Depression is one of the most prevalent disorders in the general population, causing personal and social disability and impairment. Major studies assessing the diagnosis and management of depression have shown that it is often underdiagnosed and undertreated. A pan-European study aimed at assessing the extent and consequences of depression in six different countries is reported in this article. Different types of depressive profiles are analyzed and their respective management has been compared. The importance of improving diagnosis and treatment of depression is underlined. Appropriate management of depression depends on the recognition of depressive symptoms by patients, their possibility of seeking care, and the ability of the primary care physician to recognize the disorder and prescribe the appropriate medicines. Improvement in all of these fields is necessary.

Depression is an important public health problem affecting about 15% of the general population; however, little is known about possible changes in the brain that might underlie the disorder. Neuroimaging has been a powerful tool to map actual changes in the brain structure of depressed patients that might be directly related to their symptoms of depression. Some imaging studies of brain structure have shown smaller hippocampal volume with the chronicity of depression correlating to a reduction in volume. Although the meaning of these findings is unclear, other studies have shown increased amygdala volume. Studies have found reductions in volume of the frontal cortex, with some studies showing specific reductions in subregions of the frontal cortex, including the orbitofrontal cortex. Findings of an increase in white matter lesions in elderly patients with depression have been replicated and correlated with late-onset depression, as well as impairments in social and cognitive function. These findings point to alterations in a circuit of brain regions hypothesized to include the frontal cortex, hippocampus, amygdala, striatum, and thalamus, that underlie symptoms of depression.

Basic and clinical studies over the past 10 years have lead to a fundamental shift in our understanding of mood disorders. These studies demonstrate that mood disorders and stress are accompanied by structural alterations in the brain; moreover, these structural alterations are reversible with antidepressant treatment. These alterations include changes in the length and number of neuronal processes, the number of neurons and glia, and even the rate of neurogenesis in the adult brain. Work is also being conducted to identify the molecular mechanisms underlying these changes and the adaptations that are critical to the therapeutic actions of antidepressant treatment. Some of the intracellular targets include second messengers, gene transcription factors, and neurotrophic factors that could oppose the actions of stress and depression. Taken together, this exciting new work describes and details structural alterations of limbic brain regions that are extremely dynamic and adaptive. Further understanding of the abnormalities in these systems that lead to mood disorders will provide more efficacious and possibly faster-acting therapeutic interventions.

The treatment of major depression remains problematic for several reasons. In particular, the therapeutic response to medications usually does not manifest itself until a week after administration has begun, and more than half the patients will not experience a full recovery with the first antidepressant drug administration. There are, however, some pharmacologic strategies that can accelerate antidepressant response. When facing a treatment-resistant depression, combination therapy offers a more time-efficient approach to achieve remission than drug substitution. These interventions have been devised on a better understanding of the basis for the therapeutic response obtained with the first- and second-generation antidepressants, and evidence derived from controlled clinical trials of their superior effectiveness is growing. The rationale for such approaches will be described in this article, as well as their advantages and potential inconveniences. Ongoing research in this field continues to fuel the development of novel, better-tolerated, and more effective pharmacotherapies for depression.

Studies on schizophrenia (SZ) have documented an increased presence of cavum septi pellucidi (CSP) in individuals suffering from the illness. Moreover, the presence of CSP has been cited in support of the early neurodevelopmental hypothesis in SZ. Our objective was to assess the magnetic resonance imaging (MRI) scans of first-episode patients and healthy controls to evaluate the frequency of CSP. The presence and the size of CSP were visually assessed on the MRI scans of 40 first-episode SZ patients, 19 nonpsychotic child and high-risk adolescent offspring of patients with SZ or schizoaffective disorder, and 59 controls. Our analysis revealed an absence of statistically significant differences in the occurrence of CSP between SZ patients, high-risk subjects, and controls. Even when the analysis was restricted to large CSP, no differences were found. Furthermore, no association between CSP and sex or handedness was observed. The absence of CSP abnormalities in first-episode SZ subjects might indicate that SZ is not characterized by developmentally mediated alterations in CSP. Also, family history of SZ might not increase likelihood for CSP.