Canine and Feline Epilepsy. Luisa De Risio
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href="#litres_trial_promo">Chapter 9) (Rusbridge, 2005).
In analogy with the human classification published by the ILAE in 1981 and the veterinary medical literature, focal seizures have been referred to as complex and simple depending on whether or not consciousness is altered. However, in the context of the ILAE classification, consciousness was defined as ‘the degree of awareness and/or responsiveness of the patient to externally applied stimuli’. Responsiveness was defined as ‘the ability of the patient to carry out simple commands or willed movement’ and awareness referred ‘to the patient’s contact with events during the period in question and its recall’. These functions are difficult if not impossible to assess in veterinary patients, especially based on the pet-owner description or video documentation (Berendt et al., 2004). Therefore veterinary medicine can follow the most recent recommendation of the ILAE (Berg et al., 2010) to avoid using ictal impairment of consciousness to classify specific seizure types (e.g. simple and complex focal seizures) and to describe individual seizure phenomenology accurately including impairment of consciousness/awareness, when recognized.
Focal seizures can also occur as stereotyped paroxysms of abnormal behaviour including attention-seeking or avoidance/escaping behaviour, aimless wandering, restlessness and unprovoked aggression (Licht et al., 2002; Berendt et al., 2004). Paroxysmal abnormal behaviour may result from a manifestation of sensory seizures, involvement of the limbic system or higher cerebral activity (psychic seizures according to the 1981 ILAE classification). Episodes characterized by impaired consciousness (‘trance-like staring’), abnormal behaviour, including unprovoked aggression, extreme irrational fear, compulsive tail-chasing and fly catching, have been reported as focal seizures in eight bull terriers with interictal EEG abnormalities (multiple epileptiform spikes) and moderate to severe ventriculomegaly on computed tomography (Dodman et al., 1996).
The terms complex partial (or focal) seizures, psychomotor seizures, temporal lobe and limbic seizures or epilepsy have been used interchangeably in the veterinary literature to indicate focal seizures characterized by paroxysms of abnormal behaviour with or without some degree of impairment of consciousness.
Any type of focal-onset seizure can evolve into a generalized seizure (secondarily generalize).
The onset of ictus is characterized by clinical (usually motor) manifestations consistent with the location of the seizure focus and within seconds to minutes seizure activity spreads to involve both cerebral hemispheres resulting in bilaterally symmetrical motor disturbances (usually tonic-clonic), autonomic dysfunction and (commonly) altered consciousness. The focal onset may be subtle and the secondary generalization can occur so rapidly that the initial focal component is undetected and the seizure is misclassified as a generalized-onset seizure. Close observation is essential to recognize the focal-onset of the seizure before its secondary generalization. If the terminology recently proposed by the ILAE (Berg et al., 2010) is embraced also in veterinary medicine, the term ‘secondarily generalized’ should be abandoned and replaced by a description of localization and progression of ictal events.
Focal-onset seizures have also been reported in cats (Quesnel et al., 1997; Barnes et al., 2004; Schriefl et al., 2008; Pákozdy et al., 2010). As in dogs, clinical manifestations include motor, sensory and autonomic signs, alterations of consciousness, and paroxysms of abnormal behaviour, which can occur alone or in various combinations. Reported clinical manifestations include lack of response to sensory stimuli, unilateral facial twitching (that can be limited to the ear, lip, or eyelids), turning the head to one side, repetitive movements of one or both limbs on one side of the body, mydriasis, hypersalivation, urination, abnormal behaviour suggestive of some form of hallucinations (unjustified hissing, growling, piloerection, attacking a real or imaginary object, unprovoked startle, running frantically, often blindly, into objects), self-chewing, biting and circling (Schwartz-Porsche and Kaiser, 1989; Quesnel et al., 1997). As in dogs, focal seizures have been reported to secondarily generalize in cats (Quesnel et al., 1997; Schriefl et al., 2008).
A peculiar type of feline focal seizures characterized by orofacial involvement, impaired consciousness, occurrence in clusters and frequent association with hippocampal pathology has been described (Pákozdy et al., 2011). Ictal signs include hypersalivation, facial twitching, lip smacking, chewing, licking, swallowing, mydriasis, motionless staring and vocalization. Secondary generalization occurs in the majority (12/15, 70%) of cats. The most common post-ictal and interictal signs are behavioural changes and aggression. Antibodies against voltage-gated potassium channel complexes may play a role in the pathogenesis of this type of feline focal seizure (Pakozdy et al., 2013).
In addition to a classification based on clinical manifestations, seizures have also been classified based on underlying aetiology (Table 3.3). The aetiology-based classification allows for a more specific differential diagnosis. Reported aetiologies of reactive and structural seizures in dogs and cats are described in detail in Chapters 4 and 5, respectively. Idiopathic epilepsy is presented in Chapter 6.
Veterinary classification of seizures and epilepsies based on underlying aetiology
Reactive seizures
Reactive seizures are the reaction of a normal brain to a systemic metabolic or nutritional disorder or exogenous toxin exposure (Podell et al., 1995). When the metabolic, nutritional or toxic disorder resolves, the animal does not have recurrent seizures, and therefore reactive seizures are not considered a form of epilepsy, per se (Jull et al., 2011). The authors feel that the term reactive seizure should continue to be used in veterinary medicine as the term ‘metabolic’ proposed by the ILAE 2010 may generate confusion by referring to metabolic disorders only leaving toxic and nutritional aetiologies poorly classified. In addition the term ‘metabolic’ has not been widely accepted by several expert epileptologists (Panayiotopoulos, 2012).
Animals with reactive seizures frequently have acute onset of bilateral symmetrical neurological deficits indicating diffuse fore-brain or intracranial involvement and concurrent signs of dysfunction of other body systems. Occasionally, seizures are the only obvious clinical abnormality. Aetiologies of reactive seizures are listed in Box 3.1 and described in detail in Chapter 4.
Structural (symptomatic or secondary) epilepsy
The terms symptomatic epilepsy and secondary epilepsy have both been used to indicate recurrent seizures caused by a known and identifiable structural forebrain disorder such as vascular, inflammatory/infectious, traumatic, anomalous/developmental, neo-plastic and degenerative diseases. The term structural epilepsy, introduced by the ILAE 2010 proposal, should be adopted also in veterinary medicine as its meaning indicates more clearly epilepsy resulting from structural forebrain disease. The term secondary is too generic and prone to misuse, indeed, it has sometimes been used in the veterinary literature to refer to seizures caused by structural forebrain disorders as well as metabolic or toxic disorders (Pákozdy et al., 2010) generating confusion when attempting study comparison. The term symptomatic is a truism as recurrent seizures (epilepsy) are the symptom in humans and the clinical sign in animals of an underlying disease.
Dogs and cats with structural epilepsy usually present with neurological signs (other than seizures) interictally. However, focal lesions in particular areas of the brain (‘clinically silent regions’), such as olfactory bulb and frontal lobes, can result in seizure activity without any other neurological signs (Foster et al., 1988; Smith et al., 1989). Aetiologies of structural epilepsy are listed in Box 3.2 and described in detail in