			Home About us Contact

Febrile Seizures (febrile + seizures)

Distribution by Scientific Domains

Medical Sciences	81%
Life Sciences	18%

Selected Abstracts

Prolonged Febrile Seizures Are Associated with Hippocampal Vasogenic Edema and Developmental Changes

EPILEPSIA, Issue 9 2006
Rod C. Scott
Summary:,Purpose: There is mounting evidence that a prolonged febrile seizure (PFS) can cause acute hippocampal edema although the nature of that edema remains uncertain. The principal aims of the current study were: (1) to use apparent diffusion coefficient (ADC) measurements to further characterize the hippocampal edema previously identified within 5 days of a PFS, and (2) to determine whether the age dependency of ADC in the hippocampus is different in patients when compared to a control population following a PFS. Methods: Diffusion weighted imaging was acquired in 23 children within 5 days of a PFS, and in 14 of these children a mean of 5.5 months later. Twenty-four control children were enrolled. Results: There was a reduction in ADC between the acute and follow-up investigations [mean reduction = 0.0072 mm2/s/month since PFS (95% confidence interval; 0.0001,0.014 mm2/s/month since PFS), p = 0.048] consistent with early vasogenic edema, followed by recovery in children investigated within 2 days of a PFS. In addition, the behavior of ADC with respect to age was different in patients when compared to control subjects [mean difference in slope =,0.155 mm2/s/log10 age (95% confidence interval; ,0.290,0.0203 mm2/s/log10 age), p = 0.029], in that the expected age dependence was observed only in the control subjects. Conclusion: We suggest that these latter findings are most consistent with a preexisting developmental hippocampal abnormality that may predispose individuals to having a PFS. [source]

Two Novel SCN1A Missense Mutations in Generalized Epilepsy with Febrile Seizures Plus

EPILEPSIA, Issue 9 2003
Grazia Annesi
No abstract is available for this article. [source]

Increased Plasma Levels of Pro- and Anti-inflammatory Cytokines in Patients with Febrile Seizures

EPILEPSIA, Issue 8 2002
Miia Virta
Summary: ,Purpose: Pro- and antiinflammatory cytokines regulate the febrile response during infection. Febrile seizures (FSs) conversely are associated with rapid onset of high fever. Activation of the cytokine network has been shown in previous studies of FSs and cytokines. In this study, the association between cytokines and FSs was further investigated. Methods: Interleukin-1, (IL-1,), interleukin-1 receptor antagonist (IL-1RA), interleukin-6 (IL-6), interleukin-10, and tumor necrosis factor-, plasma levels were measured with enzyme-linked immunosorbent assay in 55 children with FSs and in 20 age-matched febrile controls immediately on arrival at the hospital. Cerebrospinal fluid cytokine levels also were measured in 16 FS children. Results: The plasma IL-1RA/IL-1, ratio (mean, 2,133 vs. 119; median, 790 vs. 105; p < 0.0001) and plasma IL-6 (mean, 41.7 pg/ml vs. 16.1 pg/ml; median, 19.6 pg/ml vs. 10.5 pg/ml; p = 0.005) were significantly higher in FS patients compared with control children. Logistic regression analysis was used to find the most significant predisposing factors for FSs. In this analysis, the high plasma IL-1RA/IL-1, ratio was the most significant factor connected to FSs (OR, 41.5; 95% CI, 4.9,352.8), but high plasma IL-6 also was significantly associated with FSs (OR, 5.3; 95% CI, 1.4,20.3). Conclusions: Present results support the hypothesis that the cytokine network is activated and could have a role in the pathogenesis of FS. [source]

Febrile Seizures: Treatment and Prognosis

EPILEPSIA, Issue 1 2000
Finn Ursin Knudsen
Summary: Recent epidemiologic data indicate that the vast majority of children with febrile seizures have a normal long-term outcome. A precise knowledge of the short- and long-term outcome with or without treatment, and short- and long-term side effects is an important prerequisite for assessing the various treatment strategies. We focus on the impact of short-term or prophylactic treatment on the short- and long-term outcome of various types of febrile seizures. There is universal agreement that daily prophylaxis with antiepileptic agents should never be used routinely in simple febrile seizures, but only in highly selected cases, if at all. Intermittent diazepam (DZP) prophylaxis at times of fever may or may not reduce the recurrence rate, but it does not appear to improve the long-term outcome as compared with short-term seizure control. The treatment may be used to reduce the recurrence rate for a small arbitrarily defined group with multiple simple febrile seizures, complex febrile seizures, especially focal, prolonged or both, febrile status, and when parental anxiety is severe. However, there is no evidence that treatment of simple febrile seizures can prevent the rare cases of later epilepsy, and many children with complex febrile seizures have a benign long-term outcome, even without treatment. Many prefer a "wait and see" policy. An attractive alternative is to treat new febrile seizures with rectal DZP in solution at seizure onset, given by the parents at home to prevent febrile status. Newer, less well documented short-term strategies include nasal, oral, or rectal administration of other benzodiazepines. Short-term seizure control of febrile status and careful parental counseling are the two most important targets of treatment. [source]

Interleukin-10 is associated with resistance to febrile seizures: Genetic association and experimental animal studies

EPILEPSIA, Issue 4 2009
Yoshito Ishizaki
Summary Purpose:, Febrile seizures (FS) are the most common form of childhood convulsions. Many reports have shown that a proinflammatory cytokine, interleukin-1 (IL-1) ,, may have a facilitatory effect on the development of FS. We have previously shown that the IL1B -511C/T single nucleotide polymorphism (SNP) is associated with simple FS of sporadic occurrence. The balance between pro- and antiinflammatory cytokines influences the regulation of infections and could, therefore, play a role in the pathogenesis of FS. Here, to determine whether pro- and antiinflammatory cytokine genes are responsible for the susceptibility to FS, we have performed an association study on functional SNPs of cytokine genes in FS patients and controls. Methods:, The promoter SNPs of four inflammatory cytokine genes (IL6 -572C/G, IL8 -251A/T, IL10 -592A/C and TNFA -1037C/T) were examined in 249 patients with FS (186 simple and 63 complex FS) and 225 controls. Because the IL10 -592 SNP showed a positive association with FS, two additional SNPs (IL10 -1082A/G and -819T/C) were subjected to haplotype analysis. Furthermore, we examined the in vivo role of IL-10 in hyperthermia-induced seizures using immature animal models. Results:, The frequencies of the IL10 -592C allele and -1082A/-819C/-592C haplotype were significantly decreased in FS as compared with in controls (p = 0.014 and 0.013, respectively). The seizure threshold temperature in the IL-10,administered rats was significantly higher than that in the saline-treated control ones (p = 0.027). Conclusions:, The present study suggests that IL-10 is genetically associated with FS and, contrary to IL-1,, confers resistance to FS. [source]

Genetic Architecture of Idiopathic Generalized Epilepsy: Clinical Genetic Analysis of 55 Multiplex Families

EPILEPSIA, Issue 5 2004
Carla Marini
Summary: Purpose: In families with idiopathic generalized epilepsy (IGE), multiple IGE subsyndromes may occur. We performed a genetic study of IGE families to clarify the genetic relation of the IGE subsyndromes and to improve understanding of the mode(s) of inheritance. Methods: Clinical and genealogic data were obtained on probands with IGE and family members with a history of seizures. Families were grouped according to the probands' IGE subsyndrome: childhood absence epilepsy (CAE), juvenile absence epilepsy (JAE), juvenile myoclonic epilepsy (JME), and IGE with tonic,clonic seizures only (IGE-TCS). The subsyndromes in the relatives were analyzed. Mutations in genes encoding ,1 and ,2 ,-aminobutyric acid (GABA)-receptor subunits, ,1 and ,1 sodium channel subunits, and the chloride channel CLC-2 were sought. Results: Fifty-five families were studied. 122 (13%) of 937 first- and second-degree relatives had seizures. Phenotypic concordance within families of CAE and JME probands was 28 and 27%, respectively. JAE and IGE-TCS families had a much lower concordance (10 and 13%), and in the JAE group, 31% of relatives had CAE. JME was rare among affected relatives of CAE and JAE probands and vice versa. Mothers were more frequently affected than fathers. No GABA-receptor or sodium or chloride channel gene mutations were identified. Conclusions: The clinical genetic analysis of this set of families suggests that CAE and JAE share a close genetic relation, whereas JME is a more distinct entity. Febrile seizures and epilepsy with unclassified tonic,clonic seizures were frequent in affected relatives of all IGE individuals, perhaps representing a nonspecific susceptibility to seizures. A maternal effect also was seen. Our findings are consistent with an oligogenic model of inheritance. [source]

Increased Plasma Levels of Pro- and Anti-inflammatory Cytokines in Patients with Febrile Seizures

N -methyl- d -aspartate, hyperpolarization-activated cation current (Ih) and ,-aminobutyric acid conductances govern the risk of epileptogenesis following febrile seizures in rat hippocampus

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2010
Mohamed Ouardouz
Abstract Febrile seizures are the most common types of seizure in children, and are generally considered to be benign. However, febrile seizures in children with dysgenesis have been associated with the development of temporal lobe epilepsy. We have previously shown in a rat model of dysgenesis (cortical freeze lesion) and hyperthermia-induced seizures that 86% of these animals developed recurrent seizures in adulthood. The cellular changes underlying the increased risk of epileptogenesis in this model are not known. Using whole cell patch-clamp recordings from CA1 hippocampal pyramidal cells, we found a more pronounced increase in excitability in rats with both hyperthermic seizures and dysgenesis than in rats with hyperthermic seizures alone or dysgenesis alone. The change was found to be secondary to an increase in N -methyl- d -aspartate (NMDA) receptor-mediated excitatory postsynaptic currents (EPSCs). Inversely, hyperpolarization-activated cation current was more pronounced in naïve rats with hyperthermic seizures than in rats with dysgenesis and hyperthermic seizures or with dysgenesis alone. The increase in GABAA -mediated inhibition observed was comparable in rats with or without dysgenesis after hyperthermic seizures, whereas no changes were observed in rats with dysgenesis alone. Our work indicates that in this two-hit model, changes in NMDA receptor-mediated EPSCs may facilitate epileptogenesis following febrile seizures. Changes in the hyperpolarization-activated cation currents may represent a protective reaction and act by damping the NMDA receptor-mediated hyperexcitability, rather than converting inhibition into excitation. These findings provide a new hypothesis of cellular changes following hyperthermic seizures in predisposed individuals, and may help in the design of therapeutic strategies to prevent epileptogenesis following prolonged febrile seizures. [source]

Febrile seizures are associated with mutation of seizure-related (SEZ) 6, a brain-specific gene

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2007
Zhi-liang Yu
Abstract Genetic factors contribute significantly to the etiology of febrile seizures (FS), the most common type of seizures in childhood. However, in most patients with FS, the causative gene is unknown. The purpose of this study was to explore the relationship between human brain-specific gene SEZ-6 and FS. Through amplification of genomic DNA by PCR and sequencing of the resulting products, we screened 75 subjects for mutations in the coding region (17 exons) of the SEZ-6 gene. Fifteen subjects were healthy individuals and 60 subjects had FS. Patients with FS could be divided into sub-groups based on seizure type (42 simple and 18 complex) and family history (41 had a positive family history). All patients have been followed to date to evaluate seizure recurrence and the development of epilepsy. No mutations were found in healthy controls, but 21 of the patients with FS had mutations in SEZ-6, and the most common type of mutation was a heterozygous, cytosine insertion (frame shift mutation) at position 1435 of the cDNA. The mutation incidence was significantly higher in patients with complex FS (vs. simple FS) and in patients with a positive family history. Sixteen of 42 patients with simple FS experienced seizure recurrence during the 1,5-year follow-up period. Fifteen of 18 patients with complex FS also experienced a recurrence during this period. Among these patients with recurrences, five patients with simple FS and six patients with complex FS have developed epilepsy. The mutation incidence among these epileptic patients is 72.7%. The human SEZ-6 gene is related to the occurrence and development of FS and may be a novel candidate gene for epilepsy. Screening for mutations in SEZ-6 may be valuable in predicting FS recurrence or the development of epilepsy. © 2006 Wiley-Liss, Inc. [source]

Acute encephalopathy with biphasic seizures and late restricted diffusion on MRI in a Japanese child living in the USA

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 9 2008
David E Traul MD PhD
We report an 18-month-old Japanese female living in the USA whose clinical course and radiographic findings were consistent with acute encephalopathy with biphasic seizures and late reduced diffusion (AESD). She was initially diagnosed with complex febrile seizures. However, on day 3 of admission, she had a cluster of complex partial seizures and the onset of a global developmental regression. In contrast to the normal magnetic resonance image of the brain obtained on admission, subsequent imaging demonstrated transient subcortical diffusion-weighted abnormalities in the white matter of the bilateral posterosuperior frontal, parietal, temporal, and occipital regions, with sparing of the perirolandic area. One year later, her developmental delay, although improved, persisted and she continued to experience sporadic seizures while being treated with topiramate monotherapy. Repeat imaging showed diffuse, poorly defined, increased T2 signals in the white matter of the posterosuperior frontal, parietal, temporal and occipital regions and diffuse cerebral volume loss. Previous reports of AESD have been limited to children aged under 4 years living in Japan. With the identification of this case, it is important that all physicians, not only those in Japan, who care for children with febrile seizures be aware of AESD and its associated neurological morbidity. [source]

Sodium channel SCN1A and epilepsy: Mutations and mechanisms

EPILEPSIA, Issue 9 2010
Andrew Escayg
Summary Mutations in a number of genes encoding voltage-gated sodium channels cause a variety of epilepsy syndromes in humans, including genetic (generalized) epilepsy with febrile seizures plus (GEFS+) and Dravet syndrome (DS, severe myoclonic epilepsy of infancy). Most of these mutations are in the SCN1A gene, and all are dominantly inherited. Most of the mutations that cause DS result in loss of function, whereas all of the known mutations that cause GEFS+ are missense, presumably altering channel activity. Family members with the same GEFS+ mutation often display a wide range of seizure types and severities, and at least part of this variability likely results from variation in other genes. Many different biophysical effects of SCN1A -GEFS+ mutations have been observed in heterologous expression systems, consistent with both gain and loss of channel activity. However, results from mouse models suggest that the primary effect of both GEFS+ and DS mutations is to decrease the activity of GABAergic inhibitory neurons. Decreased activity of the inhibitory circuitry is thus likely to be a major factor contributing to seizure generation in patients with GEFS+ and DS, and may be a general consequence of SCN1A mutations. [source]

Course and outcome of childhood epilepsy: A 15-year follow-up of the Dutch Study of Epilepsy in Childhood

EPILEPSIA, Issue 7 2010
Ada Geerts
Summary Purpose:, To study the course and outcome of childhood-onset epilepsy during 15-year follow-up (FU). Methods:, We extended FU in 413 of 494 children with new-onset epilepsy recruited in a previously described prospective hospital-based study by questionnaire. Results:, Mean FU was 14.8 years (range 11.6,17.5 years). Five-year terminal remission (TR) was reached by 71% of the cohort. Course during FU was favorable in 50%, improving in 29%, and poor or deteriorating in 16%. Mean duration of seizure activity was 6.0 years (range 0,21.5 years), strongly depending on etiology and epilepsy type. Duration was <1 year in 25% of the cohort and exceeded 12 years in another 25%. Antiepileptic drugs (AEDs) were used by 86% during a mean of 7.4 years: one-third had their last seizure within 1 year of treatment, and one-third continued treatment at the end, although some had a 5-year TR. At last contact, 9% of the cohort was intractable. In multivariate analysis, predictors were nonidiopathic etiology, febrile seizures, no 3-month remission, and early intractability. Eighteen patients died; 17 had remote symptomatic etiology. Standardized mortality ratio for remote symptomatic etiology was 31.6 [95% confidence interval (CI) 18.4,50.6], versus 0.8 [95% CI 0.02,4.2] for idiopathic/cryptogenic etiology. Discussion:, In most children with newly diagnosed epilepsy, the long-term prognosis of epilepsy is favorable, and in particular, patients with idiopathic etiology will eventually reach remission. In contrast, epilepsy remains active in ,30% and becomes intractable in ,10%. AEDs probably do not influence epilepsy course; they merely suppress seizures. Mortality is significantly higher only in those with remote symptomatic etiology. [source]

Prevalence of epilepsy and seizures in the Navajo Nation 1998,2002

EPILEPSIA, Issue 10 2009
Karen Parko
Summary Purpose:, To determine the prevalence of epilepsy and seizures in the Navajo. Methods:, We studied 226,496 Navajo residing in the Navajo Reservation who had at least one medical encounter between October 1, 1998 and September 30, 2002. We ascertained and confirmed cases in two phases. First, we identified patients with International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes signifying epilepsy or seizures using Indian Health Service (IHS) administrative data. Second, we reviewed medical charts of a geographic subpopulation of identified patients to confirm diagnoses and assess the positive predictive value of the ICD-9-CM codes in identifying patients with active epilepsy. Results:, Two percent of Navajo receiving IHS care were found to have an ICD-9-CM code consistent with epilepsy or seizures. Based on confirmed cases, the crude prevalence for the occurrence of any seizure (including febrile seizures and recurrent seizures that may have been provoked) in the geographic subpopulation was 13.5 per 1,000 and the crude prevalence of active epilepsy was 9.2 per 1,000. Prevalence was higher among males, children under 5 years of age, and older adults. Discussion:, The estimated prevalence of active epilepsy in the Navajo Nation is above the upper limit of the range of reported estimates from other comparable studies of U.S. communities. [source]

Interleukin-10 is associated with resistance to febrile seizures: Genetic association and experimental animal studies

Human herpes virus 6B: A possible role in epilepsy?

EPILEPSIA, Issue 11 2008
William H. Theodore
Summary Human herpes virus 6 (HHV6) infection is nearly ubiquitous in childhood and may include central nervous system invasion. There are two variants, HHV6A and HHV6B. Usually asymptomatic, it is associated with the common, self-limited childhood illness roseola infantum and rarely with more severe syndromes. In patients with immune compromise, subsequent reactivation of viral activity may lead to severe limbic encephalitis. HHV6 has been identified as a possible etiologic agent in multiple sclerosis, myocarditis, and encephalitis. A preponderance of evidence supports an association between HHV6 and febrile seizures. An ongoing multicenter study is investigating possible links between HHV6 infection, febrile status epilepticus, and development of mesial temporal sclerosis (MTS). Investigation of temporal lobectomy specimens showed evidence of active HHV6B but not HHV6A replication in hippocampal astrocytes in about two-thirds of patients with MTS but not other causes of epilepsy. It has been suggested that HHV6B may cause "excitotoxicity" by interfering with astrocyte excitatory amino acid transport. Although conventional inflammatory changes are not found in most MTS specimens, inflammatory modulators may play a role in neuronal injury leading to MTS as well. If the link between early viral infection, complex or prolonged febrile seizures, and later development of intractable temporal lobe epilepsy is confirmed, new therapeutic approaches to a common intractable epilepsy syndrome may be possible. [source]

A Screening test for the prediction of Dravet syndrome before one year of age

EPILEPSIA, Issue 4 2008
Junri Hattori
Summary Purpose: Our aim was to develop a screening test to predict Dravet syndrome before the first birthday based on the clinical characteristics of infants and the SCN1A mutation analysis. Methods: Ninety-six patients who experienced febrile seizures before the age of one were enrolled. The patients were divided into two groups,the Dravet syndrome group (n = 46) and the non-Dravet syndrome group (n = 50). We compared the clinical characteristics before one year of age of the two groups. We analyzed all coding exons of the SCN1A gene by the direct sequencing method. Scores from 0 to 3 were assigned to each risk factor based on the odds ratio and p-value. Results: An age of onset of febrile seizure , 7 months, a total number of seizures , 5, and prolonged seizures lasting more than 10 min. were regarded as significant risk factors for Dravet syndrome. Other factors highly predictive of this syndrome were hemiconvulsions, partial seizures, myoclonic seizures, and hot water,induced seizures. A total clinical score of six or above was the cutoff value indicating a high risk of Dravet syndrome. SCN1A missense and truncated mutations were detected significantly more often in the Dravet syndrome group than in the non-Dravet syndrome group. Discussion: This simple screening test was designed to be used by general pediatricians. It could help to predict Dravet syndrome before one year of age. If the sum of the clinical risk score is , 6, then the performance of an SCN1A mutation analysis is recommended. [source]

Current Treatment of Myoclonic Astatic Epilepsy: Clinical Experience at the Children's Hospital of Philadelphia

EPILEPSIA, Issue 9 2007
Sudha Kilaru
Summary:,Purpose: Myoclonic astatic epilepsy (MAE) is a generalized epilepsy of early childhood. Little is known about the use of newer antiepileptic treatments (AET) in MAE. The purpose of this study was to describe the characteristics, treatment, and outcome of a contemporary MAE cohort exposed to the new generation AET. Methods: Charts of subjects with MAE treated between 1998 and 2005 were reviewed. Results: Twenty-three subjects (19 boys), with a median (range) follow-up of 38 (2, 86) months were identified. Thirty-nine percent had a family history of epilepsy, and 39% had family history of febrile seizures. Age at seizure onset was a median of 36 (12,24) months. Initial EEG was normal in 30%. When seizures ceased, EEG background and epileptiform abnormalities persisted in 17 and 58%, respectively. On average, each subject was exposed to five AET. The most frequently used AET was valproate (83%). Seizure freedom occurred spontaneously in three subjects, with ethosuximide and levetiracetam in one each, valproate and lamotrigine in two each, topiramate in three and the ketogenic diet (KD) in five subjects. By 36 months after seizure onset, 67% achieved seizure freedom. At the last visit, 43% were developmentally normal, 52% had mild, and 5% had moderate cognitive disabilities. Time to seizure freedom did not correlate with cognitive outcome. Conclusions: The new generation of AET may offer significant benefit to children with MAE. The KD was the most effective AET in this series, and perhaps should be considered earlier in treatment. [source]

Molecular Neuropathology of Temporal Lobe Epilepsy: Complementary Approaches in Animal Models and Human Disease Tissue

EPILEPSIA, Issue 2007
Michael Majores
Summary:, Patients with temporal lobe epilepsies (TLE) frequently develop pharmacoresistance to antiepileptic treatment. In individuals with drug-refractory TLE, neurosurgical removal of the epileptogenic focus provides a therapy option with high potential for seizure control. Biopsy specimens from TLE patients constitute unique tissue resources to gain insights in neuropathological and molecular alterations involved in human TLE. Compared to human tissue specimens in most neurological diseases, where only autopsy material is available, the bioptic tissue samples from pharmacoresistant TLE patients open rather exceptional preconditions for molecular biological, electrophysiological as well as biochemical experimental approaches in human brain tissue, which cannot be carried out in postmortem material. Pathological changes in human TLE tissue are multiple and relate to structural and cellular reorganization of the hippocampal formation, selective neurodegeneration, and acquired changes of expression and distribution of neurotransmitter receptors and ion channels, underlying modified neuronal excitability. Nevertheless, human TLE tissue specimens have some limitations. For obvious reasons, human TLE tissue samples are only available from advanced, drug-resistant stages of the disease. However, in many patients, a transient episode of status epilepticus (SE) or febrile seizures in childhood can induce multiple structural and functional alterations that after a latency period result in a chronic epileptic condition. This latency period, also referred to as epileptogenesis, cannot be studied in human TLE specimens. TLE animal models may be particularly helpful in order to shed characterize new molecular pathomechanisms related to epileptogenesis and open novel therapeutic strategies for TLE. Here, we will discuss experimental approaches to unravel molecular,neuropathological aspects of TLE and highlight characteristics and potential of molecular studies in human and/or experimental TLE. [source]

Cerebral Cortical Gyrification: A Preliminary Investigation in Temporal Lobe Epilepsy

EPILEPSIA, Issue 2 2007
Lisa Ronan
Summary:,Purpose: To introduce a measure of global cortical folding in epilepsy by using stereology. Subtle developmental abnormalities associated with temporal lobe epilepsy may encompass brain morphologic changes such as an aberrant degree of cortical folding. Methods: Stereologic methods of volume and surface-area estimation were applied to in vivo MR brain-image data of a cohort of 20 temporal lobe epilepsy (TLE) patients (10 men, 10 women), and 20 neurologically normal controls (10 men, 10 women). Indices of cerebral gyrification and cerebral atrophy were generated. The impact of side of seizure onset, age at onset, history of febrile seizures, presence or absence of lesions, and presence or absence of secondarily generalized seizures on cerebral gyrification was assessed. Results: Although no significant group mean difference was found in the degree of cerebral gyrification between patients and controls, five of 10 of male patients had an abnormal gyrification when compared with male controls. One female patient had a significant change in gyrification compared with female controls. In general, patients with TLE demonstrated a significant degree of global cerebral atrophy compared with controls. Clinical factors were not demonstrated to affect significantly any of the quantitative parameters. Conclusions: The results of this study suggest that an aberrant degree of global cerebral gyrification may occur in certain clinical groups of TLE patients. These findings have implications for general theories of developmental susceptibility in TLE. [source]

Antiepileptogenesis and Seizure Prevention Trials with Antiepileptic Drugs: Meta-Analysis of Controlled Trials

EPILEPSIA, Issue 4 2001
Nancy R. Temkin
Summary: ,Purpose: To synthesize evidence concerning the effect of antiepileptic drugs (AEDs) for seizure prevention and to contrast their effectiveness for provoked versus unprovoked seizures. Methods: Medline, Embase, and The Cochrane Clinical Trials Register were the primary sources of trials, but all trials found were included. Minimal requirements: seizure-prevention outcome given as fraction of cases; AED or control assigned by random or quasi-random mechanism. Single abstracter. Aggregate relative risk and heterogeneity evaluated using Mantel,Haenszel analyses; random effects model used if heterogeneity was significant. Results: Forty-seven trials evaluated seven drugs or combinations for preventing seizures associated with fever, alcohol, malaria, perinatal asphyxia, contrast media, tumors, craniotomy, and traumatic brain injury. Effective: Phenobarbital for recurrence of febrile seizures [relative risk (RR), 0.51; 95% confidence interval (CI), 0.32,0.82) and cerebral malaria (RR, 0.36; CI, 0.23,0.56). Diazepam for contrast media,associated seizures (RR, 0.10; CI, 0.01,0.79). Phenytoin for provoked seizures after craniotomy or traumatic brain injury (craniotomy: RR, 0.42; CI, 0.25,0.71; TBI: RR, 0.33; CI, 0.19,0.59). Carbamazepine for provoked seizures after traumatic brain injury (RR, 0.39; CI, 0.17,0.92). Lorazepam for alcohol-related seizures (RR, 0.12; CI, 0.04,0.40). More than 25% reduction ruled out valproate for unprovoked seizures after traumatic brain injury (RR, 1.28; CI, 0.76,2.16), and carbamazepine for unprovoked seizures after craniotomy (RR, 1.30; CI, 0.75,2.25). Conclusions: Effective or promising results predominate for provoked (acute, symptomatic) seizures. For unprovoked (epileptic) seizures, no drug has been shown to be effective, and some have had a clinically important effect ruled out. [source]

Epilepsy Can Be Diagnosed When the First Two Seizures Occur on the Same Day

EPILEPSIA, Issue 9 2000
Peter Camfield
Summary: Purpose: Experts have suggested that when the first two (or more) unprovoked seizures occur on the same day, they should be considered as a single event and the diagnosis of epilepsy await a further seizure. We have studied the subsequent clinical course of children with their first two seizures on the same day ("same day" group) compared with children with their first two seizures separated by more than one day ("different day" group). Method: The Nova Scotia childhood epilepsy database documented all newly diagnosed children with epilepsy from 1977 to 1985 with follow-up in 1990 and 1991. Epilepsy was defined as two or more unprovoked seizures regardless of the interval between seizures provided that consciousness fully returned between seizures. All patients had their first seizure between the ages of 1 month and 16 years. Seizure types were restricted to partial, generalized tonic-clonic, and partial with secondary generalization. Results: Of the 490 children with partial or generalized tonic-clonic seizures and follow-up of more than 2 years, 70 had their first two or more seizures on the same day and 420 had their first two seizures on different days. Eighty percent (56 of 70) of the "same day" group subsequently had one or more further seizures with (n = 14) or without (n = 42) medication; 80.9% (340 of 420) of the "different day" group had one or more further seizures with (n = 115) or without (n = 225) medication. Seizure types were nearly identical. Cause was the same (except for fewer idiopathic "genetic" cases in the "same day" group: 1 of 70 vs. 42 of 420; p = 0.02). Rates of mental handicap and previous febrile seizures were the same. Children in the "same day" group were younger on average (60 vs. 84 months; p = 0.001) and were somewhat more likely to have neurological impairment. Outcome after 7 years average follow-up was the same: 58% of the "same day" group and 56% of the "different day" group were in remission. Conclusion: If two or more unprovoked seizures (with normal consciousness between) occur on the same day, the child appears to have epilepsy and will have a clinical course identical to that of the child with a longer time interval between the first two seizures. [source]

Febrile Seizures: Treatment and Prognosis

Genetic variants in the IMPA2 gene do not confer increased risk of febrile seizures in Caucasian patients

EUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2007
M. A. Blair
Pathogenesis of febrile seizures (FS), causing the most common of types of seizures in children, remains unknown. Genetic factors appear to play a pivotal role and FS can be inherited as a monogenic or genetically complex disorder. Several risks factors have been proposed but many of the previously reported genetic associations were not replicated. Non-coding polymorphisms in the myo-inositol monophosphatase 2 gene (IMPA2) have been suggested as a susceptibility factor for FS in Japanese patients. It is unknown whether genetic variants in the same gene constitute a risk factor for FS in other ethnic groups because the frequency of FS is significantly higher in Japanese children than in Caucasian patients. We investigated the role of the IMPA2 gene in a cohort of 96 unrelated Caucasian subjects with a history of FS. We did not identify any significant differences in genotypes of cases and matched controls; no mutations or non-synonymous polymorphisms were detected in these individuals. Our data suggest that the genetic variants in the IMPA2 gene are not associated with a risk of FS in Caucasian patients and patients from various genetic groups are likely to have different genetic causes of FS. [source]

N -methyl- d -aspartate, hyperpolarization-activated cation current (Ih) and ,-aminobutyric acid conductances govern the risk of epileptogenesis following febrile seizures in rat hippocampus

Genes and loci involved in febrile seizures and related epilepsy syndromes,

HUMAN MUTATION, Issue 5 2006
Dominique Audenaert
Abstract Epilepsy is a paroxysmal disorder with a cumulative incidence of about 3%. About 13% of patients with epilepsy have a history of febrile seizures (FS). Generalized epilepsy with FS plus (GEFS+) is a familial epilepsy syndrome in which patients can have classic FS, FS that persist beyond the age of 5 years (i.e., FS+), and/or epilepsy. Both genetic and environmental factors have been shown to contribute to the pathogenesis of FS and GEFS+. During the past 10 years, molecular genetic studies have contributed a great deal to the identification of genetic factors involved in FS and GEFS+. In this study we aimed to provide a comprehensive review of currently known genes for FS and GEFS+, and the methods and approaches used to identify them. We also discuss the knowledge we currently have and hypotheses regarding the effect of the mutations on their respective protein functions. Hum Mutat 27(5), 391,401, 2006. © 2006 Wiley-Liss, Inc. [source]

Febrile seizures are associated with mutation of seizure-related (SEZ) 6, a brain-specific gene

Seizures in children after kidney transplantation: Has the risk changed and can we predict who is at greatest risk?

PEDIATRIC TRANSPLANTATION, Issue 5 2008
Lorie D. Hamiwka
Abstract:, Children undergoing kidney transplantation are at increased risk for symptomatic seizures with a previously reported incidence of approximately 20%. Little data exist to help predict which children may be at risk. We retrospectively reviewed all children who underwent kidney transplantation evaluation at our center between October 1993 and August 2007 and identified 41 children who had an EEG prior to transplant. Demographic data as well as the following were collected: immunosuppressive medications, developmental status, history of seizures, family history of seizures, post-transplant seizures and EEG results. EEGs were classified as normal or abnormal. Prior to transplantation, one child had a history of febrile seizures and six experienced afebrile seizures. Nine (22%) children identified had an abnormal EEG prior to transplant. In eight cases the EEG was non-epileptiform and in one case was epileptiform. Abnormal EEGs did not correlate with a family history of seizures. Delayed development was noted in seven children and was not associated with an epileptiform EEG. Following kidney transplantation, no child experienced a seizure. Our single center study suggests that current rates of seizures following kidney transplantation are lower than previously reported and that routine EEG as part of the pretransplant evaluation in these children is of limited use to predict those at risk. [source]

Questionnaire survey on the understanding of epilepsy among non-medical persons

PEDIATRICS INTERNATIONAL, Issue 3 2008
Akihisa Okumura
Abstract Background: A questionnaire survey was conducted on the understanding of epilepsy and febrile seizures in preschool teachers, public health nurses, and parents or caregivers of children with epilepsy. Methods: The survey was performed in three different sites at different dates. The participants were 16 preschool teachers, 25 public health nurses, and 34 parents or caregivers of children with epilepsy. Results: Seventy-seven percent of the participants thought that epilepsy was not always untreatable. Sixty-seven percent of the participants thought that epilepsy was not a hereditary disease. Sixty-one percent of the participants considered that repetitive seizures cause brain damage, and 93% of them thought that patients with epilepsy must be treated. Seventy-six percent of the participants thought that febrile seizures evolve into epilepsy if left untreated. Seventy-seven percent of the participants considered that vaccination can be performed in patients with epilepsy or febrile seizures, and 89% of them thought that swimming should not be forbidden in patients with epilepsy or febrile seizures. There was no significant difference in the answers with regard to the positions of the participants except in one question. Conclusions: The present questionnaire survey provided some information on the understanding of epilepsy among non-medical persons. A nationwide public survey is needed to clarify the problems in the public understanding of epilepsy. [source]

Immunoglobulin subgroups in children with febrile seizures

PEDIATRICS INTERNATIONAL, Issue 1 2001
Hüsey, n Çaksen
Background: The aim of the present study was to determine whether or not there was a role for immunoglobulin (Ig) or IgG subgroups in the pathogenesis of febrile seizures (FS). Methods: Serum levels of IgA, total IgG, IgM, IgE, IgG1, IgG2, IgG3 and IgG4 were measured in 34 children with FS and in 37 healthy children used as a control group. Both patients and controls were divided into two groups according to age (group I, 6,24 months; group II, 25,72 months). Results: Compared with controls, mean IgG4 levels in patients were found to be decreased in both groups I and II (group I: 95~14 vs 57~5, respectively, P=0.01; group II: 178.5~38.5 vs 65.1~24.5, respectively, P<0.01), while mean IgG2 levels were found to be decreased only in group II patients (170~16 vs 103~22; P<0.05). Conclusions: The results of the present study suggest that Ig subclass deficiencies may be responsible for the infections connected with FS or that they may be related to the pathogenesis of FS in some children. [source]

Augmented currents of an HCN2 variant in patients with febrile seizure syndromes

ANNALS OF NEUROLOGY, Issue 4 2010
Leanne M. Dibbens PhD
The genetic architecture of common epilepsies is largely unknown. HCNs are excellent epilepsy candidate genes because of their fundamental neurophysiological roles. Screening in subjects with febrile seizures and genetic epilepsy with febrile seizures plus revealed that 2.4% carried a common triple proline deletion (delPPP) in HCN2 that was seen in only 0.2% of blood bank controls. Currents generated by mutant HCN2 channels were ,35% larger than those of controls; an effect revealed using automated electrophysiology and an appropriately powered sample size. This is the first association of HCN2 and familial epilepsy, demonstrating gain of function of HCN2 current as a potential contributor to polygenic epilepsy. ANN NEUROL 2010;67:542,546 [source]