Subsequent Epilepsy Research Articles

Seroprevalence of Taenia solium infections in Croatian patients presenting with epilepsy

Epilepsy is one of the most common neurological disorders, while neurocysticercosis caused by Taenia solium infection of the central nervous system currently represents the leading cause of secondary epilepsy in Central and South America, East and South Asia, and sub-Saharan Africa. As a result of increased migration from these endemic regions, neurocysticercosis and subsequent epilepsy are becoming a growing public health problem in developed countries as well. In order to determine the prevalence of T. solium infection in patients with epilepsy in Croatia, a retrospective serological study was conducted. A total of 770 serum samples were tested for the presence of T. solium IgG antibodies using a commercial qualitative enzyme immunoassay. The Western blot technique was used as a confirmatory test for the diagnosis. The overall seroprevalence rate of T. solium infection in patients with clinically proven epilepsy was 1.5%. Although the results have shown that infection with this tapeworm is rare in Croatia, this study hopes to increase awareness about the importance of preventive measures and benefits of accurate and timely diagnosis. Intervention measures for infection control are crucial, namely sanitation improvement, control of domestic pig-breeding, detailed meat inspection, detection and treatment of tapeworm carriers, hand washing and health education.

Infectious causes of seizures and epilepsy in the developing world

Central nervous system (CNS) infections are the main cause of seizures and acquired epilepsy in the developing world. Geographical variations determine the common causes in a particular region. Acute seizures are common in severe meningitis, viral encephalitis, malaria, and neurocysticercosis, and in most cases are associated with increased mortality and morbidity, including subsequent epilepsy. Neuronal excitability secondary to proinflammatory signals induced by CNS infections are an important common mechanism for the generation of seizures, in addition to various other specific mechanisms. Newer insights into the neurobiology of these infections and the associated epilepsy could help in developing neuroprotective interventions. Management issues include prompt treatment of acute seizures and the underlying CNS infection, correction of associated predisposing factors, and decisions regarding the appropriate choice and duration of antiepileptic therapy. Strategies for the prevention of epilepsy in CNS infections such as early anti-infective and anti-inflammatory therapy need scientific exploration. Prevention of CNS infections is the only definitive way forward to reduce the burden of epilepsy in developing countries.

Transient focal cortical increase of interictal glucose metabolism in Sturge-Weber syndrome: Implications for epileptogenesis

To investigate clinical correlates and longitudinal course of interictal focal cortical glucose hypermetabolism in children with Sturge-Weber syndrome (SWS). Fluorodeoxyglucose positron emission tomography (FDG-PET) scans of 60 children (age range 3 months to 15.2 years) with Sturge-Weber syndrome and epilepsy were assessed prospectively and serially for focal hypo- or hypermetabolism. Thirty-two patients had two or more consecutive PET scans. Age, seizure variables, and the occurrence of epilepsy surgery were compared between patients with and without focal hypermetabolism. The severity of focal hypermetabolism was also assessed and correlated with seizure variables. Interictal cortical glucose hypermetabolism, ipsilateral to the angioma, was seen in nine patients, with the most common location in the frontal lobe. Age was lower in patients with hypermetabolism than in those without (p=0.022). In addition, time difference between the onset of first seizure and the first PET scan was much shorter in children with increased glucose metabolism than in those without (mean: 1.0 vs. 3.6 years; p=0.019). Increased metabolism was transient and switched to hypometabolism in all five children where follow-up scans were available. Focal glucose hypermetabolism occurred in 28% of children younger than the age of 2 years. Children with transient hypermetabolism had a higher rate of subsequent epilepsy surgery as compared to those without hypermetabolism (p=0.039). Interictal glucose hypermetabolism in young children with SWS is most often seen within a short time before or after the onset of first clinical seizures, that is, the presumed period of epileptogenesis. Increased glucose metabolism detected by PET predicts future demise of the affected cortex based on a progressive loss of metabolism and may be an imaging marker of the most malignant cases of intractable epilepsy requiring surgery in SWS.

Status epilepticus-induced pathologic plasticity in a rat model of focal cortical dysplasia

We have generated an experimental 'double-hit' model of chronic epilepsy to recapitulate the co-existence of abnormal cortical structure and frequently recurrent seizures as observed in human focal cortical dysplasia. We induced cortical malformations by exposing rats prenatally to methylazoxymethanol acetate and triggered status epilepticus and recurrent seizures in adult methylazoxymethanol acetate rats with pilocarpine. We studied the course of epilepsy and the long-term morphologic and molecular changes induced by the occurrence of status epilepticus and subsequent chronic epilepsy in the malformed methylazoxymethanol acetate exposed brain. Behavioural and electroencephalographic analyses showed that methylazoxymethanol acetate pilocarpine rats develop more severe epilepsy than naïve rats. Morphologic and molecular analyses demonstrated that status epilepticus and subsequent seizures, but not pilocarpine treatment per se, was capable of affecting both cortical architectural and N-methyl-D-aspartate receptor abnormalities induced by methylazoxymethanol acetate. In particular, cortical thickness was further decreased and N-methyl-D-aspartate regulatory subunits were recruited at the postsynaptic membrane. In addition, methylazoxymethanol acetate pilocarpine rats showed abnormally large cortical pyramidal neurons with neurofilament over-expression. These neurons bear similarities to the hypertrophic/dysmorphic pyramidal neurons observed in acquired human focal cortical dysplasia. These data show that status epilepticus sets in motion a pathological process capable of significantly changing the cellular and molecular features of pre-existing experimental cortical malformations. They suggest that seizure recurrence in human focal cortical dysplasia might be an additional factor in establishing a pathological circuitry that favours chronic neuronal hyperexcitability.

Refractory Focal Epilepsy in a Patient with Methylmalonic Aciduria: Case Report on Positive and Long-lasting Effect of Rufinamide

We report on a 5-year-old boy with methylmalonic aciduria, an autosomal recessive inborn error of metabolism leading to accumulation of methylmalonic-CoA and thereby causing intoxication with leading symptoms of hyperammonaemia and metabolic acidosis. Hyperammonemia itself causes brain oedema. In our patient, this led to a vast metabolic stroke of the left hemisphere and subsequent pharmacoresistant epilepsy. Guided by his main seizures--drop attacks--the orphan drug rufinamide (RUF) was introduced as "off-label use" and led to freedom of drop attacks and tonic-clonic seizures over a period of 14 months as well as normalisation of the electroencephalogramm. Only once during an episode of fever and diarrhoea with reduced level of RUF did some provoked seizures with focal complex semiology for the time period of infection occur. In the 16 months follow-up, the patient also improved in his development, showing a more stable gait with the hemiparesis and understanding more complex sentences.

Corpus callosum agenesis, severe mental retardation, epilepsy, and dyskinetic quadriparesis due to a novel mutation in the homeodomain of ARX

We report on a patient with agenesis of the corpus callosum (ACC), severe mental retardation, infantile spasms and subsequent intractable epilepsy, spastic/dyskinetic quadriparesis, severe limb contractures, and scoliosis. This complex, newly described phenotype, is due to a novel non-conservative missense mutation in the ARX homeodomain (c.1072A>T; p.R358W), inherited from the unaffected mother. Differently from previously reported non-conservative mutations falling within the same domain, p.R358W did not cause XLAG. It is therefore possible that differences in clinical manifestations between our patient and those with XLAG, are related to the different position of the amino acid substitution in the homeodomain, or to the different chemical properties introduced by the substitution itself. To test the hypothesis that the patient's mother was asymptomatic because of non-random X chromosome inactivation (XCI), we performed DNA methylation studies of the human androgen receptor gene, demonstrating skewing of the XCI ratio (85:15). The complex phenotype described here combines different traits that had previously been linked to various ARX mutations, including conservative missense mutations in the homeodomain and expansion in the first ARX polyalanine tract and contributes to the expanding pleiotropy associated with ARX mutations.

Long-term consequences of a prolonged febrile seizure in a dual pathology model

Clinical evidence suggests that febrile status epilepticus (SE) in children can lead to acute hippocampal injury and subsequent temporal lobe epilepsy. The contribution of febrile SE to the mechanisms underlying temporal lobe epilepsy are however poorly understood. A rat model of temporal lobe epilepsy following hyperthermic SE was previously established in our laboratory, wherein a focal cortical lesion induced at postnatal day 1 (P1), followed by a hyperthermic SE (more than 30 min) at P10, leads to hippocampal atrophy at P22 (dual pathology model) and spontaneous recurrent seizures (SRS) with mild visuospatial memory deficits in adult rats. The goal of this study was to identify the long term electrophysiological, anatomical and molecular changes in this model. Following hyperthermic SE, all cortically lesioned pups developed progressive SRS as adults, characterized by the onset of highly rhythmic activity in the hippocampus. A reduction of hippocampal volume on the side of the lesion preceded the SRS and was associated with a loss of hippocampal neurons, a marked decrease in pyramidal cell spine density, an increase in the hippocampal levels of NMDA receptor NR2A subunit, but no significant change in GABA receptors. These findings suggest that febrile SE in the abnormal brain leads to hippocampal injury that is followed by progressive network reorganization and molecular changes that contribute to the epileptogenesis as well as the observed memory deficits.

238 Long-Term Outcome of Acute Encephalitis in Childhood

Background and aims: Short-term follow-up after childhood encephalitis shows persisting symptoms in 30-60%. The aim of this study was to investigate the long-term outcome of childhood encephalitis and to find prognostic factors. Methods: Out of 93 children treated for acute encephalitis between 2000-2004, 71 were eligible for follow-up. A structured interview, using two questionnaires, was conducted with the parents. Fifteen of the children with the most severe symptoms at the time of discharge also underwent an EEG-recording and tests of reaction time and working memory. Results: Persisting symptoms were reported by 54%. The predominant symptoms were personality changes and cognitive problems. Children who made a complete recovery did so within 6-12 months. The only significant risk factor for sequelae was severity of the disease leading to admission to the ICU. The risk for subsequent epilepsy was increased for children with seizures at presentation. Most follow-up EEGs showed improvement, but in 9/15 it had not normalized. Children with encephalitis had slower reaction time compared to controls but no difference in working memory could be seen. Conclusion: Persisting symptoms after childhood encephalitis are present in a substantial number of children. Seizures increased the risk for subsequent epilepsy; the only other prognostic marker was admission to the ICU. Even children who were considered fully recovered at discharge reported persisting symptoms at follow-up and children who made a full recovery did so within 6-12 months. We suggest that all children with encephalitis should be followed for one year after the acute illness.

Long-term Outcomes of Acute Encephalitis in Childhood

The aims of this study were to investigate the long-term outcomes of childhood encephalitis and to examine possible prognostic factors. Of 93 children who were treated for acute encephalitis in 2000-2004, 71 were eligible for follow-up evaluations. A structured interview, using 2 questionnaires, was conducted with the parents. Fifteen of the children with the most-severe symptoms at the time of discharge also underwent electroencephalographic recording and tests of reaction times and working memory. Persisting symptoms were reported by 54% of children. The predominant symptoms were personality changes and cognitive problems. Children who made a complete recovery did so within 6 to 12 months. The only significant risk factor for sequelae was disease severity leading to admission to the ICU. The risk of subsequent epilepsy was increased for children with seizures at presentation. Most follow-up electroencephalograms showed improvement, but results had not normalized for 9 of 15 children. Children with encephalitis had slower reaction times, compared with control subjects, but no difference in working memory could be seen. Persisting symptoms after childhood encephalitis were present for a substantial number of children. Seizures increased the risk of subsequent epilepsy; the only other prognostic marker was admission to the ICU. Even children who were considered fully recovered at discharge reported persisting symptoms at follow-up evaluations. Children who made a full recovery did so within 6 to 12 months, which suggests that all children with encephalitis should be monitored for 1 year after the acute illness.

Epileptogenesis provoked by prolonged experimental febrile seizures: mechanisms and biomarkers.

Whether long febrile seizures (FSs) can cause epilepsy in the absence of genetic or acquired predisposing factors is unclear. Having established causality between long FSs and limbic epilepsy in an animal model, we studied here if the duration of the inciting FSs influenced the probability of developing subsequent epilepsy and the severity of the spontaneous seizures. We evaluated if interictal epileptifom activity and/or elevation of hippocampal T2 signal on magnetic resonance image (MRI) provided predictive biomarkers for epileptogenesis, and if the inflammatory mediator interleukin-1beta (IL-1beta), an intrinsic element of FS generation, contributed also to subsequent epileptogenesis. We found that febrile status epilepticus, lasting an average of 64 min, increased the severity and duration of subsequent spontaneous seizures compared with FSs averaging 24 min. Interictal activity in rats sustaining febrile status epilepticus was also significantly longer and more robust, and correlated with the presence of hippocampal T2 changes in individual rats. Neither T2 changes nor interictal activity predicted epileptogenesis. Hippocampal levels of IL-1beta were significantly higher for >24 h after prolonged FSs. Chronically, IL-1beta levels were elevated only in rats developing spontaneous limbic seizures after febrile status epilepticus, consistent with a role for this inflammatory mediator in epileptogenesis. Establishing seizure duration as an important determinant in epileptogenesis and defining the predictive roles of interictal activity, MRI, and inflammatory processes are of paramount importance to the clinical understanding of the outcome of FSs, the most common neurological insult in infants and children.

Acute symptomatic seizures—Should we retain the term?

Acute symptomatic seizures—Should we retain the term?

EEG spike activity precedes epilepsy after kainate-induced status epilepticus.

Chronic epilepsy frequently develops after brain injury, but prediction of which individual patient will develop spontaneous recurrent seizures (i.e., epilepsy) is not currently possible. Here, we use continuous radiotelemetric electroencephalography (EEG) and video monitoring along with automated computer detection of EEG spikes and seizures to test the hypothesis that EEG spikes precede and are correlated with subsequent spontaneous recurrent seizures. The presence and pattern of EEG spikes was studied during long recording epochs between the end of status epilepticus (SE) induced by three different doses of kainate and the onset of chronic epilepsy. The presence of spikes, and later spike clusters, over several days after SE before the first spontaneous seizure, was consistently associated with the development of chronic epilepsy. The rate of development of epilepsy (i.e., increase in seizure frequency) was strongly correlated with the frequency of EEG spikes and the cumulative number of EEG spikes after SE. The temporal features of EEG spikes (i.e., their presence, frequency, and pattern [clusters]) when analyzed over prolonged periods, may be a predictive biomarker for the development of chronic epilepsy after brain injury. Future clinical trials using prolonged EEG recordings may reveal the diagnostic utility of EEG spikes as predictors of subsequent epilepsy in brain-injured humans.

Assessment of Febrile Seizures in Children by the use of MEG

Event Abstract Back to Event Assessment of Febrile Seizures in Children by the use of MEG Athanasia Kotini1*, Aggelos Tsalkidis2, Photios Anninos1 and Athanasios Chatzimichael2 1 Democritus University of Thrace, Alex/polis, Lab of Medical Physics, Medical School, Greece 2 Democritus University of Thrace, Alex/polis, Dept of Pediatrics,Medical School, Greece Objective: Children with febrile seizures have a six-fold excess (3%) of subsequent afebrile seizures and epilepsy than controls. The risk is 2% after a simple and 5-10% after a complex febrile seizure. Afebrile seizures usually start within 4 years. It is well known that EEG is an unhelpful diagnostic procedure and we use it only when we want to distinguish “febrile convulsions” from convulsions with fever [1]. Methods: Our study population included 15 children (8 boys, 7 girls) within the age range of 2 - 7 years. The MEG data were recorded with a 122-channel biomagnetometer. All studies performed precisely 10 days after fever subsided for the purpose of comparison. Equivalent current dipoles (ECDs) were calculated for epileptic spikes on MEG recordings according to the single dipole model. Results: Eight out of 15 children showed ECD dipoles that located at the left - temporal, right - temporal, occipital and frontal lobe, as active regions responsible for febrile seizures. Conclusions: We assumed that one of the prognostic indicators for possible epileptic behavior in children who experienced febrile seizures is the existence of ECDs. Of course, further study in a larger number of patients is needed, before firm conclusions to be drawn.

Are psychiatric disorders independent risk factors for new-onset epilepsy in older individuals?

This retrospective study examined whether psychiatric conditions are directly related to epilepsy or, rather, are associated with underlying central nervous system (CNS) disorders linked to subsequent epilepsy. We examined data from a sample of older veterans (>65 years) receiving care from the Veterans Health Administration during fiscal year 2000. We compared individuals with new-onset epilepsy and individuals without epilepsy to examine the extent to which psychiatric disorders were associated with new-onset epilepsy; this analysis controlled for demographic and premorbid neurological risk factors previously associated with new-onset epilepsy. Premorbid psychiatric conditions occurred at higher rates in the epilepsy versus nonepilepsy groups, foremost including depression (17% vs 12%), anxiety (12% vs 8%), psychosis (12% vs 5%), and substance abuse (8% vs 4%). However, in the final model, only psychosis (OR = 1.4, CI 1.2–1.6) was significantly associated with epilepsy when controlling for neurological disorders and psychiatric conditions (e.g., stroke, dementia, brain tumor, head injury).

Progressive neurocognitive decline in two children with Dravet syndrome, de novo SCN1A truncations and different epileptic phenotypes

Dravet syndrome, often caused by mutations of SCN1A-gene, presents with prolonged clonic, generalized or unilateral seizures often occurring with fever during the first year of life, followed by usually severe epilepsy. The EEG, normal at the outset, later shows generalized and focal epileptic activities. The psychomotor development deteriorates, but little is known about the time course of the cognitive impairment and its relationship with seizures severity. We describe here the progressive neurocognitive decline in two children (one male), carrying de novo SCN1A truncating mutations and presenting with different epileptic phenotypes. The children were longitudinally assessed from the ages of 11 and 23 months until the age of 7 and 8 years, using the same scales to measure the developmental competence in various domains. Both had seizures during the first year of life, unilateral clonic in one and myoclonic in the other, but the subsequent epilepsy severity and the characteristics of the EEG diverged. One child had drug-resistant but rare generalized seizures and isolated EEG spike-wave paroxysms, while the other developed extremely frequent clusters of polymorphic seizures and generalized plus multifocal EEG epileptic activities. MRI was normal in both. A clear developmental delay begun before the age of 2 years in both children and the cognitive profile continued to worse, with some differences between different domains, irrespectively to the different course of their epileptic histories. Our observations are consistent with the hypothesis that SCN1A-mutations can be responsible not only for epilepsy, but also for early and progressive severe mental impairment.

Refractory epilepsy in tuberous sclerosis: Vagus nerve stimulation with or without subsequent resective surgery

Objective The goal of the work described here was to assess the efficacy and safety of vagus nerve stimulation in a cohort of patients with tuberous sclerosis complex with refractory epilepsy. Furthermore, we examined the impact of vagus nerve stimulation failure on the ultimate outcome following subsequent intracranial epilepsy surgery. Methods A retrospective review was performed on 19 patients with refractory epilepsy and TSC who underwent vagus nerve stimulator (VNS) implantation. There were 11 (58%) females and 8 (42%) males aged 2 to 44 years when the VNS was implanted (mean: 14.7 ± 12 years). Twelve patients underwent primary VNS implantation after having failed a mean of 7.1 antiepileptic drugs. Two patients (17%) had generalized epilepsy, one had a single seizure focus, three (25%) had multifocal epilepsy, and six (50%) had multifocal and generalized epilepsy. Seven patients were referred for device removal and evaluation for intracranial procedures. One patient in the primary implantation group was lost to follow-up and excluded from outcome analysis. Results All implantations and removals were performed without permanent complications. The duration of treatment for primary VNS implants varied from 8.5 months to 9.6 years (mean: 4.9 years). Mean seizure frequency significantly improved following VNS implantation (mean reduction: 72%, P < 0.002). Two patients had Engel Class I (18%), one had Class II (9%), seven had Class III (64%), and one had Class IV (9%) outcome. Three patients with poor response to vagus nerve stimulation therapy at our center underwent resection of one or more seizure foci (Engel Class I, two patients; Engel Class III, one patient). Seven patients referred to our center for VNS removal and craniotomy underwent seizure focus resection (6) or corpus callosotomy (1) (Engel Class II: 2, Engel III: 2; Engel IV: 3). In total, 8 of 10 (80%) patients experienced improved seizure control following intracranial surgery (mean reduction: 65%, range: 0–100%, P < 0.05). Conclusions VNS is a safe and effective treatment option for medically refractory epilepsy in patients with tuberous sclerosis complex. Nine of 11 patients (82%) experienced at least a 67% reduction in seizure burden. Lack of response to vagus nerve stimulation does not preclude subsequent improvement in seizure burden with intracranial epilepsy surgery.

The use of radiosurgery for the treatment of mesial temporal lobe epilepsy and long‐term results

To determine the efficacy of gamma knife radiosurgery in the treatment of mesial temporal lobe epilepsy due to mesial temporal sclerosis. Between November 1995 and May 1999, 14 patients underwent radiosurgical entorhinoamygdalohippocampectomy with a marginal dose of 18, 20, or 25 Gy to the 50% isodose following a standard preoperative epilepsy evaluation. One patient was classified as Engel Class Ib, three were Engel Class IIc, one was Engel Class IIIa, and two were Engel Class IVb in a subgroup of seven patients who were unoperated 2 years prior to the last visit and at least 8 years after irradiation (average 116 months). The insufficient effect of irradiation led us to perform epilepsy surgery on another seven patients an average of 63.5 months after radiosurgery. The average follow-up period was 43.5 months after the operation. Four patients are seizure-free; one is Engel Class IIb and one is Engel Class IId. One patient cannot be classified due to the short period of follow-up. The frequency of seizures tended to rise after irradiation in some patients. Collateral edema was observed in nine patients, which started earlier and was more frequent in those irradiated with higher doses. It had a marked expansive character in three cases and clinical signs of intracranial hypertension were present in three cases. We found partial upper lateral quadrant anopia as a permanent side effect in two patients. Repeated psychotic episodes (two patients) and status epilepticus (two patients) were also seen after treatment. No significant memory changes occurred in the group as a whole. Radiosurgery with 25, 20, or 18-Gy marginal dose levels did not lead to seizure control in our patient series, although subsequent epilepsy surgery could stop seizures. Higher doses were associated with the risk of brain edema, intracranial hypertension, and a temporary increase in seizure frequency.

PHENOMENOLOGY OF PROLONGED FEBRILE SEIZURES: RESULTS OF THE FEBSTAT STUDY

Background: Febrile status epilepticus (FSE) has been associated with hippocampal injury and subsequent mesial temporal sclerosis and temporal lobe epilepsy. However, little is known about the semiology of FSE. Methods: A prospective, multicenter study of the consequences of FSE included children, aged 1 month through 5 years, presenting with a febrile seizure lasting 30 minutes or more. Procedures included neurologic history and examination and an MRI and EEG within 72 hours. All information related to seizure semiology was reviewed by three epileptologists blinded to MRI and EEG results and to subsequent outcome. Inter-rater reliability was assessed by the κ statistic. Results: Among 119 children, the median age was 1.3 years, the mean peak temperature was 103.2°F, and seizures lasted a median of 68.0 minutes. Seizure duration followed a Weibull distribution with a shape parameter of 1.68. Seizures were continuous in 52% and behaviorally intermittent (without recovery in between) in 48%; most were partial (67%) and almost all (99%) were convulsive. In one third of cases, FSE was unrecognized in the emergency department. Of the 119 children, 86% had normal development, 24% had prior febrile seizures, and family history of febrile seizures in a first-degree relative was present in 25%. Conclusions: Febrile status epilepticus is usually focal and often not well recognized. It occurs in very young children and is usually the first febrile seizure. Seizures are typically very prolonged and the distribution of seizure durations suggests that the longer a seizure continues, the less likely it is to spontaneously stop. GLOSSARY: ED = emergency department; FS = febrile seizures; FSE = febrile status epilepticus; HHV = human herpesvirus; ILAE = International League Against Epilepsy; IQR = interquartile range; MTLE = mesial temporal lobe epilepsy; MTS = mesial temporal sclerosis.

Febrile seizures

Febrile seizures (FS) are the most common seizure disorder in childhood, affecting 2-5% of children between the ages of 3 and 60 months. Differentiation of FS from acute symptomatic seizures secondary to central nervous system infection is essential. Those with a focal onset, prolonged duration or which occur more than once within the same febrile illness are considered complex and have an increase in risk of subsequent epilepsy development. The vast majority of febrile convulsions are simple, lasting only a few minutes and without need of drug intervention. They have an excellent outcome with no increased risk of decline in IQ, subsequent epilepsy or increased mortality. Febrile seizure can recur, and as it often is a frightening and anxiety-provoking event for parents and caregivers, an understanding of the natural history and prognosis should enable the physician to reassure the parents providing an appropriate counselling and reassurance. Febrile seizure can recur, and as it often is a frightening and anxiety-provoking event for parent and caregivers. An understanding of the natural history and prognosis should enable the physician to reassure the parents providing an appropriate counselling and reassurance.

Seizures In Children Following an Apparent Life-threatening Event

The characteristics of seizures and epilepsy in infants who have had an apparent life-threatening event have been poorly defined. Our objective was to characterize in depth the cohort of patients with apparent life-threatening events who developed seizures. We collected data from infants hospitalized for an apparent life-threatening event, and evaluated patients for subsequent seizures or chronic epilepsy. Of 471 patients with an apparent life-threatening event, 25 (5.3%) had seizures and 17 (3.6%) developed chronic epilepsy. There was no increased risk for febrile seizures. Abnormal brain magnetic resonance imaging results and developmental delay were only found in those patients who developed chronic epilepsy. Of those who developed chronic epilepsy, 47% were diagnosed with seizures within 1 week of their apparent life-threatening event. The discharge diagnosis at the time of the apparent life-threatening event was poorly predictive of those who developed seizures. In most cases the cause of chronic epilepsy was unknown, although cortical dysplasias made up a significant percentage (12%).