Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We retrospectively reviewed the manifestations of influenza A2 in 83 hospitalized young children. Our purpose was to define the spectrum of clinical illness in this age group. Findings included fever (91%), vomiting or diarrhea (49%), pharyngitis (34%), pneumonitis (29%), otitis media (24%), conjunctivitis (13%), croup (13%), and bronchiolitis (6%). Neuromuscular manifestations occurred in 16 patients (19%) and included seizures, apnea, opisthotonos, and myositis. Three children had cerebrospinal fluid pleocytosis. Children younger than 3 months of age had fever less often and gastrointestinal symptoms more often than older children. Threee children died of progressive pneumonitis. We conclude that influenza A2 may cause a wide range of respiratory and neurologic findings in infancy and early childhood.
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PMID:Type A2 influenza viral infections in children. 62 60

Two adolescents with acute anaerobic (putrid) lung abscess were seen during an influenza epidemic. One patient, who had a history of seizures and a dental infection, had a classic predisposition to this disease. In the second patient, the abscess was apparently acquired as a complication of influenza. In both cases, the preliminary diagnosis was staphylococcal pneumonia with pneumatocele. It is suggested that failure to consider an anaerobic cause in pulmonary infections, inappropriate specimens, transport and culture of anaerobic material, and the sensitivity of oral cavity-derived anaerobes to penicillin, serve to mask the true frequency of anaerobic lung infections in childhood and adolescence.
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PMID:Anaerobic (putrid) lung abscess in adolescence. 81 18

Between Jan 15 and March 15, 1971, forty-eight grade-school patients living in western Chicago were hospitalized with an encephalopathic illness. Fourteen of these children had illnesses compatible with Reye syndrome (encephalpathy with liver impairment). Most of the children showed evidence of central nervous system (CNS) dysfunction within ten days after onset of a febrile upper respiratory tract illness. Seizures developed in 11 of the 48 patients (including 4 of the 14 with Reye syndrome). Eight of the encephalopathic patients, including 6 of the 14 with Reye syndrome, died. Two children without Reye syndrome had abnormalities of liver enzymes coincident with cerebrospinal fluid pleocytosis. Sixteen of the 24 patients tested had titer rises in serum against influenza type B only; influenza type B was isolated from throat cultures of 2 patients. This, the seventh report of CNS complications (Reye syndrome) associated with influenza type B, suggests that surveillance for neurologic sequelae should become part of the epidemiologic evaluation of influenza epidemics.
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PMID:Influenza type B-related encephalopathy. The 1971 outbreak of Reye syndrome in Chicago. 117 50

A monovalent, zonally purified, inactivated influenza B vaccine was administered to 29 children, 3 to 6 years of age, and 16 infants, 12 to 28 months of age, as a single dose of 0.25 ml containing 250 chick cell agglutinating units. The vaccine was both antigenic and well tolerated in the older group of preschool children. In the infants the vaccine was also antigenic but poorly tolerated clinically. Febrile reactions to 102 or greater were seen in 9 of the 16 infants, and two of these infants experienced a seizure following vaccination. The clinical reactions observed with the administration of influenza B vaccine in the dose used in this study would suggest significant limitations on its use in children under 3 years of age.
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PMID:Clinical reactions and serologic response following inactivated monovalent influenza type B vaccine in young children and infants. 124 39

The C57BL/10 sps/sps mouse mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps/sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca(2+)-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL/10 sps/sps mice.
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PMID:GABAergic neurotransmission in the C57BL/10 sps/sps mouse mutant: a model of absence seizures. 165 11

To develop an animal model of Reye's syndrome using a virus associated with the human disease, mice were intravenously inoculated with influenza A/PR8 virus (LD50 4000 haemagglutinin units). One to 3 days later the mice developed lethargy, seizures, coma and death. The cerebrospinal fluid cell count was normal. Serum aspartate aminotransferase levels increased 24-fold. Diffuse microvesicular fatty metamorphosis along with multiple small foci of necrosis developed in the liver. Influenza virus-like particles were seen by electron microscopy in the liver, primarily in areas of liver necrosis, but were not seen in the brain. Cerebral oedema without inflammation developed in the brain. Limited viral replication occurred within the liver. Influenza viral antigens were seen in 5-20% of hepatocytes from both necrotic and non-necrotic areas as well as in brain endothelial cells. Many of the clinical, biochemical and pathologic features of the mouse illness resemble those seen in Reye's syndrome. However, this model differs from the human disease in that focal areas of liver necrosis occurred along with limited complete viral replication in liver.
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PMID:Influenza A virus in the mouse: hepatic and cerebral lesions in a Reye's syndrome-like illness. 166 Feb 99

The clinical and laboratory findings from studies of patients with chronic fatigue syndrome (CFS) from northern Nevada are summarized. Physicians caring for these patients have estimated that greater than 400 patients with CFS from northern Nevada and nearby communities in California were identified between 1984 and 1988. As a result of these studies, a cluster of clinical and laboratory features associated with the illness in moderately to severely affected patients has been identified: profound fatigue of prolonged duration; cervical lymphadenopathy; recurrent sore throat and/or symptoms of influenza; loss of cognitive function manifested by loss of memory and loss of ability to concentrate; myalgia; impairment of fine motor skills; abnormal findings on magnetic resonance imaging brain scan; depressed level of antibody to Epstein-Barr virus (EBV) nuclear antigen; elevated level of antibody to EBV early antigen restricted component; elevated ratio of CD4 helper to CD8 suppressor cells; and strong evidence of association of this syndrome with infection with human herpesvirus 6. More-serious and longer-lasting neurologic impairments, including seizures, psychosis, and dementia, have also been observed in some of these patients.
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PMID:Chronic fatigue syndrome in northern Nevada. 185 May 42

Recombinant erythropoietin is usually associated with marked improvement in physiological and psychological well-being. Adverse effects are unusual. In this report, the unusual occurrence of seizures, increased clotting, and influenza-like syndromes is reviewed. Emphasis is given to adverse effects noted in the few available placebo-controlled studies.
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PMID:Side effects of erythropoietin therapy. 192 85

Therapy with recombinant human erythropoietin (rHuEPO) can reverse anemia and improve the quality of life in anemic hemodialysis patients. However, therapy is costly and must be used efficiently. An initial rHuEPO dose less than 50 U/kg intravenously three times weekly may be adequate to achieve a hematocrit of 30-33% in many patients. Acquired iron deficiency is a common problem during rHuEPO therapy and must be prevented with oral and parenteral iron replacement to maintain the efficacy of rHuEPO. Patients should be monitored carefully for additional problems including: an increase in blood pressure; onset of seizures or headaches; increased blood potassium, phosphate, and creatinine concentrations; enhanced coagulability resulting in dialyzer and vascular access clotting; and myalgias with a 'flu-like' syndrome.
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PMID:Practical approach to initiation of recombinant human erythropoietin therapy and prevention and management of adverse effects. 226 Jun 19

To determine whether complicated febrile seizures occur more often in children with a proven viral infection, we performed viral examinations on 144 children with febrile convulsions, of whom 112 had simple and 32 had complicated seizures. A diagnosis of virus infection was verified in 46% of the former patients and 53% of the latter. Three adenoviruses, one parainfluenza virus type 2 and one type 3, one respiratory syncytial virus, one echovirus type 11, one herpes simplex virus type 2, and one influenza B virus were isolated from the cerebrospinal fluid. A simple febrile convulsion occurred in seven children with a positive cerebrospinal fluid viral isolation, and two had a complex febrile seizure. In a follow-up of 2 to 4 years (mean 3.3 years), 21 of the 107 children with simple seizures (19.6%) and 3 of the 32 children with complicated seizures (9.4%) had recurrent febrile seizures. The children with positive evidence for a viral infection, even with a virus isolated from the cerebrospinal fluid, had no more recurrences than those without any proven viral infection. We conclude that children with a proven viral infection have no worse prognosis than those without.
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PMID:Viral infections and recurrences of febrile convulsions. 239 13


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