PubMed · 9242822
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J G Longhurst. 1997-07-26. Mania.. https://doi.org/10.1016/s0140-6736(05)62258-1
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BACKGROUND: Bipolar disorder is a common debilitating illness, characterised by acute affective episodes with full or partial inter-episode remission. Effective and acceptable treatment of acute episodes is required. Valproate has become a leading adjunctive and alternative mood stabilising treatment to lithium in bipolar disorder. OBJECTIVES: To determine the efficacy and acceptability of valproate in the treatment of acute episodes of bipolar disorder. SEARCH STRATEGY: The search included the Cochrane Collaboration Depression, Anxiety and Neurosis Controlled Trials Registrar (CCDANCTR), the Cochrane Controlled Clinical Trials Register (CCTR), reference lists of relevant papers and books, and contact with authors of trials, experts and pharmaceutical companies. SELECTION CRITERIA: Randomised controlled trials comparing valproate with placebo, other mood stabilisers and antipsychotic medication in the treatment of any bipolar affective episode. Participants were of both sexes, of all ages, with a diagnosis of bipolar affective disorder approximating to ICD 10 Code F31 and DSM IV 296. DATA COLLECTION AND ANALYSIS: Methodological quality was assessed independently by two reviewers blind to the authorship and source of papers. Ten randomised controlled trials were found comparing valproate with other interventions in mania. None was found examining its use in depression or mixed affective episodes. Data were extracted on the main outcome 'failure to respond by the end of the study' assessed by a less than 50% reduction in the Young Mania Rating Scale or the SADS-S mania scale. Three trials (316 participants) compared valproate with placebo. Three trials (158 participants) compared valproate with lithium. Two trials (363 participants) compared valproate with olanzapine. One trial (36 participants) compared valproate with haloperidol. Two trials (59 patients) compared valproate with carbamazepine. Acceptability of treatment was estimated using the outcome measure 'total number of subjects withdrawing from the study'. Three trials (321 patients) contributed to the comparison between valproate and placebo, two studies (144 patients) contributed to the comparison with lithium. One study (30 patients) provided data on this outcome in the comparison between valproate and carbamazepine. Pooled relative risks (with 95% confidence intervals) were calculated using fixed effect approaches. MAIN RESULTS: Valproate was more efficacious than placebo (RRR 38%; RR 0.62; 95% C.I. 0.51 to 0.77) in the treatment of mania. There was no significant difference between valproate and lithium (RRI 5%; RR 1.05; 95% C.I. 0.74-1.50) or between valproate and carbamazepine (RRR 34%; RR 0.66; 95% C.I. 0.38 to 1.16). Valproate was less effective than olanzapine (failure to achieve clinical response; RRI 25%; RR 1.25, 95% C.I. 1.01 to 1.54; average of 2.8 point less change on the Mania Rating Scale (95% CI 0.83 to 4.79). There were no significant differences in acceptability as measured by total number of subjects withdrawing from the study. There were significant differences in the side effect profiles of valproate and olanzapine, with more sedation and weight gain on olanzapine. REVIEWER'S CONCLUSIONS: There is consistent, if limited, evidence to suggest that valproate is an efficacious treatment for acute mania. Valproate may be less effective than olanzapine but may cause less sedation and weight gain. More well designed, randomised controlled trials investigating the relative efficacy and acceptability of valproate in the treatment of the full range of acute affective episodes occurring in bipolar disorder are required.
In the present paper we discuss the current status of drug treatment for pathological gambling and the scientific rationales underlying the various pharmacological approaches. Specifically, we summarize the treatment study results of serotonin reuptake inhibitors, mood stabilizers, opioid antagonists, and atypical antipsychotics in pathological gambling. We also discuss dosage strategies, the duration of treatment, issues surrounding medication compliance, and approaches to treatment-refractory pathological gambling, such as pharmacological and behavioral augmentation.
The clinical efficacy of lithium in the prophylaxis of recurrent affective episodes in bipolar disorder is characterized by a lag in onset and remains for weeks to months after discontinuation. Thus, the long-term therapeutic effect of lithium likely requires reprogramming of gene expression. Protein kinase C and glycogen synthase kinase-3 signal transduction pathways are perturbed by chronic lithium at therapeutically relevant concentrations and have been implicated in modulating synaptic function in nerve terminals. These signaling pathways offer an opportunity to model critical signals for altering gene expression programs that underlie adaptive responses of neurons to long-term lithium exposure. While the precise physiological events critical for the clinical efficacy of lithium remain unknown, we propose that linking lithium-responsive genes as a regulatory network will provide a strategy to identify signature gene expression patterns that distinguish between therapeutic and nontherapeutic actions of lithium.