Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comprehensive series of clinical trials have compared the unique selective NRI reboxetine with placebo and with the TCAs imipramine and desipramine, as well as with the SSRI fluoxetine. Reboxetine is clearly effective in both the short and the long term compared with placebo. Against comparator antidepressants, reboxetine is at least as effective in the treatment of patients with major depressive disorder in the adult and the elderly population and offers a significant advantage over imipramine in the treatment of melancholic patients. In severely depressed patients, reboxetine was significantly more effective than fluoxetine. Reboxetine also offers significant advantages over fluoxetine in terms of social functioning and has a significantly improved adverse event profile compared with TCAs. In comparison with fluoxetine, reboxetine has a different adverse event profile, but shows advantages in terms of agitation/nervousness/anxiety and gastrointestinal events. Reboxetine is not cardiotoxic, and it is not associated with an increased risk of seizures or of orthostatic hypotension. Overall, reboxetine offers a significant safety advantage over TCAs in the treatment of the depressed population and in subsets of the depressed population in an efficacy comparison with the SSRI fluoxetine.
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PMID:Chairman's overview. The place of reboxetine in antidepressant therapy. 981 28

Major depression (MD) is underdiagnosed and undertreated in patients with temporal lobe epilepsy (TLE). Side effects of some antidepressants, like increased risk of seizures and drug-drug interactions with anticonvulsants, contribute to undertreatment of MD in patients with TLE. We analyzed post hoc the data from 2 years of treatment of inpatients with MD and TLE. Seventy-five patients received standard treatment with citalopram, mirtazapine, or reboxetine, respectively, at recommended dosage. Examinations were done with the Hamilton Rating Scale for Depression at admission and after 4 and 20-30 weeks. Plasma levels of anticonvulsants were examined at admission and discharge. Seizures were documented. The antidepressive treatment was efficacious in all antidepressant groups. No case of serious adverse event or drug interaction occurred. There was no increase in frequency or severity of seizures. At endpoint the dropout rate for mirtazapine was significantly higher than that for reboxetine or citalopram. Reboxetine showed a trend to be more efficacious than citalopram but not mirtazapine at Week 4.
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PMID:Antidepressive treatment in patients with temporal lobe epilepsy and major depression: a prospective study with three different antidepressants. 1469 1

Apoptosis has been proposed as a contributing cellular mechanism to the structural alterations that have been observed in stress-related mood disorders. Antidepressants, on the other hand, are hypothesized to exert trophic and/or neuroprotective actions. The present study examined the regulation of the major antiapoptotic (Bcl-2, Bcl-xl) and proapoptotic (Bax) genes by repeated unpredictable stress (an animal model of depression) and antidepressant treatments (ADT). In adult rats, exposure to unpredictable stress reduced Bcl-2 mRNA levels in the central nucleus of the amygdala (CeA), cingulate (Cg), and frontal (Fr) cortices. Bcl-xl mRNA was significantly decreased in hippocampal subfields. In contrast, chronic administration of clinically effective antidepressants from four different classes, ie fluoxetine, reboxetine, tranylcypromine, and electroconvulsive seizures (ECS) upregulated Bcl-2 mRNA expression in the Cg, Fr, and CeA. Reboxetine, tranylcypromine, and ECS selectively increased Bcl-xl, but not Bcl-2 mRNA expression in the hippocampus. Chemical ADT but not ECS, robustly enhanced Bcl-2 expression in the medial amygdaloid nucleus and ventromedial hypothalamus. Fluoxetine did not influence Bcl-xl expression in the hippocampus, but it was the only ADT that decreased Bax expression in this region. In the CeA, again in direct contrast to the stress effects, exposure to all classes of ADTs significantly increased Bcl-2 mRNA. The selective regulation of Bcl-xl and Bax in hippocampal subfields and of Bcl-2 in the Cg cortex, amygdala, and hypothalamus suggests that these cellular adaptations contribute to the long-term neural plastic adaptations to stress and ADTs in cortical, hypothalamic, and limbic brain structures.
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PMID:Repeated unpredictable stress and antidepressants differentially regulate expression of the bcl-2 family of apoptotic genes in rat cortical, hippocampal, and limbic brain structures. 1770 Jun 47