A seizure (or ictus) has been defined as ’a transient occurrence of signs due to abnormal excessive or synchronous neuronal activity in the brain’ (Fisher et al., 2005). The clinical manifestations of a seizure are sudden and transient and depend on location of onset in the brain, patterns of propagation and a variety of other factors (see Chapter 1). Seizures can affect one or more of the following functions: sensory, motor, and autonomic activity, consciousness, emotional state, memory, cognition or behaviour (Fisher et al., 2005). The seizure (or ictus) may be preceded by a prodrome (or prodromal phase), which can be characterized by anxiety, restlessness, increased affection, withdrawal, aggressiveness, or vocalization, and by an aura, which is the initial manifestation of a seizure. The prodrome can occur hours to days before the seizure, the aura generally lasts seconds. The aura has been described in people as a subjective sensation, such as dizziness, tingling, and anxiety at the start of a seizure. In animals it may manifest as increased or decreased attention seeking, stereotypical sensory or motor behaviour (e.g. licking, pacing) or autonomic manifestations (e.g. salivating, vomiting, urinating). The ictus is the seizure itself and, in most cases, it lasts only a few minutes. The post-ictal period occurs soon after the seizure (or ictus) and may last seconds to days. Clinical manifestations include disorientation, aggressive behaviour, restlessness, pacing, lethargy, deep sleep, hunger, thirst, defecation, urination, ataxia, proprioceptive deficits and decreased or absent menace response with or without actual blindness.

      Epilepsy has been defined as an enduring disorder of the brain that is characterized by recurrent seizures (Blume et al., 2001; Fisher et al., 2005). As there are many causes of chronic recurrent seizures, epilepsy is not a specific disease but rather a group of heterogeneous conditions. However, not all seizures are associated with epilepsy. For instance, a seizure can be the reaction of a normal brain to a transient insult, such as intoxication or metabolic disorder. If seizures no longer occur when the metabolic or toxic disorder resolves, the patient is not considered to have epilepsy.

      A classification of seizures and epilepsies is important as clinical manifestations and aetiologies of seizures vary considerably. A standardized and uniform classification of seizure and epilepsy would allow consistency in the use of diagnostic terms, improve communication among clinicians and methods of evaluating treatment, and facilitate comparison of clinical cases and scientific studies.

      Classification of seizures and epilepsies in veterinary medicine is largely based on its human counterpart and focuses on seizure phenomenology and aetiology (Schwartz-Porsche, 1994; Podell et al., 1995; Berendt and Gram, 1999; Licht et al., 2002; Podell, 2004). The main limitations of the veterinary classification are that: (i) recognition of seizure occurrence and clinical manifestations is largely dependent on the pet-owner’s observation; (ii) electroencephalographic (EEG) data are usually not available; and (iii) no agreement has been reached for a standardized terminology in veterinary medicine. Therefore, the veterinary literature on this subject is often confusing with regard to definitions and interpretations. In addition, as in human medicine, seizure classification is an ongoing process and therefore updating is necessary.

      This chapter will initially present the definitions and classifications of seizure and epilepsy in human medicine that are relevant in order to understand how terminology and classification have been developed and could evolve in veterinary medicine. Subsequently the focus will be on proposed veterinary terminology and classification.

       Classification of Seizures and Epilepsies in Human Medicine

      In human medicine, the International League Against Epilepsy (ILAE) has appointed a task force (Commission on Classification and Terminology) for the ongoing process of seizure and epilepsy classification and terminology. Classification systems have been developed based on ictal phenomenology, associated EEG findings and on aetiology. The Commission on Classification and Terminology of the ILAE first published its classification in 1969, which has subsequently been updated in 1981 for seizures (Commission, 1981) and in 1989 for epilepsies (Commission, 1989). Advances in molecular genetics, structural and functional neuroimaging, and neurophysiologic techniques have greatly improved the knowledge and understanding of seizures and epilepsies in humans, creating the need for a more modern system. Attempts have been made to update the 1989 and 1981 classification in 2001 and 2006 (Engel, 2001, 2006), and the most recent proposal for a revised classification has been published in 2010 (Berg et al., 2010) (Table 3.1).

      Interestingly, epilepsies of unknown cause account for one-third or more of all epilepsies in humans. It is likely that several epilepsies classified as idiopathic in veterinary medicine (particularly in cats) would be more appropriately classified as unknown (or of unknown aetiology despite extensive investigations) based on the most recent ILAE classification. Future research in neuroimaging and genetics should help to further characterize and better classify these types of epilepsy (Berg et al., 2010).

      In human medicine, epilepsies have also been classified as electroclinical syndromes (Berg et al., 2010). An electroclinical syndrome has been defined as a complex of clinical features, signs and symptoms that together define a distinctive, recognizable clinical disorder (Berg et al., 2010). Electroclinical syndromes are distinctive disorders identifiable on the basis of a typical age onset, specific seizure types, EEG characteristics and other factors (such as patterns of seizure occurrence with respect to sleep, provoking or triggering factors), which, when taken together, permit a specific diagnosis. The diagnosis of an electroclinical syndrome often has implications for management, treatment and prognosis (Berg et al., 2010). One of the most distinctive and clinically relevant classifications of the currently recognized electroclinical syndromes in humans is based on typical age at onset (Berg et al., 2010).

      The subdivision of generalized seizures into tonic-clonic, tonic, clonic, myoclonic, atonic and absence seizures is overall unchanged since 1981. The 1981 subclassification of absence seizures has been simplified and altered. Absence seizures are characterized by a brief impairment of consciousness and may be associated with mild clonic, tonic, atonic and autonomic manifestations. Absence seizures are subclassified as typical, atypical and with special features (myoclonic absence and eyelid myoclonia) in the latest classification (Berg et al., 2010). Typical absence seizures occur in young patients with idiopathic generalized epilepsies and are usually associated with generalized 3–4 Hz spike-and-slow-wave