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)

A 21 year-old man presented with a history of sudden onset of aphasia and headache. CT showed a left parietal hypodensity and pallidal calcifications. The ECG showed a Wolff-Parkinson-White's syndrome. The patient then developed successively focal epileptic seizures, temper disorders, a cardiomyopathy, a pepper and salt retinopathy with hemeralopia, a left hemiplegia, deafness, and fever of unexplained origin. Left carotid angiography showed thin, irregular or occluded branches of the middle and anterior cerebral arteries. Blood muscle enzymes, lactate and pyruvate, were elevated with acidosis. Muscle biopsy revealed a mitochondrial myopathy and blood chemistry showed a severe deficiency of respiratory chain enzymes. Death occurred after 28 months. This case showed the diagnostic features of Melas, with some elements of the Kearns-Sayre syndrome. To our knowledge, this is the first case were serial angiographies allowed demonstration of arterial changes capable of explaining cerebral infarctions.
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PMID:[Mitochondrial myopathy. Encephalopathy with lactic acidosis and cerebral infarction]. 264 81

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.
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PMID:Hypernatremia. 264 64

Endocrinological emergencies in childhood include tetany - also in the form of epileptiform seizures - and Addisonian crisis. Acute tetany is treated by the administration of calcium, with subsequent calcitriol given as an adjunct. An Addisonian crisis or similar salt-loss crisis in the adrenogenital syndrome requires the administration of salt-containing solutions, replacement of gluco- and mineralocorticoids and the balancing of the acid-base household.
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PMID:[Therapy of endocrine diseases in childhood and adolescence. 6: Endocrinologic emergencies in pediatrics]. 265 79

alpha-Guanidinoglutaric acid (alpha-GGA) has been reported to occur in the cerebral cortex after epileptic seizures. No physical characteristics of alpha-GGA have been given. A practical procedure for the preparation of alpha-GGA is reported here. alpha-GGA forms a lactam in aqueous solution at 80 degrees C. It is proposed to substitute this lactam, 1-amidino-2-pyrrolidone-5-carboxylic acid (pAGlu), for pyroglutamic acid (pGlu) at the N-terminal position in neuropeptides to modify their biological characteristics. L(+)-Glutamic acid was reacted with S-methylisothiourea (I) at pH 10 in aqueous solution to form L(-)-alpha-guanidinoglutaric acid: mp 165-168 degrees C, [alpha]22D = -22.7 (C = 4, 2 M HCl). alpha-GGA reacted promptly with excess reagent to form a salt, S-methylisothiourea-alpha-guanidinoglutarate: mp 209-210 degrees C, [alpha]22D = -13.0 (C = 4, 2 M HCl). I was removed from the salt with aqueous picric acid, since I readily formed an insoluble picrate, S-methylisothiourea picrate (mp 225-228 degrees C). Alternatively, the salt was added to a cation exchange column, and the alpha-GGA was eluted with molar ammonium acetate buffer, pH 9.5. Its lactam, 1-amidino-2-pyrrolidone-5-carboxylic acid, mp 248-249 degrees C, [alpha]22D = +2.1 (C = 4, 2 M HCl), formed a picrate (mp 196-199 degrees C).
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PMID:The lactam of alpha-guanidinoglutaric acid (1-amidino-2-pyrrolidone-5-carboxylic acid). 287 49

The calcium salt of valproic acid (Valontin) has been proposed for use in the treatment of absence, myoclonic, and tonic clonic seizures of the primarily generalized type. The present study was conducted to determine the teratogenic potential of calcium valproate in rabbits. Groups of 20 Dutch-belted rabbits were given oral doses of 50, 150, or 350 mg/kg on days 6-18 of gestation. A reference group was given 350 mg/kg sodium valproate and control groups were untreated or given vehicle alone. Animals were observed daily and body weights were recorded on gestation days 0, 6, 13, 18, and 30. Litter and fetal parameters were evaluated following uterotomies on day 30. No drug-related clinical signs or deaths occurred. Postimplantation loss and the incidence of malformed vertebrae and ribs, rudimentary or absent pollices, and extra vertebrae and ribs were increased at 350 mg/kg with both calcium and sodium salts of valproic acid. At the 150-mg/kg dose level, calcium valproate markedly increased the incidence of supernumerary ribs. No teratogenic or embryotoxic effects were seen with calcium valproate at 50 mg/kg. These data indicate that the sodium and calcium salts of valproic acid exhibit teratogenic potential in rabbits.
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PMID:Teratogenesis of calcium valproate in rabbits. 309 17

Experiments were carried out on 64 nonanesthetized male Wistar rats (200-220 g). Epileptic foci were induced by the application of a filter paper saturated with a solution of benzylpenicillin sodium salt (12,000 and 20,000 U/ml) to the sensorimotor cortex. It was shown that subsequent intraperitoneal administration of verapamil (5 mg/kg and 10 mg/kg) during steady focal epileptic activity (EpA) resulted in the suppression of EpA in most animals. The antiepileptic effect of verapamil was manifested in a reduced frequency and amplitude of spike discharges, decreased power of epileptic foci and less frequent appearance of seizure (ictal) discharges. The role of Ca canals of neuronal membranes in the pathogenesis of epilepsy is discussed.
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PMID:[Effect of verapamil on focal epileptic activity in the rat cerebral cortex]. 311 8

In order to develop a percutaneous (p.c.) dosage form of valproic acid (VPA), ointments containing VPA and both VPA and its calcium salt (VPA-Ca) were prepared. The p.c. absorption was studied by determining the plasma concentrations of VPA in rabbits following application of either ointment. In addition, the in vitro penetration study with excised full-thickness rabbit skin was done to evaluate the pharmaceutical availability. VPA was readily and rapidly absorbed through the skin from the gel ointment. The plasma concentrations of VPA higher than 30 micrograms/ml were maintained for 6 h after application of 5% VPA.5% VPA-Ca gel ointment, and for 4 h after application of 5% VPA ointment. The bioavailability of VPA following dosing of both ointment was above 97%. The in vitro penetration rate through the skin and skin/solvent partition coefficient were significantly lower with 5% VPA.5% VPA-Ca solution than with 5% VPA, suggesting the slower penetration of VPA from the 5% VPA.5% VPA-Ca. A small difference was observed in the release rate of drugs from these ointments. The present results demonstrated the pharmaceutical effectiveness of the VPA.VPA-Ca ointment for seizure disorders.
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PMID:Percutaneous absorption of valproic acid and its plasma concentration after application of ointment. 312 87

The results of 373 EEG investigations were analysed. They were obtained in a period of 4 years in 222 workers with occupational exposure to metallic mercury in the synthesis of acetaldehyde and salt electrolysis. Abnormal or borderline abnormal results were found in 13% of them. Results were compared in groups differing in age, duration of occupation, working post and Hg excretion with urine. Significantly greater frequency of increased Hg absorption was found in the group with abnormal records. The authors stressed the following morphological features of EEG in those exposed to Hg: tendency for seizure activity, loss of ability of following of rhythmic flashes, unchanged frequency of background activity despite increasing degree of other abnormalities, absence of low-voltage tracings, persistence of abnormalities in the records after loss of contact with mercury.
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PMID:[Value of electroencephalographic studies for the evaluation of the neurotoxic effect of metallic mercury]. 326 31

Six patients [5 men and 1 woman, mean age 37.3 +/- 8.2 (SD) years] with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent a sequence of treatments in an effort to normalize basal serum sodium levels and thereby protect the patients against complications, including hyponatremic seizures and coma. The morning baseline group mean basal serum sodium value was 132.5 +/- 3.8 meq/liter. Over a 20-month period, the sequence of treatments was salt-added diet, lithium and phenytoin, and lithium alone. Each treatment program yielded morning group mean basal serum sodium determinations superior to baseline values, except for the program of lithium alone, which could not be tolerated. The combination of lithium and phenytoin provided a morning group mean basal serum sodium level of 140.6 +/- 3.2 meq/liter, which was superior (p less than 0.01) to all other treatment modalities. Early morning hyposthenuria persisted throughout the 20-month period of observation.
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PMID:Treatment of psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) using lithium and phenytoin. 333 51

A case of long-term acetaminophen overdosage in a six-year-old child, which contributed to her death despite optimal medical management including oral acetylcysteine therapy, is reported. Acetaminophen 325 mg every six hours was prescribed for fever associated with measles. Believing that acetaminophen was nontoxic, the child's mother progressively increased the dose over three days, first in response to fever and subsequently for abdominal pain probably secondary to unrecognized acetaminophen toxicity. On admission to the hospital, the patient's serum acetaminophen concentration was 163 micrograms/mL (11 hours after the last dose); subsequently, the acetaminophen half-life was determined to be 15 hours. A course of oral acetylcysteine therapy (a loading dose of 140 mg/kg as the sodium salt followed by 70 mg/kg every four hours for 17 doses) was begun. Hepatic and renal failure developed within two days, followed by the onset of seizures, and brain death occurred on the 11th day. Autopsy findings consistent with acetaminophen toxicity included centrilobular hepatic and renal tubular necrosis. Aspergillis fumigatus and Cryptococcus neoformans isolates from pulmonary abscesses and bronchopulmonary lymph nodes, respectively, were an unexpected finding. However, in the absence of acetaminophen overdosage, death would have been unlikely. Cryptococcal lymphadenitis was believed to have been the initial febrile illness that was treated with supratherapeutic doses of acetaminophen. Fatalities in children from a single overdose of acetaminophen have been rare, and there is only one previous report of a fatality after long-term administration of multiple excessive doses. The lethal outcome in this case illustrates the need to educate the public on the potential toxicity of nonprescription medications.
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PMID:Death of a child associated with multiple overdoses of acetaminophen. 338 45


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