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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the relationship between clinical characteristics and EEG classification in all children with febrile seizures examined at the University Pediatric Clinic, Skopje, Yugoslavia between 1982 and 1984. This is the only facility in Macedonia providing EEG or neurologic consultation for children. EEGs were classified as paroxysmally abnormal if they contained spikes, sharp waves, or spike-wave complexes considered abnormal for age. In all, 22% of the 676 children had an abnormal initial EEG. The most common basis for classification as abnormal was spike-wave complexes greater than 3 Hz; the next most common basis was the presence of spikes. Birth weight, gender, accompanying illness, and family history of seizures, and whether the index seizure was single or multiple were not associated with differences in rate of abnormal EEG. Clinically focal index seizures and longer duration were associated with EEG abnormality. Number of previous febrile seizures was associated with an increasing rate of EEG abnormality, from 18% in children with no previous seizures to 63% in those with four or more previous seizures. Age at EEG was linearly related to likelihood of paroxysmal EEG abnormality, both for the total cohort and for the 376 children with no previous seizures. In the total cohort, logistic regression identified leading predictors of abnormal initial EEG to be older age, number of previous febrile seizures, preexisting motor abnormality, and focal seizures. For children with a first febrile seizure, leading predictors were focal seizure, older age, and preexisting motor abnormality.
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PMID:Febrile seizures: clinical characteristics and initial EEG. 173 60

In a retrospective study of 411 children with cerebral convulsions over a period of 4 years, 160 patients with febrile seizures were found. This group consisted of 94 boys and 66 girls. The main purpose of this study was to establish the age of the first convulsive fit in each child. Febrile convulsions started in the first half year, increased in the second half year and culminated in the second year of life. This age dependent appearance was explained with passive immunization by maternal antibodies so that febrile convulsions appear when these antibodies decrease. The first occurrence of febrile convulsions appeared on an average of 22.9 months, in children with recurrent febrile convulsions a little earlier with 18.2 months. The most interesting fact was that children with a family history of febrile seizures showed an even earlier occurrence of the first seizure with 14.5 months. This tendency of early incidence of febrile convulsion in the group with family history and in the group of recurrent febrile convulsions could be shown as statistically significant respectively nearly significant in comparing with the group of retarded patients. A peculiar tendency for febrile convulsions seems to be documented by recurrent seizures in the patient himself, but also by a history of febrile convulsions in other family members. Both facts may lead to a very early incidence of febrile convulsions.
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PMID:[Retrospective study of 160 children with febrile convulsions]. 174 Aug 98

A cohort of 74 children three months to 16 years-old who presented with a first unprovoked seizure were followed for five years to assess the risk of recurrence. Children with febrile convulsions, immediate posttraumatic seizures, meningitis and encephalitis were not included. The risk of recurrence was 68% for a second seizure. 47% of the patients developed an epilepsy. 85% of recurrences occurred within the first 6 months and 100% within 2 1/2 years. A history of epilepsy in a first degree relative, age at first seizure, duration of seizure, initial EEG or neurologic status were not associated with significantly higher risk of recurrence.
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PMID:[Risk of recurrent seizures after the first afebrile grand mal seizure in childhood]. 174 58

The two forms of epileptic brain damage, that found in patients with chronic epilepsy (post-mortem or in an anterior temporal lobectomy specimen) and that occurring acutely after status epilepticus, have much in common but are not identical. Hippocampal lesions occurring acutely after status epilepticus show a high degree of selectivity for hilar interneurones, CA1 pyramidal neurones and CA3 pyramidal neurones. Hippocampal lesions in anterior temporal lobectomy specimens tend to involve the subfields less selectively with CA1 being only slightly more severely affected than dentate granule cells, CA3 and CA2 pyramidal neurones. The most severely damaged hippocampi may result from a combination of acute damage early in life (commonly from prolonged febrile convulsions) and cumulative damage associated with seizures. Less severe degrees of damage are probably a consequence of repeated seizures. The abnormal patterns of firing associated with epileptic activity are almost certainly responsible for cell death occurring acutely after status epilepticus; they may contribute to the progressive cell loss occurring in chronic epilepsy.
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PMID:Excitotoxicity and epileptic brain damage. 179 Jul 73

Children with febrile convulsions (FC) including 46 twin pairs, 1913 families including 393 sibling pairs, and 42 three-generation FC kindreds have been studied. Twin studies: (1) The pairwise concordance rate for FC was 69% (18/26 pairs) in monozygotic (MZ) and 20% (4/20 pairs) in dizygotic (DZ) twins (P less than 0.01). (2) The intra-pair similarity of clinical symptoms in 18 concordant MZ twin pairs showed a positive significant correlation, particularly in 4 items--duration of seizure, exogenous factors, intelligence level, and background EEG abnormality. These correlations were greater than those in sibling pairs. (3) No evident cause for discordance was detected in 8 discordant MZ twin pairs, and many dissimilar symptoms were observed in 4 concordant DZ twin pairs. Sibship studies: A large positive correlation of some clinical symptoms was observed in sibling pairs concordant for FC: age at onset of FC, degree of fever, duration of seizure, exogenous factors, and background EEG abnormality (r = +0.2- +0.6). Family history analysis: Morbidity risk among near relatives (17% in parents, 23% in siblings) than in second- (6.1%) or third-degree relatives (4.6%). The difference was found between: sibling greater than parents, uncles greater than aunts, male cousins greater than female cousins. Segregation analysis showed maternal preponderance. In 42 three-generation kindreds the morbidity risk was higher in siblings (32%), uncles/aunts (14%), and cousins (6.4%) than in relatives of other probands. Characteristic findings in FC patients with family history: Characteristic findings in FC patients with an FC parent or sibling, compared with those with no family history, were early onset of FC, lower degree of fever, longer duration of seizure, many recurrences, FC recurrence after age 3, and background EEG abnormality. Similar findings were more markedly observed in 42 3-generation kindreds. Mode of inheritance: A multifactorial mode of inheritance for FC receives some support from this study, and the heritability was estimated as 75%.
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PMID:Genetic studies of febrile convulsions: analysis of twin and family data. 181 94

We compared the etiologic factors and clinical characteristics of 30 patients with unitemporal vs those of 30 patients with bitemporal independent (minimum 20% from one side) interictal epileptiform discharges on extracranial electroencephalograms. Febrile seizures occurred significantly more frequently in the unitemporal (40%) than in the bitemporal (17%) group. Mass lesions were more common in the bitemporal group, and seven of 10 patients with mass lesions showed bitemporal interictal epileptiform discharges. There were no statistically significant differences in age at onset, frequency of seizures, duration of epilepsy, and history of central nervous system infection or trauma between the two groups. A history of febrile seizures or central nervous system infection that may be expected to cause diffuse cerebral injury does not appear to be the major factor predisposing to the development of bitemporal interictal epileptiform discharges.
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PMID:Etiologic factors for unitemporal vs bitemporal epileptiform discharges. 184 24

Major cohort studies document that the long-term prognosis for most children with febrile convulsions (FC) is excellent. The 2 main treatment alternatives so far have been long-term prophylaxis with phenobarbital or valproate or no prophylaxis at all. Phenobarbital at times of fever is ineffective and obsolete. Consensus has emerged that long-term prophylaxis with antiepileptic drugs is rarely justified in FC considering the side effects and the favourable prognosis. No treatment at all does not appear quite satisfactory either, as FC have a high recurrence rate, disrupt family life and may have emotional consequences for the family. Moreover, all FC children face a risk, although admittedly low, of subsequent long-lasting potentially central nervous system (CNS)-damaging seizures. However, 2 further options exist: treatment with rapid-acting benzodiazepines solely at times of greatest risk, i.e., at high fever or at renewed seizures. Several clinical trials have confirmed that intermittent diazepam prophylaxis by way of a few doses of the drug per year provides effective seizure control and reduces the recurrence rate by one half or two thirds. The treatment is feasible and cheap, well tolerated by the child and well accepted by the parents. Compliance problems are common and only partly abatable. Trivial side effects are frequent. Transient respiratory apnoea does occur, but 15 years' experience substantiates that serious side effects are remarkably rare. Acute anticonvulsant treatment with rectal diazepam in solution given by the parents to stop ongoing seizures and to prevent immediate recurrences is an attractive alternative. It is feasible, is probably effective and minimizes the use of drugs, but compliance problems are common and protracted seizures are not always controlled. The subsequent management should include a risk profile approach considering a combination of risk factors for new FC rather than a single factor. By means of a risk index, based on simple clinical data including age at onset, family seizure history, seizure type and frequency of fever, children may be identified as being at low, intermediate or high risk for further febrile fits. However, risk factors for new FC and not for subsequent epilepsy should be used. It is concluded that preventing or abbreviating new FC with benzodiazepines appears to be a useful, although not ideal, drug-minimizing approach in managing many children with simple or complex FC. From a health hazard viewpoint, treatment is not strictly mandatory, although advisable. A selective strategy seems rational. Intermittent diazepam prophylaxis may preferably be offered to children at high risk for new FC.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intermittent diazepam prophylaxis in febrile convulsions. Pros and cons. 185 81

The gene for autosomal dominant "benign" familial neonatal convulsions, a transient, primary epilepsy of infancy, has recently been assigned to chromosome 20q. To determine whether this disorder is genetically heterogeneous, we performed linkage analysis in two previously unreported pedigrees with benign familial neonatal convulsions in which clinical heterogeneity was evident. There were 14 affected persons in the first family, and none had seizures (febrile or afebrile) after the age of 2 months. The second family had 13 affected individuals and 2 obligate carriers; seizures frequently did not remit until 6 to 24 months, febrile convulsions occurred in at least 2 patients, apparent audiogenic seizures occurred in 4 patients, and 1 individual had refractory epilepsy until late adolescence. Linkage studies with the chromosome 20 markers D20S19 and D20S20 were performed in both families. The resulting data favored linkage of the disease and marker loci in Family 2 by a maximum odds ratio of 45:1 at 6% recombination. In Family 1, however, the odds were greater than 20,000:1 against linkage at 10% recombination or less. We conclude that the syndrome of benign familial neonatal convulsions is clinically and genetically heterogeneous. Further study will be necessary to clarify the relationship between phenotype and genotype in this disorder.
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PMID:Benign familial neonatal convulsions: evidence for clinical and genetic heterogeneity. 185 77

Recent advances in knowledge of pediatric seizure disorders, including classification of seizure types and febrile convulsions, have been the topics of major symposia. In light of these recent developments, an in-depth review is presented to aid the pediatric dentist in the treatment of these children.
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PMID:An update in pediatric seizure disorders. 188 20

An 18-year-old female presented with two seizures induced by photic stimulation. She had a positive family history for migraine and a history of febrile convulsions. Since the age of 13 she had suffered from migraine attacks with aura. A brain computerized tomography with contrast enhancement was negative and several electroencephalograms showed a photoparoxysmal response. At the age of 18 she had a partial secondary generalized seizure after photic stimulation during routine electroencephalogram. The onset of seizure was in the occipital region. Two days later, the patient presented with a typical migrainous attack with aura. Interictal apomorphine test (1.5 mg s.c.) blocked the photoparoxysmal response. According to Quesnay, dopaminergic failure of the occipital cortex may account for both epileptic and migraine features.
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PMID:Migraine with aura and photosensitive epileptic seizures: a case report. 188 72


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