Bright-light therapy (BLT) is established as the treatment of choice for seasonal affective disorder/winter type (SAD). In the last two decades, the use of BLT has expanded beyond SAD: there is evidence for efficacy in chronic depression, antepartum depression, premenstrual depression, bipolar depression and disturbances of the sleep-wake cycle. Data on the usefulness of BLT in non-seasonal depression are promising; however, further systematic studies are still warranted. In this review, the authors present a comprehensive overview of the literature on BLT in mood disorders. The first part elucidates the neurobiology of circadian and seasonal adaptive mechanisms focusing on the suprachiasmatic nucleus (SCN), the indolamines melatonin and serotonin, and the chronobiology of mood disorders. The SCN is the primary oscillator in humans. Indolamines are known to transduce light signals into cells and organisms since early in evolution, and their role in signalling change of season is still preserved in humans: melatonin is synthesized primarily in the pineal gland and is the central hormone for internal clock circuitries. The melatonin precursor serotonin is known to modulate many behaviours that vary with season. The second part discusses the pathophysiology and clinical specifiers of SAD, which can be seen as a model disorder for chronobiological disturbances and the mechanism of action of BLT. In the third part, the mode of action, application, efficacy, tolerability and safety of BLT in SAD and other mood disorders are explored.

Background: It has been proposed that aggression and especially anger attacks play an important role in the symptomatology of depression. Furthermore, it has been hypothesized that these symptoms are more prevalent in males than in females. Methods: We conducted a study in 217 depressed patients (104 females, 113 males) without psychiatric comorbidity using questionnaires. Study subjects had previously been treated as inpatients and were contacted after discharge from hospital by mail or phone. Overall response rate was 69.6%. Patients were asked to retrospectively rate their state during their last depression. Results: Males obtained higher scores on irritability (p = 0.010) and showed a tendency to overreact (p = 0.018) during their last depressive episode. They had suffered significantly more often from anger attacks than female patients (4.3 ± 7.52 versus 1.2 ± 2.97 anger attacks per month; p = 0.001). Further multivariate analyses displayed that men had significantly lower impulse control and more frequently showed symptomatic substance intake and hyperactive behavior during their depression, whereas women suffered more often from hypersomnia and heaviness in limbs (p < 0.0001). Conclusion: Our findings are indicative of gender differences in symptoms related to lowered impulse control in depressed patients. Further study is required to replicate and extend our results and to assess the significance of aggression as a gender-specific diagnostic criterion for depression.

Background:Schizophrenia has been associated with disturbances of thalamic functioning. In light of recent evidence suggesting a significant impact of the glutamatergic system on key symptoms of schizophrenia, we assessed whether modulation of the glutamatergic system via blockage of the N-methyl-d-aspartate (NMDA)-receptor might lead to changes of thalamic functional connectivity.Methods:Based on the ketamine model of psychosis, we investigated changes in cortico-thalamic functional connectivity by intravenous ketamine challenge during a 55-minute resting-state scan. Thirty healthy volunteers were measured with pharmacological functional magnetic resonance imaging using a double-blind, randomized, placebo-controlled, crossover design.Results:Functional connectivity analysis revealed significant ketamine-specific changes within the thalamus hub network, more precisely, an increase of cortico-thalamic connectivity of the somatosensory and temporal cortex.Conclusions:Our results indicate that changes of thalamic functioning as described for schizophrenia can be partly mimicked by NMDA-receptor blockage. This adds substantial knowledge about the neurobiological mechanisms underlying the profound changes of perception and behavior during the application of NMDA-receptor antagonists.