Seizures in Young Dogs and Cats

lthough the prevalence of seizures inpediatric dogs and cats is unknown, theoverall incidence in the pet population is

reportedly 2% to 3%.1,2 Seizures in young dogs andcats are a diagnostic dilemma for practitioners. Inyoung animals, seizures usually signal the onset orcoexistence of significant central nervous system(CNS) disease. A seizure in puppies and kittensoften requires prompt medical attention with spe-cial considerations for medical management. Forthe purpose of this discussion, immature or younganimals are defined as those younger than 6

months of age. Categorically,the neonatal period is 0 to 2weeks of age, the socializationperiod is 3 to 12 weeks of age,and the juvenile period is 12weeks of age to adult (i.e., 3 to 6months of age).3

Article #4

ABSTRACT:

CE

Seizures in young dogs and cats have received little attention because of the ambiguousclinical nature of seizures. In human medicine, certain aspects of brain development arenow thought to have a role in childhood seizures. Epileptogenesis (i.e., generation ofseizures) in an immature brain is influenced by inhibitory and excitatory systems, ionicmicroenvironment, and degree of myelination. Developing neurons appear to be less vul-nerable to damage and loss after seizure activity. Dogs and cats younger than 1 year ofage are more likely to have symptomatic epilepsy. Early recognition of potential causes ofseizures in young dogs and cats is important for appropriate diagnostic considerationsand timely therapeutic interventions.

PATHOPHYSIOLOGYAn immature brain is more prone to seizures

than is a mature brain because of multiplechanges that occur during development.Epileptogenesis (i.e., generation of seizures) inan immature brain is influenced by theinhibitory and excitatory systems, ionicmicroenvironment, and degree of myelination.Much of the outlined information on this hasbeen extrapolated from laboratory animalmodel studies.4 In immature animals, windowsof either decreased or increased susceptibility toseizures depend on the maturation of severalfactors within the CNS.5,6 Maturity ofinhibitory systems is crucial for cessation ofseizure activity in an immature brain. γ-Aminobutyric acid (GABA) is the predominantinhibitory neurotransmitter in the brain. TheGABA receptor may select for chloride con-

June 2005 447 COMPENDIUM

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 SpecialistsCharlotte, North Carolina

Send comments/questions via [email protected] fax 800-556-3288.

Visit CompendiumVet.com for full-text articles, CE testing, and CE test answers.

A

ductance (GABAA) or potassium conductance(GABAB).7 Ultrastructural studies comparing immaturewith adult rat brains show that GABA terminals inimmature brains are smaller and contain fewer synapticvesicles.8 Likewise, there are fewer synapses and lowerconcentrations of GABA receptors.9,10 The rate ofGABA formation and catabolism changes during matu-ration.11–13 Differences lie not in receptor compositionbut rather in maturational changes to the chloride iongradient that govern the equilibrium potential for

GABAA channels.14 Consequently, in the immaturebrain, GABAA responses result in depolarization withsubsequent activation of sodium ion (Na+) and calciumion (Ca+2) channels.6

In contrast to the inhibitory system, the excitatorysystem is overdeveloped. Glutamate is the major excita-tory neurotransmitter in the brain, and several subtypesfor the glutamate receptor exist, including N-methyl-D-aspartate (NMDA), kainate, and α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate (AMPA).15,16 Thehippocampus of the prenatal brain has an excess numberof recurrent excitatory synapses and an overabundanceof NMDA receptors.17 As the brain continues todevelop, these excitatory synapses are modulated or“pruned” to adult levels. Expression of glutamate trans-porters that play a role in glutamate uptake is also devel-opmentally regulated. Decreased expression ofglutamate transporters and variation of subtypes canlead to increased seizure susceptibility and to a lowerseizure threshold.5,18

Differences in the ionic microenvironment that sur-rounds neurons and glial cells also contribute to epilep-togenicity of the immature brain. The potassiumconcentration is increased in the extracellular fluid ofimmature brains.5 Glial function immaturity may allowthe extracellular potassium concentration to increase,causing excitability.4 Thus the action potentials in imma-ture neurons last longer because of altered potassiumchannel conductance, thereby causing a lower restingmembrane potential and increased neuronal excitability.19

Catecholamines, especially norepinephrine, play a rolein the generalization of epileptic activity during kin-dling. Lower levels of norepinephrine have been associ-

ated with loss of kindling antagonisms.4 Kindling isdefined as local, repeated, and initially subconvulsivestimulation of neurons that progresses to alter theexcitability of other nearby neurons and to develop intoa seizure focus. The threshold of kindling varies withage, and spontaneous seizures occur more readily indeveloping animals than in adults.6 The lower epineph-rine level in the immature brain may be a factor respon-sible for facilitating kindling.4

Incomplete myelination contributes to seizure expres-

sion in young animals. Myelination of the CNS beginsin the last stage of gestation and continues more rapidlyafter birth. It occurs first in phylogenetically olderregions of the brain and brain stem and later in the cor-pus callosum and neocortex.20 It is speculated that thismay have a role in poor interhemispheric synchrony ofseizure discharges.4

Can seizures cause brain damage to the immaturebrain? In humans, the neonatal CNS is particularly sus-ceptible to seizures.21 However, the immature nervoussystem is no more vulnerable and possibly more resistantto damage arising from seizures.22 The immature brainundergoing convulsive activity is capable of taking careof increased energy requirements through accelerationof glycolytic flux, thus avoiding major disruptions inoxidative metabolism.22 Cerebral high-energy phos-phates (i.e., ATP and ADP) have been preserved inpuppies with seizures.23 Nuclear magnetic resonancespectroscopy studies of the brains of puppies withseizures receiving supplemental oxygen have also shownsufficient preservation of energy balance even after pro-longed status epilepticus.24

Developing neurons are less vulnerable to neuronaldamage and cell loss.6 Thus the immature brain appearsto be more resistant to the toxic effects of glutamatethan does the mature brain.25 NMDA receptor expres-sion in neonatal rat pups shows a decreased response toglutamate associated with differences in receptor sub-types, thus indicating that the degree of calcium entryinto the neurons is directly related to age.26 This may bepartly due to the lower density of active synapses, loweruse of energy substrates, and immaturity of biochemicalcascades that subsequently cause cell death.26,27 How-

COMPENDIUM June 2005

Seizures in Young Dogs and Cats: Pathophysiology and Diagnosis448 CE

Developmental changes in the brain may increase or decreasethe window of susceptibility for seizures in young dogs and cats.

ever, there is increasing evidence that recurrent seizuresaffect neuronal development by mechanisms that altersynaptogenesis and neurogenesis.6,28

The long-term effects of continued seizure activity areunknown. Neonatal seizures can increase the suscepti-bility of the developing brain to subsequent seizure-induced injury.29,30 Experimental studies of immaturerats showed that various pathologic changes developedafter 50 short seizures.31 Histopathologic studies ofepileptic beagles have shown evidence of astrocyticswellings and ischemic changes in cerebral cortical neu-rons.32 Magnetic resonance imaging (MRI) of the brainhas shown reduced myelination in children who havehad neonatal convulsions.21,33 However, a recent analysisof humans with recurrent seizures concluded that therisk to developing individuals was low.34

CLASSIFICATIONClassifying seizures is useful in identifying the type

and determining an underlying cause. In humans, con-troversy exists over defining a solitary classificationscheme for clinically describing seizures in neonates.The scheme used in adults established by the Interna-tional League Against Epilepsy35 has been unreliableand difficult to apply to infants.36 Important differencesexist in the clinical expression of seizures in adults andneonates.37 Adults more commonly present with partialseizures, whereas neonates have postural abnormalities.Neonatal seizures are often described as subtle and frag-mentary, and some neonatal behaviors can mimic thephenomenology of true seizures.38 These seizure-likebehaviors have been referred to as reflex or release phe-

nomena and must be distinguished from true seizures.Neonatal seizures are currently classified using elec-troencephalography and simultaneous video monitoring.Neonatal seizures have been described as seizures with aclose correlation to electroencephalogram (EEG)seizure discharges, seizures with an inconsistent or norelationship to EEG ictal discharges, infantile spasms,and EEG seizures without clinical seizures.39 This hasled to classification of epileptic and nonepileptic neona-

tal seizures with further categorization according toclinical features (i.e., focal clonic, focal tonic, ormyoclonic seizures; spasms).40,41

A classification scheme for seizures according to theirclinical appearance in domestic animals has not beenthoroughly defined, and currently used schemes areextrapolated from the human literature.42,43 In veterinarymedicine, seizure types are classified into two major cat-egories: generalized and focal.44 A generalized seizureoften reflects a widespread seizure focus, producing lossof consciousness, autonomic activity, and whole bodymovements with alternating tonic and clonic phases ofmovements. A focal seizure reflects the activity of a localseizure focus in an area producing motor activity. It hasbeen believed that generalized motor seizures are themost common seizure type in dogs.42,45,46 This hasrecently been brought into question by Berendt andGram47 who applied a human classification scheme forepilepsies to dogs. Results showed that focal seizureswith and without generalization were most commonand further emphasized reevaluation of currently usedterminology for epilepsy in veterinary medicine. In pup-pies, generalized tonic seizures have been observed asearly as 4 weeks of age.48 Immaturity of the brain andneurotransmission processes may prevent more accuraterecognition of seizures in younger animals.

CAUSERecurrent seizures are more broadly defined as epilep-

sies. Podell et al42 adopted a nomenclature scheme fromhuman epilepsies based on identifiable cause. Primaryepileptic seizure (i.e., idiopathic) is the term used if an

underlying cause cannot be identified. If seizures resultfrom a structural lesion, they are defined as secondaryepileptic seizures. The term reactive epileptic seizure is usedwhen there is a reaction of the normal brain to transientsystemic insult or physiologic stresses; these seizures arenot considered recurrent. Epilepsies are also described asasymptomatic (i.e., primary, idiopathic) and sympto-matic (i.e., secondary).49 This article uses the terminol-ogy of asymptomatic and symptomatic epilepsies.

June 2005 COMPENDIUM

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

Seizures in young dogs and cats often reflect a symptomatic or anacquired cause; however, idiopathic epilepsy is being recognizedmore frequently as a diagnostic differential in younger animals.



Table 1. Causes of Seizures in Young Dogs and Catsa

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

DegenerativeLeukodystrophy 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 waterdog, beagle, Alaskan husky, Siamese cat [type 2], domesticshorthaired 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, Australianblue heeler, Australian cattle dog, Border collie, Siamese cat

Multisystemic neuronal degeneration Cocker spaniel, Rhodesian ridgeback

Hereditary quadriplegia and amblyopia Irish setter

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

sheepdog

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

Hypoglycemia Toy and miniature breeds

Hypoxemia Neonatal asphyxia

Hypocalcemia Primary hypoparathyroidism

Specific seizure types have been associated with spe-cific disease processes in humans; however, this stillneeds further evaluation in veterinary medicine. Podellet al42 found a higher probability of symptomaticepilepsy in dogs with a short interictal interval and focalseizures, supporting the belief that focal seizures are anindication of a structural cerebral lesion. Similar resultswere reported in later studies by Berendt and Gram47 aswell as Patterson et al.50 In contrast, these results addi-tionally documented that dogs considered idiopathicepileptics also exhibited focal seizures. A more recentstudy of vizslas with inherited idiopathic epilepsyshowed that focal seizures of variable frequency were thepredominant seizure type.50 Age is also a significant pre-dictor of symptomatic epileptic seizures in young dogs(i.e., <1 year of age).42 In Table 1, the DAMNIT-V clas-

sification scheme is used to summarize disorders associ-ated with or that cause seizures in immature animals.51–53

Symptomatic EpilepsiesDegenerative/Anomalous

Disorders related to neuronal migration and some formsof cranial malformations are apt to induce seizures. Brainmalformations associated with seizure activity include hy-drocephalus, Dandy-Walker syndrome, hydranencephaly,lissencephaly (Figure 1), Chiari-like malformation, intra-cranial intraarachnoid cyst, polymicrogyria, and agenesisof the corpus callosum.44,53

Congenital or acquired hydrocephalus is a commondiagnostic differential for seizures in young dogs andcats.54 Hydrocephalus was found to be the most commoncause of secondary epileptic seizures in dogs younger



Table 1. Causes of Seizures in Young Dogs and Catsa (continued)

Disorder/Category Affected Breeds/Specific Diseases

Nutritional

Thiamine deficiency Seizures in dogs fed diets mainly of meat and fish

InflammatoryViral CDV, FIP, feline panleukopenia, FIV, nonsuppurative

meningoencephalomyelitis in cats

Fungal Cryptococcus spp infection

Bacterial Infection with aerobes or anaerobes, abscessation

Protozoal Toxoplasmosis, encephalitozoonosis

Parasitic Cuterebra spp larval myiasis

Rickettsial Ehrlichiosis, Rocky Mountain spotted fever

Noninfectious inflammatory Eosinophilic meningoencephalitis, encephalitis (pug, Maltese,Yorkshire terrier), GME, periventricular encephalitis

IdiopathicEpilepsy Beagle, Belgian Tervuren, keeshond, British Alsatian, Labrador

retriever, golden retriever, collie, dachshund, vizsla

TraumaticAcute and chronic Posttraumatic epilepsy

Toxicosis Pesticides (organophosphates, carbamates, pyrethrins, metaldehyde),rodenticides (bromethalin, strychnine, rotenone, zinc phosphate,vacor), herbicides, heavy metals (lead, triethyltin, thallium), drugs,poisonous plants, mycotoxins (amanita mushrooms, penitrems A),antifreeze (ethylene glycol), disinfectants (hexachlorophene),methylxanthines, street drugs

aLists only breeds and diseases in which seizures have been clinically documented in young dogs and cats.CDV = canine distemper virus; GME = granulomatous meningoencephalomyelitis.

function. Forebrain signs include mentation changessuch as disorientation, obtundation, and stupor as well asbehavioral abnormalities that can consist of an inabilityto learn skills such as housebreaking.59 Hydrocephaluscan be diagnosed using MRI or computed tomography(CT), ultrasonography, and electroencephalography.59–61

Medical therapies can reduce the severity of clinicalsigns, presumably by altering CSF production. The goalof surgical management is shunting CSF from the ven-tricles to another space (e.g., atrium, abdominal cavity).Shunting procedures are the mainstay of therapy forhydrocephalus in human medicine and are now advo-cated in veterinary medicine.62,63

Only a few inborn errors of metabolism (e.g.,organic/mitochondrial encephalopathies) involving thecerebral cortical tissue can cause clinical signs of seizurein dogs.64–66 Neuronal metabolism is directly affectedwhen the enzyme defect is located in a major metabolicpathway. Clinical descriptions for some of theorganic/mitochondrial encephalopathies includeepisodic extensor rigidity, myoclonus, and epileptiform-like seizures.64–66 Lysosomal storage diseases causeseizures by interference of neuronal metabolism or accu-mulation of intracellular by-products. Seizure eventsthat occur with some storage disorders usually manifestat the end stage of the disease process. Storage disordersfor which seizure activity is a predominant clinical fea-



than 1 year of age.42 Internal (Figure 2) and externalhydrocephalus refer to increased fluid accumulationwithin the ventricular and subarachnoid spaces, respec-tively. Noncommunicating (i.e., obstructive) hydrocephalusrefers to increased cerebrospinal fluid (CSF) only withinthe ventricular system, and communicating refers toincreased CSF within the ventricular system and sub-arachnoid space. Congenital hydrocephalus often repre-sents 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) disor-der.56–58 Congenital hydrocephalus is associated withfusion of the rostral colliculi, causing secondary mesen-cephalic aqueductal stenosis. Head conformation ofteninvolves a dome shape and an open bregmatic fontanelle.Clinical signs of hydrocephalus vary in severity and typi-cally manifest with seizure activity and forebrain dys-

Figure 1. Gross necropsy image of a lissencephalic brainfrom a young Lhasa apso with a history of seizures. Notethe lack of gyri and sulci in the cerebral cortex. (Courtesy of Dr.Gerald R. Bratton,Texas A & M University)

Figure 2. Gross necropsy image of severe internalhydrocephalus from a 4-month-old party (multicolored)poodle. Note the enlarged lateral ventricles and collapsedcerebrocortical tissue. (Courtesy of Dr. Gayle C. Johnson,University of Missouri)

ture include ceroid lipofuscinosis, glycoproteinoses, andleukodystrophies.67

MetabolicHypoxemia in young animals is often suspected after

severe respiratory and cardiovascular compromise. Inaddition, hypoxemia may increase the anesthetic risk inpatients undergoing early spay and neuter procedures.Brain injury in newborn fetuses may be associated withhypotensive effects instead of hypoxia or acidosis.68

During the period of hypoxia–ischemia and reperfusioninjury, various cytotoxic processes include cellular energyfailure, excitoxicity, free radical damage, and intracellularcalcium accumulation.69 Hypercapnia may also be animportant component of neonatal asphyxia. Fourteen-day-old neonatal dogs had increased seizure susceptibil-ity during the recovery phase of experimentally inducedhypercapnia (i.e., partial pressure of carbon dioxide val-ues: 50 to 100 mm Hg).70

Hypoglycemia at glucose concentrations less than 40mg/dl can precipitate neuroglycopenia. Neuroglycopeniais manifested by depression, hypothermia, weakness,seizures, and coma. Factors responsible for clinical signsof neuroglycopenia include rate of decrease, level ofhypoglycemia, and duration of hypoglycemia.71 Glucoseis the predominant energy substrate for the adult andneonatal brain. Although the receptor numbers for glu-cose transport protein are low in the immature brain,the transport protein for ketone bodies as well as lactateand pyruvate is high. Studies of newborn dogs haveshown that during hypoglycemia, lactic acid is not onlyincorporated into the perinatal brain but also consumedto the extent that the metabolite can support up to 60%or more of total cerebral energy metabolism.72 Althoughthe neonatal brain can readily metabolize ketone bodies,lack of body fat and prolonged time necessary to pro-duce ketones prevent this mechanism from protectingneonates from acute hypoglycemia.73 Juvenile-onsethypoglycemia occurs because of immature hepaticenzyme systems, deficiency of glucagon, and deficiency

of gluconeogenic substrates. Fatty liver syndrome causeshypoglycemia in toy breed puppies at 4 to 16 weeks ofage.74 Persistent juvenile hypoglycemia is often relatedto a glycogen storage disorder.75 Extrinsic factors thatcause hypoglycemia include stress, hypothermia, para-sitism, and low birth weight. In addition, hypoglycemiacombined with hypoxia–ischemia is more deleterious tothe immature brain than either condition alone.76

Portosystemic shunts (PSSs) are common congenitaldefects causing hepatoencephalopathy in dogs andcats.77,78 Common clinical signs of hepatoencephalopathyinclude ataxia, circling, depression, behavior changes, andseizures. A variety of compounds have been implicatedin the pathogenesis of hepatic encephalopathy, althoughthis process is poorly understood. Postulated causesinclude elevated ammonia, altered ratios of neurotrans-mitters, and increased brain concentrations of benzodi-azepine-like neurotransmitters.79 Recent studies foundhigher concentrations of glutamine, tryptophan, and

quinolinate, a metabolite of tryptophan, in the CSF ofdogs with PSS.80 Quinolinate is an agonist of theNMDA receptor, and the developing brain is more sen-sitive to NMDA activation.81 This may play a role indevelopment of seizure activity in young dogs with PSSs.Pathologic lesions are characterized by protoplasmicastrocytic proliferation (as in Alzheimer type 2 reactions)and spongiform changes in the brains of dogs withPSSs.82 Treatment involves managing the hepatic dys-function and encephalopathy. Seizures and neurologicsequelae following PSS attenuation have been well docu-mented.83–85 Neurologic complications have been associ-ated with all of the occlusion methods.86 Potential riskfactors for neurologic complications include older dogsand dogs with single extrahepatic and portoazygousshunts.86 The pathophysiologic mechanisms of postliga-tional seizures are poorly understood.87

InflammatorySeizures occur in about 13% of dogs with CNS inflam-

matory diseases.88 Cats with seizures were frequently



An immature brain is more prone to seizures than is a mature brain because of multiple changes that occur during development.

diagnosed with inflammatory disease (47% [14 of 30] ofcats) of suspected viral or immune-mediated origin.89

Canine distemper virus (CDV) encephalitis is the mostcommon infectious inflammatory cause of seizures indogs younger than 1 year of age.42 Specifically, CDVcauses acute polioencephalitis in young dogs.90 Seizuresoften are focal, which is characterized by “chewing gum”seizures, or consist of generalized motor activity.88,90 Simi-larly, seizures have been reported with postvaccinal CDVencephalitis in puppies.91 These seizures are often pro-

gressive and refractory to antiepileptic drug therapy.Identifying the underlying inflammatory disease processis important because the disease continues to progresswithout appropriate treatment.

Dogs with noninfectious inflammatory disorders withcerebral cortical involvement clinically manifest seizureactivity. Granulomatous meningoencephalomyelitis(GME) rarely affects young dogs92 and is an inflamma-tory disease of the white matter of the brain.93–95 Thedisseminated form is usually acute and rapidly progres-sive, whereas the focal form progresses more slowly.About 20% of affected dogs have seizures along withother neurologic deficits.96 Breed-specific meningoen-cephalitis occurs in pugs,97 Yorkshire terriers,98 and Mal-teses.99 Pathologic features consist of nonsuppurativenecrotizing meningoencephalitis, with a predilection forthe cerebrum in pugs and Malteses. Seizures have alsobeen reported in Yorkshire terriers, but brain-stem signsare more commonly manifested. Young dogs are predis-posed and are usually 6 months of age or older. Dogswith the chronic form more often have clinical signs ofgeneralized or focal seizures. Definitive diagnosis of thenoninfectious inflammatory meningoencephalitides isbased on a histopathologic diagnosis.95 A diagnosis canbe suspected based on patient signalment as well asfindings 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 acat.101–103 Neurotoxic substances are released from thegranules of eosinophils, causing secondary neurologicsigns. 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 withglucocorticoid therapy.

TraumaSeizures that occur after traumatic head injury can have

an early or delayed onset. Early onset of seizures occurswithin days of the injury and may pose an increased riskof seizure activity later. Controversy exists in human andveterinary medicine regarding the role of prophylactic

antiepileptic drug therapy for patients with head injuries.Current management involves waiting to begin anti-epileptic drug therapy until seizures actually occur.

Electrical shock resulting from curious behaviors inyoung animals may induce seizures and potentially life-threatening noncardiogenic pulmonary edema.104

ToxicosisThe CNS is primarily or secondarily involved with a

variety of toxic substances. Dorman105 reported thatseizures occurred in 8.2% of all cases of suspected toxi-cosis. Inquisitive behaviors, lack of discretionary eatinghabits, and physiologic alterations in drug dispositionrender pediatric patients more susceptible to toxicantexposure.106 Neonates have a more permeable blood–brain barrier than do adults, thus increasing the poten-tial for CNS exposure to toxins.107 Skin hydration ishighest in neonates, and topical exposure to lipid-solu-ble compounds (e.g., hexachlorophene, organophos-phates) places pediatric patients at higher risk ofsignificant absorption.106 Toxins induce seizures througha number of different mechanisms: increased excitation,decreased inhibition, and interference with energymetabolism.108

Asymptomatic EpilepsyIdiopathic Epilepsy

Epilepsy is characterized by recurrent seizures.49 Theterm idiopathic epilepsy, also known as primary or asymp-tomatic epilepsy, is used when there is no identifiablecause of seizures. The term inherited epilepsy is used whenthere is a genetic cause of seizures. Epilepsy suspected ofhaving an inherited basis frequently occurs in dogs



An abnormal neurologic examination between seizures lends support for a symptomatic cause.

younger than 1 year of age. Although most dogs withidiopathic epilepsy have their first seizure at 1 to 5 yearsof age, seizures have been reported in Labrador retrieversas young as 2 months of age.42,109 An inherited basis,familial transmission, or a higher incidence has been rec-ognized in many breeds. Based on pedigree analysis, agenetic basis is strongly suspected in keeshonds,110 Bel-gian Tervurens,111 Alsatian shepherds,112 Labrador andgolden retrievers,113,114 vizslas,50 and a colony of labora-tory-raised beagles.115 The mode of inheritance has beensuggested in some breeds. Hall and Wallace116 found evi-dence of a single recessive gene contributing to a predis-position of epilepsy in keeshonds. Statistics suggest thatseizures in Belgian Tervurens result from a complex pat-tern of inheritance.117,118 A polygenic multifactorial modeof inheritance is suggested in golden and Labradorretrievers.113,114 An autosomal recessive pattern of inheri-tance is suspected in vizslas with idiopathic epilepsy.50 Inhumans, genes have been identified for ion channeldefects in some epilepsies.119

DIAGNOSTIC CONSIDERATIONSThe appropriate diagnostic procedures for seizures in

young animals are variable and depend on the mostlikely differentials.44,53 Tests may be subdivided into pro-cedures that do and do not require anesthesia (Figure 3).The minimum database should include patient signal-ment, history, physical and neurologic examinations, andclinical pathology. The patient’s history plays an impor-tant 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 neurologicexaminations lend support for symptomatic causes ofseizures and more extensive diagnostic testing. Neu-roanatomic localization for seizure activity is in the fore-brain. Neurologic examination findings may revealforebrain dysfunction or evidence of a multifocal or dif-fuse disease process. A funduscopic examination mayshow active or previous signs of chorioretinitis. Clinicalpathology testing should include a complete blood count

(CBC), serum chemistry profile, and urinalysis. Abnor-mal findings may further support a metabolic or toxiccause of seizures. Screening tests in a serum biochemicalprofile should include blood urea nitrogen, alkalinephosphatase, alanine transaminase, calcium, and bloodglucose levels. Interpretation of results should also takeinto account an animal’s age because adult and immatureanimals have different serum values. Based on clinico-pathologic abnormalities, additional diagnostic testing isindicated when specific organ pathology is suspected.Liver function tests, such as pre- and postprandial bileacid concentrations and blood ammonia levels, can pro-vide evidence of hepatic dysfunction. Scintigraphy andultrasonographic studies can further aid in identifying aPSS.120 Profiles for metabolic screening of blood, urine,and CSF are useful when storage disorders or inbornerrors of metabolism are suspected.121,122

Serology and immunologic testing may indirectly lendfurther support to infectious causes.123 Overall, viralcauses are difficult to definitively diagnose with less inva-sive diagnostic testing. Results of serologic testing are alsodifficult to interpret because of the presence of circulatingantibodies from maternal immunity, vaccination, or envi-ronmental exposure. Immunofluorescent antibody stain-ing of epithelial cells from the conjunctiva has reportedlyidentified about 54% of dogs with CDV infection.90,124

Additional neurodiagnostic testing can further deter-mine the type and extent of intracranial pathology.Ultrasonography is useful in animals with an open breg-matic fontanelle or intracranial arachnoid cysts.125,126

Findings of only mild hydrocephalus should be carefullyinterpreted because this may not be the inciting cause.

Advanced imaging such as CT or MRI can aid in diag-nosing structural abnormalities related to cranial andintracranial malformations, inflammatory disorders, andneoplasms. MRI is more ideal for identifying soft tissueabnormalities. In human medicine, the efficacy of usingCT in children after the first nonfebrile seizure has beenquestioned based on lack of abnormal findings.127

Electroencephalography in animals may show charac-teristic patterns in disease, such as hydrocephalus and



It is important to identify the underlying inflammatory or metabolic disease because clinical signs continue to

progress without appropriate treatment.

ease is a more likely differential than neoplasia in youngeranimals, CSF analysis may more often provide a greaterdiagnostic yield than imaging procedures alone. CSF can becollected by puncturing the cerebellomedullary cistern.Analysis should include a nucleated cell count, protein con-centration, and cytologic evaluation within 30 minutes ofsample collection. Unfortunately, results of CSF analysistend to be nonspecific for some disease processes. Intrathe-cal antibody production can be determined to further assistin diagnosing some infectious diseases.123

encephalitis.61,128 However, an animal’s age should becarefully considered because EEG patterns in younganimals can mimic patterns associated with disease. Anelectroencephalograph can develop the pattern of anadult dog by approximately 5 months of age.129 In ourexperience, continual electroencephalography is alsouseful in monitoring persistent seizure activity and ade-quate response to therapy.

CSF analysis is particularly useful in identifying the pres-ence of inflammatory disease.88 Because inflammatory dis-



SEIZURE ACTIVITY

Signalment and history

Fundic examination

Serology

Glucoseevaluation

Electrolytemonitoring

Liver functiontesting

Metabolic screening forinborn errors of metabolism

Ultrasonography/scintigraphy

Clinical pathology(CBC, serum chemistry, urinalysis;

blood urea nitrogen, alkaline phosphatase, alaninetransaminase, calcium, and glucose levels)

EEG

Ultrasonographyof the cranium

Advanced imaging(CT, MRI)

CSF analysis

Physical and interictal neurologic examination

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

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

CONCLUSIONEarly recognition of the cause of seizures in young

dogs and cats is important for appropriate therapeuticintervention. Inappropriate therapy can delay cessationof seizures and increase patient morbidity and mortality.

Watch for an upcoming article on managingseizures in young dogs and cats.

REFERENCES1. Bunch SE: Anticonvulsant drug therapy in companion animals, in Kirk RW

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1. Which statement regarding inhibitory and exci-tatory 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 GABAA receptor results in repo-

larization of the immature neuron.e. Expression of NMDA receptors is increased in the

prenatal brain.



ARTICLE #4 CE TESTThis article qualifies for 2 contact hours of continuingeducation credit from the Auburn University College ofVeterinary Medicine. Subscribers may purchase individualCE tests or sign up for our annual CE program.Those who wish to apply this credit to fulfill state relicensurerequirements should consult their respective stateauthorities 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.

CE

2. Which of the following occurs within the ionicmicroenvironment 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 potassiumchannel conductance.

d. Glial function immaturity results in a decreasedextracellular potassium concentration.

e. An increased extracellular potassium concentrationresults in neuronal hyperpolarization.

3. An area within the brain in which myelination iscompleted last is thea. cerebrum.b. brain stem.c. olfactory region.d. hippocampus.e. pyriform lobe.

4. _________________ is the most common causeof secondary epilepsy in young dogs.a. Lissencephalyb. Hepatic encephalopathyc. Hydranencephalyd. Hypoglycemiae. Hydrocephalus

5. Which statement regarding glucose use in theimmature brain is correct?a. Receptor numbers for the glucose transport pro-

tein 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 pro-

tein are low.e. The neonatal brain has a readily available source of

ketones to prevent acute hypoglycemia.

6. Which statement regarding CDV encephalo-myelitis is correct?a. CDV encephalomyelitis is the most common inflam-

matory cause of seizures in dogs younger than 1year of age.

b. CDV causes acute leukoencephalomyelitis in youngdogs.

c. Seizure activity is characterized only by “chewinggum” seizures.

d. Seizures are often controlled well with antiepilepticdrug therapy.

e. Seizure activity has not been associated with post-vaccinal CDV encephalitis.

7. Which noninfectious inflammatory disorder isleast likely to occur in young dogs with seizureactivity? a. pug encephalitisb. Yorkshire terrier encephalitisc. Maltese encephalitisd. steroid-responsive meningoencephalomyelitise. GME

8. Which factor is likely to predispose young dogsand cats to toxin exposure?a. increased blood–brain barrier permeabilityb. increased skin hydrationc. inquisitive behaviord. alterations in drug dispositione. all of the above

9. Which statement regarding primary epilepsy iscorrect?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 greaterdiagnostic yield if an inflammatory disorder issuspected of causing seizures in young animals?a. serologyb. CBCc. CSF analysisd. funduscopic examinatione. CT or MRI

June 2005 Test answers now available at CompendiumVet.com COMPENDIUM


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Seizures in Young Dogs and Cats