Epilepsy is one of the most common complain in referring neurology; it is also a common complain in a general practice. However, numerous veterinarians fail to deal properly with epilepsy. Although owner are aware of "grand mal" type of seizures and able to recognize them as such, they often miss the point when partial, focal or complex episodes occur in their pets. The contact with the owner of a pet which has had, and will most likely have other seizures, must be multidirectional: 1) Explain what is occurring; 2) Explain the cause of seizures; 3) Explain the raisons why complementary tests are essentials to obtain a causal diagnosis; and finely, 4) Explain the minimal of pharmacology necessary to understand the therapeutical approach.

What are seizures?

We have to realize that most dogs or cats are being diagnosed as epileptic on the basis of their owner descriptions. If the veterinarian does not has the reflex "strange behaviour" may be a form of "seizure", then he may miss many cases of epilepsy. Seizures, common word used for epileptic manifestations, may present as numerous forms; only part of them are recognized as such by the common owner or sometime the veterinarian. Epilepsy is characterized by paroxysmal real or "presumed" discharges in the EEG that are sometimes accompanied by clinical signs: alteration of consciousness, movement disorders in hypo or hyper, autonomic signs, psychic disturbances presumed to be associated with sensory disturbances. Clinical epilepsy often ends as generalized and owners usually describe them as "grand mal seizures". More rarely, owners will notice the first seconds of their pet's seizure, and describe a focal onset. They will not recognize it as being part of an epileptiform episode if it is not followed by a generalised form. A lot of the "generalized" seizures do have focal onset (facial twitching, paw trembling, ...) but owner do not pick them up.

Making a diagnosis of epilepsy, especially (psychomotor, temporal lobe, or limbic epilepsy) based on only complex clinical signs, without EEG confirmation of paroxysmal discharges is also very unscientific. Ictal EEG recordings are the most diagnostic tool to confirm that what our patient is having is a seizure. Interictal recordings would have to be performed too in order to confirm that patients with atypical forms of seizures, autonomic, psychomotor, simple focal, etc..., are epileptic and must be treated as such. In the conventional veterinary EEG montages, the piriform lobe is totally inaccessible, because the anatomical origin of this kind of epilepsy is ventral to the area covered by electrodes. EEG interictal recording are also necessary to record dissociated forms (brain electrical activity without clinical manifestations) or control treatment efficacy. However, if we call epilepsy only cases with EEG confirmation of paroxysmal discharges, epileptic patients would be rarely diagnosed. EEG rarely gives information that changed how to dealt with the case. They all ends treated based on the clients description of the events. The response to therapy helps also with the diagnosis. If the owner description is a little confusing, a video camera allows to see what the owner is talking about.

What about the owner contact, what he thinks he knows about epilepsy and what he does not know?

A lot of owners are aware of epileptic "grand mal", i.e., toni-clonic generalized seizures. They know and are able to describe the "fit". Some of them will also describe the pre-aural period when the pet appears worried, try to hide or stick to his owner's legs. The clinician, thus, must be aware and pick up from the owner comments that can be reliable to partial simple or complex episodes. He sometime knows that epilepsy may be a non-curable disease that will occurs more or less regularly.

The major part of owners is not aware that partial, focal, simple or complex seizures occurs and will not describe them in the proper way. The clinician will have to retrieve theses information among other unclear descriptions of what is wrong with the pet and recognize them as part of a seizure. The common owner has no idea about why the seizures occur and that multiple reasons may be hypothesized. He usually thinks that seizure is a disease in se. He also has no idea that a symptomatic (anti-epileptic) treatment is sometime the only possibility when no etiological treatment can be proposed.

How to explain when and why complementary exams are necessary?

Seizures are clinical signs of a prosencephalic deregulation. The origin of the deregulation may be intracranial or extracranial. When extracranial, the origins of the seizures are either toxic or metabolic in nature. In the first instance, the history brings information about the nature or the possibility of a contact with a molecule susceptible of being epileptogenic. In the second instance, the signalment of the animal, the history and often the waxing and waning occurrence of the episodes drive the clinician to suspect a metabolic abnormality; hypoglycemia, hepatic encephalopathy, hypocalcemia, hyperviscosity are among the most common extracranial causes of recurring seizures. Complementary tests are relevant to confirm or infirm such hypothesis. All the data already collected from the owner, the general or the neurological examinations are sometime not sufficient to propose a highly suspected diagnosis. When an extracranial cause has been ruled out, an intracranial cause may be suspected. A structural lesion may sometime be at the origin of an epileptogenic focus; trauma, inflammation, neoplasia are among the most common cause of intracranial structural causes of epilepsy; vascular infarct or hemorrhage, or congenital macroscopic or microscopic defect are rare. In such cases, the neurological examination is rarely normal; deficits usually help to suspect a focal structural lesion. Cerebrospinal fluid tap, serology or PCR, and imaging techniques are necessary to drive the clinician to one most probable origin. Finally, if no extracranial or structural intracranial cause has been found, idiopathic or primary epilepsy will be suspected. The terminology "idiopathic" must be used when all possible causes have been ruled out, the patient presenting or not neurological deficits. In this instance, a cause exists however the diagnostic procedures that should be used to confirm it either have been nondiagnostic, either do not exist. The terminology "primary" must be used only when a non-structural intracranial cause of epilepsy is suspected. Some breeds have a known predisposition to develop epilepsy; some other have a known hereditary form of epilepsy. In such cases, the seizure characteristics are often similar: first episode before 7 years of life, grand mal episodes without focal manifestation, often at night or during rest, often cyclic in occurrence, normal mentation and physical ability in between the episodes, ... Ideally even such cases should be worked out to rule out extracranial or structural intracranial causes.

What pharmacological rules should be explained?

The owner has rarely some bases of pharmacology. When an intracranial structural or extracranial cause has been diagnosed, a curative treatment may sometime be obtained if the cause may be eliminated. It is the case with intoxication, hepatic encephalopathy, puerperal hypocalcemia, benign neoplastic or inflammatory processes, ... In some instance, only a control of the cause may be proposed: hepatic encephalopathy, insulinoma, malignant neoplasm, inflammatory process, ... Sometime, the cause may be gone (vascular accident) or perfectly controlled (head trauma) however structural sequela are still present. In this instance, as well as in all other cases, a symptomatic treatment must be proposed to control the kindling effect. Such a treatment is the only treatment possible in front of a idiopathic or primary epilepsy. The symptomatic treatment goal is only to control, as well as possible, the epileptic condition. To do so, one should use drugs which pharmacology has been well documented, cheap because the treatment may be long, without secondary effect superior to the beneficial effect, and if possible without health consequences. Phenobarbital and potassium bromide are such drugs. They can be used initially alone or potentially in synergy. These two drugs do not have a definitive dosage; because animal will metabolise them differently, a blood level must be regularly performed to control if the concentration is within, under or above a therapeutical range. Because of a long half life, they will not be effective until they reach the lower value of the therapeutical range. Because of its enzymatic induction, Phenobarbital dosage will have to be readjusted with time. Because of its renal excretion, animals on bromide will have to receive a strict and constant diet. These drugs have secondary effects. Excessive thirst and appetite and in consequence, possible incontinence or weight gain are the most common side effect. The sedative effect noted during the beginning of the treatment or when dosages are changed is often temporary. The other anti-epileptic drugs on the market are either not used because they have a too short half life and cannot be technically used in dogs, either not studied enough, either too expensive.

What the owner should know by the end of the consultation?

1.  Grand mal seizures are one form of epileptic manifestations; other manifestations may be considered as been epilepsy.

2.  To have seizure only means that something is wrong with the brain; it is a clinical signs and not a disease in se.

3.  It is rare that the history, the general examination and the neurological examination are sufficient to give a final diagnosis; complementary tests are often necessary to precise the origin of the seizures.

4.  Therapy in an epileptic patient must be directed against the seizures (symptomatic treatment) and, when known and possible, the origin of the cerebral dysfunction must be addressed (causative treatment). These treatments may last for the animal' life.

5.  The goal of the symptomatic treatment is to reduce the intensity, the number and the occurrence of the seizures, i.e., to control the situation rather than to cure it. This goal must be determined and chosen with the owner

6.  The common anti-epileptic drugs necessitate days to reach a therapeutical level and thus, the control may be poor during the beginning of the treatment

7.  Excessive sedation is a common secondary effect when the treatment is initiated. The number of seizures and the drug combination are responsible. It will disappear with time; however, to be sedated is better that to seize!!! Increase of thirst and appetite may be more difficult to control when dosage is high.

8.  Because there is no definite dosage for these drugs, a tentative dosage must be initiated and adjusted according to the control obtained. Blood measurement of the drug level will help to understand why the control is not satisfying.

9.  Failure in control means either poor treatment administration, either too low blood level, or possible causative diagnostic error.

10.  A regular life and a regular contact with the veterinarian is the key to long life.

Conclusion

The first consultation with an owner who's pet has experienced seizure must be a 30 to 45 minutes consultation. If the regular clinician has no such time, it is the referring veterinarian's work to set good communication basis and return the owner to the first one for regular control.