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1 ion and psychosis with the use of divalproex sodium (valproate).
2 development of the child exposed in utero to sodium valproate.
3 e concentrations of the HDACIs vorinostat or sodium valproate.
4 and carbamazepine and greater than those of sodium valproate.
5 tivators in common clinical use--lithium and sodium valproate.
6 ncy over older AEDs namely carbamazepine and sodium valproate.
7 orarginine and histone deacetylase inhibitor sodium valproate.
8 , and typically responsive to treatment with sodium valproate.
9 whether single or multiple administration of sodium valproate, a GABA agonist, would prevent the expr
11 ood stabilizers (lithium, carbamazepine, and sodium valproate) and plasma levels of these drugs to fu
16 gnancy registers has not only confirmed that sodium valproate is teratogenic but also that it may be
17 tising neurologists had long suspected--that sodium valproate is the most effective drug in the treat
19 is undoubtedly a phamacogenetic component to sodium valproate's teratogenic and neurodevelopmental ef
20 disorders in children exposed to monotherapy sodium valproate (VPA) (6/50, 12.0%; aOR 6.05, 95%CI 1.6
21 etiracetam (LEV) 1.00 (0.16 to 1.84) p=0.02; sodium valproate (VPA) 0.74 (0.10 to 1.38) p=0.02; topir
25 Therefore, we have examined the effect of sodium valproate, which enhances GABA function, on the d
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