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Neonatal seizure

Phenobarbital is the drug of choice for neonatal seizures, but in other situations it is reserved for patients who have failed other AEDs. [Pg.608]

Marangos PJ, Daval JL, Weiss SRB, et al Carbamazepine and brain adenosine receptors, in Neonatal Seizures. Edited by Wasterlain CG, Vert P. New York, Raven, 1990, pp 203-209... [Pg.690]

Phenobarbital Enhances phasic GABAa receptor responses reduces excitatory synaptic responses Nearly complete absorption not significantly bound to plasma proteins peak concentrations in Vi to 4 h no active metabolites tjy2 varies from 75 to 125 h Generalized tonic-clonic seizures, partial seizures, myoclonic seizures, generalized seizures, neonatal seizures, status epilepticus Toxicity Sedation, cognitive issues, ataxia, hyperactivity Interactions Valproate, carbamazepine, felbamate, phenytoin, cyclosporine, felodipine, lamotrigine, nifedipine, nimodipine, steroids, theophylline, verapamil, others... [Pg.529]

Some cases of neonatal seizures, respiratory depression, vomiting, and diarrhea have been reported in infants whose mothers received carbamazepine during pregnancy... [Pg.51]

Painter, M.J. Pippenger, C.E. Wasterlein, C. Barmada, M. Pitlick, W. Carter, G. Aberin, S. Phenobarbital and phenytoin in neonatal seizures Metabolism and tissue distribution. Neurology 1981, 31, 1107-1112. [Pg.2649]

Molybdenum cofactor deficiency (MoCoD) is an autosomal recessive, fatal neurological disorder, characterized by the combined deficiency of sulphite oxidase, xanthine dehydrogenase, and aldehyde oxidase. No therapy is known for this rare disease, which results in neonatal seizures and other neurological symptoms identical to sulfite oxidase deficiency. Heterozygous carriers of a MoCo deficiency allele do not display any symptoms (Reiss et al. 1999). [Pg.470]

Unclassified epileptic seizures (includes some neonatal seizures)... [Pg.765]

There is also considerable evidence for a higher susceptibility to domoic acid toxicity during early postnatal development in rats [92,110,116,117,131]. Domoic acid induces a time-dependent behavioral toxicity in neonatal rats that is characterized by hyperactivity, stereotypic scratching, convulsions, and death at exposures 40-50 times lower by body weight in neonates than that reported in adults [116,117]. However, acute toxicity with domoic acid does not appear to cause structural alteration in the brain of neonates as assessed by Nissl staining and cupric silver histochemistry [117]. This is consistent with numerous other studies of neonatal seizures that demonstrate a generalized resistance to excitotoxic damage [135,136],... [Pg.416]

Phenobarbital ° (PB) is FDA approved for the treatment of partial and generalized seizure disorders. PB is also frequently used for treatment of neonatal seizures not due to proven superior efficacy, but to familiarity of use. [Pg.247]

Reduced neurogenesis after neonatal seizures. J Neurosci 21(6) 2094-2103 McIntyre, D.C., Hutcheon, B., Schwabe, K., and Poulter, M.0.2002. Divergent GABA(A) receptor-mediated synaptic transmission in genetically seizure-prone and seizure-resistant rats. J Neurosci 22(22) 9922-9931... [Pg.132]

In six neonates (body weight over 2000 g, gestational age over 30 weeks) in a prospective pilot study on the use of oral levetiracetam as monotherapy in the treatment of neonatal seizures the dose was increased by 10 mg/kg day over 3 days [206 ]. There were no clear adverse events during the study. There was mild sedation during titration in one neonate taking concomitant phenobarbital. [Pg.106]

Ramantani G, Ebinger F, Philippi H, Poschl J, Schubert S, Rating D, Bast T. Levetiracetam in the treatment of neonatal seizures a pilot study. Seizure 2010 19(3) 185-9. [Pg.136]

Torres, O.A., Miller, V.S., Buist, N.M., and Hyland, K., 1999. Folinic acid-responsive neonatal seizures. Journal of Child Neurology. 14 529-532. [Pg.555]

D-bifunctional protein deficiency (D-BP), the second peroxisomal -oxidation disorder, was only delineated recently [6-9]. All patients identified sofar (>40 see [10]) show severe clinical abnormalities including hypotonia, craniofacial dysmorphia, neonatal seizures, hepatomegaly, and developmental delay. Most patients with D-BP deficiency die in the first year of life. A remarkable observation is that patients with D-BP deficiency show disordered neuronal migration as in ZS. [Pg.485]

Vieker S, Thiel M, Tangier A. Neonatal seizures caused by lamotrigin withdrawal Geburtshilfe Neonatol 2009 213(2) 62-3. [Pg.190]


See other pages where Neonatal seizure is mentioned: [Pg.129]    [Pg.230]    [Pg.687]    [Pg.686]    [Pg.30]    [Pg.129]    [Pg.2649]    [Pg.2980]    [Pg.676]    [Pg.258]    [Pg.1024]    [Pg.130]    [Pg.45]    [Pg.484]    [Pg.696]    [Pg.364]    [Pg.256]   
See also in sourсe #XX -- [ Pg.470 ]




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