EPILEPSY in DOGS and in CATS

A seizure is a paroxysmal clinical manifestation resulting from an abnormal, excessive or synchronous discharge of a population of brain neurons; it is a sudden and transient event whose symptoms depend on the brain area affected by this abnormal activity. The pathophysiological mechanism underlying the epileptic seizures is therefore always the same, but the symptoms vary according to the site involved.

The term epilepsy, instead, refers to a chronic neurological pathology characterised by the persistent predisposition to develop epileptic seizures and the relative consequences.

Epileptic seizures based on frequency are divided into SINGLE (the interval between two successive seizures is greater than 24 hours) and CLUSTER (the interval between one seizure and the next is less than 24 hours); we then speak of a STATE OF EPILEPTIC DISEASE when the ictal phase, the convulsive manifestation, lasts for more than 5 minutes or there is no complete recovery between one seizure and another.

With reference to clinical manifestations, FOCAL seizures are defined as those that originate in neuronal circuits limited to a single hemisphere and these will be simple or complex depending on the mental state which may be normal or altered respectively. When, on the other hand, from the onset there is an immediate and widespread involvement of the brain structures, the seizures are called GENERALISED. It may happen that a seizure begins as focal and then goes towards a subsequent generalisation.

In the context of generalised seizures, they are distinguished by loss of consciousness, or in which there is an alteration of the state of consciousness. This is not easy to identify in pets. The veterinarian will have to distinguish between atonic seizures, cataplexy and syncopal seizures as the animal undergoes a sudden loss of tone in the limbs and body. Then there are also tonic, clonic and tonic-clonic seizures.

The etiological factors involved in the genesis of epileptic disease have been grouped into three broad categories: GENETIC, METABOLIC / STRUCTURAL, UNKNOWN.

In dogs, most of the epileptic forms can be traced back to idiopathic epilepsy; relatively less common are structural epilepsies that are subject to vascular causes, mostly ischemic, infectious (Cimurro, Toxoplasmosis, Cryptococcosis), inflammatory (Meningoencephalitis of unknown etiology, granulomatous, necrotising), traumatic, congenital (degenerative hydrocephalus), neoplastic (storage disorders, organic aciduria). Conditions of hypoglycemia due to insulinoma or iatrogenic, hypocalcemia due to hypoparathyroidism or renal insufficiency or pancreatitis, hepatic encephalopathy and intoxication by metaldehyde, organophosphates and strychnine are responsible for the forms of metabolic epilepsy.

In approaching the diagnosis of a dog or cat with epileptic disease, the veterinarian must accurately and correctly collect all the information that will direct him towards a diagnosis (age of onset, breed, frequency of seizures, any diagnostic and therapeutic paths undertaken in the past, etc.).

With the physical examination, the doctor aims to understand if the problem presented is actually due to an epileptic disease or if it is of another nature.

Then the conditions of the cardiovascular and respiratory systems will be assessed by chest x-rays, ECG, echocardiography and possibly a dynamic ECG will be performed if arrhythmias or cardiac function abnormalities are found (in this case a syncopal form would be assumed).

Excluding non-neurological causes, it must be established whether you are dealing with an idiopathic-genetic epilepsy or a condition secondary to structural or metabolic pathologies. The neurological examination will help the veterinarian look for signs of involvement of the forebrain region; in fact, convulsive activity always indicates a functional or structural alteration of this region and in particular of the frontal and temporal lobe. A negative neurological examination will more likely indicate a metabolic or idiopathic origin of the crisis, conversely, the identification of neurological deficits with prosencephalic localisation will suggest the presence of an intracranial lesion.

We proceed with blood chemistry tests that can highlight any metabolic diseases that justify the symptoms and that define the patient's metabolic status for anaesthetic and therapeutic purposes.

If a structural lesion of the brain is suspected, MRI will be recommended and if it reveals the presence of inflammatory changes or particular pictures, the Cephalorachidian Liquor examination will be used.

Chest X-ray and ultrasound of the abdomen will be proposed later for the identification of any masses in the case of a diagnosis of neoplastic disease; on the other hand, if the patient's picture is suggestive of infectious or metabolic diseases, specific confirmation tests will be performed.

A treatment can now be set. It is agreed that the frequency of two seizures per semester is the threshold for the start of treatment for a patient with Idiopathic Epilepsy, on the other hand for a subject who already presents cluster of seizures or a state of epileptic disease at the onset, we would start immediately and moreover with high doses to be reduced at a later stage.

Another common tendency is to intervene in the first instance with a monotherapy, resorting to polypharmacological schemes when a state of resistance or poor responsiveness to the treatment up to that moment is established.

The antiepileptic drugs most commonly used in dog epilepsy are phenobarbital and bromide. More recently used molecules are imepitoin, zonisamide and levetiracetam.

The target that we try to reach, through antiepileptic treatment, is the reduction of at least 50% in the frequency of seizures after treatment, with one or two drugs, which has a good balance between symptom control and drug-related side effects (it is important to monitor the patient during treatment).

In the case of deciding suspension of treatment, it is not always easy to make that decision because of the rebound effect that often triggers upon discontinuation of treatment. However It is possible to consider the possibility of a suspension in animals that have not had seizures for a year; the interruption must be reached gradually, reducing the dosages each time by 25% and ensuring a monitoring period of 6 months between one reduction and the next. If there is a return of the symptoms, it is necessary to return to the initial posology.

Gandini G., L’epilessia del cane: un moderno approccio clinico e terapeutico parte I: definizione, classificazione, patogenesi, approccio clinico in “Veterinaria”, Anno 29, n. 1 (February 2015)

Gandini G., L’epilessia del cane: un moderno approccio clinico e terapeutico parte II: Diagnosi differenziali e terapia, in “Veterinaria”, Anno 29, n. 1 (February 2015)

Nelson - Couto - Grauer - Hawkins - Johnson - Lappin - Scott Moncrieff – Taylor, Medicina interna del cane e del gatto, Edra-Masson, 2015