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)

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Total muscle phosphorus content fell from 28.0+/-1.3 to 26.1+/-2.5 mmol/dg fat-free dry solids. Sodium, chloride, and water contents rose. These changes resembled those observed in patients with subclinical alcoholic myopathy. When studied after 3 days of hyperalimentation, the animals not receiving phosphorus showed weakness, tremulousness, and in some cases, seizures. Serum phosphorus fell, the average lowest value was 0.8 mg/dl (P <0.001). CPK activity rose from 66+/-357 to 695+/-1,288 IU/liter (P <0.001). Muscle phosphorus content fell further to 21.1+/-7.7 mmol/dg fat-free dry solids (P <0.001). Muscle Na and Cl contents became higher (P <0.01). Sections of gracilis muscle showed frank rhabdomyolysis.6 of the 23 phosphorus- and calorie-deprived dogs were also given 140 kal/kg per day but in addition, each received 147 mmol of elemental phosphorus. These dogs consumed their diet avidly and displayed no symptoms. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. The gracilis muscle appeared normal histologically in these animals. These data suggest that a subclinical myopathy may set the stage for rhabdomyolysis if acute, severe hypophosphatemia is superimposed. Neither acute hypophosphatemia nor rhabdomyolysis occur if abundant phosphorus is provided during hyperalimentation.
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PMID:Hypophosphatemia and rhabdomyolysis. 74 77

1. Sodium di-n-propylacetate (DPA) treatment induced significant increases in brain contents of gamma-aminobutyric acid (GABA), 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA). Furthermore, the threshold for pentylenetetrazol (PTZ) clonic convulsions was also increased in response to DPA administration. 2. Pretreatment with inhibitors of monoamine synthesis alpha-methyl-p-tyrosine (AMPT) and p-chlorophenylalanine (PCPA) did not alter the anticonvulsant activity of DPA, but when given alone, both AMPT and PCPA caused significant decreases in brain monoamine contents and PTZ threshold seizures. 3. Experiments using probenecid suggest that the increases in 5-HIAA and HVA seen after DPA treatment could have resulted from inhibition of their active transport out of the brain. These data indicate that the anticonvulsant action of DPA is not dependent on changes in monoamine metabolism in the brain.
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PMID:Anticonvulsant activity of di-n-propylacetate and brain monoamine metabolism in the rat. 169 53

The heterogenous psychoses in epilepsies, caused by well known conditions, are not rare but associated with regularly a few of seizure-types not with the nature and development of attacks. Polar transitional ranks and converging courses of schizophrenic (accentuated) syndromes in epilepsies and idiopathic schizophrenias are rather frequent. Also (sub-)acute schizophrenic psychoses are corresponding to the complete palette of first and second rank symptoms (K. Schneider) of idiopathic schizophrenias. After manifestations of epilepsy these syndromes can appear at any time. It is given a profile of risks. Progressive avoidance of a. phenylaceturea, b. mixtures of antiepileptics did not put an end to psychotic syndromes: Long-term therapies with 1. Polytherapy, 2. Primidone and Phenytoin (dosedependant) as well as 3. Ethosuximide (-monotherapy) cause a disorder of feed back mechanisms, especially a disturbed regulation of vigilance and sleeping-waking-cycle and their psychological correlates. Carbamazepine and Sodium Valproate are, plasma-level-controlled of preventive antipsychotic effect. Selected neuroleptics of rather slight epileptogenic potency are of going down importance. Benzodiazepines are required mostly in prepsychotic syndromes, Lithium compounds in selected cases. There is no more alternative seizures or psychosis.
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PMID:[Psychoses in epilepsy]. 198 Oct 95

Sodium diphenylhydantoin (DFH-Na) is the drug of choice to control convulsive seizure disorders. Beneficial as well as adverse effects of DFH-Na have been reported to occur since 1938. Thus, the present article deals with the effect that 2.5, 5, 10, 15, 20 and 100 mg/kg/day (2.5, 5, 10, 15, 20 and 100) might cause on Cerebrum (C), Cerebellum (Cb) and liver (L) DNA [DNA] and Protein [Pr] concentration. Our results showed that: 1) DNA-C-14 (15, 20 and 100) were found decreased when compared to control (p less than 0.001) and [DNA]-C-30 (15, 20 and 100) as well (p less than 0.001). [Pr]-C-7, 14, 30 (2.5, 5, 10, 15, 20 and 100) showed no statistically important differences. 2) [DNA]-Cb-14 (15 and 20) were found lower than control (p less than 0.05) and [DNA]-Cb-30 (15 and 20) as well (p less than 0.05). [Pr]-Cb-14,30 (100) was found decreased (p less than 0.05). 3) [DNA]-L-14 (10, 15, 20 and 100) was found decreased when compared to control (p less than 0.001) and [DNA]-L-30 (10, 15, 20 and 100) as well (p less than 0.001). [Pr]-L-7, 14 and 30 (2.5, 5, 10, 15, 20 and 100) were found lower than control (p less than 0.05). A bimodal pattern of [DNA] of C. Cb and L was demonstrated to occur with i.p. injected DFH-Na.
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PMID:[Sodium diphenylhydantoin changes the concentrations of DNA and proteins in the cerebrum, cerebellum and liver]. 222 13

Sodium phenobarbitone (20 and 70 mg/kg) had a significant anticonvulsant action against pentylenetetrazole-induced seizures, which persisted for 21 days of treatment. On drug withdrawal there was a significant decrease in seizure threshold below control level 24-48 h after the last dose of 70 mg/kg. Phenytoin (40 mg/kg) had a significant anticonvulsant action after 7 days of treatment and this persisted for 21 days of treatment. On drug withdrawal there was a significant decrease in seizure threshold 48 h after the last dose. Lorazepam (0.1 mg/kg) had a significant anticonvulsant action, but the group tested after 21 days of treatment did not differ from the controls, indicating that tolerance had developed to this effect; on drug withdrawal there was a decrease in seizure threshold from 24 to 72 h. The only drug to increase aggressive behaviour was sodium phenobarbitone (70 mg/kg); this reached significance after 14 and 21 days of treatment and occurred 8 h after drug administration; 0.5 h after drug administration phenobarbitone (70 mg/kg) abolished aggressive behaviour. After 7 days of treatment phenobarbitone (70 mg/kg) increased social behaviour 0.5 h after administration and this was still increased after 21 days of treatment. On drug withdrawal, there were no changes in aggressive behaviour, but there were significant decreases in social behaviour 24 and 48 h after phenobarbitone (70 mg/kg) withdrawal and 24, 48 and 72 h after lorazepam (0.1 mg/kg) withdrawal.
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PMID:Changes in seizure threshold and aggression during chronic treatment with three anticonvulsants and on drug withdrawal. 230 12

Three days after systemic administration of kainic acid (15 mg/kg, s.c.), selected cholinergic markers (choline acetyltransferase, acetylcholinesterase, muscarinic acetylcholine receptor, and high-affinity choline uptake) and GABAergic parameters [benzodiazepine and gamma-aminobutyric acid (GABA) receptors] were studied in the frontal and piriform cortex, dorsal hippocampus, amygdaloid complex, and nucleus basalis. Kainic acid treatment resulted in a significant reduction of choline acetyltransferase activity in the piriform cortex (by 20%), amygdala (by 19%), and nucleus basalis (by 31%) in comparison with vehicle-injected control rats. A lower activity of acetylcholinesterase was also determined in the piriform cortex following parenteral kainic acid administration. [3H]Quinuclidinyl benzilate binding to muscarinic acetylcholine receptors was significantly decreased in the piriform cortex (by 33%), amygdala (by 39%), and nucleus basalis (by 33%) in the group treated with kainic acid, whereas such binding in the hippocampus and frontal cortex was not affected by kainic acid. Sodium-dependent high-affinity choline uptake into cholinergic nerve terminals was decreased in the piriform cortex (by 25%) and amygdala (by 24%) after kainic acid treatment. In contrast, [3H]flunitrazepam binding to benzodiazepine receptors and [3H]muscimol binding to GABA receptors were not affected 3 days after parenteral kainic acid application in any of the brain regions studied. The data indicate that kainic acid-induced limbic seizures result in a loss of cholinergic cells in the nucleus basalis that is paralleled by degeneration of cholinergic fibers and cholinoceptive structures in the piriform cortex and amygdala, a finding emphasizing the important role of cholinergic mechanisms in generating and/or maintaining seizure activity.
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PMID:Changes in cholinergic but not in GABAergic markers in amygdala, piriform cortex, and nucleus basalis of the rat brain following systemic administration of kainic acid. 254 59

The Lennox-Gastaut Syndrome is one of the most refractory form of epilepsy and a variety of compounds, such as traditional antiepileptics, "new anticonvulsants" and non-anticonvulsant drugs has been tested. ACTH and, among the traditional antiepileptics. Clonazepam and Sodium Valproate showed the most favorable effects. The immediate (within 6 months) therapeutic response to ACTH and Clonazepam is satisfactory, with a more than 50% reduction of seizures in about one half of patients; after one year, however, only a small percentage of cases (7-10%), rather close to that with spontaneous remission, shows some therapeutic benefit. Valproate, when used as a single drug, produces a decrease in seizures (greater than 50%) in 25-30% of pts. A list of compounds, such as amphetamine, taurine, amantadine, allopurinol and, among the new putative antiepileptics, cinromide and gamma-vinyl-GABA, has been tested with some occasionally observed improvement in seizure control. None of these compounds, however, is of really proven efficacy. An acquired general rule of treatment is to avoid complex polypharmacy and overdose; there is in fact good evidence that making the child drowsy will greatly increase the number of fits.
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PMID:[Lennox-Gestaut syndrome: therapeutic aspects]. 270 Aug 41

In this study we describe a preparation in which we examined directly, using tight-seal whole-cell recording, sodium currents from embryonic Drosophila neurons maintained in culture. Sodium currents were expressed in approximately 65% of the neurons prepared from wild-type Drosophila embryos when examined at room temperature, 24 hr after plating. While current density was low, other features of the sodium current in wild-type neurons, including the voltage sensitivity, steady-state inactivation, macroscopic time course, and TTX sensitivity were similar to those found in other excitable cells. Physiological and biochemical evidence has led to the suggestion that mutations in the nap, seizure, and tip-E loci of Drosophila may affect voltage-dependent sodium channels. There was no significant difference in the percentage of neurons expressing sodium currents in cultures prepared from embryos with mutations at the nap, sei or tip-E loci compared with wild-type cultures. Sodium currents recorded from napts appeared similar in all of the properties examined to those in wild-type cells. However, neuronal sodium current density was 40-60% lower in cultures prepared from both tip-E and seits1 embryos. The voltage dependence and gating properties of these sodium channels, as well as the TTX sensitivity, appear similar to wild type. These results indicate that both the tip-E and sei loci are important in regulation of sodium current density in embryonic neurons.
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PMID:Voltage-clamp analysis of sodium channels in wild-type and mutant Drosophila neurons. 284 3

The results of therapy have been analyzed in a series of 192 patients admitted for status epilepticus over 7 years in two intensive care units. Most (142 cases without any prior epilepsy) corresponded to secondary forms. In 2/3 of the cases, the patients were admitted because of failure of benzodiazepines and/or phenobarbitone. Sodium thiopentone achieved control of seizures in 75%; short-acting barbiturates should be especially prescribed in grand mal status with impending brain anoxia. Diphenylhydantoin would appear suitable in non-life-threatening conditions such as serial seizures or partial status. Chlormethiazole often succeeds in controlling convulsive status which has proved refractory to other treatment. Supportive management is mandatory: 52% of patients required respiratory assistance. Fatalities (36%) exclusively correspond to the underlying cerebral conditions and systemic disorders.
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PMID:[Treatment of status epilepticus in the adult. Retrospective analysis of 192 cases treated in intensive care units]. 286 66

The authors report the results obtained in 42 patients affected by infantile spasms syndrome during treatment with Sodium Dipropylacetic acid. The subjects were divided into two groups according to the aetiology: idiopathic and secondary. In the first group the use of DPK as determined the disappearance of the seizures in 6 cases (40%), reduction of the crises beyond 50% in 7 cases (46.6%), while in 2 subjects (13.3%) the crises persisted. In the secondary group the crises ceased in 3 cases (11.1%), in 17 (62.9%) there were a reduction of the crises beyond 50%, no response to the drug was observed in 7 subjects (25.9%). In 10 patients the anticonvulsant treatment was progressively diminished and was substituted with hormonal treatment. The long term follow up (1-6 years) gives the following results: the seizures persisted in 2 cases (18.18%) among the idiopathic form and in 6 cases (28.57%) among the secondary group. Mental retardation was found in 4 subjects (36.36%) among the idiopathic group and in 12 patients (57.14%) among the secondary group. The authors shortly report the side effect of the hormonal treatment: they prefer the initiation of treatment of I.S. with anticonvulsant drug and suggest to resort to the ACTH when the initial treatment is unsuccessful.
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PMID:[Therapy of infantile spasms (West syndrome) with sodium dipropylacetate]. 301 74


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