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Seizures and Movement Disorders
Michael Podell, DVM, DACVIM (Neurology)

MedVet, Worthington, OH, USA

Seizures since the early 1980s. The standardized classification
scheme for seizures and epilepsy established by the
Pathophysiology International League Against Epilepsy (ILAE) in the
1980s provided the first basis for a taxonomic foundation
Epilepsy is a heterogeneous disease of diverse etiology, for an analytic approach in the diagnosis and treatment
electrophysiologic and behavioral seizure patterns, and of epilepsy. The proposed diagnostic scheme consists of
responses to treatment. As such, the pathogenesis of five levels or axes as proposed by Engel and revised by
epilepsy is multifactorial. Genetically determined sei- Berg et al. for people and Podell for dogs (Box 70.1).
zure susceptibility factors play a crucial role in the
response of the brain to triggering or precipitating fac- Axis 1: Seizure (Ictal) Phenomenology
tors, also known as the seizure threshold. A seizure can be defined as a nonspecific, paroxysmal,
A basic tenet in the mechanism of epilepsy is the pres- abnormal event of the body. An epileptic seizure is
ence of an imbalance in excitatory and inhibitory neuro- defined by the ILAE as a transient occurrence of signs
transmission. A seizure develops when the balance shifts and/or symptoms due to abnormal excessive or synchro-
towards excessive excitation. Glutamate is the principal nous neuronal activity in the brain. Thus, an epileptic
excitatory neurotransmitter and gamma‐aminobutyric seizure has a specific neural origin. Absolute confirma-
acid (GABA) is the main inhibitory neurotransmitter tion that a seizure is epileptic may be difficult as it
involved in this process in the brain. Conditions leading requires simultaneous observation of behavioral and
to excessive excitation or loss of inhibition result in electroencephalographic changes. As a result, historical
depolarization of neurons without normal regulatory information is often used to diagnose an epileptic sei-
feedback mechanisms. The result is a paroxysmal depo- zure. The clinical features of epileptic seizures can be
larization shift of a neuronal aggregate. In response to separated into four components.
this sudden change in brain activity, local surrounding
inhibitory zones are established to try to prevent the 1) The prodrome is the period prior to the onset of
spread of this epileptogenic activity. If inhibition is seizure activity. Owners report that they can “predict”
unsuccessful, other neuronal aggregates are excited the onset of their pet’s seizures based on behavior
through thalamocortical recruitment, intrahemispheric exhibited during this time, such as increased anxiety‐
association pathways or interhemispheric commissural related behavior (i.e., attention seeking, whining),
pathways. Successful recruitment of a critical number of reluctance to perform normal activity patterns, and
areas with synchronized depolarization then leads to a increased hiding (especially in cats).
seizure (Figure 70.1). 2) The aura is the initial manifestation of a seizure.
During this period, which can last from minutes to
hours, animals can exhibit stereotypical sensory or
History and Clinical Signs
motor behavior (e.g., pacing, licking), autonomic patterns
Classification of seizures and epilepsy into a universally (e.g., salivating, urinating, vomiting) and even unu-
accepted, coherent and relevant scheme for clinicians sual psychiatric events (e.g., excessive barking,
has been an ongoing dynamic process in human epilepsy increased/decreased attention seeking).

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical