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Off-label use of sodium valproate for schizophrenia.

ABSTRACT: BACKGROUND: Off-label use of a drug not according to its regulatory labeling has become common in medicine, especially in the field of psychiatry. Mood stabilizers are intended to be used to attenuate mood fluctuations in bipolar disorder, but their use has spread to patients with schizophrenia, as it provides greater control of impulsivity and aggressiveness. Sodium valproate is one of the most frequently used mood stabilizers in psychiatry. This study determined the prevalence of off-label use of sodium valproate for schizophrenia and schizoaffective disorder in Abarbanel Psychiatric Hospital and the demographic and clinical characteristics associated with its use. METHODS: Retrospective study of patients hospitalized in 2011-2012 with a diagnosis of schizophrenia or schizoaffective disorder in one of three general psychiatric wards. RESULTS: Valproate use was significantly lower in the geriatric group (11.6% vs. 20.1%, chi square = 4.7, p = .03), in patients with schizophrenia (14.1% vs. schizoaffective disorder (35.2%), chi square = 29, p<.001) and in patients receiving both atypical and typical antipsychotics (23.3% vs. 16.4%, p = .04). In multivariate logistic regression analysis, diagnosis and the combination of atypical and typical antipsychotics predicted the use of sodium valproate. The number of other medications prescribed did not predict sodium valproate use. CONCLUSIONS: Off-label use of sodium valproate in psychiatric patients with schizophrenia or schizoaffective disorder is extensive, especially in younger patients and those with schizoaffective disorder. More research is needed to determine whether it is being prescribed appropriately.

SUBMITTER: Horowitz E

PROVIDER: S-EPMC3963914 | biostudies-other | 2014

REPOSITORIES: biostudies-other

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Project description:Status epilepticus has been shown to activate the proliferation of neural stem cells in the hippocampus of the brain, while also causing a large amount of neuronal death, especially in the subgranular zone of the dentate gyrus and the subventricular zone. Simultaneously, proliferating stem cells tend to migrate to areas with obvious damage. Our previous studies have clearly confirmed the effect of sodium valproate on cognitive function in rats with convulsive status epilepticus. However, whether neurogenesis can play a role in the antiepileptic effect of sodium valproate remains unknown. A model of convulsive status epilepticus was established in Wistar rats by intraperitoneal injection of 3 mEq/kg lithium chloride, and intraperitoneal injection of pilocarpine 40 mg/kg after 18-20 hours. Sodium valproate (100, 200, 300, 400, 500, or 600 mg/kg) was intragastrically administered six times every day (4-hour intervals) for 5 days. To determine the best dosage, sodium valproate concentration was measured from the plasma. The effective concentration of sodium valproate in the plasma of the rats that received the 300-mg/kg intervention was 82.26 ± 11.23 μg/mL. Thus, 300 mg/kg was subsequently used as the intervention concentration of sodium valproate. The following changes were seen: Recording excitatory postsynaptic potentials in the CA1 region revealed high-frequency stimulation-induced long-term potentiation. Immunohistochemical staining for BrdU-positive cells in the brain revealed that sodium valproate intervention markedly increased the success rate and the duration of induced long-term potentiation in rats with convulsive status epilepticus. The intervention also reduced the number of newborn neurons in the subgranular area of the hippocampus and subventricular zone and inhibited the migration of newborn neurons to the dentate gyrus. These results indicate that sodium valproate can effectively inhibit the abnormal proliferation and migration of neural stem cells and newborn neurons after convulsive status epilepticus, and improve learning and memory ability.

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Off-label use of sodium valproate for schizophrenia.

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