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

In a prospective study of thirty-two children with seizures treated with phenytoin (diphenylhydantoin), five had low levels of serum-IgA before treatment. All of these were among the fifteen who had had febrile convulsions in infancy. IgA levels fell significantly during 6 months treatment in the fourteen patients studied sequentially. Treated children with low serum-IgA had normal numbers of lymphocytes with surface IgA. This suggests that phenytoin causes failure of terminal differentiation of B lymphocytes, and is the first known cause of this, the commonest mechanism of immunoglobulin deficiency.
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PMID:IgA deficiency, epilepsy, and phenytoin treatment. 5 4

Three single CSF proteins with different molecular size (albumin, immunoglobulin G, and alpha2-macroglobulin) were determined by the method of electroimmunoassay in 61 children with febrile convulsions (FC) in order to evaluate the permeability of the blood-CSF barrier (B-CSF-B). Forty-two children with acute extracerebral infection served as controls. In contrast to a group of 22 children who suffered from acute meningoencephalitis or encephalitis, the CSF values of 48 children with FC were within normal limits. Thus even a very mild form of inflammatory encephalopathy-undetectable with conventional CSF investigation-was excluded in the majority of the children with FC. In 11 patients, however, CSF concentrations of albumin and alpha2-macroglobulin were abnormally raised, indicating a B-CSF-B distrubance. Elevated albumin values were found most frequently. In several children with FC lasting more than 20-30 min, B-CSF-B damage was probably caused by prolonged seizure activity since there is a linear correlation between albumin concentration and duration of convulsions. Several other factors known to raise the children's risk of developing epilepsy in later life were associated with the protein pattern of B-CSF-B disturbance in some of the children. In these cases, the cause of abnormal permeability of B-CSF-B is unknown and the condition might have existed prior to the occurrence of seizures.
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PMID:Febrile convulsions and blood-cerebrospinal fluid barrier. 7 3

One hundred and five children admitted to hospital with convulsions were studied prospectively. A convulsion was designated febrile if an axillary temperature of 38 degrees C or more occurred after the fit. Twenty-two children had an initial non-febrile convulsion and five of them (22.7 percent) have developed recurrent nonfebrile seizures. In the febrile group of 83 only two children (2.4 percent) have so far had non-febrile convulsions. Both their initial convulsions were uncomplicated. There was no difference between the groups of convulsion or EEG result. Investigations in hospital, including lumbar puncture, rarely revealed a diagnosis not clinically suspected. In previously healthy children with convulsions that are not prolonged, pyrexia is the only factor of prognostic significance by 12 months follow up.
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PMID:Prospective study of convulsions in childhood. 28 62

The duration of cardiac asystole induced by ocular compression was measured in 100 consecutive children referred for electroencephalographic examination after one or more febrile convulsions (FC). The children were classified into three groups-namely, those with anoxic FCs, those with epileptic FCs, and "others"-according to the appearances of the FC and the electroencephalogram (EEG). In 14 children the description of the FC suggested non-epileptic anoxic cerebral seizures such as are seen after prolonged syncope or breath-holding. In 35 children the FCs were assumed to be epileptic in mechanism on the basis of unilateral (hemiclonic) twitching, known cerebral disease, a family history of epilepsy, or spikes on the EEG. In the 51 "others" the FCs could not be classified. Definitely abnormal asystole (four seconds or over) was induced by ocular compression in half the anoxic group, in 16% of the "others," but in none of the epileptic group. The differences between the degree of asystole induced in each of the three groups was highly significant (P=0.005).These results support the hypothesis that vagal-mediated cerebral ischaemic anoxia is implicated in the genesis of FCs that resemble anoxic seizures and in a substantial number of those without an obvious epileptic mechanism. The significance, genetics, management, and prognosis of FCs must now be re-examined in this light.
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PMID:Two types of febrile seizure: anoxic (syncopal) and epileptic mechanisms differentiated by oculocardiac reflex. 35 95

203 epileptic children (127 boys, 76 girls), who had demonstrated at least once focal sharp waves in the EEG during the course were investigated regarding clinical and historical data as well as familial morbidity for seizures. Expectedly, the seizure symptomatology was multiform: focal seizures of different type, especially secondarily generalized, grand mal, psychomotor fits, infantile spasms etc. Organic brain lesions play an important role. In 23% of cases a familial seizure affliction can be registered. The morbidity (close family) is significantly lower than in families of patients with spike wave absences (2.5 and 4.4% resp., Doose et al. 1973). Like in spike wave absence epilepsies mothers and mothers' siblings are more often affected than fathers and fathers' siblings. Among the affected relatives grand mal epilepsies predominate. The increase of febrile convulsions and spike wave absences observed in the families of absence epileptics is not present. In probands with onset of epilepsy during early childhood a significantly increased familial affliction can be observed. A more extensive discussion of the results will follow in a second paper deeling with EEG findings in probands and siblings.
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PMID:Genetic factors in childhood epilepsy with focal sharp waves. I. Clinical data and familial morbidity for seizures. 40 82

The marriage rate of epileptic patients was 62% in males and 78% in females. Compared with the rates in the general population, the male patients had a 15% lower rate, but there was no difference in females. There were 263 patients with at least one offspring selected for the study. There were 234 sons and 272 daughters (506 total, 1.9 per patient). Distribution by types of seizure was awakening grand mal, absence or myoclonic petit mal in 24%, grand mal with no aura in 21%, grand mal during sleep in 23%, diffuse grand mal in 7%, grand mal with aura in 13%, psychomotor seizure in 9%, and focal seizure in 3%. The probands were composed of 79% idiopathic and 21% symptomatic in pathogenetic classification. An epileptic EEG abnormality was demonstrated in 22% of male and 44% of female probands. The incidence of seizures among offspring was 2.4% (4.2% age-corrected) in a narrow sense (epilepsy) and 9.1% in a broad sense including febrile convulsions. The latter morbidity was 11.0% for the idopathic and 3.2% for the symptomatic group; 11.0% for female and 6.9% for male probands; 10.2% for sons and 8.1% for daughters. The figure was higher for the probands with the age range at onset of seizure of 0--4 years (20.6%) and 20--29 years (12.6%) than for those with other age ranges; higher for those with awakening grand mal, absence, myoclonic petit mal, for those with family history of epilepsy than those without it. Possible correlation of types of seizure between probands and offspring was demonstrated. Thirty-seven percent of offspring exhibited epileptic EEG abnormalities, and the ratio of epileptic EEG abnormalities to clinical manifestation is about 4:1. Possible existence of familial aggregation of EGG abnormalities and of two kinds of families with large or small epileptic predisposition was indicated. The importance of the role of hereditary and environmental factors in epileptic pathogenesis is proved, and the results of an investigation of congenital malformation among offspring of epileptic mothers are presented. These results were considered to be useful for genetic counseling of epileptic patients.
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PMID:Incidence of seizures and EEG abnormalities among offspring of epileptic patients. 40 30

A cohort of 666 children who had convulsions with fever were followed to determine the risks of subsequent epilepsy. High risks were found in children with preexisting cerebral palsy or mental retardation. Other major risk factors were atypical features of the febrile convulsions (such as focal seizures) and duration of febrile seizures for 10 minuts or more. The risk of developing epilepsy by age 20 was about 6 percent for all children who had experienced febrile convulsions. However, this risk figure consisted of a combination of 2.5 percent of children without prior neurologic disorder or atypical or prolonged seizures, and 17 percent of those with such complications.
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PMID:The risk of epilepsy following febrile convulsions. 57 73

Out of 500 patients with febrile convulsions, 41 were found to have a spike focus on E.E.G., 35 of these were then followed up. The clinical features of the seizure in these 35 children did not differ from the group in general. The initial focus was practically always unilateral, except for one case with an asynchronous bioccipital focus. The most frequent site was occipital (43 p. 100). Migration of the focus was relatively rare. In 35 patients the focus disappeared, in 45 p. 100 within a year and in 88 p. 100 within 3 years. Following the disappearance of the focus, generalised sharp wave activity was seen in 30 p. 100 cases, all 35 children being under treatment. All the seizures with the exception of two children who have become epileptic were benign rendering long term anticonvulsant therapy unnecessary.
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PMID:["Spike focus" during the evolution of febrile convulsion: an electrophysiological and clinical study of 35 patients (author's transl)]. 61 92

The relationship of febrile seizures to later intellectual and academic performance was examined in a sibling-control study. Amont 431 sibling pairs tested at the age of 7 years, the mean full scale IQ on the Vechsler Intelligence Scales for Children was not different for children who had febrile seizures as compared with siblings who were seizure-free. Neither recurrent seizures nor those lasting 30 minutes or longer were associated with IQ deficit. Poor academic achievement, defined as Wide Range Achievement Test performance more than one grade level below school placement in children with IQs of 90 or above, was equally frequent in index cases and control patients. Febrile seizures were not associated with a decrement in IQ or early academic performance, as judged by comparison of affected children with their siblings.
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PMID:Febrile seizures and later intellectual performance. 61 68

In only a small proportion of young children with brief, generalized, febrile convulsions do afebrile seizures develop, but this fraction is several times the prevalence of epilepsy in an unselected population. The risk of another febrile convulsion is approximately 30%. Febrile status epilepticus during a subsequent infection is a potential source of serious morbidity and mortality. Intermittent phenobarbital administration during subsequent, febrile illnesses confers little protection against recurrent, febrile convulsions. Continuous phenobarbital administration during the preschool years is indicated for most children who have had a simple febrile convulsion.
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PMID:Continuous phenobarbital treatment after a 'simple febril convulsion'. 62 69


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