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

Reye's syndrome in infancy is not a well-defined entity and is infrequently diagnosed. Eight infants 6 months of age or younger had a prodromal viral illness followed by the rapid onset of lethargy, seizures, and coma, resulting in the diagnosis of Reye's syndrome. All had abnormal results of liver function tests including elevations of blood ammonia level. Three patients had pathological studies that confirmed fatty visceral infiltration. The data on these patients, as well as a review of the literature, indicate that the most prominent clinical findings in Reye's syndrome in infancy include marked respiratory abnormalities with tachypnea and apneic episodes; frequent occurrence of seizures in the early stages of the illness; and hypoglycemia in most cases. A strong socioeconomic bias was noted in these patients, with the infants coming primarily from lower socioeconomic, urban environments, while older children with Reye's syndrome have been observed to be predominantly middle-class and from suburban or rural areas.
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PMID:Reye's syndrome in infancy. 68 88

The clinical picture of Reye's syndrome, characterized by an acute severe disease of brain and liver, initially has nonspecific generalized symptoms with cough, myalgia, and fever. The prognosis is poor. The disease starts with an infection, quickly followed by vomiting and loss of consciousness. In this phase the serum bilirubin is moderately raised, the transaminases markedly so. In addition to gastro-intestinal bleeding there may be hypoventilation, hypoglycaemia and seizures. Morbid anatomically there is a small-drop fatty infiltration of the liver and other organs with cerebral oedema. Aetiology and pathogenesis remain uncertain. Numerous therapeutic measures have been proposed.
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PMID:[Reye's syndrome in adults (author's transl)]. 68 69

The hospital course and therapy of 369 patients with Reye's syndrome were evaluated. Eighty-three percent of patients had deepening coma during hospitalization. Stage of coma on admission, evidence of increased intracranial pressure, and blood ammonia levels greater than 300 microgram/100 ml were all significantly associated with increasing mortality. Among survivors of Reye's syndrome, 30% of those who developed either decerebrate posturing or seizures during hospitalization had serious neurologic sequelae upon discharge. When analyzed by (1) stage of coma during admission (2) progression of coma during hospitalization, (3) degree of blood ammonia level elevation, and (4) presence of increased intracranial pressuring, no significant differences were noted between patients receiving intensive supportive care and those receiving exchange transfusions and/or peritoneal dialysis.
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PMID:Reye's syndrome: clinical progression and evaluation of therapy. 91 33

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

General principles of thermoregulation, the pathophysiology of fever, controversies concerning the use of antipyretic therapy, and nonpharmacologic and pharmacologic treatments commonly used for antipyresis in the pediatric population are reviewed. Several arguments can be made for not ameliorating the febrile response. Fever is an important diagnostic and prognostic clinical sign that may have beneficial effects for the host. In addition, body temperatures of < or = 41 degrees C (105.8 degrees F) are relatively harmless. Reasons for treating fever include patient discomfort, the potential for adverse sequelae, the possibility of seizures, and the possibility that fever could affect the pharmacokinetic profiles of drugs. Nonpharmacologic treatment for fever includes environmental measures to enhance dissipation of body heat and sponging. Aspirin and acetaminophen are the agents used most frequently for antipyresis in pediatric patients. However, aspirin use in children with a viral illness has been associated with development of Reye's syndrome. As a result, its use in children has declined in the United States. Acetaminophen is relatively free of adverse effects and is considered first-line pharmacologic antipyresis therapy. Ibuprofen suspension should be considered as second-line antipyretic therapy. Combination therapy with acetaminophen and aspirin may be considered if the patient fails to respond to other nonpharmacologic and pharmacologic therapies; however, combination therapy may result in increased risk of drug toxicity, increased probability of adverse reactions, and increased risk of intoxication. Aspirin, acetaminophen, and ibuprofen are equally effective for antipyresis in pediatric patients. However, because acetaminophen is the safest medication, it is currently the therapy of choice.
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PMID:Antipyretic therapy in the febrile child. 128 50

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

A four year old girl manifested with seizures, raised intracranial tension and altered consciousness. Laboratory investigations suggested Reye's syndrome. Later she developed fatal hypothermia. Rarity of such a case is highlighted. Probable pathogenesis of hypothermia in Reye's syndrome is discussed.
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PMID:Hypothermia: an unusual manifestation of Reye's syndrome. 226 14

Monitoring of intracranial pressure (ICP) and efforts to keep the ICP below the critical level are vital in the treatment of Reye's syndrome. Continuous monitoring of ICP was carried out in 21 cases of Reye's syndrome who were at or beyond stage III at the time of admission to the Veterans General Hospital, between January 1981 and August 1986. Seventeen had ICP ranging from 15 mmHg to 67 mmHg. Three patients died, 1 in stage V with an ICP of 67 mmHg received a craniectomy, and 2 others were in stage IV with ICP's of 66 mmHg and 25 mmHg, respectively. The fatality rate was 14% (3/21). Among 18 patients, 5 had moderate psychomotor retardation (PMR), 4 had severe PMR and 2 had mild PMR. The remaining 7 patients survived without sequelae. Blood exchange transfusion could further reduce ICP and seemed to improve neurologic outcome. Blood ammonia higher than 400 micrograms% is indicative of a bad prognosis. Hyperventilation was the most rapid and effective means of reducing moderate degrees of increased ICP. During intensive supportive care, we also found that coughing, endotracheal intubation, seizures, asynchronous respiration to an artificial respirator, suction of the airway and any painful stimulation caused further increases in ICP and worsened the situation. Care should be given to avoid these factors.
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PMID:Continuous monitoring of intracranial pressure in Reye's syndrome--5 years experience. 228 26

Neuron-specific enolase (NSE) has recently proved to be a useful marker of neuron damage. We determined NSE levels in the serum and CSF of 117 children with various neurological disorders (43 with febrile convulsion, 25 with seizure disorder, 32 with meningitis, 3 with brain tumor, 2 with Reye syndrome, 3 with congenital CNS malformation and 9 with other disorders). The purpose of this study is to assess the potential usefulness of NSE in diagnosis and prognosis. Twenty CSF and serum samples of children without neurological problem served as a control. The mean values of the NSE levels in the CSF and serum of the control group were 5.00 +/- 1.65 ng/ml and 8.34 +/- 4.40 ng/ml respectively. The peak values were found in cases with brain tumor. A patient died of Reye syndrome didn't show a very high level of NSE in the serum or CSF. However, we found significant differences in NSE levels between the patients with febrile convulsions and those with seizure disorders (non-febrile, abnormal EEG). Most of our patients with febrile convulsions were cases of simple febrile convulsion, and their NSE levesin the CSF and serum were 4.55 +/- 1.00 and 8.06 +/- 3.18 ng/ml. Cases with non-febrile seizure disorders had significantly higher level of NSE in both CSF and serum (P less than 0.05). Patients with purulent meningitis usually had higher levels than those with aseptic meningitis. Our study can be summarized thus: 1. A normal level of NSE does not exclude severe neuron damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies of neuron-specific enolase levels in serum and cerebrospinal fluid of children with neurological diseases. 234 56

Brain water content was measured by gas-chromatography in rats following intraperitoneal injection of drugs and fatty acids related to the etiology of Reye syndrome. A statistically significant increase in brain water content was observed following injection of 5% glucose solution, valproic acid, acetyl salicylic acid, calcium hopantenate, margosa oil, 4-pentenoic acid, linolenate and arachidonate. Seizures occurred in all animals given valproic acid, margosa oil and 4-pentenoic acid, and in 25% of those given 5% glucose solution + anti-diuretic hormone. The results of these studies may help in the selection of appropriate agents for experimental induction of acute encephalopathy and brain edema in animal models of Reye syndrome.
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PMID:Effects of drugs and fatty acids related to Reye syndrome on brain water content in rats. 251 90


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