support either view strongly.
• A seizure may start in a focal region of the brain only to spread throughout both cerebral hemispheres, resulting in a focal seizure with secondary generalization.

Acute presentation

• Status epilepticus Status epilepticus.

Cost considerations

• Cross-sectional imaging of the brain, if required, may be expensive.
• Long-term antiepileptic medication may be required.

Special risks

• Refractory epilepsy will often result in a decision for euthanasia.
• Death can occur during status epilepticus.
• Discontinuing antiepileptic medication abruptly may trigger ‘abstinence syndrome’. This involves central nervous system hyerexcitability; motor, autonomic and behavioral changes; and potentially withdrawal seizures.

Etiology

• Biochemical imbalance of neurotransmitters, disrupted intracellular energy metabolism, altered membrane properties due to:
  • Intracranial: congenital or acquired brain damage.
  • Extracranial: circulating toxic substance, eg uremia Uremia, hepatic encephalopathy Hepatic encephalopathy, or metabolic disturbance, eg hypoglycemia Hypoglycemia, affecting brain function.

Intracranial(iestructural/symptomatic or functional)

• Idiopathic epilepsy Epilepsy: idiopathic.
• Congenital diseases (eghydrocephalus Hydrocephalus, porencephaly/hydranencephaly, storage diseases Storage disease, arachnoid cyst).
• Infectious meningoencephalitis, (egFIP Feline infectious peritonitis, non-specific viruses, cryptococcus, toxoplasmosis Toxoplasmosis, FeLV Feline leukemia virus disease, FIV Feline immunodeficiency virus disease, Borna disease Borna virus infection: Non-suppurative meningoencephalitis).FeLV and FIV are rarely direct causes of seizures.
• Non-infectious meningoencephalitis (iemeningoencephalitis of unknown origin such as granulomatous meningoencephalitis).
• Vascular (egFeline cerebral ischemic encephalopathy Feline ischemic encephalopathy, cerebrovascular accidentsuch as an infarct or hemorrhage).
• Central nervous system neoplasia (egglioma, meningioma Meningioma, oligodendroglioma).
• Nutritional (egthiamine deficiency Thiamine deficiency).
• Trauma.

Extracranial(iemetabolic, toxic or anoxic seizures)

• Metabolic disease:
  • Hypoglycemia Hypoglycemia(eginsulinoma, sepsis, hepatic insufficiency, hypoadrenocorticism, insulin overdose, juvenile hypoglycemia, xylitol toxicity, paraneoplastic cause).
  • Hypocalcemia Hypocalcemia (egeclampsia, renal failure, pancreatitis, ethylene glycol intoxication, primary hypoparathyroidism)
  • Hypernatremia Hypernatremia (ieexcess intake or renal/gastrointestinal loss)
  • Hepatic encephalopathy Hepatic encephalopathy(egportosystemic shunt or severe hepatic insufficiency).
  • UremiaUremia.
  • Hyperproteinemia.
  • Hyperthyroidism Hyperthyroidism.
  • Hyperlipoproteinemia (egfamilial or secondary to hypothyroidism).
  • Hypertensive encephalopathy.
  • Polycythemia.
• Toxicity:
  • Lead Lead toxicity.
  • Metaldehyde Metaldehyde poisoning.
  • Ethylene glycol Ethylene glycol poisoning.
  • Strychnine Strychnine toxicity.
  • Chlorinated hydrocarbons (carbamate).
  • Bromethalin Bromethalin poisoning.
• Anoxic:
  • Hypoxia, eg cardiac Heart: congestive heart failureor respiratory insufficiency.

Pathophysiology

• Epilepsy can be caused by an intracranial (iecongenital or acquired brain damage) or extracranial problem (iea problem with the content or supply of blood to the brain) Seizures: extra- and intracranial causes.
• The normal brain cell maintains an unevenly distributed electrical charge across the cell membrane. The interior of the cell is negative with respect to the exterior, and this difference is maintained in the resting state primarily via the Na+-K+ ATPase pump that removes three sodium ions in exchange for two potassium ions into the cell.
• The resting potential of the neuron refers to the difference between the voltage inside and outside the neuron.
• The resting potential of the average neuron is around -70 millivolts, indicating that the inside of the cell is 70 millivolts less than the outside of the cell.
• When the cell is excited, the sodium channels open and positive sodium ions surge into the cell. Once the cell reaches a certain threshold (depolarisation), an action potential will fire, sending an electrical signal down the axon.
• After the neuron has fired, there is a refractory period in which another action potential is not possible.
• During this time, the potassium channels open and the sodium channels close, gradually returning the neuron to its resting potential. Once the neuron has returned to the resting potential, it is possible for another action potential to occur.
• There are neurons that are either excitatory or inhibitory.
• The excitation of neurons is mainly mediated by the glutamate neurotransmitters (also aspartate and acetylcholine) and their receptors – creating excitatory post-synaptic potentials (EPSPs)
• The inhibition of neurons is mediated by the GABA neurotransmitter (γ-aminobutyric acid; also glycine, taurine and noradrenaline) and their receptors - creating inhibitory post-synaptic potentials (IPSPs).
• The neuronal membrane potential is determined by the balance of EPSPs and IPSPs - if this balance is compromised, an epileptic seizure will result.
• The basic pathophysiological processes that result in seizures are excessive excitation or loss of inhibition (disinhibition):
  • Hypoglycemia→ loss of energy substrate for the Na+-K+ ATPase pump, failure to extrude Na+, increasing cell positivity resulting in depolarisation (excessive excitation).
  • In a disease process where inhibitory transmitters are unable to function (eghepatic encephalopathy), the lack of inhibition allows for unregulated depolarisation.
• Two interesting phenomena that occur due to seizure activity include:
  • Mirror focus - where a seizure focus creates similar activity in a hom*ologous area of the contralateral hemisphere.
  • Kindling - where one seizure increases the likelihood of further seizures. With time both mirror foci and kindled foci may become autonomous and form a new, independent seizure focus.
• Why seizures terminate as rapidly as they begin is not known. Metabolic exhaustion of neurons is not an adequate explanation. Extracortical inhibitory centers, such as within the cerebellum, may play a role. Ablations of the cerebellum, for example, facilitate seizure activity. Phenytoin, a commonly used antiepileptic medication in humans, dramatically increases the rate of firing of Purkinje neurons. Other areas such as the caudate and parts of the thalamus and reticular formation may also help to terminate seizure activity.
• It is often noted that seizures occur in the middle of the night in cats. One explanation suggests that during low levels of awareness, drowsiness and dreamless sleep, decreased activity in the reticular formation allows for reverberating circuits between the thalamus and the cortex to synchronise. Additionally, groups of neurons which are only mildly hyperactive in the awake state become excitable and fire consistently during sleep.

Publications

Refereed papers

• Recent references from PubMed and VetMedResource.
• Arrol L, Penderis J, Garosi Let al (2012) Aetiology and long-term outcome of juvenile epilepsy in 136 dogs. Vet Rec 170 (13),335 PubMed.
• Bush W W, BarrC S, Darrin E Wet al(2002) Results of cerebrospinal fluid analysis, neurological examination findings, and age at the onset of seizures as predictors for results of magnetic resonance imaging of the brain in dogs examined because of seizures: 115 cases (1992-2000). JAVMA 220 (6), 781-784 PubMed.
• Steffen F & Grasmueck S (2000)Propofol for treatment of refractory seizures in dogsand acatwi