A retrospective study of the efficacy of zonisamide in controlling seizures in 57 cats.

BACKGROUND: Evidence-based recommendations for antiepileptic drug selection in cats beyond phenobarbital are limited, and additional studies are needed for cats where seizures remain inadequately controlled by administration of phenobarbital alone or for cats that cannot safely receive phenobarbital. OBJECTIVE: To compare seizure frequency in cats before and after oral administration of zonisamide and describe adverse clinical or clinicopathologic effects in this cohort. ANIMALS: Fifty-seven cats with a history of seizures. METHODS: Multicenter, retrospective study. Median number of seizures per month and number of seizure days per month were compared before and after administration of zonisamide in all cats, a subgroup of cats with idiopathic epilepsy (IE), and a subgroup of cats receiving zonisamide as sole therapy. Clinical and clinicopathologic adverse effect data were also reported. RESULTS: A median decrease of 1 (P = .001, 95% confidence interval (CI) [-1.0, -0.5]) seizure per month, and 1 (P = .003, 95% CI [-1.5, -0.2]) seizure days per month was found across all cats after oral administration of zonisamide. The subgroup with IE showed median decreases of 1 (P = .03, 95% CI [-2.0, -0.5]) and 2 (P = .01, 95% CI [-2.5, -1.0]), respectively. The most common clinical adverse effects were sedation (17%), ataxia (11%), hyporexia (17%), and emesis (5%). One cat developed mild nonregenerative anemia, 2 cats developed mild metabolic acidosis, and 6 cats showed mild increases in ALT and ALP. CONCLUSION: Zonisamide was well tolerated and efficacious in controlling seizure activity in most cats.

Juvenile idiopathic epilepsy in Egyptian Arabian foals, a potential animal model of self-limited epilepsy in children.

BACKGROUND: Juvenile idiopathic epilepsy (JIE) is categorized as a generalized epilepsy. Epilepsy classification entails electrocortical characterization and localization of epileptic discharges (ED) using electroencephalography (EEG). HYPOTHESIS/OBJECTIVES: Characterize epilepsy in Egyptian Arabian foals with JIE using EEG. ANIMALS: Sixty-nine foals (JIE, 48; controls, 21). METHODS: Retrospective study. Inclusion criteria consisted of Egyptian Arabian foals: (1) JIE group diagnosed based on witnessed or recorded seizures, and neurological and EEG findings, and (2) control group of healthy nonepileptic age-matched foals. Clinical data were obtained in 48 foals. Electroencephalography with photic stimulation was performed under standing sedation in 37 JIE foals and 21 controls. RESULTS: Abnormalities on EEG were found in 95% of epileptic foals (35 of 37) and in 3 of 21 control asymptomatic foals with affected siblings. Focal ED were detected predominantly in the central vertex with diffusion into the centroparietal or frontocentral regions (n = 35). Generalization of ED occurred in 14 JIE foals. Epileptic discharges commonly were seen during wakefulness (n = 27/37 JIE foals) and sedated sleep (n = 35/37 JIE foals; 3/21 controls). Photic stimulation triggered focal central ED in 15 of 21 JIE foals. CONCLUSIONS AND CLINICAL IMPORTANCE: Juvenile idiopathic epilepsy has a focal onset of ED at the central vertex with spread resulting in clinical generalized tonic-clonic seizures with facial motor activity and loss of consciousness. Electroencephalography with photic stimulation contributes to accurate phenotyping of epilepsy. Foals with this benign self-limiting disorder might serve as a naturally occurring animal model for self-limited epilepsy in children.

Clinical characterization of epileptic seizures in Pomeranians with idiopathic epilepsy or epilepsy of unknown cause.

BACKGROUND: Focal epileptic motor seizures manifested by limb contraction have been recognized anecdotally in Pomeranians. OBJECTIVES: To investigate clinical features of idiopathic epilepsy (IE) and epilepsy of unknown cause (EUC) in Pomeranians as well as the ADAM23 haplotype frequency previously reported as a common risk haplotype for epilepsy in several breeds of dogs. ANIMALS: Twenty-eight Pomeranians, including 15 with IE and 13 with EUC. Nine Pomeranians with epilepsy and 8 control Pomeranians were used for ADAM23 risk haplotype analysis. METHODS: Case series study including both retrospectively and prospectively collected cases. The ADAM23 haplotype was determined by direct sequencing of PCR amplicons. Data were analyzed descriptively. RESULTS: Focal epileptic seizures (FS) were the predominant type of seizure in 22 of 28 dogs (78.6%). Among these, 12 of the IE dogs (80.0%) and 10 of the EUC dogs (76.9%) showed FS. Notably, 21 of 22 Pomeranians with FS (95.5%) showed limb contraction during ictal periods. Some dogs with FS also showed immobility, generalized tremors, difficulty walking or moving, autonomic signs, orofacial automatisms or some combination during ictal events. Ten dogs with FS and limb contraction had electroencephalography (EEG) performed, and interictal epileptiform discharges were identified in 9 dogs. The haplotype frequency of ADAM23 in cases was lower (27.8%) than that of the controls (56.3%). CONCLUSIONS AND CLINICAL IMPORTANCE: In our study, FS was the predominant type of seizure in Pomeranians, and almost all cases with FS showed limb contraction, regardless of whether having IE or EUC.

Neurosurgery in canine epilepsy.

Epilepsy surgery is functional neurosurgery applied to drug-resistant epilepsy. Although epilepsy surgery has been established and achieves fair to good outcomes in human medicine, it is still an underdeveloped area in veterinary medicine. With the spread of advanced imaging and neurosurgical modalities, intracranial surgery has become commonplace in the veterinary field, and, therefore, it is natural that expectations for epilepsy surgery increase. This review summarizes current standards of intracranial epilepsy surgery in human medicine and describes its current status and expectation in veterinary medicine. Intracranial epilepsy surgery is classified generally into resection surgery, represented by cortical resection, lobectomy, and lesionectomy, and disconnection surgery, such as corpus callosotomy and multiple subpial transection. In dogs with drug-resistant epilepsy, corpus callosotomy is available as a disconnection surgery for generalized epilepsy. However, other types of disconnection and resection surgeries for focal epilepsy are limited to experimental studies in laboratory dogs and/or anecdotal case reports of lesionectomy, such as tumor or encephalocele removal, without epileptogenic evidence. Veterinary epilepsy surgery is a new and challenging neurosurgery field; with the development of presurgical evaluations such as advanced electroencephalography and neuroimaging, it may become more readily practiced.

Focal epilepsy with fear-related behavior as primary presentation in Boerboel dogs.

BACKGROUND: Focal seizures with fear as a primary ictal manifestation, their diagnostic challenges, and impact on quality of life are well described in human medicine. Reports focusing on ictal fear-like behavior in animals are scarce. OBJECTIVE: To describe the clinical and histopathological characteristics of a novel focal epilepsy in Boerboel dogs. ANIMALS: Five client-owned Boerboel littermates presented for evaluation of sudden episodes of severe fear-related behavior. METHODS: Clinical examination, complete blood cell count, routine blood biochemistry, and urinalysis were performed in all dogs. Magnetic resonance imaging (MRI) scans of the brain were performed in 3 affected Boerboels. In addition, in 2 affected Boerboels, metabolic screening, cerebrospinal fluid (CSF) analysis, and necropsy were performed. RESULTS: Onset of signs was 3 months of age in all affected Boerboels. All Boerboels howled loudly, had an extremely fearful facial expression and trembled during seizures. All affected Boerboels also had autonomic or motor signs. Results of laboratory investigations, diagnostic imaging, and metabolic screening were generally unremarkable. Histopathology showed moderate numbers of single large vacuoles in the perikaryon of neurons throughout the brain, specifically in the deeper cerebral cortical regions. Family history, pedigree analysis, and the homogenous phenotype were suggestive of autosomal recessive inheritance. CONCLUSIONS AND CLINICAL IMPORTANCE: The observed paroxysmal fear-related behavior represents a newly recognized hereditary focal epilepsy in dogs with distinctive clinical and histopathologic features. Veterinarians should be aware that sudden episodes of unusual behavior can represent focal epilepsy.

Mining continuous intracranial EEG in focal canine epilepsy: Relating interictal bursts to seizure onsets.

OBJECTIVE: Brain regions are localized for resection during epilepsy surgery based on rare seizures observed during a short period of intracranial electroencephalography (iEEG) monitoring. Interictal epileptiform bursts, which are more prevalent than seizures, may provide complementary information to aid in epilepsy evaluation. In this study, we leverage a long-term iEEG dataset from canines with naturally occurring epilepsy to investigate interictal bursts and their electrographic relationship to seizures. METHODS: Four dogs were included in this study, each monitored previously with continuous iEEG for periods of 475.7, 329.9, 45.8, and 451.8 days, respectively, for a total of >11,000 h. Seizures and bursts were detected and validated by two board-certified epileptologists. A published Bayesian model was applied to analyze the dynamics of interictal epileptic bursts on EEG and compare them to seizures. RESULTS: In three dogs, bursts were stereotyped and found to be statistically similar to periods before or near seizure onsets. Seizures from one dog during status epilepticus were markedly different from other seizures in terms of burst similarity. SIGNIFICANCE: Shorter epileptic bursts explored in this work have the potential to yield significant information about the distribution of epileptic events. In our data, bursts are at least an order of magnitude more prevalent than seizures and occur much more regularly. Our finding that bursts often display pronounced similarity to seizure onsets suggests that they contain relevant information about the epileptic networks from which they arise and may aide in the clinical evaluation of epilepsy in patients.

Risk factors for survival in a university hospital population of dogs with epilepsy.

BACKGROUND: Although a common neurological disorder in dogs, long-term outcome of epilepsy is sparsely documented. OBJECTIVES: To investigate risk factors for survival and duration of survival in a population of dogs with idiopathic epilepsy or epilepsy associated with a known intracranial cause. ANIMALS: One hundred and two client owned dogs; 78 dogs with idiopathic epilepsy and 24 dogs with epilepsy associated with a known intracranial cause. METHODS: A retrospective hospital based study with follow-up. Dogs diagnosed with epilepsy between 2002 and 2008 were enrolled in the study. Owners were interviewed by telephone using a structured questionnaire addressing epilepsy status, treatment, death/alive, and cause of death. RESULTS: Median life span was 7.6 years, 9.2 years, and 5.8 years for all dogs, and dogs with idiopathic epilepsy or dogs with epilepsy associated with a known intracranial cause (P < .001), respectively. Survival time for dogs with idiopathic epilepsy was significantly (P = .0030) decreased for dogs euthanized because of epilepsy (median: 35 months) compared to dogs euthanized for other reasons (median: 67.5 months). Neutered male dogs with idiopathic epilepsy had a significant (P = .031) shorter survival (median: 38.5 months) after index seizure compared to intact male dogs (median: 71 months). Treatment with two antiepileptic drugs (AED's) did not negatively influence survival (P = .056). CONCLUSION AND CLINICAL IMPORTANCE: Dogs with idiopathic epilepsy can in many cases expect a life span close to what is reported for dogs in general. In dogs where mono-therapy is not sufficient, the need for treatment with two AED's is not linked to a poor prognosis.

Cerebral glucose utilization measured with high resolution positron emission tomography in epileptic Finnish Spitz dogs and healthy dogs.

In human epileptic patients, changes in cerebral glucose utilization can be detected 2-deoxy-2-[(18) F] fluoro-D-glucose positron emission tomography (FDG-PET). The purpose of this prospective study was to determine whether epileptic dogs might show similar findings. Eleven Finnish Spitz dogs with focal idiopathic epilepsy and six healthy dogs were included. Dogs were examined using electroencephalography (EEG) and FDG-PET, with epileptic dogs being evaluated during the interictal period. Visual and semi-quantitative assessment methods of FDG-PET were compared and contrasted with EEG findings. Three independent observers, unaware of dog clinical status, detected FDG-PET uptake abnormalities in 9/11 epileptic (82%), and 4/8 healthy dogs (50%). Occipital cortex findings were significantly associated with epileptic status (P = 0.013). Epileptic dogs had significantly lower standardized uptake values (SUVs) in numerous cortical regions, the cerebellum, and the hippocampus compared to the control dogs. The lowest SUVs were found in the occipital lobe. White matter normalized and left-right asymmetry index values for all pairs of homologous regions did not differ between groups. Visual evaluation of the EEGs was less sensitive (36%) than FDG-PET. Both diagnostic tests were consensual and specific (100%) for occipital findings, but EEG had a lower sensitivity for detecting lateralized foci than FDG-PET. Findings supported the use of FDG-PET as a diagnostic test for dogs with suspected idiopathic epilepsy. Visual and semiquantitative analyses of FDG-PET scans provided complementary information. Findings also supported the theory that epileptogenesis may occur in multiple brain regions in Finnish Spitz dogs with idiopathic epilepsy.

A longitudinal study of survival in Belgian Shepherds with genetic epilepsy.

BACKGROUND: Belgian Shepherds have focal genetic epilepsy. The prevalence of epilepsy has been estimated as 9.5% in the breed and as 33% in the family investigated. Dogs with epilepsy might have an increased risk of premature death. OBJECTIVE/HYPOTHESIS: To investigate survival and selected risk factors for premature death in a Belgian Shepherd family with genetic epilepsy. ANIMALS: One hundred ninety-nine related Belgian Shepherds. METHODS: Longitudinal observational study, 2009-2011. Follow-up telephone interviews were all conducted using a structured questionnaire addressing epilepsy, including seizure history and phenomenology, possible remission, possible death, and cause of death. RESULTS: The life span of epileptic dogs was not significantly shortened by the presence of epilepsy (P = .87). Epilepsy was the predominant cause of death in the population (19/75 = 25%) and epilepsy-related deaths accounted for 70% (19/27) of all deaths in the group of dogs with epilepsy. Two probable sudden unexpected deaths related to epilepsy occurred in dogs with generalized seizures. Cluster seizures occurred in 33% (17/51) but did not significantly influence the life span of epileptic dogs. Dogs with epilepsy had an epilepsy remission proportion of 13.7%. CONCLUSION AND CLINICAL IMPORTANCE: The Belgian Shepherds investigated in the present study display a focal genetic epilepsy with an overall benign course. The life span was not significantly affected by the presence of epilepsy.

Canine epilepsy genetics.

There has been much interest in utilizing the dog as a genetic model for common human diseases. Both dogs and humans suffer from naturally occurring epilepsies that share many clinical characteristics. Investigations of inherited human epilepsies have led to the discovery of several mutated genes involved in this disease; however, the vast majority of human epilepsies remain unexplained. Mouse models of epilepsy exist, including single-gene spontaneous and knockout models, but, similar to humans, other, polygenic models have been more difficult to discern. This appears to also be the case in canine epilepsy genetics. There are two forms of canine epilepsies for which gene mutations have been described to date: the progressive myoclonic epilepsies (PMEs) and idiopathic epilepsy (IE). Gene discovery in the PMEs has been more successful, with eight known genes; six of these are orthologous to corresponding human disorders, while two are novel genes that can now be used as candidates for human studies. Only one IE gene has been described in dogs, an LGI2 mutation in Lagotto Romagnolos with a focal, juvenile remitting epilepsy. This gene is also a novel candidate for human remitting childhood epilepsy studies. The majority of studies of dog breeds with IE, however, have either failed to identify any genes or loci of interest, or, as in complex mouse and human IEs, have identified multiple QTLs. There is still tremendous promise in the ongoing canine epilepsy studies, but if canine IEs prove to be as genetically complex as human and murine IEs, then deciphering the bases of these canine epilepsies will continue to be challenging.

Complex partial cluster seizures in cats with orofacial involvement.

Seventeen cats were presented with acute onset of complex partial seizures with orofacial involvement (salivation, facial twitching, lip smacking, chewing, licking or swallowing), motor arrest (motionless starring) and behavioural changes. In 11 cats hippocampal necrosis (HN) was confirmed by histopathology. In a further six cats hippocampal changes were suggested by magnetic resonance imaging. The mean monitoring time of eight cats which were not euthanased in the acute phase of the disease, was 408 days (60-908): four cats are still alive. In all surviving cases, the owners reported a good quality of life. We conclude that an acute cluster of complex partial seizures with orofacial involvement are often associated with HN and that HN is not necessarily a fatal condition. Supportive and antiepileptic therapy can result in remission. The long-term outcome can be good to excellent; therefore, euthanasia should be avoided in the acute phase of the signs.

Focal epilepsy in the Belgian shepherd: evidence for simple Mendelian inheritance.

OBJECTIVES: To establish the mode of inheritance and describe the clinical features of epilepsy in the Belgian shepherd, taking the outset in an extended Danish dog family (199 individuals) of Groenendael and Tervueren with accumulated epilepsy. METHODS: Epilepsy positive individuals (living and deceased) were ascertained through a telephone interview using a standardised questionnaire regarding seizure history and phenomenology. Living dogs were invited to a detailed clinical evaluation. Litters more than five years of age, or where epilepsy was present in all offspring before the age of five, were included in the calculations of inheritance. results: Out of 199 family members, 66 dogs suffered from epilepsy. The prevalence of epilepsy in the family was 33%. Fifty-five dogs experienced focal seizures with or without secondary generalisation, while four dogs experienced primary generalised seizures. In seven dogs, seizures could not be classified. The mode of inheritance of epilepsy was simple Mendelian. CLINICAL SIGNIFICANCE: This study identified that the Belgian shepherd suffers from genetically transmitted focal epilepsy. The seizure phenomenology expressed by family members have a strong resemblance to what has been reported for familial partial (focal) epilepsy in humans with variable foci with suggestion of linkage to chromosome 2 and chromosome 22q12.

Levetiracetam as an adjunct to phenobarbital treatment in cats with suspected idiopathic epilepsy.

OBJECTIVE: To assess pharmacokinetics, efficacy, and tolerability of oral levetiracetam administered as an adjunct to phenobarbital treatment in cats with poorly controlled suspected idiopathic epilepsy. DESIGN-Open-label, noncomparative clinical trial. ANIMALS: 12 cats suspected to have idiopathic epilepsy that was poorly controlled with phenobarbital or that had unacceptable adverse effects when treated with phenobarbital. PROCEDURES: Cats were treated with levetiracetam (20 mg/kg [9.1 mg/lb], PO, q 8 h). After a minimum of 1 week of treatment, serum levetiracetam concentrations were measured before and 2, 4, and 6 hours after drug administration, and maximum and minimum serum concentrations and elimination half-life were calculated. Seizure frequencies before and after initiation of levetiracetam treatment were compared, and adverse effects were recorded. RESULTS: Median maximum serum levetiracetam concentration was 25.5 microg/mL, median minimum serum levetiracetam concentration was 8.3 microg/mL, and median elimination half-life was 2.9 hours. Median seizure frequency prior to treatment with levetiracetam (2.1 seizures/mo) was significantly higher than median seizure frequency after initiation of levetiracetam treatment (0.42 seizures/mo), and 7 of 10 cats were classified as having responded to levetiracetam treatment (ie, reduction in seizure frequency of >or=50%). Two cats had transient lethargy and inappetence. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that levetiracetam is well tolerated in cats and may be useful as an adjunct to phenobarbital treatment in cats with idiopathic epilepsy.

Intracranial neoplasia in 61 cats: localisation, tumour types and seizure patterns.

The purpose of this study was to analyse retrospectively a feline population with intracranial neoplastic diseases, to document seizure patterns in these animals and to determine whether partial seizures were more frequently associated with structural brain lesions then generalised seizures. In addition, a comparison was made within the population with intracranial neoplasia between two groups of cats: one with and one without seizures. Special emphasis was given to the evaluation of tumour type, localisation and size of the lesion and its correlation with seizure prevalence. Sixty-one cats with histopathological diagnosis of intracranial tumour were identified. Fourteen cats (23%; group A) had a history of seizure(s). Forty-seven cats (77%; group B) had no history of seizure(s). Generalised tonic-clonic seizures were seen in eight cats (57%) and were the most common seizure pattern in our cats with intracranial neoplasia. Clusters of seizures were observed in six cats. Status epilepticus was observed in one patient. The mean age of the cats was 7.9 years within group A (median 8.5) and 9.3 years (median 10) within group B. The cats with lymphoma within both groups were significantly younger than cats with meningioma. In both groups meningioma and lymphoma were confirmed to be the most frequent tumour type, followed by glial cell tumours. The prevalence of the seizures in patients with glial cell tumours was 26.7%, 26.3% in patients with lymphomas and 15% in cases with meningiomas. In 33 cases (54.1%) the tumours were localised in the forebrain, 15 tumours (24.6%) were in the brainstem, four (6.6%) in the cerebellum and nine tumours (14.7%) had multifocal localisation. Parietal lobe and basal ganglia mostly affected group A. In group B tumours were most frequently located in the parietal and frontal lobes as well as in the diencephalon. A positive association was documented between the localisation of a tumour in the forebrain and seizure occurrence.

Magnetic resonance imaging findings in Finnish Spitz dogs with focal epilepsy.

Eleven Finnish Spitz dogs with focal seizures and 3 healthy controls were evaluated. General clinical and neurological examinations, blood examination, urinalysis, cerebrospinal fluid examination, electroencephalography (EEG), and magnetic resonance imaging (MRI) of the brain were performed on all dogs. On EEG examination, focal epileptic activity was found in 7 of 11 dogs (64%), and generalized epileptic activity was observed in 4 of 11 dogs (36%). MRI (performed with 1.5 T equipment) detected changes in 1 epileptic dog. Mild contrast enhancement after gadolinium injection was identified in this dog's right parietal cortex. However, no such changes were observed in repeated magnetic resonance images. Special emphasis was given to seizure history to determine any correlations between seizure intervals and MRI findings. Our results indicate that Finnish Spitz dogs with focal seizures suffer from focal idiopathic epilepsy and have nondetectable findings on MRI or pathology. MRI showed poor sensitivity in detecting epileptogenic areas in our patients with focal seizures. Reversible MRI changes in 1 dog could have been caused by seizures.

Necrosis of hippocampus and piriform lobe: clinical and neuropathological findings in two Italian cats.

The present paper reports the clinical and neuropathological findings in two cats with a neuropathologically confirmed diagnosis of necrosis of the hippocampus and piriform lobe. The cats were presented because of acute onset of behavioural changes and complex partial seizures. The neurological examination suggested a forebrain lesion. The results of blood examination were within the normal range, and the cerebrospinal fluid (CSF) analysis and computed tomography (CT) scan in one cat did not show any abnormality. Despite therapy with diazepam (Valium; Roche) there was deterioration of the clinical signs and the cats were euthanased. The neuropathological examination revealed hippocampal necrosis that included the piriform lobe.

Characteristics and phenomenology of epileptic partial seizures in dogs: similarities with human seizure semiology.

Dogs with spontaneous occurring epilepsy with partial seizures express symptomatology resembling what is found in humans with partial epileptic seizures. Questionnaires on clinical signs from 70 dogs, with a confirmed diagnosis of epilepsy with partial seizures with or without secondary generalization, were reviewed in order to characterize and classify clinical signs of partial seizure activity in dogs and compare them to partial seizure phenomenology in humans. Signs of partial seizure activity were distributed into three categories: motor signs, autonomic signs and paroxysms of behavioral signs. Motor signs were described in 48 dogs (69%), autonomic signs in 16 dogs (23%) and paroxysms of behavioral signs in 56 dogs (80%). The majority of dogs expressed signs from more than one group. Sixty-one dogs (87%) had partial seizures with secondary generalization. Nine dogs (13%) had partial seizures without secondary generalization. The study shows a remarkable resemblance between the seizure phenomenology expressed in humans and canines with partial epileptic seizures.

Behavioral changes associated with suspected complex partial seizures in bull terriers.

OBJECTIVES: To identify and treat a range of abnormal behavior, including tail chasing, unprovoked aggression, and extreme irrational fear, in Bull Terriers and to correlate the behavioral signs with electroencephalogram (EEG) or anatomic evidence of abnormal brain geometry or deafness. DESIGN: Prospective clinical study. ANIMALS: 8 affected and 5 unaffected (control) Bull Terriers. PROCEDURE: All dogs were examined neurologically, including use of EEG, brainstem auditory-evoked response, and computed tomography or postmortem examination of the brain. In addition, plasma concentrations of zinc, copper, and iron, and the activity of zinc- and copper-dependent enzymes (alkaline phosphatase and ceruplasmin oxidase) were measured in affected and control dogs. RESULTS: An abnormal EEG was found in 7 of 7 affected dogs and in none of the control dogs subjected to this examination. Seven of 8 affected dogs and 2 of 3 controls had various degrees of hydrocephalus. Metal ion and enzyme concentrations were not different between affected and control dogs. Treatment with phenobarbital was effective in 5 of 7 dogs. CLINICAL IMPLICATIONS: Bull Terriers with compulsive tail chasing and extreme affective disorders should be regarded as neurologically disturbed, with partial seizures perhaps underlying their behavior. Treatment with anti-convulsants is a logical first step in treatment.

Diagnosis of partial epilepsy in a goat.

A seizure disorder of 4.5 years' duration in a 6-year-old female Nubian goat was diagnosed as partial epilepsy on the basis of history, focal electroencephalogram (EEG) abnormalities, convulsive response to ketamine, and necropsy findings. The goat appeared to maintain consciousness during her seizures. A 1.5-day period of continuous seizures during a pregnancy at age 1.5 years may have resulted in a postanoxic seizure focus responsible for the seizures. A morphologic cause for the seizures was not detected. Two spontaneous seizures and 2 drug-induced seizures were detected during 1 month of observation after donation. The amplitude of the EEG over the left frontocentral cortex was depressed, and periodic bursts of high-frequency interictal spiking were detected over the same site. Acepromazine, intermittent photic stimulation, or ketamine after acepromazine failed to elicit seizures or EEG abnormalities, but ketamine alone (50 mg, IV) twice elicited seizures. Seizure severity appeared to parallel plasma estrogen concentration.