Felis ISSN 2398-2950

Seizures

Synonym(s): Convulsion, Fit

Contributor(s): Agnes Delauche, Laurent Garosi, David Godfrey, Rosanna Marsella, Mark Lowrie

Introduction

  • 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: a seizure 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 epilepsy Epileptic seizures and epilepsy to give to your client.

Pathogenesis

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 (ie structural/symptomatic or functional)

Extracranial (ie metabolic, toxic or anoxic seizures)

Pathophysiology

  • Epilepsy can be caused by an intracranial (ie congenital or acquired brain damage) or extracranial problem (ie a 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 (eg hepatic 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 homologous 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.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Arrol L, Penderis J, Garosi L et al (2012) Aetiology and long-term outcome of juvenile epilepsy in 136 dogs. Vet Rec 170 (13), 335 PubMed.
  • Bush W W, Barr C S, Darrin E W et 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 dogs and a cat with intracranial disorders.​ JSAP 41 (11), 496-499 PubMed.
  • Bagley R S, Gavin P R, Moore M P et al (1999) Clinical signs associated with brain tumors in dogs: 97 cases (1992-1997). JAVMA 215 (6), 818-819 PubMed.
  • Berendt M & Gram L (1999) Epilepsy and seizure classification in 63 dogs: A reappraisal of veterinary epilepsy terminology. JVIM 13 (1), 14-20 PubMed.
  • March P A (1998) Seizures: Classification, etiologies, and pathophysiology. Clin Tech Small Anim Pract 13 (3), 119-131 PubMed.
  • Bagley R S, Harrington M L & Moore M P (1996) Surgical treatments for seizure: Adaptability for dogs. Vet Clin North Am Small Pract 26 (4), 827-842 PubMed.
  • Podell M (1996) Seizures in dogs. Vet Clin North Am Small Pract 26 (4), 779-809 PubMed.
  • Podell M, Fenner W R & Powers J D (1995) Seizure classification in dogs from a non-referral based population. JAVMA 206 (11), 1721-1728 PubMed.
  • Parent J M (1988) Clinical management of canine seizures. Vet Clin North Am Small Pract 18 (4), 947-964 PubMed.


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