In contemporary psychiatry, depression and mania are conceived as different entities. They may occur together, as in bipolar disorder, or they may occur separately, as in unipolar depression. This view is partly based on a narrow definition of mania and a rather broad definition of depression. Generally, depression is seen as more prominent, common, and problematic; while mania appears uncommon and treatment-responsive. We suggest a reversal: mania viewed broadly, not as simply episodic euphoria plus hyperactivity, but a wide range of excitatory behaviors; and depression seen more narrowly. Further, using pharmacological and clinical evidence, and in contrast to previous theories of mania interpreted as a flight from depression, we propose the primacy of mania hypothesis (PM): depression is a consequence of the excitatory processes of mania. If correct, current treatment of depressive illness needs revision. Rather than directly lifting mood with antidepressants, the aim would be to suppress manic-like excitation, with depression being secondarily prevented. Potential objections to, and empirical tests of, the PM hypothesis are discussed.

The purpose of the present study was to investigate the factor structure of the Beck Depression Inventory-II (BDI-II) in pregnancy and postpartum. Women were asked to fill in the BDI-II in their last trimester of pregnancy and at 3 months after delivery. A total of 331 pregnant women, with a mean age of 29.7 years (SD = 4.6), and 354 mothers, aged 30.6 years (SD = 4.6 years), answered the BDI-II. The first group was mainly nulliparas (65.6%) and the second group was mostly primiparas (57.4%). Factor analyses with principal components solution and varimax rotation were performed. Based on the scree test of Cattell a 2-factor solution and a 3-factor solution were explored. The 2-factor solution was identical in pregnancy and postpartum. Items loading in the Cognitive–Affective factor and in the Somatic–Anxiety factor were almost the same, though the Cognitive–Affective factor explained more of the BDI-II total variance in pregnancy, whereas in postpartum both factors explained similar total variances. The 3-factor solution of the BDI-II in pregnancy and postpartum slightly diverged. Besides the Cognitive–Affective and the Somatic–Anxiety factors, a third factor, Fatigue, was obtained in pregnancy while Guilt was the third factor identified in postpartum. This study reveals that the BDI-II 3-factor solution might be more appropriate to assess depressive symptoms in pregnancy and postpartum.

The majority of the adults with ADHD have chronic difficulty to go to bed on time. This leads to a shorter sleep duration and daytime sleepiness that may aggravate the inattention problems of ADHD. This sleep pattern is also known as a delayed sleepphase, and the patients as ‘eveningtypes’. The other way round, eveningtypes have been associated with impulsiveness. The scope of this presentation is to study the impact of this sleep pattern in adults with ADHD on mood (i.e. seasonal affective disorder), eating habits (like timing of meals and binge eating), activity patterns (like nightshift work and light at night) and health in general, i.e. obesity and cancer.

People with severe mental illnesses, such as schizophrenia, depression or bipolar disorder, have worse physical health and reduced life expectancy compared to the general population. The excess cardiovascular mortality associated with schizophrenia and bipolar disorder is attributed in part to an increased risk of the modifiable coronary heart disease risk factors; obesity, smoking, diabetes, hypertension and dyslipidaemia. Antipsychotic medication and possibly other psychotropic medication like antidepressants can induce weight gain or worsen other metabolic cardiovascular risk factors. Patients may have limited access to general healthcare with less opportunity for cardiovascular risk screening and prevention than would be expected in a non-psychiatric population. The European Psychiatric Association (EPA), supported by the European Association for the Study of Diabetes (EASD) and the European Society of Cardiology (ESC) published this statement with the aim of improving the care of patients suffering from severe mental illness. The intention is to initiate cooperation and shared care between the different healthcare professionals and to increase the awareness of psychiatrists and primary care physicians caring for patients with severe mental illness to screen and treat cardiovascular risk factors and diabetes.

It is now acknowledged that Attention-deficit Disorder with Hyperactivity (ADHD) is not limited to children or adolescents. Regardless of culture, up to 4% of the adults in the general population might be diagnosed with ADHD, a disorder often accompanied by comorbid psychiatric disorders. Among those is Substance Abuse including cigarette smoking. Indeed, ADHD patients tend to start with drugs earlier than normal controls. Pharmacological treatments of ADHD chiefly encompass amphetamine salts, methylphenidate and atomoxetine with a good tolerance and effectiveness. These treatments are even better tolerated now that long-acting, extended-release formulations and transdermal delivery systems become available. But it is likely that some patients will still not respond, especially when comorbid disorders are associated. Other agents are being tested as future pharmacotherapies of ADHD. Here we propose a review of the literature concerned with the relationships between cigarette smoking and ADHD in adolescent and adult patients, and an overview of the future pharmacotherapies of ADHD related with nicotine receptor agonists.

Attention-deficit/hyperactivity disorder (ADHD) encompasses a broad constellation of behavioral and learning problems. These patients are also characterized by low blood long-chain polyunsaturated fatty acid concentrations; however their supplementation effect on ADHD symptoms is not clear. It was recently (1) shown in children with inattention that consumption of n-3 phosphatidylserine (PS) for 3-mo favorably affected their visual sustained attention performance. We aimed to evaluate in children with ADHD the effect of n-3 PS on ADHD symptoms and wellbeing.

ADHD is a neurodevelopmental disorder that impairs executive functions, leads to maladaptive behavior and, in about 50%, has a livelong persistence. Nevertheless, adult ADHD is a very much under-diagnosed condition.

We conducted a study aimed to identify ADHD in a special population of adults. Questionnaires were applied to the parents of children attending CADIn, a Clinical Centre for Developmental Disorders for evaluation or intervention (48% of their children were diagnosed as having ADHD and 22% were diagnosed as having Pervasive Developmental Disorder). We expected a higher incidence of ADHD in this population as well as a better awareness for the condition.

We used the Adult ADHD Self-report Scale (ASRS-v1.1) and the questionnaires contained questions concerning degree of impairment, persistence of symptoms and comorbid psychiatric conditions. 114 parents were inquired, 29% fathers, 68% mothers 3% missed gender. 17% of the parents quoted above the cut-off-point for the ASRS-v1.1 screener and amongst those, 45% referred the ADHD symptoms as causing them severe impairment. Only 3 subjects had been previously diagnosed as ADHD. The prevalence of ADHD symptoms was similar for males and females. 56% of the ADHD population was diagnosed formerly as suffering from psychiatric disorder, compared to 35% of the total population. The more common diagnoses were depression (45%) and anxiety (30%).

We conclude that ADHD is much under-diagnosed in the adult population. Considering its high heritability, a closer evaluation of the parents of children diagnosed with ADHD is suggested.

There have been a number of recent findings that elucidate the ways repeated episodes relate to cognitive impairment and poor functioning in Bipolar Disorder. While available treatments are undoubtedly helpful, many patients are still lacking improvement and adequate prophylaxis even when adherence to treatment is accomplished. New research point to neural glial cells resilience and connectivity as major contributors to the pathophysiology of the disorder. In this context, growth factors such as the brain-derived neurotrophic factor (BDNF) have been pointed out as potential targets for the development of new treatments. In the psychological domain, better assessment of the cognitive decline associated with the disorder is a major issue. Once cognitive disability is present, interventions with the potential to recover functioning have been put forward. In the biological domain, strategies aiming at reducing neural damage and with the potential to regenerate connectivity among brain cell are promising avenues for the development of new treatments. Another important development would be the incorporation of biological markers as a means to help staging the degree of severity of the disorder and guide the pharmacological treatment. These topics and their relationship to the clinical context will be discussed in this session.

While we continue to refine our understanding of the pathophysiology of bipolar disorder (BD), several hypotheses have been postulated including a role for monoamines, gamma-amino butyric acid, glutamate, and second messenger signaling pathways. Recently, mitochondrial dysfunction and oxidative stress have been identified by a number of studies, as an important etiological factor in this disorder. Mitochondria play a crucial role in ATP production through oxidative phosphorylation, a process carried out by the electron transport chain (ETC) complexes. During the transfer of electrons along this ETC, the ROS can be generated, especially in complex I and III4. Growing body of evidence suggests the association of mitochondrial dysfunction and BD. Recent DNA microarray analysis in post-mortem frontal cortex and hippocampus revealed that the expression of several mRNAs coding for ETC complexes I-V subunits was decreased in subjects with BD. Supporting the key involvement of oxidative damage in BD, assays conducted with peripheral blood samples have demonstrated that BD is associated with alterations in antioxidant enzymes and increased lipid peroxidation. Recently we found that oxidative damage to lipid is present in the frontal cortex of BD subjects. A meta-analysis suggested that the levels of lipid peroxidation are elevated in BD providing support for oxidative stress hypothesis of BD. Furthermore, BD subjects showed increased DNA damage, as well as, upregulation of apoptotic genes. These data not only suggest that oxidative mechanisms may form unifying common pathogenic pathways in psychiatric disorders, but also introduce new targets for the development of therapeutic interventions.

Repeated stress induces structural remodeling in brain regions involved with memory and emotions, such as hippocampus, amygdala and prefrontal cortex. Under chronic stress, hippocampal and prefrontal volumes are frequently diminished, whereas the size of the amygdala is increased. Related anatomical changes have been described in patients with bipolar disorder. New data indicate that episodes of depression and mania are associated with decreases neurotrophic and increases in proapoptotic pathways. Such stress- and episode-induced alterations in emotional circuitry may lead to a dysfunctional processing of information, which may render BD patients more vulnerable to subsequent environmental stressors, episodes, and substances of abuse. Allostasis means literally keeping stability through change. Allostatic load refers to the bodily wear and tear that emerges with sustained allostatic states. This concept provides an explanatory link to apparently unrelated findings such as cognitive impairment and higher rates of physical co-morbidity and mortality that occur in the course of bipolar disorder and further highlight the importance of effective long-term prophylaxis.