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1 ion and psychosis with the use of divalproex sodium (valproate).
2 th other medications such as clobazam and/or sodium valproate.
3 development of the child exposed in utero to sodium valproate.
4 e concentrations of the HDACIs vorinostat or sodium valproate.
5 and carbamazepine and greater than those of sodium valproate.
6 tivators in common clinical use--lithium and sodium valproate.
7 ncy over older AEDs namely carbamazepine and sodium valproate.
8 orarginine and histone deacetylase inhibitor sodium valproate.
9 , and typically responsive to treatment with sodium valproate.
10 whether single or multiple administration of sodium valproate, a GABA agonist, would prevent the expr
12 ood stabilizers (lithium, carbamazepine, and sodium valproate) and plasma levels of these drugs to fu
18 gnancy registers has not only confirmed that sodium valproate is teratogenic but also that it may be
19 tising neurologists had long suspected--that sodium valproate is the most effective drug in the treat
21 OR, 0.32 [95% CI, 0.15-0.67]; P = .003), and sodium valproate (OR, 0.33 [95% CI, 0.15-0.71]; P = .004
22 ated seizures and increased spiking, whereas sodium valproate reduced spiking, mirroring drug respons
23 is undoubtedly a phamacogenetic component to sodium valproate's teratogenic and neurodevelopmental ef
24 disorders in children exposed to monotherapy sodium valproate (VPA) (6/50, 12.0%; aOR 6.05, 95%CI 1.6
25 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
27 atal exposure to the anti-seizure medication sodium valproate (VPA) is associated with an increased r
30 rbamazepine, lamotrigine, levetiracetam, and sodium valproate) was defined using routinely collected
32 Therefore, we have examined the effect of sodium valproate, which enhances GABA function, on the d