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

Seizure is a common problem evaluated in pediatric emergency departments. Serum chemistry analysis is often performed as a routine part of the diagnostic evaluation of children who arrive in the ED with seizure. From this retrospective study, we sought to determine 1) how often serum electrolytes (Na, K, Cl, CO2), total calcium, magnesium, ammonia, and glucose chemistries were performed, 2) the frequency of abnormalities detected, and 3) whether abnormalities resulted in a change in patient care. Three hundred eight ED charts from 12 consecutive months were reviewed. Data collected included age, sex, ED diagnosis, medical history, and physical examination. Charts were also reviewed for diagnostic tests ordered and patient management. Children were classified as having febrile (FS) or nonfebrile seizures (NFS) to establish diagnostic evaluation practices for each group as well as to determine rates of laboratory abnormalities. Three hundred eight children were enrolled, 108 (35%) FS and 200 (65%) NFS. The mean ages of FS and NFS patients were 2.1 and 5.7 years, respectively (P less than 0.05, t-test). One hundred twenty-four of 308 (40%) children had at least one test performed; no abnormal test was thought to have caused seizure; none was treated. One hundred five of 308 (34%) were experiencing their first seizure. There was no difference in the likelihood of having a test ordered for children with a first seizure, regardless of seizure category. We concluded that 1) abnormal serum electrolytes, total calcium, magnesium, and glucose rarely cause seizure in children and 2) routine use of these tests in the ED is costly and does not contribute to seizure therapy.
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PMID:Emergency department laboratory evaluation of children with seizures: dogma or dilemma? 160 83

Changes in amino acids (AA) and ammonia were investigated in the cerebral cortex and striatum of rats after the following conditions: 1) one hyperbaric oxygen (HBO)-induced seizure (6 ATA O2); 2) exposure to 6 ATA air; and 3) exposure to atmospheric pressure (no seizures in both latter groups). Exposure to 6 ATA air produced no change with respect to atmospheric pressure. After HBO seizure, AA levels (except for gamma-amino butyric acid, GABA, and glutamine), with respect to 6 ATA air levels, were altered in the striatum with a concomitant rise in ammonia (+70%) at variance with the cortex. These changes could be explained by increased oxidative deamination in the striatum. Decrease in taurine content (-66%) in the striatum, where HBO lipoperoxidation exists, suggests an alteration of glial function leading to blockade of uptake and loss of released products in interstitial fluid. This pattern of change recalls the one seen in ischemic conditions, but cannot be confirmed in the absence of measurements of extracellular amino acid levels under HBO conditions. The maintenance in the level of GABA would favor its role in controlling seizure. In the cortex, only a few AA levels decreased, along with a nonsignificant trend for ammonia to increase. The remaining abnormalities in the striatum, after the first HBO seizure, may explain the already known repetition of seizures in continuously exposed animals and are consistent with previous data on the important role of the striatum.
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PMID:Changes in striatal and cortical amino acid and ammonia levels of rat brain after one hyperbaric oxygen-induced seizure. 161 Mar 39

From 65 reported cases of medium chain acyl-CoA dehydrogenase deficiency, we found an average presenting age of 13.5 months and a mean age at death of 18.5 months. One quarter of patients died of a Reye-like syndrome and/or sudden infant death. In half the cases there had been at least one sibling death. Asymptomatic cases were not uncommon (12% of cases). The crises were generally induced by a prolonged fast and after a viral prodromal phase in three quarters of cases. The crises consisted of somnolence progressing to lethargy which could lead to coma. Vomiting was frequent (60% of cases). Seizures, which were found in 29% of cases, represented a bad prognosis. The physical examinations revealed frequently a variable and regressive anicteric hepatomegaly. Blood and urine analysis revealed in most instances hypoglycaemia (96% of cases) with hypoketonuria and sometimes metabolic acidosis. Hepatic and muscular cytolytic enzymes were frequently raised, as were plasma ammonia, urea, and uric acid. Plasma total or free carnitine concentrations, especially non-fasting, were diminished in most cases. Plasma saturated medium chain fatty acids and particularly unsaturated cis-4-decenoate were on the other hand raised during the crises or during fasting. Urinary organic acid analysis revealed a characteristic profile of medium chain aciduria: C6-C10 dicarboxylic acids, hydroxy acids, glycine conjugates, and carnitine conjugates. Oral loading tests with carnitine or phenylpropionate allow a precise diagnosis. The diagnosis is confirmed by specific assays in various tissues. Avoidance of prolonged fasting seems to be the mainstay of treatment.
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PMID:Medium chain acyl-CoA dehydrogenase deficiency. 173 32

Administration of ammonium acetate to mice caused seizures and alterations of brain energy metabolites. Pretreatment of animals with L-carnitine suppressed the frequency of the seizures and prolonged the latency to the first fit. When examined using the 'freeze clamp' method, brain energy metabolites were well preserved and the elevation of ammonia was less marked on administration of L-carnitine. Thus, L-carnitine suppresses ammonia-induced seizures and biochemical alterations of the brain in mice.
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PMID:Suppression of neurotoxicity of ammonia by L-carnitine. 181 38

A case of propionic acidemia is reported. The main features of this patient were recurrent vomiting, ketosis and occasional episodes of seizure. Serum concentrations of propionic acid and glycine were within the normal range. Blood ammonia was slightly elevated. Characteristic organic acids were present in the patient's urine. they were: 3-hydroxypropionic acid, propionylglycine, methyl-citric acid, tiglyglycine, 3-hydroxyvaleric acid, etc. The etiology, pathogenesis, clinical features, diagnosis, and treatment of propionic acidemia are briefly discussed.
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PMID:[Propionic acidemia: one case report]. 183 12

A 24-year-old man was admitted to our hospital, because two days before the admission he had abruptly lost consciousness following generalized convulsive seizures. He had a past history of transient amnesia and a favor for peanuts. His grandparents had a record of consanguinity. On admission, he was comatose and flaccid with his four extremities. Laboratory examination revealed the followings; mild degree of abnormal liver function, slight elevation of blood ammonia, irregular theta basic rhythm on EEG, marked brain edema on CT and a normal liver ultrasonography. From the second hospital day, in addition to antiepileptic drugs and adrenocorticosteroids, branched chain amino acid was administered to reactivate damaged brain functions. Thereafter, the concentration of blood ammonia increased to more than 3,000 micrograms/dl, and as a result he fell into status epilepticus. On the fourth hospital day, the levels of citrulline in the plasma and urine taken on the first hospital day were found to have increased by 20 and 100 times, respectively. Although the transfusion of branched chain amino acid was stopped, he died while in coma on the 12th hospital day. Enzymatic analyses of necropsied liver specimens revealed that the quantitative activity of argininosuccinate synthetase had decreased to less than 10% in his urea cycle. In this patient, it was noted that, after transfusion of branched chain amino acid, his brain activities turned worse and blood ammonia was markedly elevated. There is a possibility that intravenous administration of branched chain amino acid may interrupt the urea cycle balance in an adult patient of citrullinemia with dysfunction of the brain, kidney and muscle, especially with brain edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Adverse effects of branched chain amino acid transfusion on type-II citrullinemia--report of an adult case]. 191 26

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

Congenital hyperargininaemia is a rare condition transmitted as an autosomal dominant trait. Following a one-year free interval, repeated vomiting, psychomotor regression and spastic paraparesis with talipes equinus progressively develop. The diagnosis, confirmed by arginine assays in blood and urine, is probably often missed. We report a case of homozygous arginase deficiency belatedly diagnosed at the age of 18 years, when treatment with sodium valproate (VPA) was instituted. This female patient presented with psychomotor regression since the age of 15 months and with paraparesis since she was 3 years' old. These symptoms rapidly became worse. At the age of 18 years, when she was bed-ridden, she was hospitalized for subintrant tonic seizures. EEG showed generalized, continuous spike-wave discharges at the rate of 3.5 c/s. Treatment with VPA was instituted. Five days later, she went into a state of stupor. Blood ammonia level was elevated at 362 mumol/l. VPA was discontinued, and this was followed by a regression of disturbances of consciousness and by a decrease in arterial ammoniaemia, although the ammonia levels remained high, fluctuating between 40 and 100 mumol/l. Several months after VPA treatment was interrupted, the patient had a second episode of stupor, and her ammoniaemia was 500 mumol/l. Serum amino acid chromatography showed hyperargininaemia at 501 mumol/l (N = 30-150 mumol/l). The diagnosis of arginase deficiency was confirmed by the rise of arginine in red cells, cerebrospinal fluid and urine and, above all, by the finding of a deeply depressed arginase activity in erythrocytes. In all cases of intolerance to VPA, arterial ammoniaemia should be measured after withdrawal of VPA, some time after the acute episode.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Late diagnosis of congenital argininemia during administration of sodium valproate]. 229 Oct 40

Monoamines (catecholamines, serotonin, and metabolites) and ammonia were studied within two areas of the rat brain--the frontal cortex (FC) and the striatum (SA)--after exposure to hyperbaric oxygen (HBO) at 6 ATA up to the first seizure. An increase of norepinephrine (NE), dopamine (DA), and metabolites (HVA, DOPAC) measured by the HPLC/EC method were found in SA with a parallel increase of ammonia at variance with the FC where no monoamine changes, but a slight increase of ammonia, were found. Blood ammonia did not change with HBO. So, 20 min after one HBO seizure, there are regional differences in the brain, which are consistent with the previous findings of an SA start of electrocortical abnormalities at the onset of a seizure. Elevated DA, and possibly NE, levels may contribute to the accumulation of ammonia in the brain. During prolonged HBO exposure, this rise of ammonia could be one of the mechanisms involved in the relapse of seizures. It might also be implicated in initiation of the first seizure. By their situations and contents, SA glial cells could play an important role in brain HBO susceptibility.
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PMID:Ammonia and monoamine concentrations in two brain areas in rats after one hyperoxic seizure. 230 23

A previous study of the patterns of visual evoked responses (VERs) in rats was interpreted as providing support for the synergistic neurotoxins hypothesis of the pathogenesis of hepatic encephalopathy (HE) due to fulminant hepatic failure (FHF). In contrast, other studies of the patterns of VERs in rabbits with different encephalopathies were interpreted as providing support for the concept that increased GABA-ergic tone may contribute to the neural inhibition of HE due to FHF. To attempt to resolve the discordant findings in these studies, additional studies of VERs have been undertaken in rats. To induce increased tissue levels of ammonia, mercaptans and fatty acids which are found in HE due to FHF, carefully predetermined doses of urease, dimethyldisulphide and octanoic acid were administered. The (pre-seizure) encephalopathy induced by these three agents was associated with abnormalities of the VER waveform that were fundamentally different from the abnormalities of the VER waveform associated with HE due to thioacetamide-induced FHF. However, the VER waveform in this model of HE due to FHF resembled closely that associated with pentobarbital-induced encephalopathy. These findings are in satisfactory agreement with those in the previous analogous studies in rabbits. They do not provide support for the synergistic neurotoxins hypothesis of the pathogenesis of HE, but are entirely consistent with increased GABA-ergic tone contributing to the neural inhibition of HE due to FHF.
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PMID:Hepatic encephalopathy. Application of visual evoked responses to test hypotheses of its pathogenesis in rats. 303 57


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