In the last two decades enormous progress has been made in the characterization of premature ejaculation (PE). Although lifelong (primary) PE and acquired (secondary) PE has been known since the 1980s, a new classification of PE has been proposed in 2006 by Waldinger et al., who distinguished two other PE subtypes, e.g., premature-like ejaculatory disfunction and natural variable PE. In 1943, Bernhard Schapiro noted that family members of men with PE often have PE as well. In 1998, Waldinger et al postulated that lifelong PE, and particularly the short intravaginal ejaculation latency time (IELT), may be genetically determined. They postulated that the IELT is distributed according to a continuum, from men who always ejaculate very rapidly to men who always ejaculate after a very long intravaginal ejaculation time. Research in male rats showed this continuum. In two stopwatch studies, such a continuum was also shown in a random sample of men. In 2009, Janssen et al. publish ed a DNA study performed in men with lifelong PE. This study showed that 5-HTT polymorphism was involved in the ejaculation latency time. It appeared that in men with lifelong PE, males with LL genotype had a 100% faster ejaculation time than men with an SS genotype. It is postulated that the IELT is genetically determined by a cluster of genetic polymorphisms of the 5-HTT, 5-HT receptors, 5-HT enzymes and/or polymorphisms of other neurotransmitter systems.

Studies in humans and animals have suggested that the central dopaminergic system is involved in all components of male and female sexual behavior: desire, erection, orgasm and satisfaction. Copulating activity enhances DA release in the nucleus accumbens as measured by microdialysis in male rats. This rise in DA release lasts until ejaculation and then declines during the refractory period.

Dopaminergic agonists such as L-dopa, apomorphine, amantadine, bupropion, amphetamines and cocaine have been reported to arouse sexual behavior. Short term use of cocaine and other drugs that increase dopaminergic activity (Marijuana, MDMA) facilitate sexual desire and erection and delay ejaculation. These effects are reversed in chronic abuse when brain DA is depleted.

Central dopaminergic blockers, like first generation antipsychotics suppress sexual functioning via the D2 receptors blockade and the corresponding elevation in plasma prolactin levels. Due to their weak antagonistic activity at D2 receptors, second generation antipsychotics are associated with fewer sexual side effects and thus provide an option in the treatment of patients with schizophrenia.

Enhancement of dopaminergic activity by the addition of the DA agonists or bupropion, a norepinephrine-dopamine reuptake inhibitor, has been reported as an effective approach in the management of antidepressant-induced sexual dysfunction. The significant facilitating role of the DA system on sexual function should not be viewed independently. The dopaminergic system interacts with other systems like gonadal hormones, Nitric Oxide and serotonine in the complex neurobiology of sexual function.

The research of neurobiology and treatment of various disorders requires certain degree of homogeneity of the studied entities. In an ideal word, common etiology and/or pathogenesis would help to define homogenous entities. As our understanding of etiology and/or pathogenesis of mental disorders and diseases is lacking, we rely on various diagnostic systems to help us reach some degree of homogeneity.

The diagnostic criteria of sexual dysfunction(s) in the DSM-IV are rather vague and imprecise. Interestingly, we are not even clear when a sexual problem becomes a sexual dysfunction. As the new versions of the diagnostic systems (e.g., DSM-V) are being prepared, the classification and definitions of sexual disorders/dysfunctions are being considered.

The general classification issues that need to be and are addressed are specific duration of sexual dysfunctions, use of distress s a diagnostic criterion and quantification of severity and frequency. Strengthening and clarifying these three classification issues would probably help in defining more homogenous entities.

The broader yet more specific issues to be considered are inclusions of new diagnostic entities (persistent genital arousal disorder in women; adjustment disorder with disturbed sexual functioning; coercive paraphilic disorder), possible removal or reclassification of some sexual dysfunctions (e.g., sexual aversion disorder - remove or reclassify as specific phobia); collapsing some entities into one (dyspareunia and vaginismus into genitor-pelvic pain/penetration disorder) changing the names of some dysfunctions (premature ejaculation to rapid ejaculation); and redefining some dysfunctions (e.g. sexual desire and subjective sexual arousal in women).

Reigning theories about how the brain governs sexual behavior are the product of experimental investigations and observations in rodents. However, there is a growing appreciation of the fact that these animal models can not account for the sheer complexity of human sexuality. The need for human studies coincides with the exponential growth of the use of medical scanners for the purpose of visualizing human brain activity in vivo. Over the last decade, some 50 of these brain imaging - or neuroimaging - studies have appeared in the field of sexuality research.

In this lecture I will give an overview of the contribution neuroimaging has made to knowledge about the sexual brain. These studies cover a large area of human sexuality, including sexual orientation and preference, sexual desire and arousal, genital stimulation and orgasm, as well as sexual dysfunction and paraphilic disorders. Significant progress, relative to animal studies, has been made in understanding the role of the cerebral cortex, the prefrontal cortex in particular. At the end of the lecture, I will touch upon possible future research directions in the field of human neurosexology.

There is a high prevalence of panic disorder (PD) in the community. The National Comorbidity Survey, a US study of over 8000 adults in the general population, found a lifetime prevalence rate of 3.5%. This is a higher prevalence than that reported in earlier epidemiological studies, which documented lifetime prevalence rates of between 1.2 and 2.4%. Panic disorder is typically a disorder of young adults, with an impact on quality of life, in terms of social, personal, and economic consequences, at least comparable to that of major depression. Benzodiazepines, as well as selective serotonine reuptake inhibitors (SSRIs) have been studied thoroughly in acute and long-term PD. However, there is a lack of data to answer the question if there is an enhanced efficacy with the combination of psychological treatments as well as to guide the clinicians what to do after non-response.

Generalized anxiety disorder (GAD) is a chronic illness with an estimated one year prevalence of approximately 3%, and a lifetime prevalence of approximately 6%. GAD (without depression comorbidity) is associated with significant impairment in quality of life and functioning which has been found to be comparable to major depressive disorder, and chronic medical illnesses such as diabetes and arthritis. At least 5 classes of drugs are available for the pharmacologic management of GAD (Bandelow et al., 2008), each acting via different mechanisms: (1) benzodiazepines (diazepam, lorazepam, alprazolam, etc) which augment inhibitory GABAergic activity; (2) monoaminergic reuptake inhibitors, consisting of SSRI drugs with serotonin selectivity (paroxetine, escitalopram, sertraline), SNRI drugs with dual serotonin/ norepinephrine activity (venlafaxine-XR, duloxetine), as well as some first generation tricyclics (imipramine); (3) azapirones (buspirone) which modulate monoaminergic transmission; and (4) pregabalin, which acts presynaptically to inhibit excitatory neurotransmission. Two other classes of medication (antihistamines such as hydroxyzine; antipsychotics such as quetiapine) and recently a herbal remedy, silexan, have also demonstrated efficacy in the treatment of GAD. Cross-study comparisons suggest that each class of drug has a different benefit-risk profile. However, relatively few double-blind, placebo-controlled head-to-head trials have been published which provide direct comparisons of the efficacy and safety profiles of drugs in each class.

Based on the sound knowledge of clinical psychiatry neuroscientists embark since over 20 years to discover the biological bases of mental disorders. Whereas the “window to the brain” was firstly dominated by neuroendocrine and biochemical models, we now have the possibility to use sophisticated brain imaging techniques which span from electrophysiology to techniques derived from nuclear medicine. Furthermore, the combination of brain imaging techniques with genetic variables promises to have a close insight into brain-environment interactions. For treatment of psychiatric diseases, multidimensional criteria for selection of a psychotropic medication is necessary to not only judge the clinical phenotype but also the functional phenotype and finally the genotype. Whereas the clinical phenotype is characterized by psychiatric syndromes including psychiatric and somatic comorbidity, the functional phenotype can be uncovered with neuroendocrine measurements, sleep physiology, imaging techniques as well as proteomics. Finally, the genotype can be characterized by single nucleotid polymorphisms (SNP), coupling as well as the determination of candidate genes. Imaging genetics is a new way to achieve insight in the genetic variables of changes on a cellular level which thereafter influence information processing and finally are represented in complex functional interaction of human behavior. Based on this knowledge it is evident that psychiatrists not only should be determined to the clinical symptomatology of their patients but also on the underlying biological processes which can in turn be influenced to various degress with pharmacological as well as non-pharmacological treatment modalities, since the brain has a specified way to get better.

Over than 20 randomised controlled trials (RCTs) showed that cognitive behaviour therapy (CBT) is the most efficacy treatment for adults with bulimia nervosa (BN). CBT-BN is more effective than delayed treatment, pharmacotherapy, and as effective as, or more effective than, all the psychological treatments evaluated. The leading alternative treatment is interpersonal psychotherapy which is comparable in its effects but much slower to act. However, CBT-BN is not effective enough: at best, only half the patients make a full remission and it has not been designed for treating anorexia nervosa (AN), and eating disorder (ED) not otherwise specified patients, that together represent 2/3 of ED patients. CBT-Enhanced (CBT-E) has been designed to overcome these limits. CBT-E adopts more modern and potent procedures and strategies to address ED psychopathology, and it is suitable for all forms of clinical EDs. CBT-E has been originally designed for adults in standard outpatient settings, but it has been adapted for use with younger patients (under 18 years), with patients with medical and psychiatric comorbidity, and with patients treated in intensive settings (e.g. intensive outpatient, day-hospital and inpatient. Data from a recent RCT show that CBT-E is effective both for BN and not underweight EDNOS. Emerging data shows that CBT-E is a also a promising treatment for outpatient AN and for severe inpatient ED patients.

Prevention of mental ill health has been declared a major task by the European Commission; and an early detection and intervention in psychosis in terms of an indicated (secondary) prevention in persons already seeking help for mental problems is increasingly approached across Europe both on research as well as clinical level, a mixture of both dominating. The growing interest in this field of research across Western and Western-Central Europe becomes apparent in the rapidly increasing number of publications on this topic since the turn of the century that has nearly increased by the factor of 5. The 3 leading European countries in this are Germany, the United Kingdom and Switzerland.

Despite the very well reception of the ‘prevention idea’ by clinicians, researchers, relatives of patients with psychosis and clients and first promising results of early detection and/or early intervention studies, critics caution against the percentage of false-positive predictions by current prodromal criteria and the possibly unnecessary initiation of an antipsychotic psychological and/or pharmacological treatment along with its risks of unwanted side effects including early stigmatization. Supporters, however, argue that these short-comings will be overcome in the course of time and that the potential of new benign preventive interventions was just about to be discovered as well as caution against self-stigmatization by odd, eccentric behaviours and loss of functioning not recognized as part of an illness but attributed to the person him-/herself.

In future, joint efforts across clinical and scientific disciplines as well as countries will be required to enhance predictive accuracy, to develop broadly applicable and risk-adapted interventions, to provide help to all in need, to extend preventive efforts to other psychiatric disorders and to possibly reach the ultimate aim, a primary prevention of mental disorders.

Schema Therapy (ST) for Borderline Personality Disorder (BPD) is a (cost-) effective treatment compared to a psychodynamic specialized treatment and treatment as usual (TAU). This presentation focuses on recent development in ST for BPD. First the results of the BPD RCT by Giesen-Bloo et al. (2006) will be presented. Then the new results of an implementation study of ST for BPD in regular practice will be presented. This study also tested to what degree telephone availability of the therapist in case of crisis had a medium of large effect on the results of ST (Nadort et al., 2009). Thirdly, a special group format seems to catalyze the processes of change used by ST. We will present results of a recent RCT comparing group ST for BPD to TAU and discuss the specific ingredients of this group-ST approach (Farrell et al. 2009).

There have been a number of recent changes in training and education in psychiatry in the UK in the last decade. A new regulator has emerged called the Postgraduate Medical Education and Training Board (PMETB), which is independent of government and has responsibility for the standards and quality assurance of all postgraduate education, training and assessment in medicine and dentistry. In April 2010 this body will merge with the General Medical Council, which has the regulatory powers for registration, keeping the specialist register and approving medical school curricula. There will be the addition of another year called Foundation year 2, where trainees learn more generic skills prior to choosing their specialty training. After completion of the Foundation Programme, trainees will enter a specialist training programme leading directly to the award of a Certificate of Completion of Training (CCT). Entry to the programme will be competitive, but subject to satisfactory progress, no other further competition will be needed before the completion of training. These changes have a serious impact on selection, recruitment and retention of trainees. Comparisons with other European countries will be discussed, along with the potential advantages of educational networks.

To assess the efficacy of psychiatric treatments, rating scales are essential. In this presentation, methodological and statistical problems associated with the use of rating scales in psychiatry are discussed, by taking the anxiety disorders as an example.

Not only standard symptom-specific rating scales, such as the Hamilton Anxiety Scale (HAMA), but also global measures such as the Clinical Global Impression Scale (CGI) and Quality of Life scales are used, as not only improvement of single symptoms, but also an overall increase of a patient's well-being should be the focus of a clinical trial. However, due to high placebo response rates in anxiety disorders, the use of rating scales is determined by the need for an instrument, which is sensitive enough to detect differences between active drugs and placebo (or between a certain psychological treatment and a psychological placebo). Quality of Life scales often do not detect such differences, as domains such as partnership or employment do not show rapid changes within the 8-12 weeks of a clinical study. Moreover, when using too many different scales, problems of multiple testing occur.

The outcome of a clinical study is often described by the number of patients who responded or remitted, as these endpoints are easily understood by patients. “Response” is commonly defined as a ≥ 50% reduction on these standard scales. However, this definition is arbitrary, and cut-off points should rather be founded on empirical data than on a thumb rule. The definition of “remission” on standard scale scores varies from study to study and is also very subjective. An analysis of available treatment studies in patients with anxiety disorders revealed that these definitions do not necessarily reflect clinical reality. Also, “number needed to treat” is an endpoint, which may lead to inaccurate assessments from a statistical point of view, because it is based on a subjective definition of remission. The adequate use of rating scales also touches ethical questions.

As nowadays, the introduction of novel psychotropic drugs is a relatively rare event, the use of those presently available should be optimised in order to increase their efficiency. Ideally, medication should be personalized, in order to obtain a maximal efficacy and minimal risks for adverse effects. Knowledge about the neurobiological basis of the major psychoses and the biological consequences of pharmacological treatments has dramatically increased. This situation has prompted the development of tests in patients, to be carried out at baseline and during the treatment, in the aim to improve the diagnosis of the underlying disease, to select the optimal treatment and to monitor the clinical evolution of the patient. These tests are available both on the pharmacodynamic and on the pharmacokinetic level: (1) analysis of neurotransmitters (biogenic amines, neuropeptides, hormones) in blood or CSF; (2) pharmacogenetic tests at the pharmacodynamic (receptor proteins, neurotransmitter transporter proteins) and the pharmacokinetic (drug metabolising enzymes (e.g. cytochrome P-450), drug transporter proteins (e.g. P-glycoprotein)) levels; 3) monitoring techniques (drug receptor binding in the brain using imaging techniques, therapeutic drug monitoring in the blood, phenotyping for metabolising enzymes). There is much evidence about the usefulness of these techniques for diagnostic and monitoring purposes, but also about their limits in the clinical context and in their performance regarding sensitivity and specificity. In particular, there is a lack of studies, which combine pharmacodynamic and pharmacokinetic tests. The present state of research suggests that tests in relationship with the pharmacokinetic behaviour of a drug are useful tools to personalise drug treatment.

This presentation highlights the need for a close link between the psychiatrists and the dermatologists. There is undoubtedly a high prevalence of psychiatric conditions amongst both the dermatology outpatients and the inpatients. The psychiatric symptoms can be either a manifestation of distress secondary to the primary dermatological pathology or a primary psychiatric condition presenting as dermatological pathology. In both the cases, the risk has to be recognised as the distress can lead to a suicide attempt and therefore, it can be challenging to both the treating dermatologist and the psychiatrist as the patient can actively refuse treatment because of the stigma associated with the label of having a psychiatric ailment. This presentation mentions various psychiatric conditions with regard to dermatology and specific issues about the psychotropic and dermatological medications.

Mental disorders which can present in the dermatology clinics are anxiety, depression, obsessive-compulsive disorder, body dysmorphic disorder, delusional parasitosis or delusional infestation and dermatitis artefacta. It can be quite helpful for the dermatologist to be aware of the symptoms of these disorders whether primarily psychiatric or secondary to the dermatological pathology. The issues regarding medication are specifically with regard to Isotretinoin and combination treatments. An association had been reported between oral isotretinoin and mood changes, particularly depression and suicide but a recent systematic review did not find any conclusive evidence for such an association. Combination of cytotoxic agents with clozapine can exacerbate the risk of reduction in white blood cell counts. There is an increased risk of ventricular arrhythmias with the combination of erythromycin and antipsychotics. An increased risk of convulsions with a combination of erythromycin and clozapine has been mentioned. There are particular concerns about the over the counter use of St. John's wort, used in mild and moderate depressions with regard to interaction with various dermatological agents.

In summary, a close liaison between dermatologists and psychiatrists is essential to provide holistic care for patients presenting with dermatological pathology.

Bipolarity might be underdiagnosed by the DSM-IV. This could particularly pertain for young adults, when the disorder is in early stages and the manifestations of hypomania are not typical. Additionally, the current DSM-IV-based instruments are not sufficiently sensitive for detecting hypomania. Support comes from epidemiological and clinical studies, which showed that subthreshold BPD is common and clinically significant. In the National-Comorbidity-Survey-Replication (NCS-R) the overall prevalence of BPD increased from 2.1% up to 4.4% if subthreshold BPD was considered. Role impairment, comorbidity (alcohol abuse, panic disorder, impulse control), and family history of mania are the validators of subthreshold bipolarity. In the small prospective Zurich Study a stepwise broadening of the criteria for hypomania allocated almost half of the subjects with MDE to a broadly defined bipolar group. In bigger samples, such as 2300 patients presenting recurrent or resistant depressions, the hypomania rate, when dimensionnaly rated (by using the hypomania checklist) was more than 60%.

DSM-IV “Bipolar II disorder” and “Cyclothymia” are still ill defined with a great confusion among the territory of “Soft Bipolar Spectrum”, and clinicians need a more practical approach.

The Kahlbaum-Hecker syndrome of cyclothymia includes depressive (dysthymia), hypomanic (hyperthymia), and mixed hypomanic-depressive phases. According to French experts, Deny and Kahn (1909) supported the hypothesis that Cyclothymia represents a special constitution, which can be considered nowadays as particular affective temperament with close continuum with subtrheshold bipolarity.

The great idea of Kahlbaum, Hecker, Deny is to combine the following variables: 1) premorbid temperament; 2) age of onset, 3) time course of an illness (cyclicity / intermittence). Applying this combination, bipolar spectrum could be currently divided into 2 categories: “Typical BP-I/II” (episodic mania or hypomania with free intervals) versus “Cyclothymia” (radically instable form with continuous ups and downs). This intra-bipolar dichotomy seems to be closer to the clinical reality of mood disturbances. Cyclothymia is probably the most frequent expression of bipolar disorder (more than 30% of major depressions). Repeated brief swings with high mood instability and rapid switching seemed to be a distinct entity with early onset, irritable (“dark”) hypomania and high suicide risk. This condition emerged as the most prevalent and severe expression of the bipolar spectrum.

Coercive treatment in European inpatient psychiatric facilities remains to be used in daily practice with high variety of its frequency, type and legal background. Use of coercive measures is sometimes sharply criticized by various bodies. It was proclaimed that these procedures are regarded as signaling failures in care. Others are of that opinion, that even if elimination of restraint and seclusion should be a goal, it may be difficult to accomplish it if we endeavor to treat individuals with acute psychosis who have a history of violence and whose recent violent behavior led to hospitalization.

In last decade in many countries several programs minimizing use of coercive measure during psychiatric treatment were launched and published to be successful. However, the ideal of avoiding all coercive measures in facilities hospitalizing all acute patients from defined catchment area seems to be an unrealistic goal for the time being. Country socio-cultural traditions as well as treatment habits in individual psychiatric facilities play decisive role in this very sensitive area. Future research projects should identify those factors in legislation and clinical practice that could be specifically relevant for achieving more constructive cooperation of all engaged parties. But even at present time it is necessary to introduce programs and practice guidelines that would rationalize and minimize use of coercive measures in psychiatric facilities. In any case, patient’s rights should be granted and interventions be provided according to the principle of the “least restrictive alternative”.

Environmental factors and both common and rare genetic variants increasing risk for schizophrenia are being discovered, but the neural mechanisms that mediate their impact are only now coming into focus. We discuss work from a translational genetics approach, with a focus on neuroimaging, delineating mechanisms of genetic risk through interaction of prefrontal cortex with striatum, midbrain and hippocampus. Using social status as an example, we identify dissociable neural responses to perceived social rank using functional magnetic resonance imaging (fMRI) in an interactive, simulated social context. In both stable and unstable social hierarchies, viewing a superior individual differentially engaged perceptual-attentional, saliency, and cognitive systems, notably dorsolateral prefrontal cortex. In the unstable hierarchy setting, additional regions related to emotional processing (amygdala), social cognition (medial prefrontal cortex), and behavioral readiness were recruited. Furthermore, social hierarchical consequences of performance were neurally dissociable and of comparable salience to monetary reward, providing a neural basis for the high motivational value of status. Finally, we discuss GEI impacting on these circuits, with a focus on validating epidemiologically identified GEI on the neural circuit level.