Seizures In Cats Research Articles

A retrospective evaluation of phenobarbital-induced hematologic changes in 69 cats.

Phenobarbital (PB) is used as a first-line treatment for recurrent epileptic seizures in cats. While hematologic abnormalities are well-known side effects of antiepileptic therapy with PB in humans and dogs, little is known about such alterations in cats. The aim of this retrospective study was to investigate the prevalence and clinical relevance of cytopenia during PB treatment in cats. In this single-center, retrospective clinical study, 69 cats-with suspected idiopathic epilepsy admitted to the Small Animal Clinic of the University of Veterinary Medicine in Vienna (VMU)-were included. A complete blood count for each patient was performed, and changes in hematocrit, leukocytes, neutrophils, and thrombocytes were documented and graded. Fifty-three out of 69 cats (76.8%) showed cytopenias with a reduction of at least one cell fraction during PB treatment. The most frequent change was neutropenia (60%), followed by leukopenia (49.3%), thrombocytopenia (24.1%), and anemia (20.3%). Most of the changes were mild or moderate; only one patient (1.5%) showed severe leukopenia and neutropenia, and one was a life-threatening neutropenia (1.5%) with a serum PB concentration within or even below the therapeutic range. These patients did not present with clinical symptoms other than those related to epileptic episodes. Cats who received combination therapy showed lower hematocrits than those who received monotherapy. A tendency for leukocytes and neutrophils to decrease during PB treatment was also seen. Blood cytopenias may frequently occur in cats on chronic PB therapy, even when serum drug levels are within the therapeutic range. However, clinical signs are typically mild to moderate and rarely severe.

Investigation of the effect and availability of ketamine on electroencephalography in cats with temporal lobe epilepsy.

In recent years, electroencephalography (EEG) in veterinary medicine has become important not only in the diagnosis of epilepsy, but also in determining the epileptogenic focus. In cats, sedation and immobilization, usually with medetomidine or dexmedetomidine, are necessary to place the electrodes and to obtain stable scalp EEG recordings. In this study, we hypothesized that, for cats with temporal lobe epilepsy (TLE), ketamine, a sedative/anesthetic and N-methyl-D-aspartate (NMDA) antagonist that activates the limbic system and is also used to treat refractory status epilepticus in dogs, would induce sufficient sedation and immobilization for EEG, as well as induce interictal epileptiform discharges (IEDs) that are more pronounced than those induced with medetomidine. We obtained EEG recordings from TLE cats and healthy cats administered either ketamine or medetomidine alone (study 1) or ketamine after medetomidine sedation (study 2). In study 1, the frequency of IEDs showed no statistically significant difference between ketamine and medetomidine in both TLE and healthy cats. Seizures were observed in 75% (9/12) cats of the TLE group with ketamine alone. When ketamine was administered after sedation with medetomidine (study 2), 3/18 cats in the TLE group developed generalized tonic-clonic seizure and 1/18 cats showed subclinical seizure activity. However, no seizures were observed in all healthy cats in both study 1 and study 2. Slow wave activity at 2-4 Hz was observed in many individuals after ketamine administration regardless studies and groups, and quantitative analysis in study 2 showed a trend toward increased delta band activities in both groups. While there was no significant difference in the count of IEDs between medetomidine and ketamine, ketamine caused seizures in cats with TLE similar to their habitual seizure type and with a higher seizure frequency. Our results suggest that ketamine may activate epileptiform discharges during EEG recordings. However, caution should be used for cats with TLE.

Transient hyperammonaemia following epileptic seizures in cats

The aim of this study was to determine whether transient postictal hyperammonaemia exists in cats. The medical records of all feline patients that presented at a Swedish veterinary hospital between 2008 and 2018 were retrospectively reviewed to find those that had a recent or ongoing epileptic seizure. To qualify for inclusion, the medical record had to include information on at least one ammonia value taken in close proximity to, or during, an active seizure, the cat must have exceeded the normal upper limit of blood ammonia concentration on initial testing (reference interval 0-95 μmol/l), and there needed to be a follow-up ammonia value available within a maximum of 3 days. Five cats were included in the study, and they had blood ammonia concentrations on initial testing ranging from 146 to 195 µmol/l. They were all retested within a period of 2 h to 3 days of the original reading. All five cats had a spontaneous decrease in ammonia levels without any specific treatment for hyperammonaemia. Pursuant to the findings of this retrospective study, transient hyperammonaemia may be noted after epileptic seizure in cats. Consequently, a differential diagnostic list in feline patients with hyperammonaemia could, depending on the context, include non-hepatic-related pathologies, such as epileptic seizures.

Feline Epilepsy: An update

Epileptic seizures are the most common neurological disorder in the clinical setting. Their etiology is multifactorial and is mainly divided into structural, reactive and idiopathic epilepsy. Structural epilepsy can be caused by vascular events, inflammatory conditions (encephalitis), traumatic injuries, neoplasia, congenital and inherited (degenerative) disorders. Reactive epilepsy is caused by exposure in toxins or metabolic derangements. Although idiopathic epilepsy was thought to be rare in cats, it is now established as a common cause. Epileptic seizures in cats appear with various clinical presentations including generalized, focal with or without secondary generalization epileptic seizures. Diagnostic investigation is crucial in order to establish final diagnosis and to determine the therapeutic plan. Diagnostics include physical and neurological examination with detailed history (drug or toxin exposure), routine hematology (CBC, biochemistry, urinalysis), specific laboratory tests if concurrent or metabolic disease are suspected, advanced diagnostic imaging (CT/MRI) whether intracranial disease is suspected and cerebrospinal fluid (CSF) analysis. Most commonly used antiepileptic drugs (AED) in cats are phenobarbital and levetiracetam. Bromide is contraindicated in cats due to severe respiratory disease caused as an adverse life-threatening reaction. Diazepam is an emergency AED used to eliminate cluster seizures or status epilepticus but it should be avoided as a long-term medication because it has been associated with fatal hepatotoxicity. Gabapentin in another potential antiepileptic drug however its longterm efficacy has to be evaluated. Prognosis depends on the underlying etiology and treatment response. In most cats quality of life is improved and (>50% reduction of epileptic seizures) regardless of etiology. The complete remission of epileptic seizures in cats is rare and most cats should be maintained on anti-epileptic therapy.

Feline Epilepsy: An Update

Seizures are the most common neurological disorder in the clinical setting. Its etiology is multifactorial and is mainly divided into primary and secondary epilepsy. Secondary epilepsy can be caused by vascular events, inflammatory conditions (encephalitis), toxins, traumatic injuries, metabolic derangements, neoplasia, congenital and inherited (degenerative) disorders. Although primary (idiopathic) epilepsy was thought to be rare in cats, it is now established as a common cause. Seizures in cats appear with various clinical presentations including the typical generalized tonic-clonic, focal with or without secondary generalization seizures, or solely as behavioral changes. Type of seizures is not indicative of their etiology. Diagnostic investigation is crucial in order to establish final diagnosis and to determine the therapeutic plan. Diagnostics include physical and neurological examination with detailed history (drug or toxin exposure), routine hematology (CBC, biochemistry, urinalysis), specific laboratory tests if concurrent or metabolic disease are suspected, advanced diagnostic imaging (CT/MRI) whether intracranial disease is suspected and cerebrospinal fluid (CSF) analysis. Most commonly used antiepileptic drugs (AED) in cats are phenobarbital and levetiracetam. Bromide is contraindicated in cats due to severe respiratory disease caused as an adverse life-threatening reaction. Diazepam is an emergency AED used to eliminate cluster seizures or status epilepticus but it should be avoided as a long-term medication because it has been associated with fatal hepatotoxicity. Gabapentin in another potential antiepileptic drug however its long-term efficacy has to be evaluated. Prognosis depends on the underlying etiology and treatment response. In most cats quality of life is improved and (>50% reduction of seizures) regardless of etiology. The complete remission of seizures in cats is rare and most cats should be maintained on anti-epileptic therapy.

Reactive seizures in cats: A retrospective study of 64 cases

Epileptic seizures are a common indication for neurological evaluation. This retrospective study reviewed 789 cats referred for epileptic seizure evaluation to the Department of Small Animal Medicine and Surgery of the University of Veterinary Medicine in Hannover, between 1998 and 2017. The aim of this study was to determine common causes for reactive seizures (RS) in cats.Reactive seizures were diagnosed in 62 (7.9%) of 789 feline patients. The most common cause of RS was presumptive or confirmed intoxication (n=34/62; 54.8%). Toxins included permethrin (n=5/62; 8.1%), fipronil (n=1/62; 1.6%), and pesticide (n=1/62; 1.6%). Other common causes were hepatic and renal encephalopathy (n=6/62; 9.7% each), hypertension (n=5/62; 8.1%), hyperthyroidism (n=3/62; 4.8%), hypoglycaemia (n=3/62; 4.8%), and hyperglycaemia (n=1/62; 1.6%). Most commonly, cats with RS presented with generalised tonic–clonic seizures (n=25/62; 40.3%). A single status epilepticus was observed in 9.7% (n=6/62) and 4.8% (n=3/62) presented only with cluster seizures. Focal seizures were the only presenting sign in 3.2% (n=2/62) of cases, however in 4.8% (n=3/62) they were accompanied by tonic–clonic seizures. The mean age of all cats presented for RS was 10.8 years. In the intoxication group, the mean age was 2.9 years. Intoxication (confirmed or presumptive) was the most common cause of RS identified. Clinicians should suspect intoxication when other causes of RS are excluded; when there are appropriate historical findings; when the cat is frequently unobserved by the owner; when symptomatic treatment leads to cessation of epileptic seizures; and when seizures do not recur after treatment has been discontinued.

Recurrent seizures in cats: Diagnostic approach - when is it idiopathic epilepsy?

This review of recurrent seizures in cats is intended for all veterinarians who are facing the challenges of seizure diagnosis and management in the feline patient. Evidence base: Recommendations for diagnosis and management of feline seizure disorders have historically been extrapolated from the canine and human literature. The information and guidance provided in this two-part series is based on a review of the recent published literature addressing seizure disorders and antiepileptic treatment in cats, as well as the authors' clinical experience.

Recurrent seizures in cats: Treatment - which antiepileptic drugs are recommended?

This review of recurrent seizures in cats is intended for all veterinarians who are facing the challenges of seizure diagnosis and management in the feline patient. Evidence base: Recommendations for diagnosis and management of feline seizure disorders have historically been extrapolated from the canine and human literature. The information and guidance provided in this two-part series is based on a review of the recent published literature addressing seizure disorders and antiepileptic treatment in cats, as well as the authors' clinical experience.

Feline Temporal Lobe Epilepsy: Review of the Experimental Literature.

Accumulating evidence suggests that epileptic seizures originating from the temporal lobe (TL) occur in cats. Typically, affected animals have clinically focal seizures with orofacial automatisms including salivation, facial twitching, lip smacking, chewing, licking, and swallowing. Motor arrest and autonomic and behavioral signs also may occur. Many affected cats have magnetic resonance imaging (MRI) changes within the hippocampus or histopathologically confirmed hippocampal sclerosis or necrosis. From the 1950s to the 1980s, cats frequently were used as animal models for neurophysiological experiments and electrophysiological studies, from which important basic knowledge about epilepsy originated, but which has been rarely cited in clinical veterinary studies. These studies were reviewed. Experimental research on cats showed the widespread anatomical connections among TL structures. The ictal clinical signs originating from the hippocampus, amygdala, or lateral temporal cortex are similar, because of their dense interconnections. The ictal signs can be divided into autonomic, somatic, and behavioral. For research purposes, a 6‐stage system was established, reflecting the usual sequential progression from focal to generalized seizure: attention response (1), arrest (2), salivation, licking (3), facial twitching (4), head turning or nodding (5), and generalized clonic convulsions (6). Knowledge of this data may help in recognizing low‐stage (stage 1 or stage 2) epileptic seizures in clinical practice. Early experimental research data are in accordance with recent clinical observations regarding ictal clinical signs of TL epileptic seizures in cats. Furthermore, the research data supports the idea that TL epilepsy represents a unique clinical entity with a specific seizure type and origin in cats.

Magnetic resonance imaging findings in epileptic cats with a normal interictal neurological examination: 188 cases

Epilepsy is a common neurological condition in dogs and cats. Although an increased likelihood of significant brain lesions with age has been identified in neurologically normal dogs with epileptic seizures,...

Audiogenic reflex seizures in cats.

ObjectivesThis study aimed to characterise feline audiogenic reflex seizures (FARS).MethodsAn online questionnaire was developed to capture information from owners with cats suffering from FARS. This was collated with the medical records from the primary veterinarian. Ninety-six cats were included.ResultsMyoclonic seizures were one of the cardinal signs of this syndrome (90/96), frequently occurring prior to generalised tonic–clonic seizures (GTCSs) in this population. Other features include a late onset (median 15 years) and absence seizures (6/96), with most seizures triggered by high-frequency sounds amid occasional spontaneous seizures (up to 20%). Half the population (48/96) had hearing impairment or were deaf. One-third of cats (35/96) had concurrent diseases, most likely reflecting the age distribution. Birmans were strongly represented (30/96). Levetiracetam gave good seizure control. The course of the epilepsy was non-progressive in the majority (68/96), with an improvement over time in some (23/96). Only 33/96 and 11/90 owners, respectively, felt the GTCSs and myoclonic seizures affected their cat’s quality of life (QoL). Despite this, many owners (50/96) reported a slow decline in their cat’s health, becoming less responsive (43/50), not jumping (41/50), becoming uncoordinated or weak in the pelvic limbs (24/50) and exhibiting dramatic weight loss (39/50). These signs were exclusively reported in cats experiencing seizures for >2 years, with 42/50 owners stating these signs affected their cat’s QoL.Conclusions and relevanceIn gathering data on audiogenic seizures in cats, we have identified a new epilepsy syndrome named FARS with a geriatric onset. Further studies are warranted to investigate potential genetic predispositions to this condition.

Seizures and epilepsy in cats.

Seizures are a common presenting complaint in cats, although causes and options for the treatment of seizures in this species have been historically poorly described in the veterinary literature. Seizure manifestation in cats may be different than what is typically seen in dogs, but the underlying causes of seizure activity are the same. These include primary epilepsies, structural epilepsies, and reactive seizures. Although primary epilepsy was once believed to be rare in cats, we now commonly appreciate this syndrome, albeit at a lower frequency than in dogs. Because of this, a complete diagnostic work-up is recommended for all cats presenting for initial evaluation of seizures. Symptomatic treatment of seizures in cats is similar to dogs, with only a few limitations related to species-specific antiepileptic drug toxicities. The goal of this review is to summarize the recent veterinary literature related to feline seizures, with a focus on seizure classification, clinical manifestation, diagnostic evaluation, and treatment options.

Evaluation of therapeutic phenobarbital concentrations and application of a classification system for seizures in cats: 30 cases (2004–2013)

To determine the percentage of cats with a phenobarbital (PB) concentration between 15 and 45 μg/mL that had a ≥ 50% reduction in the number of seizures and to investigate applicability of the 2011 International League Against Epilepsy (ILAE) classification system in cats. Retrospective case series. 30 cats with suspected or confirmed epilepsy. Medical records for 2004 to 2013 at 3 veterinary hospitals were searched. Information collected included signalment, duration of observation before treatment, frequency of seizures before PB administration, seizure phenotype, dose of PB, serum PB concentration, number of seizures after PB administration, duration of follow-up monitoring, and survival time. A modified 2011 ILAE classification system was applied to all cats. Seizure control was achieved in 28 of 30 (93%) cats with a serum PB concentration of 15 to 45 μg/mL. This comprised 10 of 11 cats with structural epilepsy, 14 of 15 cats with unknown epilepsy, and 4 of 4 cats with presumptive unknown epilepsy. Thirteen cats had no additional seizures after initiation of PB treatment. Seizure control was achieved in most cats with a serum PB concentration between 15 and 45 μg/mL, regardless of the cause of the seizures. A modified 2011 ILAE classification was applied to cats with seizures and enabled classification of cats without specific genetic testing and without identified structural or inflammatory disease. This classification system should be incorporated into veterinary neurology nomenclature to standardize communication between veterinarians and improve comparisons among species.

Suspected Limbic Encephalitis and Seizure in Cats Associated with Voltage‐Gated Potassium Channel (VGKC) Complex Antibody

Treatment-resistant complex partial seizures (CPS) with orofacial involvement recently were reported in cats in association with hippocampal pathology. The features had some similarity to those described in humans with limbic encephalitis and voltage-gated potassium channel (VGKC) complex antibody. The purpose of this pilot study was to evaluate cats with CPS and orofacial involvement for the presence of VGKC-complex antibody. Client-owned cats with acute orofacial CPS and control cats were investigated. Prospective study. Serum was collected from 14 cats in the acute stage of the disease and compared with 19 controls. VGKC-complex antibodies were determined by routine immunoprecipitation and by binding to leucine-rich glioma inactivated 1 (LGI1) and contactin-associated protein-like 2 (CASPR2), the 2 main targets of VGKC-complex antibodies in humans. Five of the 14 affected cats, but none of the 19 controls, had VGKC-complex antibody concentrations above the cut-off concentration (>100 pmol/L) based on control samples and similar to those found in humans. Antibodies in 4 cats were directed against LGI1, and none were directed against CASPR2. Follow-up sera were available for 5 cats in remission and all antibody concentrations were within the reference range. Our study suggests that an autoimmune limbic encephalitis exists in cats and that VGKC-complex/LGI1 antibodies may play a role in this disorder, as they are thought to in humans.

Prevalence of seizures in cats after head trauma

To determine the prevalence of seizures in cats after head trauma. Retrospective cross-sectional study. 52 cats with head trauma. Information was obtained from medical records of cats with head trauma and via telephone interviews of owners at least 2 years after cats had head trauma. Severity of head trauma in cats was classified with the modified Glasgow coma scale (mGCS), and the association between scores and development of seizures was determined. 9 cats had moderate head trauma (mGCS score, 9 to 14), and 43 cats had mild head trauma (mGCS score, 15 to 18). None of the cats developed seizures during the follow-up period (≥ 2 years after head injury). The calculated 95% confidence interval for prevalence of seizures in cats after head injury was 0% to 5.6%. There was no significant relationship between severity of head trauma and the risk of seizures in cats. Results indicated the probability that cats with mild to moderate head trauma would develop posttraumatic seizures was low. However, clinicians should monitor cats with a history of head trauma for development of secondary epilepsy.

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 408days (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.

Biofeedback in the treatment of epilepsy

This review traces the application of electroencephalographic (EEG) operant conditioning, or biofeedback, from animal research to its emergence as an alternative treatment for the major types of seizure disorder. Initial animal studies focusing on brain mechanisms that mediate learned behavioral inhibition revealed a uniquely correlated 12- to 15-Hz EEG rhythm localized to sensorimotor cortex. We labeled this the sensorimotor rhythm, or SMR. The similarity of the SMR to the known EEG spindle pattern during quiet sleep led to the novel idea of attempting to increase the SMR using EEG operant conditioning. The hypothesis was that this might produce a corresponding increase in sleep spindle activity, thus establishing a common EEG marker for the state of motor inhibition. Results supported this hypothesis but led also to the accidental discovery of an anticonvulsant effect on drug-induced seizures in cats and monkeys. Continuing animal studies identified a pattern of neurophysiologic responses correlated with the SMR in primary motor pathways. These and other findings were indicative of reduced motor excitability. Simultaneously, we undertook studies in human epileptic subjects that documented a significant reduction in seizure incidence and severity, together with EEG pattern normalization. This work expanded internationally, resulting in numerous well-controlled group and single-case studies summarized in recent meta-analyses. Exciting new findings in functional neuroimaging/EEG correlation studies provide a rational model for the basis of these clinical effects. In recognition of the diversity of clinical applications of EEG biofeedback and the complexity of seizure disorders, this review also details specific methods used in our EEG biofeedback program.

EPSP depression following neocortical seizures in cat

To study the possible mechanism(s) underlying unresponsiveness following neocortical seizures, we recorded excitatory postsynaptic potentials (EPSPs) of cortical neurons evoked by ipsilateral cortical stimulation before and after spontaneous or elicited seizures. Regular-spiking neurons (n = 32) were intracellularly recorded in association area five of cats under ketamine-xylazine or barbiturate anesthesia. Compared with control responses, cortically evoked EPSPs were characterized by decreased amplitude after electrographic seizures. Synaptic responses and intrinsic properties were measured by applying extracellular electrical stimuli followed by intracellular hyperpolarizing current pulses. The input resistance decreased during seizures but quickly recovered to control level after the paroxysms, whereas the amplitude of evoked EPSPs remained lower following seizures, generally for 2-12 min, suggesting that the decreased EPSPs were not due to an alteration of intrinsic response. Data demonstrate a long-lasting decreased synaptic responsiveness following generalized spike-wave seizures slowly recovering in time.

Hyperexcitability of intact neurons underlies acute development of trauma-related electrographic seizures in cats in vivo.

Cortical trauma can lead to development of electrographic paroxysmal activities. Current views of trauma-induced epileptogenesis suggest that chronic neuronal hyperexcitability and extensive morphological reorganization of the traumatized cortex are required for the generation of electrographic seizures. However, the mechanisms responsible for the initiation of electrographic seizures shortly after cortical injury are poorly understood. Here we show that, in the experimental model of partially deafferented (undercut) cortex, an increase in intrinsic and synaptic excitability of neurons in areas adjacent to the undercut cortex is sufficient for the generation of electrographic paroxysmal activity within few hours after partial cortical deafferentation. Locally increased and spatially restricted neuronal excitability arose from the increased incidence of intrinsically bursting neurons, enhanced intrinsic and synaptic neuronal responsiveness, and slight disinhibition. These mechanisms only operate in neurons located in the vicinity of partially deafferented sites because, after the cortical injury, partially deafferented neurons are mostly silent and hypoexcitable. Our results suggest that trauma-induced electrographic seizures first arise in cortical fields that are closest to the site of injury and such seizures do not require long-term neuronal reorganization.

Neocortical very fast oscillations (ripples, 80-200 Hz) during seizures: intracellular correlates.

Multi-site field potential and intracellular recordings from various neocortical areas were used to study very fast oscillations or ripples (80-200 Hz) during electrographic seizures in cats under ketamine-xylazine anesthesia. The animals displayed spontaneously occurring and electrically induced seizures comprising spike-wave complexes (2-3 Hz) and fast runs (10-20 Hz). Neocortical ripples had much higher amplitudes during seizures than during the slow oscillation preceding the onset of seizures. A series of experimental data from the present study supports the hypothesis that ripples are implicated in seizure initiation. Ripples were particularly strong at the onset of seizures and halothane, which antagonizes the occurrence of ripples, also blocked seizures. The firing of electrophysiologically defined cellular types was phase-locked with ripples in simultaneously recorded field potentials. This indicates that ripples during paroxysmal events are associated with a coordination of firing in a majority of neocortical neurons. This was confirmed with dual intracellular recordings. Based on the amplitude that neocortical ripples reach during paroxysmal events, we propose a mechanism by which neocortical ripples during normal network activity could actively participate in the initiation of seizures on reaching a certain threshold amplitude. This mechanism involves a vicious feedback loop in which very fast oscillations in field potentials are a reflection of synchronous action potentials, and in turn these oscillations help generate and synchronize action potentials in adjacent neurons through electrical interactions.