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Seizures in Young Dogs and Cats: 

Pathophysiology and Diagnosis 

Joan R. Coates, DVM, MS, DACVIM (Neurology) 

University of Missouri, Columbia 

Robert L. Bergman, DVM, MS, DACVIM (Neurology) 

Carolina Veterinary Specialists 

Charlotte, North Carolina 

ABSTRACT: 

Seizures in young dogs and cats have received little attention because of the ambiguous 

clinical nature of seizures. In human medicine, certain aspects of brain development are 

now thought to have a role in childhood seizures. Epileptogenesis (i.e., generation of 

seizures) in an immature brain is influenced by inhibitory and excitatory systems, ionic 

microenvironment, and degree of myelination. Developing neurons appear to be less vulnerable 

to damage and loss after seizure activity. Dogs and cats younger than 1 year of 

age are more likely to have symptomatic epilepsy. Early recognition of potential causes of 

seizures in young dogs and cats is important for appropriate diagnostic considerations 

and timely therapeutic interventions. 

lthough the prevalence of seizures in 

pediatric dogs and cats is unknown, the 

overall incidence in the pet population is 

reportedly 2% to 3%. 1,2 A 

Seizures in young dogs and 

cats are a diagnostic dilemma for practitioners. In 

young animals, seizures usually signal the onset or 

coexistence of significant central nervous system 

(CNS) disease. A seizure in puppies and kittens 

often requires prompt medical attention with special 

considerations for medical management. For 

the purpose of this discussion, immature or young 

animals are defined as those younger than 6 

months of age. Categorically, 

the neonatal period is 0 to 2 

weeks of age, the socialization 

period is 3 to 12 weeks of age, 

and the juvenile period is 12 

weeks of age to adult (i.e., 3 to 6 

months of age). 3 

PATHOPHYSIOLOGY 

An immature brain is more prone to seizures 

than is a mature brain because of multiple 

changes that occur during development. 

Epileptogenesis (i.e., generation of seizures) in 

an immature brain is influenced by the 

inhibitory and excitatory systems, ionic 

microenvironment, and degree of myelination. 

Much of the outlined information on this has 

been extrapolated from laboratory animal 

model studies. 4 In immature animals, windows 

of either decreased or increased susceptibility to 

seizures depend on the maturation of several 

factors within the CNS. 5,6 Maturity of 

inhibitory systems is crucial for cessation of 

seizure activity in an immature brain. γ-Amino 

butyric acid (GABA) is the predominant 

inhibitory neurotransmitter in the brain. The 

GABA receptor may select for chloride con- 

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Seizures in Young Dogs and Cats: Pathophysiology and Diagnosis 

ductance (GABA A) or potassium conductance 

(GABA B). 7 Ultrastructural studies comparing immature 

with adult rat brains show that GABA terminals in 

immature brains are smaller and contain fewer synaptic 

vesicles. 8 Likewise, there are fewer synapses and lower 

concentrations of GABA receptors. 9,10 The rate of 

GABA formation and catabolism changes during maturation. 

11–13 Differences lie not in receptor composition 

but rather in maturational changes to the chloride ion 

gradient that govern the equilibrium potential for 

GABA A channels. 14 Consequently, in the immature 

brain, GABA A responses result in depolarization with 

subsequent activation of sodium ion (Na + ) and calcium 

ion (Ca +2 ) channels. 6 

In contrast to the inhibitory system, the excitatory 

system is overdeveloped. Glutamate is the major excitatory 

neurotransmitter in the brain, and several subtypes 

for the glutamate receptor exist, including N-methyl-Daspartate 

(NMDA), kainate, and α-amino-3-hydroxy-5methyl-4-isoxazoleproprionate 

(AMPA). 15,16 The 

hippocampus of the prenatal brain has an excess number 

of recurrent excitatory synapses and an overabundance 

of NMDA receptors. 17 As the brain continues to 

develop, these excitatory synapses are modulated or 

“pruned” to adult levels. Expression of glutamate transporters 

that play a role in glutamate uptake is also developmentally 

regulated. Decreased expression of 

glutamate transporters and variation of subtypes can 

lead to increased seizure susceptibility and to a lower 

seizure threshold. 5,18 

Differences in the ionic microenvironment that surrounds 

neurons and glial cells also contribute to epileptogenicity 

of the immature brain. The potassium 

concentration is increased in the extracellular fluid of 

immature brains. 5 Glial function immaturity may allow 

the extracellular potassium concentration to increase, 

causing excitability. 4 Thus the action potentials in immature 

neurons last longer because of altered potassium 

channel conductance, thereby causing a lower resting 

membrane potential and increased neuronal excitability. 19 

Catecholamines, especially norepinephrine, play a role 

in the generalization of epileptic activity during kindling. 

Lower levels of norepinephrine have been associ- 

ated with loss of kindling antagonisms. 4 Kindling is 

defined as local, repeated, and initially subconvulsive 

stimulation of neurons that progresses to alter the 

excitability of other nearby neurons and to develop into 

a seizure focus. The threshold of kindling varies with 

age, and spontaneous seizures occur more readily in 

developing animals than in adults. 6 The lower epinephrine 

level in the immature brain may be a factor responsible 

for facilitating kindling. 4 

Incomplete myelination contributes to seizure expres- 

Developmental changes in the brain may increase or decrease 

the window of susceptibility for seizures in young dogs and cats. 

sion in young animals. Myelination of the CNS begins 

in the last stage of gestation and continues more rapidly 

after birth. It occurs first in phylogenetically older 

regions of the brain and brain stem and later in the corpus 

callosum and neocortex. 20 It is speculated that this 

may have a role in poor interhemispheric synchrony of 

seizure discharges. 4 

Can seizures cause brain damage to the immature 

brain? In humans, the neonatal CNS is particularly susceptible 

to seizures. 21 However, the immature nervous 

system is no more vulnerable and possibly more resistant 

to damage arising from seizures. 22 The immature brain 

undergoing convulsive activity is capable of taking care 

of increased energy requirements through acceleration 

of glycolytic flux, thus avoiding major disruptions in 

oxidative metabolism. 22 Cerebral high-energy phosphates 

(i.e., ATP and ADP) have been preserved in 

puppies with seizures. 23 Nuclear magnetic resonance 

spectroscopy studies of the brains of puppies with 

seizures receiving supplemental oxygen have also shown 

sufficient preservation of energy balance even after prolonged 

status epilepticus. 24 

Developing neurons are less vulnerable to neuronal 

damage and cell loss. 6 Thus the immature brain appears 

to be more resistant to the toxic effects of glutamate 

than does the mature brain. 25 NMDA receptor expression 

in neonatal rat pups shows a decreased response to 

glutamate associated with differences in receptor subtypes, 

thus indicating that the degree of calcium entry 

into the neurons is directly related to age. 26 This may be 

partly due to the lower density of active synapses, lower 

use of energy substrates, and immaturity of biochemical 

cascades that subsequently cause cell death. 26,27 How- 

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ever, there is increasing evidence that recurrent seizures 

affect neuronal development by mechanisms that alter 

synaptogenesis and neurogenesis. 6,28 

The long-term effects of continued seizure activity are 

unknown. Neonatal seizures can increase the susceptibility 

of the developing brain to subsequent seizureinduced 

injury. 29,30 Experimental studies of immature 

rats showed that various pathologic changes developed 

after 50 short seizures. 31 Histopathologic studies of 

epileptic beagles have shown evidence of astrocytic 

swellings and ischemic changes in cerebral cortical neurons. 

32 Magnetic resonance imaging (MRI) of the brain 

has shown reduced myelination in children who have 

had neonatal convulsions. 21,33 However, a recent analysis 

of humans with recurrent seizures concluded that the 

risk to developing individuals was low. 34 

CLASSIFICATION 

Classifying seizures is useful in identifying the type 

and determining an underlying cause. In humans, controversy 

exists over defining a solitary classification 

scheme for clinically describing seizures in neonates. 

The scheme used in adults established by the International 

League Against Epilepsy 35 has been unreliable 

and difficult to apply to infants. 36 Important differences 

exist in the clinical expression of seizures in adults and 

neonates. 37 Adults more commonly present with partial 

seizures, whereas neonates have postural abnormalities. 

Neonatal seizures are often described as subtle and fragmentary, 

and some neonatal behaviors can mimic the 

phenomenology of true seizures. 38 These seizure-like 

behaviors have been referred to as reflex or release phe- 

nomena and must be distinguished from true seizures. 

Neonatal seizures are currently classified using electroencephalography 

and simultaneous video monitoring. 

Neonatal seizures have been described as seizures with a 

close correlation to electroencephalogram (EEG) 

seizure discharges, seizures with an inconsistent or no 

relationship to EEG ictal discharges, infantile spasms, 

and EEG seizures without clinical seizures. 39 This has 

led to classification of epileptic and nonepileptic neona- 

Seizures in Young Dogs and Cats: Pathophysiology and Diagnosis CE 449 

tal seizures with further categorization according to 

clinical features (i.e., focal clonic, focal tonic, or 

myoclonic seizures; spasms). 40,41 

A classification scheme for seizures according to their 

clinical appearance in domestic animals has not been 

thoroughly defined, and currently used schemes are 

extrapolated from the human literature. 42,43 In veterinary 

medicine, seizure types are classified into two major categories: 

generalized and focal. 44 A generalized seizure 

often reflects a widespread seizure focus, producing loss 

of consciousness, autonomic activity, and whole body 

movements with alternating tonic and clonic phases of 

movements. A focal seizure reflects the activity of a local 

seizure focus in an area producing motor activity. It has 

been believed that generalized motor seizures are the 

most common seizure type in dogs. 42,45,46 This has 

recently been brought into question by Berendt and 

Gram 47 who applied a human classification scheme for 

epilepsies to dogs. Results showed that focal seizures 

with and without generalization were most common 

and further emphasized reevaluation of currently used 

terminology for epilepsy in veterinary medicine. In puppies, 

generalized tonic seizures have been observed as 

early as 4 weeks of age. 48 Immaturity of the brain and 

neurotransmission processes may prevent more accurate 

recognition of seizures in younger animals. 

CAUSE 

Recurrent seizures are more broadly defined as epilepsies. 

Podell et al 42 adopted a nomenclature scheme from 

human epilepsies based on identifiable cause. Primary 

epileptic seizure (i.e., idiopathic) is the term used if an 

Seizures in young dogs and cats often reflect a symptomatic or an 

acquired cause; however, idiopathic epilepsy is being recognized 

more frequently as a diagnostic differential in younger animals. 

underlying cause cannot be identified. If seizures result 

from a structural lesion, they are defined as secondary 

epileptic seizures. The term reactive epileptic seizure is used 

when there is a reaction of the normal brain to transient 

systemic insult or physiologic stresses; these seizures are 

not considered recurrent. Epilepsies are also described as 

asymptomatic (i.e., primary, idiopathic) and symptomatic 

(i.e., secondary). 49 This article uses the terminology 

of asymptomatic and symptomatic epilepsies. 

June 2005 COMPENDIUM

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Table 1. Causes of Seizures in Young Dogs and Cats a 

Disorder/Category Affected Breeds/Specific Diseases 

Developmental Anomalies 

Hydrocephalus Boston terrier, Chihuahua, English bulldog, Maltese, Lhasa apso, 

Pomeranian, toy poodle, Cairn terrier, pug, Pekingese, Siamese cat 

Hydranencephaly, porencephaly Secondary to infection 

Lissencephaly Lhasa apso, Irish setter, wire fox terrier, domestic shorthaired cat, 

Korat cat 

Polymicrogyria Poodle 

Agenesis of corpus callosum Domestic shorthaired cat, Labrador retriever 

Dandy-Walker syndrome Not breed specific in dogs and cats 

Chiari malformation Cavalier King Charles spaniel, other small-breed dogs 

Intracranial arachnoid cyst Not breed specific 

Degenerative 

Leukodystrophy Dalmatian, Labrador retriever, Shetland sheepdog, Samoyed, silky 

terrier 

Alexander’s disease (Scottish terrier, miniature poodle, 

Burmese Mountain dog, Labrador retriever) 

Metachromatic leukodystrophy Domestic shorthaired cat 

Subacute necrotizing encephalomyelopathy Australian cattle dog, Alaskan husky, Maltese 

(mitochondrial encephalopathy) 

Spongiform encephalopathy Saluki, Labrador retriever, silky terrier, Egyptian Mau cat 

Glycogen storage disease Type 1 (silky terrier dog, domestic shorthaired cat, toy breeds), 

type 2 (domestic shorthaired cat), type 4 (Norwegian forest cat) 

Lysosomal storage disease GME1 gangliosidosis (German shorthaired pointer, Portugese water 

dog, beagle, Alaskan husky, Siamese cat [type 2], domestic 

shorthaired cat [types 1 and 2], Korat cat [type 2]) 

GME2 gangliosidosis (Siamese cat, domestic short-haired cat, Korat cat) 

Fucosidosis (English springer spaniel) 

Glycoproteinosis (Lafora’s disease; Basset hound, miniature poodle, 

beagle) 

Ceroid lipofuscinosis (infantile, juvenile) Chihuahua, Dalmatian, English setter, dachshund, saluki, Australian 

blue heeler, Australian cattle dog, Border collie, Siamese cat 

Multisystemic neuronal degeneration Cocker spaniel, Rhodesian ridgeback 

Hereditary quadriplegia and amblyopia Irish setter 

Metabolic 

Portosystemic shunting Yorkshire terrier, Maltese, schnauzer, Irish wolfhound, Old English 

sheepdog 

Hepatic microvascular dysplasia Poodle, schnauzer, dachshund, Yorkshire terrier, shih tzu, cocker 

spaniel 

Hypoglycemia Toy and miniature breeds 

Hypoxemia Neonatal asphyxia 

Hypocalcemia Primary hypoparathyroidism 


Specific seizure types have been associated with specific 

disease processes in humans; however, this still 

needs further evaluation in veterinary medicine. Podell 

et al 42 found a higher probability of symptomatic 

epilepsy in dogs with a short interictal interval and focal 

seizures, supporting the belief that focal seizures are an 

indication of a structural cerebral lesion. Similar results 

were reported in later studies by Berendt and Gram 47 as 

well as Patterson et al. 50 In contrast, these results additionally 

documented that dogs considered idiopathic 

epileptics also exhibited focal seizures. A more recent 

study of vizslas with inherited idiopathic epilepsy 

showed that focal seizures of variable frequency were the 

predominant seizure type. 50 Age is also a significant predictor 

of symptomatic epileptic seizures in young dogs 

(i.e.,

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Figure 1. Gross necropsy image of a lissencephalic brain 

from a young Lhasa apso with a history of seizures. Note 

the lack of gyri and sulci in the cerebral cortex. (Courtesy of Dr. 

Gerald R. Bratton,Texas A & M University) 

than 1 year of age. 42 Internal (Figure 2) and external 

hydrocephalus refer to increased fluid accumulation 

within the ventricular and subarachnoid spaces, respectively. 

Noncommunicating (i.e., obstructive) hydrocephalus 

refers to increased cerebrospinal fluid (CSF) only within 

the ventricular system, and communicating refers to 

increased CSF within the ventricular system and subarachnoid 

space. Congenital hydrocephalus often represents 

a secondary manifestation of a developmental (e.g., 

Chiari type 1–like malformation) 55 or an acquired (e.g., 

perinatal exposure to toxins or infectious disease) disorder. 

56–58 Congenital hydrocephalus is associated with 

fusion of the rostral colliculi, causing secondary mesencephalic 

aqueductal stenosis. Head conformation often 

involves a dome shape and an open bregmatic fontanelle. 

Clinical signs of hydrocephalus vary in severity and typically 

manifest with seizure activity and forebrain dys- 

Figure 2. Gross necropsy image of severe internal 

hydrocephalus from a 4-month-old party (multicolored) 

poodle. Note the enlarged lateral ventricles and collapsed 

cerebrocortical tissue. (Courtesy of Dr. Gayle C. Johnson, 

University of Missouri) 

function. Forebrain signs include mentation changes 

such as disorientation, obtundation, and stupor as well as 

behavioral abnormalities that can consist of an inability 

to learn skills such as housebreaking. 59 Hydrocephalus 

can be diagnosed using MRI or computed tomography 

(CT), ultrasonography, and electroencephalography. 59–61 

Medical therapies can reduce the severity of clinical 

signs, presumably by altering CSF production. The goal 

of surgical management is shunting CSF from the ventricles 

to another space (e.g., atrium, abdominal cavity). 

Shunting procedures are the mainstay of therapy for 

hydrocephalus in human medicine and are now advocated 

in veterinary medicine. 62,63 

Only a few inborn errors of metabolism (e.g., 

organic/mitochondrial encephalopathies) involving the 

cerebral cortical tissue can cause clinical signs of seizure 

in dogs. 64–66 Neuronal metabolism is directly affected 

when the enzyme defect is located in a major metabolic 

pathway. Clinical descriptions for some of the 

organic/mitochondrial encephalopathies include 

episodic extensor rigidity, myoclonus, and epileptiformlike 

seizures. 64–66 Lysosomal storage diseases cause 

seizures by interference of neuronal metabolism or accumulation 

of intracellular by-products. Seizure events 

that occur with some storage disorders usually manifest 

at the end stage of the disease process. Storage disorders 

for which seizure activity is a predominant clinical fea- 


ture include ceroid lipofuscinosis, glycoproteinoses, and 

leukodystrophies. 67 

Metabolic 

Hypoxemia in young animals is often suspected after 

severe respiratory and cardiovascular compromise. In 

addition, hypoxemia may increase the anesthetic risk in 

patients undergoing early spay and neuter procedures. 

Brain injury in newborn fetuses may be associated with 

hypotensive effects instead of hypoxia or acidosis. 68 

During the period of hypoxia–ischemia and reperfusion 

injury, various cytotoxic processes include cellular energy 

failure, excitoxicity, free radical damage, and intracellular 

calcium accumulation. 69 Hypercapnia may also be an 

important component of neonatal asphyxia. Fourteenday-old 

neonatal dogs had increased seizure susceptibility 

during the recovery phase of experimentally induced 

hypercapnia (i.e., partial pressure of carbon dioxide values: 

50 to 100 mm Hg). 70 

Hypoglycemia at glucose concentrations less than 40 

mg/dl can precipitate neuroglycopenia. Neuroglycopenia 

is manifested by depression, hypothermia, weakness, 

seizures, and coma. Factors responsible for clinical signs 

of neuroglycopenia include rate of decrease, level of 

hypoglycemia, and duration of hypoglycemia. 71 Glucose 

is the predominant energy substrate for the adult and 

neonatal brain. Although the receptor numbers for glucose 

transport protein are low in the immature brain, 

the transport protein for ketone bodies as well as lactate 

and pyruvate is high. Studies of newborn dogs have 

shown that during hypoglycemia, lactic acid is not only 

incorporated into the perinatal brain but also consumed 

to the extent that the metabolite can support up to 60% 

or more of total cerebral energy metabolism. 72 Although 

the neonatal brain can readily metabolize ketone bodies, 

lack of body fat and prolonged time necessary to produce 

ketones prevent this mechanism from protecting 

neonates from acute hypoglycemia. 73 Juvenile-onset 

hypoglycemia occurs because of immature hepatic 

enzyme systems, deficiency of glucagon, and deficiency 


of gluconeogenic substrates. Fatty liver syndrome causes 

hypoglycemia in toy breed puppies at 4 to 16 weeks of 

age. 74 Persistent juvenile hypoglycemia is often related 

to a glycogen storage disorder. 75 Extrinsic factors that 

cause hypoglycemia include stress, hypothermia, parasitism, 

and low birth weight. In addition, hypoglycemia 

combined with hypoxia–ischemia is more deleterious to 

the immature brain than either condition alone. 76 

Portosystemic shunts (PSSs) are common congenital 

defects causing hepatoencephalopathy in dogs and 

cats. 77,78 Common clinical signs of hepatoencephalopathy 

include ataxia, circling, depression, behavior changes, and 

seizures. A variety of compounds have been implicated 

in the pathogenesis of hepatic encephalopathy, although 

this process is poorly understood. Postulated causes 

include elevated ammonia, altered ratios of neurotransmitters, 

and increased brain concentrations of benzodiazepine-like 

neurotransmitters. 79 Recent studies found 

higher concentrations of glutamine, tryptophan, and 

An immature brain is more prone to seizures 

than is a mature brain because of multiple 

changes that occur during development. 

quinolinate, a metabolite of tryptophan, in the CSF of 

dogs with PSS. 80 Quinolinate is an agonist of the 

NMDA receptor, and the developing brain is more sensitive 

to NMDA activation. 81 This may play a role in 

development of seizure activity in young dogs with PSSs. 

Pathologic lesions are characterized by protoplasmic 

astrocytic proliferation (as in Alzheimer type 2 reactions) 

and spongiform changes in the brains of dogs with 

PSSs. 82 Treatment involves managing the hepatic dysfunction 

and encephalopathy. Seizures and neurologic 

sequelae following PSS attenuation have been well documented. 

83–85 Neurologic complications have been associated 

with all of the occlusion methods. 86 Potential risk 

factors for neurologic complications include older dogs 

and dogs with single extrahepatic and portoazygous 

shunts. 86 The pathophysiologic mechanisms of postligational 

seizures are poorly understood. 87 

Inflammatory 

Seizures occur in about 13% of dogs with CNS inflammatory 

diseases. 88 Cats with seizures were frequently 


454 CE 


diagnosed with inflammatory disease (47% [14 of 30] of 

cats) of suspected viral or immune-mediated origin. 89 

Canine distemper virus (CDV) encephalitis is the most 

common infectious inflammatory cause of seizures in 

dogs younger than 1 year of age. 42 Specifically, CDV 

causes acute polioencephalitis in young dogs. 90 Seizures 

often are focal, which is characterized by “chewing gum” 

seizures, or consist of generalized motor activity. 88,90 Similarly, 

seizures have been reported with postvaccinal CDV 

encephalitis in puppies. 91 These seizures are often pro- 

gressive and refractory to antiepileptic drug therapy. 

Identifying the underlying inflammatory disease process 

is important because the disease continues to progress 

without appropriate treatment. 

Dogs with noninfectious inflammatory disorders with 

cerebral cortical involvement clinically manifest seizure 

activity. Granulomatous meningoencephalomyelitis 

(GME) rarely affects young dogs 92 and is an inflammatory 

disease of the white matter of the brain. 93–95 The 

disseminated form is usually acute and rapidly progressive, 

whereas the focal form progresses more slowly. 

About 20% of affected dogs have seizures along with 

other neurologic deficits. 96 Breed-specific meningoencephalitis 

occurs in pugs, 97 Yorkshire terriers, 98 and Malteses. 

99 Pathologic features consist of nonsuppurative 

necrotizing meningoencephalitis, with a predilection for 

the cerebrum in pugs and Malteses. Seizures have also 

been reported in Yorkshire terriers, but brain-stem signs 

are more commonly manifested. Young dogs are predisposed 

and are usually 6 months of age or older. Dogs 

with the chronic form more often have clinical signs of 

generalized or focal seizures. Definitive diagnosis of the 

noninfectious inflammatory meningoencephalitides is 

based on a histopathologic diagnosis. 95 A diagnosis can 

be suspected based on patient signalment as well as 

findings from advanced imaging and CSF analysis. 100 

Serology can assist in ruling out infectious causes. 

Eosinophilic meningoencephalitis is characterized by 

eosinophilic pleocytosis of the CSF in dogs and a 

cat. 101–103 Neurotoxic substances are released from the 

granules of eosinophils, causing secondary neurologic 

signs. This disease has been reported in young dogs. 

Neurologic signs are variable, but seizures can be a pre- 

senting sign. The diagnosis is based on CSF analysis. 101 

Recovery or remission of clinical signs can occur with 

glucocorticoid therapy. 

Trauma 

Seizures that occur after traumatic head injury can have 

an early or delayed onset. Early onset of seizures occurs 

within days of the injury and may pose an increased risk 

of seizure activity later. Controversy exists in human and 

veterinary medicine regarding the role of prophylactic 

An abnormal neurologic examination between 

seizures lends support for a symptomatic cause. 

antiepileptic drug therapy for patients with head injuries. 

Current management involves waiting to begin antiepileptic 

drug therapy until seizures actually occur. 

Electrical shock resulting from curious behaviors in 

young animals may induce seizures and potentially lifethreatening 

noncardiogenic pulmonary edema. 104 

Toxicosis 

The CNS is primarily or secondarily involved with a 

variety of toxic substances. Dorman 105 reported that 

seizures occurred in 8.2% of all cases of suspected toxicosis. 

Inquisitive behaviors, lack of discretionary eating 

habits, and physiologic alterations in drug disposition 

render pediatric patients more susceptible to toxicant 

exposure. 106 Neonates have a more permeable blood– 

brain barrier than do adults, thus increasing the potential 

for CNS exposure to toxins. 107 Skin hydration is 

highest in neonates, and topical exposure to lipid-soluble 

compounds (e.g., hexachlorophene, organophosphates) 

places pediatric patients at higher risk of 

significant absorption. 106 Toxins induce seizures through 

a number of different mechanisms: increased excitation, 

decreased inhibition, and interference with energy 

metabolism. 108 

Asymptomatic Epilepsy 

Idiopathic Epilepsy 

Epilepsy is characterized by recurrent seizures. 49 The 

term idiopathic epilepsy, also known as primary or asymptomatic 

epilepsy, is used when there is no identifiable 

cause of seizures. The term inherited epilepsy is used when 

there is a genetic cause of seizures. Epilepsy suspected of 

having an inherited basis frequently occurs in dogs 


younger than 1 year of age. Although most dogs with 

idiopathic epilepsy have their first seizure at 1 to 5 years 

of age, seizures have been reported in Labrador retrievers 

as young as 2 months of age. 42,109 An inherited basis, 

familial transmission, or a higher incidence has been recognized 

in many breeds. Based on pedigree analysis, a 

genetic basis is strongly suspected in keeshonds, 110 Belgian 

Tervurens, 111 Alsatian shepherds, 112 Labrador and 

golden retrievers, 113,114 vizslas, 50 and a colony of laboratory-raised 

beagles. 115 The mode of inheritance has been 

suggested in some breeds. Hall and Wallace 116 found evidence 

of a single recessive gene contributing to a predisposition 

of epilepsy in keeshonds. Statistics suggest that 

seizures in Belgian Tervurens result from a complex pattern 

of inheritance. 117,118 A polygenic multifactorial mode 

of inheritance is suggested in golden and Labrador 

retrievers. 113,114 An autosomal recessive pattern of inheritance 

is suspected in vizslas with idiopathic epilepsy. 50 In 

humans, genes have been identified for ion channel 

defects in some epilepsies. 119 

DIAGNOSTIC CONSIDERATIONS 

The appropriate diagnostic procedures for seizures in 

young animals are variable and depend on the most 

likely differentials. 44,53 Tests may be subdivided into procedures 

that do and do not require anesthesia (Figure 3). 

The minimum database should include patient signalment, 

history, physical and neurologic examinations, and 

clinical pathology. The patient’s history plays an important 

role, especially if toxin exposure is a consideration. 

The history can also help identify vaccination status, 

pedigree information, environmental factors, and seizure 

patterns. Abnormal findings on physical and neurologic 

examinations lend support for symptomatic causes of 

seizures and more extensive diagnostic testing. Neuroanatomic 

localization for seizure activity is in the forebrain. 

Neurologic examination findings may reveal 

forebrain dysfunction or evidence of a multifocal or diffuse 

disease process. A funduscopic examination may 

show active or previous signs of chorioretinitis. Clinical 

pathology testing should include a complete blood count 


(CBC), serum chemistry profile, and urinalysis. Abnormal 

findings may further support a metabolic or toxic 

cause of seizures. Screening tests in a serum biochemical 

profile should include blood urea nitrogen, alkaline 

phosphatase, alanine transaminase, calcium, and blood 

glucose levels. Interpretation of results should also take 

into account an animal’s age because adult and immature 

animals have different serum values. Based on clinicopathologic 

abnormalities, additional diagnostic testing is 

indicated when specific organ pathology is suspected. 

Liver function tests, such as pre- and postprandial bile 

acid concentrations and blood ammonia levels, can provide 

evidence of hepatic dysfunction. Scintigraphy and 

ultrasonographic studies can further aid in identifying a 

PSS. 120 Profiles for metabolic screening of blood, urine, 

and CSF are useful when storage disorders or inborn 

errors of metabolism are suspected. 121,122 

Serology and immunologic testing may indirectly lend 

further support to infectious causes. 123 Overall, viral 

causes are difficult to definitively diagnose with less invasive 

diagnostic testing. Results of serologic testing are also 

difficult to interpret because of the presence of circulating 

antibodies from maternal immunity, vaccination, or environmental 

exposure. Immunofluorescent antibody staining 

of epithelial cells from the conjunctiva has reportedly 

identified about 54% of dogs with CDV infection. 90,124 

Additional neurodiagnostic testing can further determine 

the type and extent of intracranial pathology. 

Ultrasonography is useful in animals with an open bregmatic 

fontanelle or intracranial arachnoid cysts. 125,126 

Findings of only mild hydrocephalus should be carefully 

interpreted because this may not be the inciting cause. 

It is important to identify the underlying inflammatory 

or metabolic disease because clinical signs continue to 

progress without appropriate treatment. 

Advanced imaging such as CT or MRI can aid in diagnosing 

structural abnormalities related to cranial and 

intracranial malformations, inflammatory disorders, and 

neoplasms. MRI is more ideal for identifying soft tissue 

abnormalities. In human medicine, the efficacy of using 

CT in children after the first nonfebrile seizure has been 

questioned based on lack of abnormal findings. 127 

Electroencephalography in animals may show characteristic 

patterns in disease, such as hydrocephalus and 


456 CE 


Figure 3. Algorithm of diagnostic considerations regarding seizures in young dogs and cats. 

Electrolyte 

monitoring 

EEG 

Ultrasonography 

of the cranium 

Glucose 

evaluation 

encephalitis. 61,128 However, an animal’s age should be 

carefully considered because EEG patterns in young 

animals can mimic patterns associated with disease. An 

electroencephalograph can develop the pattern of an 

adult dog by approximately 5 months of age. 129 In our 

experience, continual electroencephalography is also 

useful in monitoring persistent seizure activity and adequate 

response to therapy. 

CSF analysis is particularly useful in identifying the presence 

of inflammatory disease. 88 Because inflammatory dis- 

SEIZURE ACTIVITY 

Signalment and history 

Physical and interictal neurologic examination 

Clinical pathology 

(CBC, serum chemistry, urinalysis; 

blood urea nitrogen, alkaline phosphatase, alanine 

transaminase, calcium, and glucose levels) 

Advanced imaging 

(CT, MRI) 

CSF analysis 

Liver function 

testing 

Ultrasonography/ 

scintigraphy 

Fundic examination 

Serology 

Metabolic screening for 

inborn errors of metabolism 

Diagnostic procedures above the dashed line do not require anesthesia; those below the dashed line do. 

ease is a more likely differential than neoplasia in younger 

animals, CSF analysis may more often provide a greater 

diagnostic yield than imaging procedures alone. CSF can be 

collected by puncturing the cerebellomedullary cistern. 

Analysis should include a nucleated cell count, protein concentration, 

and cytologic evaluation within 30 minutes of 

sample collection. Unfortunately, results of CSF analysis 

tend to be nonspecific for some disease processes. Intrathecal 

antibody production can be determined to further assist 

in diagnosing some infectious diseases. 123 


CONCLUSION 

Early recognition of the cause of seizures in young 

dogs and cats is important for appropriate therapeutic 

intervention. Inappropriate therapy can delay cessation 

of seizures and increase patient morbidity and mortality. 

Watch for an upcoming article on managing 

seizures in young dogs and cats. 

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ARTICLE #4 CE TEST 

This article qualifies for 2 contact hours of continuing CE 

education credit from the Auburn University College of 

Veterinary Medicine. Subscribers may purchase individual 

CE tests or sign up for our annual CE program. Those 

who wish to apply this credit to fulfill state relicensure 

requirements should consult their respective state 

authorities regarding the applicability of this program. 

To participate, fill out the test form inserted at the end 

of this issue or take CE tests online and get real-time 

scores at CompendiumVet.com. 

1. Which statement regarding inhibitory and excitatory 

synapses in the immature brain is correct? 

a. The GABA terminals are smaller, and the synapses 

are fewer. 

b. The excitatory synapses are underdeveloped. 

c. The rate of GABA metabolism remains the same 

during CNS maturation. 

d. Stimulation of the GABA A receptor results in repolarization 

of the immature neuron. 

e. Expression of NMDA receptors is increased in the 

prenatal brain. 


460 CE 


2. Which of the following occurs within the ionic 

microenvironment of the immature brain? 

a. The resting membrane potential is increased. 

b. The potassium concentration is increased in the 

extracellular fluid of immature brains. 

c. The action potentials for immature neurons are of 

short duration because of prolonged potassium 

channel conductance. 

d. Glial function immaturity results in a decreased 

extracellular potassium concentration. 

e. An increased extracellular potassium concentration 

results in neuronal hyperpolarization. 

3. An area within the brain in which myelination is 

completed last is the 

a. cerebrum. 

b. brain stem. 

c. olfactory region. 

d. hippocampus. 

e. pyriform lobe. 

4. _________________ is the most common cause 

of secondary epilepsy in young dogs. 

a. Lissencephaly 

b. Hepatic encephalopathy 

c. Hydranencephaly 

d. Hypoglycemia 

e. Hydrocephalus 

5. Which statement regarding glucose use in the 

immature brain is correct? 

a. Receptor numbers for the glucose transport protein 

are high. 

b. Lactic acid can support 60% of cerebral energy 

metabolism. 

c. Receptor numbers for the ketone body transport 

protein are low. 

d. Receptor numbers for the lactic acid transport protein 

are low. 

e. The neonatal brain has a readily available source of 

ketones to prevent acute hypoglycemia. 

6. Which statement regarding CDV encephalomyelitis 

is correct? 

a. CDV encephalomyelitis is the most common inflammatory 

cause of seizures in dogs younger than 1 

year of age. 

b. CDV causes acute leukoencephalomyelitis in young 

dogs. 

c. Seizure activity is characterized only by “chewing 

gum” seizures. 

d. Seizures are often controlled well with antiepileptic 

drug therapy. 

e. Seizure activity has not been associated with postvaccinal 

CDV encephalitis. 

7. Which noninfectious inflammatory disorder is 

least likely to occur in young dogs with seizure 

activity? 

a. pug encephalitis 

b. Yorkshire terrier encephalitis 

c. Maltese encephalitis 

d. steroid-responsive meningoencephalomyelitis 

e. GME 

8. Which factor is likely to predispose young dogs 

and cats to toxin exposure? 

a. increased blood–brain barrier permeability 

b. increased skin hydration 

c. inquisitive behavior 

d. alterations in drug disposition 

e. all of the above 

9. Which statement regarding primary epilepsy is 

correct? 

a. Inherited epilepsy can manifest with seizures in dogs 

younger than 1 year of age. 

b. Inherited epilepsy is a rare form of idiopathic 

epilepsy. 

c. Epilepsy does not occur in Labrador retrievers. 

d. All inherited epilepsies have an autosomal recessive 

mode of inheritance. 

e. Inherited epilepsy is a form of symptomatic epilepsy. 

10. Which diagnostic method can provide a greater 

diagnostic yield if an inflammatory disorder is 

suspected of causing seizures in young animals? 

a. serology 

b. CBC 

c. CSF analysis 

d. funduscopic examination 

e. CT or MRI 

June 2005 Test answers now available at CompendiumVet.com COMPENDIUM

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