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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 complexes on EEG. Atypical absence seizures occur in patients with cryptogenic or structural generalized epilepsies and are often associated with slow spike-wave complexes of 1.5–2.5 Hz. Motor manifestations are more pronounced in patients with atypical absence seizures than in those with typical absence seizures.

Table 3.1. Comparison of major changes between the 1981 and 1989 Classification and Terminology and the newly proposed Classification and Terminology (Commission, 1981, 1989; Berg et al., 2010).

ILAE 1981 and 1989	ILAE 2010
Generalized seizures are those in which the first clinical and electroencephalographic changes indicate initial involvement of both cerebral hemispheres.	Generalized seizures are conceptualized as originating at some point within and rapidly engaging bilaterally distributed networks. Such bilateral networks can include cortical and subcortical structures, but do not necessarily include the entire cortex.
Focal seizures (previously termed as partial) are those in which the first clinical and electroencephalographic changes indicate initial activation of a system of neurons limited to a part of one cerebral hemisphere.	Focal seizures are conceptualized as originating at some point within networks limited to one hemisphere. They may be discretely localized or more widely distributed. Focal seizures may originate in subcortical structures.
Idiopathic epilepsy: there is no underlying cause other than a possible hereditary predisposition. Idiopathic epilepsies are defined by age-related onset, clinical and electroencephalographic characteristics, and a presumed genetic aetiology.	Genetic epilepsy: the epilepsy is, as best as understood, the direct result of a known or presumed genetic defect(s) in which seizures are the core symptom of the disorder. This attribution must be supported by specific forms of evidence (e.g. specific molecular genetic studies or family studies).
Structural epilepsy: this type of epilepsy is the consequence of a known or suspected disorder of the central nervous system.	Structural and metabolic epilepsy: this type of epilepsy is the secondary result of a distinct structural or metabolic condition. These structural or metabolic disorders may be of acquired or genetic origin (as is the case for malformations of cortical development and certain metabolic disorders).
Cryptogenic (probable structural) epilepsy: this refers to a disorder whose cause is hidden or occult. Cryptogenic epilepsies are presumed to be structural.	Unknown epilepsy: the nature of the underlying cause is as yet unknown; it may have a fundamental genetic basis (e.g. a previously unrecognized channelopathy) or it may be the consequence of an unrecognized structural or metabolic disorder not yet identified.

The 1981 classification subdivided focal seizure types into: complex (with impairment of consciousness), simple (without impairment of consciousness) and secondarily generalized (when the initially focal ictal event progresses to involvement of the entire body resulting in a generalized seizure) (Commission, 1981). The most recently proposed classification (Berg et al., 2010) recommends to abandon this terminology (simple, complex, secondarily generalized) and to describe focal seizure semiology accurately, including impairment of consciousness/awareness, when recognized, and localization and progression of ictal events.

The most recently proposed classification of seizure and epilepsies (Berg et al., 2010) has been met with considerable dissatisfaction from several expert epileptologists and therefore the previous ILAE classifications are likely to continue to be used until a more widely accepted proposal has been developed (Panayiotopoulos, 2011, 2012). Among the criticisms to the ILAE 2010 proposal (Berg et al., 2010) the comments that are most relevant to the current veterinary classification involve:

• The need to maintain, although update, a specific classification of focal seizures rather than recommend to abandon the previous classification and use only a description of the clinical manifestations (Panayiotopoulos, 2011);

• The aetiologic classification of seizures and epilepsies should remain unchanged. The terms ‘idiopathic’, ‘symptomatic’ and ‘cryptogenic’ should not be abandoned, although their correct definition should be reiterated. The term ‘genetic’ should be introduced, not to replace ‘idiopathic’ but to represent a new category in addition to the other three in a revised classification of epilepsies (Panayiotopoulos, 2012).