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Epilepsy: traumatic



  • Traumatic epilepsy is one that occurs secondary to head injury.
  • A seizure is defined as a paroxysmal, transitory disturbance of brain function that has a sudden onset, ceases spontaneously, and has a tendency to recur.
  • Seizures are usually associated with autonomic disturbances such as urination, salivation and defecation.
  • Epilepsy is a recurrent seizure disorder irrespective of cause.
  • Traumatic epilepsy is postulated to be associated with a previous contusion or damage to the forebrain resulting in a seizure focus.
  • Relative to the prevalence of epilepsy in the general dog population, dogs with traumatic brain injury (TBI) may be at increased risk of developing seizures (1.4% vs 10%).
  • Cause: trauma to head.
  • Signs: recurrent seizures, or may present in status epilepticus.
  • History of physical trauma to head, eg road traffic accident (RTA) or fall.
    In all cases of traumatic injury warn owner of potential complications at time of injury.
  • Diagnosis: recurrent seizures.
  • Treatment: symptomatic, antiepileptic therapy.
  • Prognosis: guarded.



  • Damage within the brain predisposing to an area with spontaneous depolarization of neurons.

Predisposing factors



  • Depressed skull fracture → compression and injury to brain.
  • Acceleration injury → impact of brain on skull causes damage.
  • Hemorrhage → compression of brain.
  • 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).
  • 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+2-K+ ATPase pump that removes 3 sodium ions in exchange for 2 potassium ions into the cell.
  • The resting potential of the neuron refers to the difference between the voltage inside and outside the neruon.
  • 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 excitatiry or inhibitory.
  • The excitation of neurons is mainly mediated by the glutamate neurotransmitters (also aspartate and acetylcholine) and their receptors - creating excitatiry 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.


  • Acute (associated with traumatic injury).
  • Up to 3 years after traumatic incident.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Steinmetz S, Tipold A, Löscher W (2013) Epilepsy after head injury in dogs: a natural model of posttraumatic epilepsy. Epilepsia 54 , 580-588 PubMed.
  • Friedenberg S G, Butler A L, Wei L et al (2003) Seizures following head trauma in dogs: 259 cases (1999-2009). JAVMA 241, 1479-83 PubMed.
  • Berendt M, Gram L (1999) Epilepsy and seizure classfication 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.
  • Dyer K R, Shell L G (1993) Anticonvulsant therapy: a practical guide to medical management of epilepsy in pets. Vet Med 88 (7), 647-653 VetMedResource.
  • Koestner A (1989) Neuropathology of canine epilepsy. Probl Vet Med (4), 516-534 PubMed.

Other sources of information

  • Platt S R, Adams V, Garosi L Set al(2003)Gabapentin as adjunctive therapy for refractory idiopathic epilepsy in dogs.Proc ECVN Annual Symposium.

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