Reactive Seizures Research Articles

Evaluation of Blood C Reactive Protein (CRP) and Neutrophil-to-Lymphocyte Ratio (NLR) Utility in Canine Epilepsy.

The role of neuroinflammation in epileptogenesis has been previously explored, and several biomarkers have been identified as being relevant in assessing the intensity of the inflammatory process. In human medicine, an increased C reactive protein (CRP) blood concentration and/or neutrophil-to-lymphocyte ratio (NLR) is considered a constant finding of epileptic activity. In veterinary medicine, only a few studies have been published regarding both of these topics. Our aim was to assess the C reactive protein blood concentration and the neutrophil-to-lymphocyte ratio in epileptic dogs, regardless of etiology. This retrospective study was based on changes in routine blood parameters in 59 dogs with epileptic activity. An increased C reactive protein concentration was observed mostly in the dogs affected by structural epilepsy, and all epileptic dogs displayed abnormal neutrophil-to-lymphocyte values. Based on the authors' knowledge, this is the first report regarding the NLR in epileptic dogs. Both the CRP concentration and the NLR might be considered feasible non-specific markers of the neuroinflamation involved in epileptogenesis and might be used in the diagnosis of and therapeutic approach to cluster seizures in dogs with idiopathic epilepsy and in patients with structural epilepsy. Dogs diagnosed with IEis and high CRP concentrations and NLRs may be subject to non-documented cluster seizures. Both CRP and the NLR have limited diagnostic value in dogs with reactive seizures.

Phenotype of Idiopathic Epilepsy in Great Swiss Mountain Dogs in Germany-A Retrospective Study.

Genetic predisposition of idiopathic epilepsy (IE) has been demonstrated in individual breeds. According to the responsible breeding association in Germany, the average incidence of registered Great Swiss Mountain Dogs (GSMDs) with seizures between the years 1999 and 2019 is 2.56%, a genetic predisposition in this breed is suspected. To describe the seizure phenotype and to examine seizure causes, a retrospective, questionnaire-based study was performed. In cooperation with the Swiss Mountain Dog Association of Germany e.V. (SSV e.V.), 114 questionnaires filled in by owners of GSMD displaying seizures and filled in by their respective veterinarians between the years 2005–2021 were evaluated. Seizure characteristics, clinical and further examinations, treatment, treatment responses, and pedigree information were collected. In this study, 94 (83.06%) dogs had IE (suspected genetic epilepsy) confirmed with confidence level TIER 1, 2, or 3. The remaining 20 dogs showed the signs of structural epilepsy, reactive seizures, or epilepsy of unknown cause and were therefore excluded from further analysis. The average age at seizure onset was 28.83 months. Male GSMDs were significantly more often affected by IE than females. The most common seizure type was focal evolving into generalized seizures (64.5%). Seizures often began with vomiting, retching, or salivation. Cluster seizures (CS) (48.9%) and status epilepticus (SE) (37.2%) were observed in a large proportion of dogs. During the observation time, a total of 49 animals (52.13%) died. Out of those, 19 dogs (20.21%) were euthanized in SE or during CS and 14 dogs (14.9%) died spontaneously during CS or SE. The median age at death was 4 years, and the median survival time for the time, when the dog was suffering from seizures, was found to be 18 months. Both occurrence of CS (p = 0.0076) and occurrence of SE (p = 0.0859) had an impact on survival time. In GSMD, idiopathic epilepsy presents with a severe phenotype with frequently occurring CS and SE. This study could serve as basis for further genetic evaluations as well as to provide individual treatment recommendations.

Response to Levetiracetam Treatment and Long-Term Follow-Up in Dogs With Reactive Seizures Due to Probable Exogenous Toxicity

Limited information is available on the long-term follow-up and seizure recurrence in dogs with reactive seizures due to suspected exogenous toxicity. The purpose of this study was to report the long-term follow-up of 13 dogs referred to a single referral hospital, diagnosed with reactive seizures and treated with a standardized levetiracetam protocol. All dogs received a loading levetiracetam dose of 60 mg/kg/IV once, followed by a maintenance dose of 20 mg/kg every 8 h as part of an open-label clinical study. Levetiracetam was withdrawn after a 6-months seizure-free period by reducing levetiracetam to 20 mg/kg every 12 h for a 4-week seizure-free period, followed by levetiracetam 20 mg/kg every 24 h for a 4-week seizure-free period, before levetiracetam treatment was stopped. No adverse effects of the treatment were reported. No dogs experienced any seizures after discharge or after levetiracetam withdrawal. Median follow-up time from time of discharge was of 78 months (=6 years 6 months). The result of this study supports the use of levetiracetam for treatment of reactive seizures due to exogenous substance intoxication. Moreover, our results do not support the need for long-term antiepileptic treatment in cases of reactive seizures due to exogenous intoxication.

SEIZURES IN DOGS AND CATS

When dogs or cats get seizures, epileptic seizures and epilepsy are usually thought of. However, it is important to take into account the existence of seizures that are similar to epileptic seizures but do not belong to epileptic seizures (non-epileptic seizures). Nonepileptic seizures occur suddenly, are short-term, disappear as quickly as they occur, recur and have no epileptic etiology and can be of non-neurological and neurological origin. Unlike non-epileptic seizures, epileptic seizures have a specific neural origin and represent excessive, synchronous, usually self-limiting epileptic activity of brain neurons. Epileptic seizures should be distinguished from reactive seizures because reactive seizures occur as a natural response of a healthy brain to transient disorders (metabolic or toxic in nature) and they disappear after the cause ceases to act. Absolute confirmation that it is an epileptic seizure can be difficult because it requires both visualization of the seizure and registration of changes on the EEG. In practice, the suspicion that epileptic seizures occurs is based on information from the medical history and videos. In making a differential diagnosis when an seizure occurs, it is necessary to take into account the age of infected animals, the presence of clinical signs other than the seizure, the presence or absence of disease progression, video recording, blood counts and blood biochemical parameters results, CST test results, and X-ray, MRI or CT findings. The first step in a diagnosis is to determine whether the lesion that leads to the onset of the seizure is localized extracranially or intracranially. If the lesion is localized extracranially, it should be determined whether the problem originates outside the body (poisoning with xylitol, organophosphates, chocolate) or from the body (hypothyroidism, hypocalcemia, kidney disease, etc.). If the process is localized intracranially, it should be determined whether the process is progressive (tumor, inflammation, hydrocephalus, etc.) or not.

Reactive seizures in 40 dogs: A clinical study

Seizures are the most common neurological disorders in dogs. Based on the etiology the epileptic dogs were classified as idiopathic epilepsy, reactive seizures and structural epilepsy. In this study 40/179 dogs were diagnosed with reactive seizures. They were grouped in to different age and sex. The different etiologies of reactive seizures in this study were hepatic encephalopathy, cardiomyopathy, uremic encephalopathy, infectious, hypothyroidism, hypocalcemia, verminous, hypoglycaemia, tetanus and anemia. This categorisation will guide the clinician to treat for the primary cause and plan the antiepileptic treatment accordingly.

Reactive Seizures Due to Hyperlipidemia in a Maltese Dog

Background: Primary hyperlipidemia is a condition that affects some specific breeds. It has been previously described in Miniature Shnauzer, Beagles, Shetland Shepdog and West Highland White Terrier. There are no reports of primary hyperlipidemia in Maltese dogs. It is a hereditary disorder of lipoprotein metabolism. The etiology is unknown and may be related to a genetic problem in lipoprotein lipase or to the absence of apaprotein CII. Clinical signs include spontaneous arterosclerosis, retinal lipemia, cutaneous xanthomas, abdominal pain, lethargy, vomiting and / or diarrhea. Neurological manifestations such as seizures and behavioral changes may also occur. The aim of this report is to describe a case of reactive seizures due to hyperlipidemia in a dog.Case: A 5-year-old male Maltese dog was admitted with a history of seizures. Hypertension and abdominal distension with large amounts of intestinal gases were found in general physical examination. Neurological examination revealed impaired nasal septum sensory perception, which was slightly bilaterally reduced, and pain on cervical palpation and in the brachial plexus region. Based on history and clinical examination, it was possible to locate the lesion in the thalamocortical region and to suspect idiopathic epilepsy, reactive seizures, and symptomatic epilepsy due to meningoencephalitis of unknown origin. The diagnosis of primary hyperlipidemia was made by exclusion with the aid of laboratory tests and ultrasound. After the establishment of a fat restriction diet, bezafibrate, phenobarbital, and omega-3 supplementation, the animal improved significantly with the reduction of epileptic seizures.Discussion: The initial clinical suspicion was hyperadrenocorticism as the primary cause of hyperlipidemia. This suspicion was based on the presence of polyphagia, polydipsia, polyuria and abdominal distension, together with laboratory results of thrombocytosis, increased ALT and AF, and hyposenuria; but ultrasound images and ACTH stimulation test ruled out this differential diagnosis. Hypothyroidism was also ruled out since LDL values were normal and the animal was extremely active. Regarding nephrotic syndrome, it was also excluded for some alterations would be present, such as severe proteinuria, cholesterol reduction and hypoalbuminemia. As for diabetes mellitus, it was discarded because of the dog’s young age and due to the absence of suggestive clinical signs. The suspicion of primary hyperlipidemia was based on increased levels of triglycerides, and the presumptive diagnosis was of reactive seizures due to hyperlipidemia. It is essential, when treating hyperlipidemia, to readjust to a low-calorie diet with fat concentration below 8% and protein level above 18%. Generally, these restricted diets are for life. Omega-3 supplementation can be performed to help maintain low levels of triglycerides. Drug therapy is usually carried out with bezafibrate, which is used in human medicine as treatment for hypertriglyceridemia, and has showed good results in the control of hypertriglyceridemia and hypercholesterolemia in dogs with primary and secondary hyperlipidemia. Six months after the beginning of the treatment, the animal no longer presented abdominal distension and pain, cholesterol values and its fractions were controlled, as well as triglycerides. Seizures were also under control. Therefore, hyperlipidemia is an important differential diagnosis in cases of patients presenting seizures, especially when dealing with young animals showing signs of metabolic diseases.

Continuous rate infusion of midazolam as emergent treatment for seizures in dogs.

BackgroundMidazolam delivered by continuous rate infusion (CRI) might be effective in dogs with cluster seizures (CS) or status epilepticus (SE).ObjectiveTo describe the use and safety of midazolam CRI in dogs with CS or SE.AnimalsOne‐hundred six client‐owned dogs presenting to a veterinary teaching hospital with CS or SE.MethodsRetrospective review of medical records for dogs with CS or SE treated with a midazolam CRI.ResultsSeventy‐nine dogs presented with CS and 27 dogs had SE. Seizure control was achieved in 82/106 dogs (77.4%) receiving a midazolam CRI. The median dose associated with seizure control was 0.3 mg/kg/h (range, 0.1‐2.5 mg/kg/h). The median duration of CRI was 25 hours (range, 2‐96 hours). Seizures were controlled in 34/40 dogs (85%) with idiopathic epilepsy, 32/43 dogs (74%) with structural epilepsy, 12/16 dogs (75%) with unknown epilepsy, and 4/7 dogs (57%) with reactive seizures (P = .20). Seizure control was achieved in 81% of dogs with CS and 67% in dogs with SE (P = .18). Dogs with idiopathic/unknown epilepsy were more likely to survive than those with structural epilepsy (87% vs 63%, P = .009). Adverse effects were reported in 24 dogs (22.6%) and were mild in all cases.Conclusions and Clinical ImportanceMidazolam CRI is apparently safe and might be an effective treatment in dogs with CS or SE.

Seizures in dogs under primary veterinary care in the United Kingdom: Etiology, diagnostic testing, and clinical management.

BackgroundAlthough seizures are common in dogs, limited published information is available on the classifications of seizures, diagnostic approaches, or clinical management of seizure‐affected patients in the veterinary primary care setting.ObjectivesExplore seizure etiology, diagnostic testing, and clinical management of seizure‐affected dogs in the primary care veterinary setting.AnimalsA total of 455 553 dogs in VetCompass.MethodsCross‐sectional analysis by cohort clinical data.ResultsFrom 2834 incident seizure cases, we identified 579 (20.5%) dogs with epilepsy based on the International Veterinary Epilepsy Task Force (IVETF) classification system, including 484 (17.1%) with idiopathic epilepsy, 95 (3.4%) with structural epilepsy, and 179 dogs (6.3%) with reactive seizures. In their clinical first opinion records, 245 (8.6%) cases were recorded with epilepsy. Overall, 1415 (49.9%) cases received diagnostic evaluation equivalent to or higher than IVETF Tier 1 diagnostic testing.Being <12 years of age and being insured were risk factors for receiving IVETF Tier 1 or higher diagnostic evaluation among seizure cases. Anti‐seizure drug (ASD) treatment was not prescribed for 1960/2834 (69.2%) dogs in association with the incident seizure event. Of the remainder, 719 (25.3%) dogs received 1 ASD, whereas 155 (5.5%) an ASD combination.Conclusion and clinical importanceThe differences between seizure classifications in the clinical records and those retrospectively assigned by the researchers support the need for clearer diagnostic guidelines in clinical practice. Insured dogs and dogs <12 years of age were more likely to receive advanced diagnostic evaluation, suggesting that financial and perceived prognostic factors influence case management.

Small Animal Review

Introduction: Cats showing seizure activity at under 12 months of age are more likely to have primary (structural) epilepsy than idiopathic epilepsy or reactive seizures. Advanced diagnostic imaging is recommended for cats with juvenile-onset seizures once metabolic and toxic causes have been excluded.

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.

Seizure etiologic classification and long-term outcome for cats with juvenile-onset seizures.

OBJECTIVE To identify seizure etiologic classification for cats that developed seizures at < 12 months of age and describe the long-term outcome of affected cats. DESIGN Retrospective cohort study. ANIMALS 15 client-owned cats with seizures that began at < 12 months of age. PROCEDURES Information on each cat was obtained from the medical records, veterinarians, and owners. Inclusion required an onset of seizures before 12 months of age and a complete medical record, including a final diagnosis. RESULTS 7 of the 15 cats had structural epilepsy, 4 had idiopathic epilepsy, and 4 had reactive seizures. Median age at seizure onset was 27 weeks (range, 0.4 to 41 weeks). Cluster seizures were reported in 6 cats, and status epilepticus was reported in 2. Age at the onset of seizures, presence of cluster seizures, and seizure semiology (ie, generalized vs focal seizures) were not significantly associated with seizure etiologic classification. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that cats that developed seizures at < 12 months of age were more likely to have structural epilepsy than idiopathic epilepsy or reactive seizures. Therefore, advanced diagnostic imaging is recommended in cats with juvenile-onset seizures if metabolic and toxic causes are excluded.

Clinical Risk Factors for Early Seizure Recurrence in Dogs Hospitalized for Seizure Evaluation.

BackgroundEpileptic seizures are a common cause for neurological evaluations in dogs.Hypothesis/ObjectivesTo determine the timing, frequency, and risk factors for early seizure recurrence (ESR) among dogs admitted to the hospital for seizure evaluation and to facilitate rapid decision making about whether dogs should be placed in the intensive care unit (ICU) or day ward.AnimalsNine‐hundred twenty‐two dogs referred for seizure investigation; 214 patients were included.MethodsRetrospective study. Medical records between 2000 and 2017 were reviewed to determine risk factors for ESR. Findings were compared among dogs diagnosed with idiopathic epilepsy (IE), structural epilepsy (StE) and reactive seizures (RS), as well as in all selected cases together.ResultsFifty percent of dogs had a seizure while hospitalized. In the group 53.1 and 52.2% in the StE group, whereas in the RS 40.44% had ESR. The average time to ESR was 7 hours. In IE group, abnormal postictal neurological examination with prosencephalon signs predicted ESR. In StE group, a single generalized or focal seizure 72 hours before hospital admission and abnormal neurologic examination predicted ESR. In the RS group, ERS was predicted by long‐term antiepileptic monotheraphy. When all dogs were analyzed together, abnormal neurological examination, the occurrence of cluster seizures, status epilepticus, or combination of them 72 hours before presentation predicted ESR.Conclusions and Clinical ImportanceEpileptic seizures recurred in 50% of patients within a mean time of 7 hours. In general, when cluster seizures, status epilepticus or both occurred 72 hours before presentation and neurological examination was abnormal upon presentation, the dog should be placed in ICU for observation.

Update on Cysticercosis Epileptogenesis: the Role of the Hippocampus.

Neurocysticercosis (NCC) is the most common helminthic infection of the nervous system and a frequent cause of reactive seizures and epilepsy worldwide. In many cases, multiple episodes of focal seizures related to an identifiable parenchymal brain cyst (and likely attributable to local damage) continue for years after the cyst resolves. However, cases where seizure semiology, interictal EEG abnormalities, and parasites location do not correlate raise concerns about the causal relationship between NCC and either reactive seizures or epilepsy, as well as the epileptogenic potential of parasites. Neurosurgical series of patients with intractable epilepsy and cross-sectional population-based studies have shown a robust association between NCC and hippocampal sclerosis (HS), which might contribute to the above-referred inconsistencies. Current information does not allow to define whether in patients with NCC, HS could result from recurrent seizure activity from a local or distant focus or from chronic recurrent inflammation. In either case, HS may become the pathological substrate of subsequent mesial temporal lobe epilepsy (MTLE). Longitudinal clinical- and population-based cohort studies are needed to evaluate the causal relationship between NCC and HS and to characterize this association with the occurrence of MTLE. If a cause-and-effect relationship between NCC and HS is demonstrated, NCC patients could be assessed to examine neuronal mechanisms of hippocampal epileptogenesis in comparison with animal models, to identify biomarkers of hippocampal epileptogenesis, and to develop novel interventions to prevent epilepsy in NCC and perhaps in other forms of acquired epilepsy.

International veterinary epilepsy task force consensus proposal: diagnostic approach to epilepsy in dogs.

This article outlines the consensus proposal on diagnosis of epilepsy in dogs by the International Veterinary Epilepsy Task Force. The aim of this consensus proposal is to improve consistency in the diagnosis of epilepsy in the clinical and research settings. The diagnostic approach to the patient presenting with a history of suspected epileptic seizures incorporates two fundamental steps: to establish if the events the animal is demonstrating truly represent epileptic seizures and if so, to identify their underlying cause. Differentiation of epileptic seizures from other non-epileptic episodic paroxysmal events can be challenging. Criteria that can be used to make this differentiation are presented in detail and discussed. Criteria for the diagnosis of idiopathic epilepsy (IE) are described in a three-tier system. Tier I confidence level for the diagnosis of IE is based on a history of two or more unprovoked epileptic seizures occurring at least 24 h apart, age at epileptic seizure onset of between six months and six years, unremarkable inter-ictal physical and neurological examination, and no significant abnormalities on minimum data base blood tests and urinalysis. Tier II confidence level for the diagnosis of IE is based on the factors listed in tier I and unremarkable fasting and post-prandial bile acids, magnetic resonance imaging (MRI) of the brain (based on an epilepsy-specific brain MRI protocol) and cerebrospinal fluid (CSF) analysis. Tier III confidence level for the diagnosis of IE is based on the factors listed in tier I and II and identification of electroencephalographic abnormalities characteristic for seizure disorders. The authors recommend performing MRI of the brain and routine CSF analysis, after exclusion of reactive seizures, in dogs with age at epileptic seizure onset <6 months or >6 years, inter-ictal neurological abnormalities consistent with intracranial neurolocalisation, status epilepticus or cluster seizure at epileptic seizure onset, or a previous presumptive diagnosis of IE and drug-resistance with a single antiepileptic drug titrated to the highest tolerable dose.This consensus article represents the basis for a more standardised diagnostic approach to the seizure patient. These recommendations will evolve over time with advances in neuroimaging, electroencephalography, and molecular genetics of canine epilepsy.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-015-0462-1) contains supplementary material, which is available to authorized users.

Seizure Disorders in 43 Cattle

BackgroundLarge animals have a relatively high seizure threshold, and in most cases seizures are acquired. No published case series have described this syndrome in cattle.ObjectivesTo describe clinical findings and outcomes in cattle referred to the Veterinary Teaching Hospital of the University of Turin (Italy) because of seizures.AnimalsClient‐owned cattle with documented evidence of seizures.MethodsMedical records of cattle with episodes of seizures reported between January 2002 and February 2014 were reviewed. Evidence of seizures was identified based on the evaluation of seizure episodes by the referring veterinarian or 1 of the authors. Animals were recruited if physical and neurologic examinations were performed and if diagnostic laboratory test results were available.ResultsForty‐three of 49 cases fulfilled the inclusion criteria. The mean age was 8 months. Thirty‐one animals were male and 12 were female. Piedmontese breed accounted for 39/43 (91%) animals. Seizures were etiologically classified as reactive in 30 patients (70%) and secondary or structural in 13 (30%). Thirty‐six animals survived, 2 died naturally, and 5 were euthanized for reasons of animal welfare. The definitive cause of reactive seizures was diagnosed as hypomagnesemia (n = 2), hypocalcemia (n = 12), and hypomagnesemia‐hypocalcemia (n = 16). The cause of structural seizures was diagnosed as cerebrocortical necrosis (n = 8), inflammatory diseases (n = 4), and lead (Pb) intoxication (n = 1).Conclusion and Clinical ImportanceThe study results indicate that seizures largely are reported in beef cattle and that the cause can be identified and successfully treated in most cases.

Hippocampal sclerosis: the missing link of cysticercosis epileptogenesis?

A closed workshop was held in Atahualpa, Ecuador, with support from Universidad Espiritu Santo—Ecuador. Aims of the workshop were to gain more insights on the suggested association between neurocysticercosis (NCC), epilepsy, and hippocampal sclerosis (HS), and to design a study that will help to better characterize this association, namely, is there a causal relationship between NCC and HS, and, if so, is this association linked to chronic unprovoked seizures? Investigators have long been concerned with the lack of correlation between location of parenchymal brain cysticerci, seizure semiology, and electroencephalography (EEG) findings in a sizable proportion of patients with epilepsy and NCC. In addition, many patients with parenchymal brain cysts or calcifications have never had seizures. This led some authors to suggest that both epilepsy and NCC might merely occur by chance in areas where this parasitic disease is endemic. Although this is theoretically possible, there is some evidence suggesting a causal relationship between NCC and seizures, including the higher prevalence of epilepsy in cysticercotic-endemic areas when compared with nonendemic regions and the occurrence of inflammatory changes surrounding calcified cysticerci immediately after a seizure in about 50% cases.1 Information from surgical series of patients with medically refractory epilepsy and NCC suggest that chronic seizures often come from an associated ipsilateral HS and not from the calcified parasite. In many of such patients, seizure freedom was achieved by resection of the affected hippocampus alone,2, 3 although some authors have reported that resection of both the hippocampus and the calcified cysticercus was associated with a better outcome.4 In the presence of HS, however, it is unclear whether resection of the cyst alone is sufficient to eliminate seizures. It is plausible that recurrent reactive seizures (or status epilepticus) from repeated inflammation of the parasite induce HS, which then becomes responsible for the chronic epileptic disorder. Cysticerci are not necessarily located within limbic circuits, requiring a remote deleterious effect of reactive seizures on hippocampal neurons.5 Alternatively, calcified cysticerci could lead to inflammation-mediated hippocampal damage without causing seizures.6 In this case, periodic exposure of trapped parasitic antigens to the host's immune system might account for recurrent inflammatory events that trigger HS. Experimental evidence showing that repeated endotoxin exposure correlate with hippocampal damage, support this hypothesis.7 Figure 1 is a diagram depicting the complex circuit of events associating NCC, seizures, and HS. The panel agreed that a population-based cohort study would be the best way to confirm a causal relationship between NCC and HS, and to characterize this association with the occurrence of chronic epilepsy. For this, adults residing in cysticercotic-endemic villages should undergo neuroimaging studies to identify those with a single calcified parenchymal brain cysticercus (case patients). The selection of individuals with a single lesion would provide a better model for assessing the role of either the cysticercus or the HS in epileptogenesis. Case patients and similar numbers of age- and sex-matched individuals with no evidence of NCC (controls) have to be evaluated with repeated neuroimaging at the end of the study (5 years) to assess the numbers of persons who develop HS in the follow-up. In addition, epilepsy prevalence at enrollment and incidence during the follow-up must be assessed in all participants (irrespective of their case/control status), as well as characterization of clinical and neurophysiologic patterns, initially and at completion of the study. If isolated calcifications can cause HS and mesial temporal lobe epilepsy, it will be of great value to elucidate the epileptogenic mechanisms involved. This could not only lead to novel treatments to prevent epilepsy in people with NCC, but promote the development of antiepileptogenic interventions in other forms of acquired epilepsy. This study was partially supported by University Espiritu Santo—Ecuador, Guayaquil, Ecuador. H.H. Garcia is supported by a Wellcome Trust International Senior Fellowship in Public Health and Tropical Medicine. None of the authors has any conflict of interest to disclose. We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.

Effects of traumatic brain injury on reactive astrogliosis and seizures in mouse models of Alexander disease

Alexander disease (AxD) is the only known human pathology caused by mutations in an astrocyte-specific gene, glial fibrillary acidic protein (GFAP). These mutations result in abnormal GFAP accumulations that promote seizures, motor delays and, ultimately, death. The exact contribution of increased, abnormal levels of astrocytic mutant GFAP in the development and progression of the epileptic phenotype is not clear, and we addressed this question using two mouse models of AxD. Comparison of brain seizure activity spontaneously and after traumatic brain injury (TBI), an effective way to trigger seizures, revealed that abnormal GFAP accumulation contributes to anomalous brain activity (increased non-convulsive hyperactivity) but is not a risk factor for the development of epilepsy after TBI. These data highlight the need to further explore the complex and heterogeneous response of astrocytes towards injury and the involvement of GFAP in the progression of AxD.

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.

Investigating epilepsy in dogs

WHEN a dog is presented with recurrent seizures, investigation proceeds to find an underlying cause. Symptomatic epilepsy occurs secondarily to a structural disorder of the central nervous system (CNS), eg,...

Aetiology and long-term outcome of juvenile epilepsy in 136 dogs

The aetiology and outcome of dogs with juvenile-onset seizures were investigated. One hundred and thirty-six dogs whose first seizure occurred before the age of one year were investigated. One hundred...