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 controlled clinical trial of the anti-epileptic efficacy and toxic side effects of diphenylsilanediol was conducted on 24 client-owned epileptic dogs. Data obtained from an abbreviated procedural treatment program indicated that diphenylsilanediol compared favorably with primidone as an anti-epileptic compound, but had limiting toxic side effects to the liver, pancreas, and possibly to other tissues. There was a mean reduction of 60.7% in seizure frequency in 15 epileptic dogs treated with diphenylsilanediol when compared with their pretreatment frequency. There was a mean reduction of 55.6% in seizure frequency in 9 spileptic control dogs treated with primidone. Samples of blood obtained from the dogs in the program on the 4th, 8th, 12th, 24th, and 36th weeks of treatment were examined for complete blood cell count, blood urea nitrogen, liver function, and pancreatic function. Toxic side effects were not seen among the primidone-treated control dogs, with the exception of occasional dose-related drowsiness. Among the diphenylsilanediol-treated dogs, 3 developed liver disease, 2 developed definite pancreatic changes, and 2 showed evidence of bone marrow suppression. Four dogs died during treatment with diphenylsilanediol, whereas no deaths occurred during the same interval of primidone therapy.
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PMID:Clinical evaluation of the new compound diphenylsilanediol for ani-epileptic efficacy and toxicity. 704 6

A five-year retrospective study was conducted to review 91 emergency patients with first time major motor seizures who were hospitalized. Patients were reviewed with regard to etiology of seizures, evaluation, and hospital course. Our objectives were to compare admission and discharge diagnoses, to establish a screening survey which might determine the need for immediate admission, and to evaluate the sensitivity of tests used in diagnostic evaluation. The emergency department diagnosis was in agreement with the discharge diagnosis in 89% of cases. A screening system included a history, physical examination, urinalysis, complete blood cell count, electrolytes, blood urea nitrogen, glucose, electrocardiogram, and arterial blood gases more than one hour post-seizure. When applied to the cases, it distinguished need for admission in 90 of 91 patients. Skull radiographs, electroencephalograms, CAT scans, brain scans, and lumbar punctures were helpful in making a specific diagnosis, but not in determining the need for immediate admission.
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PMID:First time major motor seizures in an emergency department. 736 74

The effects of alpha-guanidinoglutaric acid (GGA), the levels of which were increased in the cobalt-induced epileptic focus tissue in the cerebral cortex of cats, on brain nitric oxide synthase (NOS) activity were observed. GGA inhibited NOS activity in a linear mixed manner (Ki = 2.69 microM) and was as effective as NG-monomethyl-L-arginine (MeArg; Ki = 3.51 microM), a well-known NOS inhibitor. Although MeArg was synthesized by substituting the guanidino nitrogen of L-arginine (Arg), GGA was a non-guanidino nitrogen-substituted guanidino compound. On the other hand, Arg, which is an endogenous NOS substrate, elevates the threshold of seizures induced by GGA. There is evidence that GGA is an endogenous, potent, and non-guanidino nitrogen-substituted NOS inhibitor and that suppression of nitric oxide biosynthesis may be involved in GGA-induced convulsions. Therefore, GGA may be a useful tool in elucidating the chemical nature of NOS and the physiological function of nitric oxide.
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PMID:alpha-Guanidinoglutaric acid, an endogenous convulsant, as a novel nitric oxide synthase inhibitor. 752 94

L-Arginine-derived nitrogen monoxide (NO) formation was determined in different regions of the rat brain during kainate-induced seizures. NO was trapped in vivo as a paramagnetic mononitrosyl-iron diethyldithiocarbamate complex, the concentration of which was determined ex vivo by cryogenic electron spin resonance spectroscopy. Basal NO formation (0.3-0.8 nmol g-1 tissue 30 min-1) was detected in the brain of control rats. In kainate-injected rats NO formation was increased six-fold within 30-60 min in the amygdala/temporal cortex region, and up to 12-fold, though more slowly, in the remaining cortex. The kainate-elicited convulsions and NO formation were attenuated in animals pretreated with either 7-nitroindazole, a specific inhibitor of neuronal NO synthase, or diazepam. These findings identify NO as a proconvulsant mediator in kainate-evoked seizures.
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PMID:Nitric oxide promotes seizure activity in kainate-treated rats. 753 56

A series of (fluorobenzyl)triazolo[4,5-c]pyridines was synthesized and tested for activity against maximal electroshock-induced seizures in rodents. The most promising compound, 14 (BW 534U87), which is a carbon-nitrogen isoster of a purine anticonvulsant, has a profile in rodents that suggests 14 will be free of emesis and useful in the treatment of seizure disorders for which phenytoin is presently indicated.
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PMID:1-(Fluorobenzyl)-4-amino-1H-1,2,3-triazolo[4,5-c]pyridines: synthesis and anticonvulsant activity. 756 50

Congenital duodenal webs are rare lesions, usually detected during early infancy because of signs of high intestinal obstruction. The occasional patient escapes both symptoms and detection until adolescence or adulthood. This report concerns two cases of congenital duodenal web at different ages and with different clinical manifestations. Case 1, a six-month-old male, was admitted because of abdominal distention and vomiting. Case 2, a 13-year-old boy, was referred here for further evaluation of recurring seizure attacks, elevated blood urea nitrogen and creatinine and hyponatremia. Duodenotomy and excision of the web performed for both patients. Complete amelioration of all symptoms was then observed at Outpatient Clinic follow-up for one year.
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PMID:Congenital duodenal web in late infancy and childhood: a report of two cases. 803 46

A 9-year-old sexually intact male Boxer was euthanatized because of progressive, generalized seizures that were refractory to medical treatment. To try to preserve the breeding line, postmortem epididymal semen extraction was attempted. The testes were excised after the dog was euthanatized, and semen was extracted, frozen, and stored in liquid nitrogen. Approximately 3.5 months later, a suitable recipient was identified, and surgical intrauterine insemination was performed. Fifty-seven days after insemination, a viable pup was born.
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PMID:Conception by use of postmortem epididymal semen extraction in a dog. 805 Sep 45

Ifosfamide, a nitrogen mustard derived alkylating agent commonly used in the treatment of solid tumors, has been associated with neurotoxicity in 5-33% of treated patients. Encephalopathy most often occurs during or shortly following drug administration, with increased drowsiness or irritability, confusion, hallucinations, visual blurring, extrapyramidal dysfunction, cranial nerve abnormalities, incontinence, generalized muscle twitching, seizures, and coma reported in infants, children, and older adults. While most reported neurologic abnormalities associated with ifosfamide have been reversible, encephalopathy resulting in death has occurred. We now report an infant who developed ifosfamide-induced encephalopathy, loss of developmental milestones, progressive brain atrophy, and cessation of cranial growth. This is the first case of cerebral atrophy and loss of developmental milestones that has been reported in a pediatric patient treated with ifosfamide. Given the efficacy of this anti-neoplastic agent and its increasing use in pediatrics, further investigation is indicated, especially in infants where brain growth is ongoing.
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PMID:Cerebral atrophy in an infant following treatment with ifosfamide. 805 12

In an effort to detect active renal tubular dysfunction in 74 epileptic patients being treated with antiepileptic drugs (AEDs), we measured the urinary activity of two lysosomal enzymes, N-acetyl-beta-glucosaminidase (NAG) and beta-galactosidase (beta-gal). The heterogeneity of the types of seizures and therapeutic regimens permitted us to examine the potential differences in AED effects. We also examined the chronological changes in the urinary excretion rates of NAG and beta-gal in 132 healthy controls, aged 3 months to 37 years. Increased NAG excretion rates (defined as > or = 2 S.D. compared with age-matched controls) were found in 36.5% of the patients. Valproic acid was highly associated with this increase, and in combination with potassium bromide caused the highest levels of NAG excretion. Among the patients taking carbamazepine, only 11.1% exhibited high levels of NAG in urine. Children under 1 year of age showed higher levels of NAG excretion than older patients. In spite of the abnormally high urinary excretion of NAG, we could not detect any signs of renal dysfunction by urinalysis and measurement of blood urea nitrogen and serum electrolytes. We cannot exclude the possibility that the increased levels of urinary NAG in epileptic patients might be due to renal tubular enzyme induction by AEDs.
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PMID:Urinary excretion of N-acetyl-beta-glucosaminidase and beta-galactosidase by patients with epilepsy. 821 37

Studies have demonstrated that 2-substituted N-benzyl-2-acetamidoacetamides (2) are potent anticonvulsants. A recent investigation has led to the hypothesis that an important structural feature in 2 for maximal anticonvulsant activity is the placement of a small, substituted heteroatom moiety one atom from the C(2) site. This paper validates this hypothesis. Twelve derivatives of N-benzyl-2-acetamidopropionamide have been prepared in which six different heteroatom substituents (chloro, bromo, iodo, oxygen, nitrogen, and sulfur) were incorporated at the C(3) site. Highly potent activities were observed for the two oxygen-substituted derivatives, N-benzyl-2-acetamido-3-methoxypropionamide (18) and N-benzyl-2-acetamido-3-ethoxypropionamide (19). The ED50 values in mice following intraperitoneal (i.p.) dosing for the maximal electroshock-induced seizure test for 18 and 19 were 8.3 and 17.3 mg/kg, respectively. These values compared favorably to the ED50 value found for phenytoin (ED50 = 6.5 mg/kg). Comparable activities were observed for 18 and 19 upon oral (p.o.) administration to rats (18, ED50 = 3.9 mg/kg; 19, ED50 = 19 mg/kg; phenytoin, ED50 = 23 mg/kg). Evaluation of the individual stereoisomers for 18 demonstrated that the principal anticonvulsant activity resided in the (R)-stereoisomer. The ED50 value for (R)-18 was 4.5 mg/kg, and the ED50 for (S)-18 exceeded 100 mg/kg. This difference in activity for the two stereochemical isomers surpassed comparable values for other members within this class of compounds. The protective indices (PI = TD50/ED50) (where TD50 represents a neurotoxic dose impairing rotorod performance) for (R)-18 in mice (i.p.) and in rats (p.o.) were 6.0 and > 130, respectively.
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PMID:Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives. 862 14


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