The switch from IR to OROS methylphenidate was associated with an improvement in both adherence and effectiveness. There were no differences between IR and OROS methylphenidate in terms of tolerability.

Values are expressed as mean T SD, t tests, P values (week 24: responders only). Covance laboratory upper limit of normal range for adolescents: males 16.1 Kg/L, females 29.0 Kg/L. LOCF indicates last observations carried forward; NA, not applied.

We present the case of a schizophrenic patient with severe insomnia that had a partial response to high doses of benzodiazepines and sedating antipsychotics. Treatment with agomelatine allowed to suspend benzodiazepine treatment and restore quality of sleep. Case report: Mr. Y is a 36 year old male patient diagnosed with simple schizophrenia that has complained of insomnia since the age of sixteen. During the last three years the treatment that the patient was following was stable and consisted of 100 mg of diazepam, 300 mg of levomepromazine and 120 mg of clotiapine every night. During the last year 60 mg of duloxetine were added to treat a moderate depression. His mood improved with the prescribed treatment, but eleven months later it worsened. In an attempt to simultaneously treat the mood and the sleep disorder, during a period of 4 days, a dosis of 12.5 mg of aglomelatin at dinner was introduced while the morning dose of duloxetine was reduced to 30mg. On the fifth day, agomelatine was increased to 25 mg at dinner while duloxetine was suspended. The antipsychotic treatment was kept stable while the patient was instructed to reduce 10 mg of diazepam every week until next appointment one month later. In the next appointment the patient had completely suspended diazepam one week before the appointment. The patient referred improved sleep quality and no rebound insomnia. Conclusion: Agomelatine may be a valid treatment of insomnia in schizophrenia.

Introduction: S100B is a 21 kDa protein expressed primarily in astrocytes and has been related with brain dysfunction. There is evidence for increased S100B in schizophrenia, including first-episode psychosis (FEP), and in epilepsy specially after seizures. Pico and nanomolar levels of S100B are neurotrophic and micromolar levels are toxic and apoptotic. Objective: To assess serum levels of S100B at admission and at discharge in a patient with FEP who had comorbid juvenile myoclonic epilepsy (JME). Methods and results: A 23 year-old male was admitted for injury delusions, suspicion and auditory hallucinations that had started in the last three months. In the last year the patient presented progressive social isolation and stopped attending classes. He was diagnosed JME at age 14 and was treated with 1300 mg valproic acid per day. The last seizure was two years ago. Risperidone was started up to 8 mg per day and valproic acid was continued. He had a progressive clinical improvement and in two weeks was discharged. Serum levels of S100B were determined at admission (3528.23 pg/ml) and discharge (3553.78 pg/ml). Conclusions: This patient had high levels of serum S100B both at admission and discharge. These levels were ten times higher than previous studies in epilepsy (without psychosis), hundred times higher than previous in psychosis and thousands times higher than in healthy subjects. We interpret these results as an intense activation of astrocytes by a double brain insult. Monitoring this patient during more time will show the evolution of S100B with antipsychotic treatment.

IntroductionAntidepressants can induce SIADH and it can be a serious complication. It is frecuently asociated with SSRIs (Selective Serotonin Reuptake Inhibitors) but this syndrome can be caused by another antidepressants, drugs and another causes can be involved.ObjectivesWe report the clinical course of an antidepressants induced SIADH with SSRIs and Mirtazapine and propose psychopharmacologic alternatives.MethodsWe describe the case of a 25 years old man, hypertensive in treatment with thiazides, polytraumatized as a result of a suicide attempt. The patient was treated with Sertraline and a SIADH occurred. Stopped Sertraline and diuretics and then, the patient was treated with Mirtazapine and Bisoprolol but hyponatremia was persistent. Then we use Trazodone and the sodium levels were normalized.ResultsHyponatremia is a potentially dangerous side effect of antidepressants and is not exclusive to SSRIs. Current evidence suggests a relatively higher risk of hyponatremia with SSRIs and venlafaxine, especially when combined with patient risk factors. In our case, the risk was increased by the polytrauma and thiazide diuretics. Although, according to the literature, the risk associated with mirtazapine is moderate, in our case, hyponatremia was persistent and sodium levels were normalized when stopped Mirtazapine and started Trazodone.ConclusionWe have to take into account risk factors associated with SIADH and modify them as far as possible. Trazodone could be an alternative treatment for patients with SIADH.