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

There are many causes of lens dislocation in man. Amongst these are two inborn errors of sulfur amino acid metabolism, viz., homocystinuria and sulfite oxidase deficiency. To date nine patients have been found in whom a combined deficiency of sulfite oxidase and xanthine dehydrogenase was observed. This inherited disease is due to a defective synthesis of molybdenum cofactor, an essential component for the assembly of both enzymes. The main clinical symptoms of these patients were: facial dysmorphic features, severe feeding difficulties, mental retardation, abnormal muscle tone, severe seizures and myoclonia. Four out of nine patients had dislocated eye lenses. The main biochemical findings included hypouricemia, xanthinuria, an increased excretion of sulfite, thiosulfate, S-sulfocysteine, taurine and a decreased excretion of inorganic sulfate. The prognosis of the disease is poor; various attempts at treatment were not successful so far. Prenatal diagnosis by assay of sulfite oxidase in cultured amniotic fluid cells and by direct measurement of amniotic fluid S-sulfocysteine is possible.
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PMID:Absence of hepatic molybdenum cofactor. An inborn error of metabolism associated with lens dislocation. 387 98

Male Long-Evans rats were kindled via daily electrical stimulation of the left prepyriform cortex. The animals were then used in two experiments which examined the pharmacological basis of cocaine's effects on three mutually exclusive components of the kindled seizure, which were the following: (a) latency to clonus, (b) clonus duration, and (c) duration of AD outlasting clonus. The first experiment compared the effects produced by cocaine HCl (20 mg/kg, IP), lidocaine HCl (20 mg/kg, IP), and amphetamine sulfate (2.5 mg/kg, IP). The results indicated that both cocaine and lidocaine reduced the duration of kindled AD, latency to clonus, and duration of AD persisting beyond clonus, thus suggesting that these cocaine effects are mediated by local anesthetic mechanisms. Only cocaine reduced clonus duration, which suggests that this cocaine effect is not produced by a local anesthetic action. The second experiment examined the effects of cocaine following the administration of three dose levels of the monoamine antagonists haloperidol, prazosin, yohimbine, propranolol, or metergoline (selected for their ability to block dopamine, alpha-1-norepinephrine, alpha-2-norepinephrine, beta-norepinephrine, and serotonin receptors, respectively). The results of this experiment found no support for a monoaminergic contribution to cocaine's effect on clonus latency or AD after clonus. However, results for prazosin, which reduced clonus duration and exhibited an additive effect with cocaine on this variable, suggest that cocaine's norepinephrine action (especially on the alpha-norepinephrine systems) may modulate clonus duration.
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PMID:Monoaminergic and local anesthetic components of cocaine's effects on kindled seizure expression. 399 58

Previous studies from this laboratory have shown that pyridoxal-5'-sulphate, the synthetic analogue of pyridoxal phosphate, causes epileptic seizures including tonic-clonic convulsions. These seizure activities are prevented or reversed by GABA or muscimol. In an attempt to delineate the biochemical basis of these seizure processes further, we have studied and shown that pyridoxal sulphate is a competitive inhibitor of glutamic acid decarboxylase. In addition, the chronic administration of pyridoxal sulphate was shown to reduce the concentration of pyridoxal phosphate in the cerebellum, the cerebrum, and basal ganglion, but not in the hippocampus. The activity of hippocampal glutamic acid decarboxylase was reduced after 1, 3, and 5 days of chronic application of pyridoxal sulphate. The inhibition was demonstrated, whether glutamic acid decarboxylase was assayed in the presence or absence of its coenzyme pyridoxal phosphate. Unlike findings in the hippocampus, the activity of glutamic acid decarboxylase in other brain regions was unaffected following chronic application of pyridoxal sulphate. The selective toxic effects of pyridoxal sulfate to the hippocampus, a brain area well known for its high susceptibility to seizure discharges, deserve additional indepth investigation.
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PMID:Pyridoxal phosphate-unrelated inhibition of hippocampal glutamic acid decarboxylase by convulsant pyridoxal sulphate. 400 Mar 91

A retrospective study of 781 alcoholics detoxified at two treatment centers suggested that magnesium sulfate was significant in preventing seizures and that benzodiazepines were essential in minimizing other complications. Future investigations should determine the most effective mineral dosage levels for alcohol detoxification.
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PMID:Clinical experience with 781 cases of alcoholism evaluated and treated on an inpatient basis by various methods. 403 Jan 78

The use of magnesium sulfate as an anticonvulsant remains controversial. The effect of parenteral magnesium sulfate on established penicillin-induced seizure foci in anesthetized cats was studied. After induction of an epileptic focus by application of penicillin to the cerebral cortex, experimental animals were infused intravenously with magnesium sulfate, whereas control animals received normal saline solution at an equivalent rate. Experimental animals achieved a mean serum magnesium level of 11.73 +/- 2.00 mg/dl. Analysis of the electroencephalogram recordings demonstrated no significant difference in epileptic spike activity between the experimental and control groups. The critical importance of adequate controls in studies of this type is stressed.
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PMID:Effect of parenteral magnesium sulfate on penicillin-induced seizure foci in anesthetized cats. 403 7

Neurotoxicity is a well-recognized and commonly observed side effect associated with the use of vincristine sulfate in cancer chemotherapy. The clinical manifestations of vincristine neuropathy cover a wide spectrum of peripheral neurologic dysfunctions that have been described to be reversible and cumulative in most instances (1, 2). Paresthesias, loss of tendon reflexes, and progressive weakness are the most common clinical features (3, 4). Sensory impairment, cranial nerve palsies, gastrointestinal disturbances, and autonomic dysfunctions including atonic bladder, impotence, and orthostatic hypotension may occur (5). Acute CNS complications, usually presenting as generalized seizures, are extremely rare and only a few cases have been reported which were without underlying biochemical or structural abnormalities (1, 5-9). We describe the case of a woman with multiple myeloma, who developed fulminant encephalopathy following 4 days of continuous vincristine, adriamycin, and day 1-4 pulse dexamethasone (VAD) combination therapy.
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PMID:Acute encephalopathy associated with continuous vincristine sulfate combination therapy: case report. 406 27

All adult cardiopulmonary resuscitations attended by the pharmacy department at a 486-bed tertiary-care institution were analyzed over a 24-month period. Data describing patient demographics, drug and equipment use, and patient survival were collected on 516 consecutive adult arrests. These data were recorded on a report form by a pharmacy technician and were classified as cardiac, respiratory, trauma, or other. Trauma included arrests caused by motor-vehicle accidents and gunshot wounds, and other included arrests caused by anaphylaxis or seizures. The majority of arrests (70%) were classified as cardiac, 24% as respiratory, and 6% as other. Overall, 54.5% of the patients suffering from arrests were resuscitated successfully. There was an equal distribution of arrests throughout the day. The mean duration of the resuscitation efforts was 38 minutes with a trend toward greater patient survival when resuscitation efforts lasted less than 15 minutes. Arterial blood-gas determinations were made in 81% of the arrests, defibrillations in 40%, and pacemaker or chest tube insertion in less than 10%. Sodium bicarbonate was the most frequently administered medication, followed by calcium salts and atropine sulfate. Lidocaine was used in 83% of the cases requiring antiarrhythmic therapy. Pressor support was required in 44.6% of the cases; norepinephrine bitartrate was the first-line pressor agent. Drugs not categorized as essential according to the American Heart Association's Advanced Cardiac Life Support (ACLS) standards were administered infrequently. Hospitals may benefit from arrest data in assessing their equipment and supply needs, staffing patterns, and personnel training programs.
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PMID:Evaluation of 516 cardiopulmonary resuscitation attempts. 407 65

Two neonates suffered from generalized seizures during the course of intravenous morphine sulfate for post-operative analgesia. They received morphine in doses of 32 micrograms/kg/hr and 40 micrograms/kg/hr larger than a group of 10 neonates who received 6-24 micrograms/kg/hr and had no seizures. Plasma concentrations of morphine in these neonates was excessive (60 and 90 mg/ml). Other known reasons for seizures were ruled out and the convulsions stopped a few hours after cessation of morphine and did not reoccur in the subsequent 8 months. It is suggested that post-operative intravenous morphine should not exceed 20 micrograms/kg/ml in neonates.
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PMID:Morphine-induced seizures in newborn infants. 408 66

Mice of the DBA/2/M strain are audio-sensitive only for a short period (5 to 10 days). When this period is over, 100 p. 100 audiogenic seizures can be obtained with experimental magnesium deficiency. When AKR/R, OF1 and C57BL/R mice were deprived of magnesium for 15 or 21 days, they manifested an audiogenic attack only when given amphetamine sulfate, caffeine or isonicotinylhydrazine. If they had been deprived for 43 days, it was no longer necessary to administer these substances. The audiogenic attack could be prevented by correcting the deficiency with magnesium chloride or by preliminary administration of a single dose of various barbiturics, anti-convulsives, tranquillizers or parachlorophenylalanine, but not neuroleptics.
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PMID:[Audiogenic seizure in the mouse according to strain and sex: the effect of the magnesium ration and neuromediators]. 613 May 80

The effects of pyridoxal phosphate, pyridoxine and hydrazine were studied on homocysteine-induced seizures in mice. Both of the B6 vitamers significantly decreased the latency and increased the severity, lethality and duration of seizures induced by homocysteine. The B6 inhibitor hydrazine sulfate, which is normally a convulsant, prevented the tonic component of the convulsions and increased the latency to the clonic component. This experiment indicates that a vitamin B6 dependent step is critically involved in the metabolic changes which precede homocysteine seizures.
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PMID:Homocysteine induced convulsions: enhancement by vitamin B6 and inhibition by hydrazine. 626 Mar 8


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