Objective: Increased impulsivity has been shown to be a trait feature of adults with bipolar disorder (BD), yet impulsivity has received little study in adolescents with BD. Thus, it is unknown whether it is a trait feature that is present early in the course of the disorder. We tested the hypotheses that self-reported impulsiveness is increased in adolescents with BD, and that it is present during euthymia, supporting impulsiveness as an early trait feature of the disorder.

Methods: Impulsiveness was assessed in 23 adolescents with BD and 23 healthy comparison (HC) adolescents using the self-report measure of impulsivity, the Barratt Impulsiveness Scale (BIS), comprised by attentional, motor and non-planning subscale scores. Effects of subscale scores and associations of scores with mood state and course features were explored.

Results: Total and subscale BIS scores were significantly higher in adolescents with BD than HC adolescents. Total, attentional and motor subscale BIS scores were also significantly higher in the subset of adolescents with BD who were euthymic, compared to HC adolescents. Adolescents with BD with rapid-cycling and chronic mood symptoms had significantly higher total and motor subscale BIS scores than adolescents with BD without these course features.

Conclusion: These results suggest increased self-reported impulsiveness is a trait feature of adolescents with BD. Elevated impulsivity may be especially prominent in adolescents with rapid-cycling and chronic symptoms.

Objective: Although depressive symptoms are preponderant in the course of bipolar (BP) disorders, the treatment of BP depression remains a controversial issue with different clinical approaches available. This review addresses the issues of whether antidepressants (ADs) are effective in treating acute and long-term BP depression, risks linked to ADs and what alternatives to ADs are available.

Methods: We searched the MEDLINE databases using the following syntax: [bipolar depression AND unipolar depression AND (antidepressants OR anticonvulsants OR lithium OR antipsychotics OR dopamine-agonists OR psychoeducation OR psychotherapy OR electroconvulsive therapy OR transcranial magnetic stimulation)]. The search included studies published up to 31 May 2009 and conducted on adults.

Results: In the acute treatment of BP depression ADs are effective with no differences among drug classes. However, neither the switch into (hypo)mania induction rate nor the suicide risk linked to AD use are definitely established. The effectiveness of long-term AD use is limited to highly selected samples of patients with positive acute response. The risk of long-term ADs causing cycle acceleration and rapid cycling induction concerns a subpopulation of patients. Valid alternatives to ADs in treating acute BP depression are quetiapine, an olanzapine–fluoxetine combination, and electroconvulsive therapy for more severe patients. Lamotrigine is effective and safe in preventing depressive relapses. Psychotherapy and psychoeducation represent effective adjunctive treatments.

Conclusion: In the treatment of BP depression there is not a specific effective treatment for all the patients. Interventions should therefore be personalised and the scientific evidence should be adapted to each patient's clinical features.

Objective: To compare the scientific content of recent general media articles on tryptophan, diet and depression, with recent empirical research into dietary manipulation of tryptophan published in the scientific literature.

Method: A review of the recent empirical research into the role of tryptophan in depression, focusing on dietary methods to influence tryptophan levels. In parallel, a review of recent articles in the general English language media regarding tryptophan and mood.

Results: Empirical evidence for improving mood through dietary manipulation of tryptophan is lacking, and it is difficult to change plasma tryptophan levels through diet alone. Tryptophan supplementation and depletion studies suggest that altering tryptophan levels may only benefit certain groups of patients who have a personal or family history of depression. Scientific studies also focus on elucidating mechanisms in depression, rather than treating depression by changing tryptophan levels. However, general media articles often recommend diets and foods to increase blood tryptophan levels and raise brain serotonin levels. Such recommendations are not supported by scientific studies.

Conclusion: It is very difficult to alter blood tryptophan levels through dietary methods alone, outside of a laboratory or research setting. Only a small number of lay articles provide sound advice, with general media reports on tryptophan often being hyperbolic and misleading. A clinician should be aware of the type of (mis)information a patient may have accessed and have the scientific knowledge to explain the impracticalities of influencing tryptophan levels through diet alone.

Objectives: Bipolar disorder (BD) is a mental illness associated with higher rates of suicide. The present study aims to investigate the brain mitochondrial respiratory chain activity in an animal model of mania induced by ouabain.

Methods: Adult male Wistar rats received a single intracerebroventricular administration of ouabain (10−3 and 10−2 M) or vehicle. Locomotor activity was measured using the open field test. Mitochondrial respiratory chain activity was measured in the brain of rats 1 h and 7 days after ouabain administration.

Results: Our results showed that spontaneous locomotion was increased 1 h and 7 days after ouabain administration. Complexes I, III and IV activities were increased in the prefrontal cortex, hippocampus and striatum immediately after the administration of ouabain, at the concentration of 10−3 and 10−2 M. Moreover, complex II activity was increased only in the prefrontal cortex at the concentration of 10−2 M. On the other hand, no significant alterations were observed in complex I activity 7 days after ouabain administration. However, an increase in complexes II, III and IV activities was observed only in the prefrontal cortex at the concentration of 10−2 M.

Conclusion: Our findings suggest an increase in the activities of mitochondrial respiratory chain in this model of mania. A possible explanation is that these findings occur as a rebound effect trying to compensate for a decrease of ATP deprivation in BD. The present findings suggest that this model may present good face validity and a limitation in construct validity.

Objectives: Depression and dementia are highly prevalent in the elderly. Language impairment is an inherent component of Alzheimer's disease (AD), which can also be encountered in depressed patients. The aim of this study wasto compare the profiles of language abilities in late-onset depression and mild AD groups.

Methods: We studied 25 patients with late-onset depression (mean age 73.6 ± 6.6 years; schooling 9.1 ± 5.7 years) and 30 patients with mild AD (77.6 ± 5.4 years; 7.5 ± 7.1 years) using the Arizona Battery for Communication Disorders of Dementia (ABCD), compared to a group of 30 controls (73.8 ± 5.8 years; 9.1 ± 5.4 years). Cut-off scores to discriminate between Controls × Depression and Depression × AD were determined.

Results: Depressed patients' scores were similar to AD in confrontation naming, concept definition, following commands, repetition and reading comprehension (sentence). Episodic memory and mental status subtests were useful in differentiating depressed patients from AD, a result that was reproduced when using analysis of covariance to control for the effect of age in the same subtests (p = 0.01 and 0.04, respectively).

Conclusion: Language impairment resembling AD was found in the aforementioned language subtests of the ABCD in elderly depressed patients; the mental status and episodic memory subtests were useful to discriminate between AD and depression. The ABCD has proven to be a suitable tool for language evaluation in this population and should aid in the differentiation of AD and pseudodementia (as that of depression).