Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009952 (febrile convulsions)
 1,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Since the introduction of oral polio vaccine in 1962, 30 cases of convulsions were registered within 30 days after the immunisation in Hamburg. 29 further cases from the surroundings came also to our attention. The majority of these cases occurred within 8 days after the vaccination (44 cases), afterwards only single cases were recorded. 33 patients were males, 24 females (2 cases sex unknown). The majority of the patients had the postvaccinal convulsions between 7 to 36 months of age, a characteristic period for febrile convulsions. 28 patients showed a course typical for febrile convulsions. In some cases intercurrent infections (pneumonia, otitis media purulenta) could also explain the nerval reactions. In 11 cases encephalopathy or encephalitis (1 case due to mumps) had been diagnoses. 8 patients suffered later from a convulsive disorder. Between 1964 and 1974 165,000 children born in Hamburg, were immunised thrice with OPV. In this period 19 convulsions and 3 permanent convulsive disorders were observed (1 case per 8,600 vaccinees; 1 convulsive disorder per 55,000 vaccinees).
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PMID:Convulsions following oral polio immunisation. 52 Jun 68

A multidisciplinary workshop held from September 29 to October 1, 1989, at Airlie House, Warrenton, Virginia, considered the neurologic complications of whooping cough and pertussis vaccine. Pertussis mortality in the U.S. in 2-3/1000 cases. Seizures occur in 1.9% of cases, and encephalopathy in 0.3%. Reviewing all data, it appears likely that a combination of one or more bacterial toxins, asphyxia, CO2 retention and loss of cerebral vascular autoregulation is responsible for neurologic symptoms. The timing of the encephalopathy suggests that it results from increased lysis of bacteria, and release of endotoxin. The encephalopathy is not confined to the paroxysmal phase. In evaluating side-reactions to the vaccine, the following must be kept in mind: 1. Vaccines are not standardized between manufacturers. 2. For a given manufacturer, vaccines are not standard from one batch to the next. 3. Unless the vaccine is properly prepared and refrigerated, its potency and reactivity varies with shelf life. In fact, the whole question of vaccine detoxification has never been systematically investigated. Listed in order of increasing severity, observed adverse reactions include irritability, persistent, unusually high pitched crying, somnolence, seizures, a shock-like "hypotensive, hyporesponsive" state, and an encephalopathy. Since the neurologic picture is not specific for pertussis vaccination, its temporal relationship to the vaccination is the critical variable for determining causation. Although the majority of seizures following pertussis vaccination are associated with fever, it was the consensus of the neurologists attending the workshop, that these do not represent febrile convulsions, but are non-benign convulsions. The incidence of post-vaccine encephalopathy is difficult to ascertain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Workshop on neurologic complications of pertussis and pertussis vaccination. 198 Dec 51

Nosological confusion within the epilepsies with myoclonic manifestations occurring in early life has led several epileptologists to separate more rigorously true myoclonic seizures from pseudomyoclonic ones and to identify clusters of homogeneous parameters that may lead to the formulation of syndromatic groupings. In recent years, four neonatal, infantile, and early myoclonic syndromes have been proposed: early myoclonic encephalopathy (EME), early infantile epileptic encephalopathy (EIEE), benign infantile myoclonic epilepsy (BIME), and severe infantile myoclonic epilepsy (SIME). These are reviewed critically, historically, and in the context of personal observations. The author's conclusions are that there is some justification to support, provisionally, a nosological place for the EME syndrome, that a nosologically separate position for the EIEE syndrome appears less firm, and that it seems safer to consider it at this time as an early variant of the West syndrome. From personal observations it appears that BIME and SIME, while justifiably constituting recognizable entities, may best be combined into a single syndrome of "infantile myoclonic epilepsy following febrile convulsions," with variable clinical outcomes.
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PMID:Early myoclonic encephalopathy, early infantile epileptic encephalopathy, and benign and severe infantile myoclonic epilepsies: a critical review and personal contributions. 212 Feb 81

The pattern of epilepsy and other convulsive disorders in 1,000 consecutive Saudi nationals is described. These disorders were common with a hospital frequency rate of 8 per 1,000. Men were more frequently affected than women and 60% of the patients were under 10 years old at the onset of their illness. The epilepsies were the commonest type (74%). Febrile convulsions (20%) presented mainly between the ages of one and five years. Isolated seizures (3%) and acute symptomatic convulsions (3%) were uncommon. In the epileptic group, generalised seizures (71%) were more frequent than partial (29%) and complex partial seizures occurred mainly in those above 21 years old. Absences (4%), infantile spasms (3%) and atonic seizures (3%) were uncommon. No specific etiology of the epilepsy was determined in the majority of the cases (63%). The identified major etiologic factors of the epilepsies were perinatal encephalopathy (21%), cerebral trauma (11%), sequelae of meningitis or encephalitis (2%), brain tumors (0.5%), and vascular lesions such as stroke and arteriovenous malformation. Perinatal encephalopathy accounted for 40% of the epilepsies in children less than 5 years old, and trauma for 20% of those above 20 years old. A family history of epilepsy in close relations was obtained in 23% of the cases, and the consanguinity rate among the parents was 53%. The high incidence of associated perinatal encephalopathy found in this study suggests that perinatal factors play a major role in the pathogenesis of epilepsy in Saudi Arabia. The high frequency of cerebral trauma was also striking. Although consanguinity of the parents appeared not to be a major factor in the genetics of convulsive disorders in this environment, it might have potentiated the tendency of familial aggregation of convulsive disorders in this community. Consanguinity may be an important factor in the production of some of these disorders but its precise role has not been determined.
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PMID:Epilepsy and other convulsive disorders in Saudi Arabia: a prospective study of 1,000 consecutive cases. 212 16

Pertussis vaccine was originally accused of provoking a short latency explosive encephalopathy with serious mental and physical consequences. Reports of recurrence of encephalopathy, worse after each dose, strengthened the notion of causality. Anecdotal associations can be no more than hypothesis-generating. With no distinctive clinical or pathological neurology, a major epidemiological study was necessary to answer the question "Does whooping cough vaccine cause brain damage in children"? The British national Childhood Encephalopathy Study (NCES) seemed to indicate that very rarely the answer was yes. Unfortunately the NCES confused disorders which might be notified as "encephalopathy" with actual brain damaging events, imaging a continuum of injury. Close scrutiny of the individual cases, as was possible during the recent test case in the High Court of London, shows that all the temporally associated cases with permanent sequelae had either viral encephalitis or Reye's syndrome. No cases were unexplained. There was an apparent excess of febrile convulsions in the first 24 hours, but all these children were normal at follow-up. The short latency explosive encephalopathy with adverse outcome predicted by the earlier case series did not occur. The NCES gives no support to the idea that pertussis vaccine damages children's brains. Contra-indications to DTP should be the same as to DT.
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PMID:A neurologist looks at neurological disease temporally related to DTP immunization. 307 4

An ad hoc panel of the American Medical Association prepared a report to identify severe, irreversible pertussis vaccine reactions and to establish criteria for attributing such reactions to the vaccine. Severe but reversible reactions, their likely duration and effects, and the clinical criteria for attribution were also examined. Three types of reactions which may produce residual brain damage lasting more than one year are encephalopathy, complex febrile convulsions, and afebrile convulsions. Serious pertussis vaccine reactions which are unlikely to have persistent adverse effects are simple febrile convulsions, anaphylaxis, and shock collapse. The panel also noted that there is no evidence that killed vaccine such as the pertussis vaccine can cause any insidious, delayed harmful effects.
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PMID:Pertussis vaccine injury. AMA Ad Hoc Panel on Pertussis Vaccine Injury. 405 31

Epileptic seizures are frequently reported (4-32%) in autism. These values are higher than in the normal population of children and adolescents (0.5%). In the literature there is no uniform description of epilepsy in autism. We examined 106 patients with autistic disorder divided into three groups on the basis of presence or absence of EEG paroxysmal abnormalities (PA) and / or epilepsy including febrile convulsions (FG). Our patients presented an autistic syndrome unrelated to clear congenital or acquired encephalopathy. The prevalence of epilepsy and EEG PA was 23.6% and 18.9%, respectively. Significant differences between the three groups appeared for (i) familial antecedents for epilepsy / FC and neurologic and psychiatric diseases (P < 0.004), (ii) a different proportion between the three groups for mental retardation (P < 0.03), (iii) and EEG fast activity (P < 0.04). Our patients showed several types of epilepsy, including idiopathic forms with seizure onset after the age of 10 in 45% of cases. Seizures were mainly partial, not frequent and controllable by anti-epileptic drugs. PA were mostly focal and multifocal and in 45% of cases were typical of benign childhood partial epilepsy with centro-temporal spikes. The higher incidence of epilepsy and EEG PA is apparently not related to organic pre-, peri- and postnatal antecedents or cerebral lesions. On the contrary, genetic factors responsible for autism and epilepsy seem important in the genesis of these two disorders.
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PMID:EEG features and epilepsy in patients with autism. 857 26

A case of early epileptic encephalopathy (EIEE) with suppression-bursts or Ohtahara's syndrome, associated with focal cortical dysplasia is reported. Infantile spasms and brief tonic unilateral seizures began on the fifth day of life. Interictal EEG demonstrated an asymmetrical "suppression-burst" pattern with no wake or sleep cycling. Seizures were refractory to all antiepileptic drug (AED) and steroid therapy. Magnetic resonance imaging (MRI) showed right frontotemporal cortical thickening. After three weeks of an ineffective medical treatment a preoperative evaluation with single photon emission computed tomography (SPECT) and electrocorticography (ECoG) was performed to characterize epileptogenic focus. Surgical resection of the precentral area was performed at age 1 month. Neuropathologic examinations confirmed diagnosis of focal cortical dysplasia by identifying cytoarchitectural disarray and ectopic neurons located deep in subcortical white matter. During follow-up, 1-year postoperative the child had a single febrile seizure. Neurologic examination showed minor developmental delay and slight left-sided weakness.
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PMID:Surgical treatment of an early epileptic encephalopathy with suppression-bursts and focal cortical dysplasia. 800 6

To determine the recurrence risk of West syndrome (WS), we studied the familial antecedents of consecutively referred patients. Among siblings, there was an increased incidence of WS but not of febrile convulsions. Familial incidence of epilepsy was intermediate between the epileptic and nonepileptic control groups. When cases resulting from a genetically determined disease were excluded, incidence of epilepsy among siblings was similar to that in normal controls. Five of the 11 familial cases of WS were due to an identifiable cause: twin pregnancy, tuberous sclerosis, and recurrent maternal toxemia. In 4 of the remaining families, the clinical picture included spasms, erratic myoclonus, and postnatal microcephaly, suggestive of a previously unidentifiable progressive encephalopathy. Therefore, when identifiable familial diseases were excluded, the recurrence risk was < 1%.
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PMID:Genetic predisposition to West syndrome. 833 May 85


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