The goal of this training workshop is to give an introduction in recent developments of wisdom psychology and their bearing for cognitive psychotherapy of adjustment disorders.

Negative life events like divorce, dead of a beloved one, job loss etc. require enhanced coping. If this is not sufficient it can result in adjustment or other mental disorders. One factor which often contributes to pathological developments in the context of negative life events is embitterment because of the feeling of having been treated unfair, been let down or been humiliated. If embitterment is present then there is a tendency not to recover spontaneously but rather to take a chronic course.

There is a new approach in the treatment for such adjustment disorders which is based on recent developments in wisdom psychology. Wisdom has been defined as the capacity to cope with unsolvable and serious problems and questions in life. It has been shown:

1. a. that persons who are not successful in coping with negaive life events lack wisdom capacities,

2. b. that wisdom capacities can be trained, and

3. c. that cognitive treatment which uses wisdom strategies is helpful in the treatment of adjustment disorders and especially those with prolonged embitterment reactions.

This training workshop will:

• • inform about the clincial features of adjustment disorders and especially posttraumatic embitterment disorders;

• • give an introduction in recent developments of wisdom psychology;

• • teach the esentials of wisdom psychotherapy.

The discussion on the use of coercive interventions such as seclusion and restraint accompanies the history of psychiatry from its beginning. It is the oldest and still topical issue of psychiatric institutions. Nowadays, the political growing together of Europe puts questions of common ethical standards on the agenda. The quality of psychiatric care and particularly the use of freedom-restricting coercive measures for mentally ill people are a challenge for modern civilized societies. There is a wide variety in the use of coercive interventions in different European countries in the past and the presence. An important supra-national institution dealing with the issue of coercive interventions in mental health care is the CPT (Committee for the Prevention of Inhumane or degrading Treatment or Punishment). Available data on the use of coercive interventions in different countries were found by literature review. The percentage of admissions exposed to seclusion or restraint varies from zero (Iceland) to 35% (Austria). The median duration of a coercive measure varies from 15 minutes (physical restraint, UK) to 16 days (seclusion, Netherlands). Recently, in several European countries (Finland, Germany, Netherlands, Norway, Switzerland, UK) initiatives have emerged to reduce seclusion and restraint. Obstacles for decreasing coercion in clinical psychiatry are discussed, suggestions for action are given.

Sound humanitarian psychiatry has for long, perhaps always struggled with the conflict between being therapeutical with the patients best interest at hand and the demand for restricting and applying coercive measures against the patients will and autonomy for the sake of protecting the integrity and security of not only the patient, but also her/his surroundings. This conflict includes a number of ethical issues such as preserving the patients’ autonomy, safeguarding the autonomy and security of the patients’ family as well as societal interests.

At the same time, some psychiatric research deals with the evidence of psychiatrically motivated restrictive and coercive measures and their possible therapuetic effect. Recent reviews have found that there is no evidence for the therapeutic effect of coercive measures. In view of the reasons for coercive measures, the issue of its therapeutical effects seems wrongly addressed.

It will be argued in this presentation that the issue is how psychiatry intended for the most severely disturbed patients should live up to delivering ethically sound services is a question of proper supervision. The presentation will problematise these issues as well as arguing that psychiatry intended for the most severely disturbed has to be politically controled within the frame of a democratic society with sound ethical human principles.

The presentation will adress the following questions: 1.Do coercive measures in European countries increase? 2.Could coercive measures be minimized? 3.Are coercive measures less effective than voluntary measures? 4.Are alternatives to coercive measures available, and if so which ones? 5.Is coercion always coercion, and does it influence prognosis? 6.What is the current status of the development of clinical guidelines pertaining to the use of coercive measures? 7.Is the use of coercive measures an indicator for the quality of mental health care? 8.Are the main legal problems associated with the use of coercive measures solved? 9.What are the consequences of having answered questions 1.-8.? 10. Are there issues in the field of coercion in psychiatry which have gained recent importance?

Psychopathology is a central tool for psychiatry, in clinical practice as well as in research. And phenomenological psychopathology is an important theoretical and methodological approach. However, both terms may carry very different and even contradictory meanings. In this lecture I shall trace the historical roots of both concepts and argue for their significance beyond the historical dimension. Especially regarding the necessity to link neuroscientific data with the clinical level, i.e. with the individual patient, psychopathology in general and phenomenological aspects in particular are likely to gain influence in the future. This will be discussed in detail and exemplified by recent publications.

Nancy Andreasen (2007) published a bleak assessment of the consequences of introducing operational criteria for psychiatric diagnosis (DSM-III and subsequent editions). She lists a widespread ignorance of features that are not themselves criteria, dehumanisation of psychiatric praxis, and unquestioned belief in reified rigidly conceived diagnostic categories with poor validity.

Moreover, we could add that subjectivity-aversive stance has had a negative consequence for etiological, preventive and therapeutic efforts in schizophrenia. As an example of phenomenological approach, integrated with empirical design, a series of studies of disorders of self-experience in schizophrenia is presented.

The term ‘psychopathology’ is used with different meanings. In the most trivial sense it refers to the object of psychiatry, i.e. pathologies of the psyche. In continental Europe Psychopathology is the formal taxonomy of the modalities of abnormal experience. We have three levels or profiles of Psychopathology. First, General Psychopathology, rooted in Jaspers’ work:

1. i. sorts out, defines and differentiates abnormal psychic phenomena, actualized and sistematically described in specific terms; and

2. ii. classifies groups of phenomena according to their phenomenological affinities, i.e. in terms of the patients’ self-descriptions, and the modes in which the experience comes to expression.

Second, Clinical Psychopathology, rooted in Kurt Schneider's work, aims at becoming the psychopathological doctrine linking symptoms and diagnosis. Clinical Psychopathology is essentially aimed at the identification of symptoms which are significant in view of nosographical distinctions. Third, we have Phenomenological Psychopathology, whose task is organizing different kinds of a person's abnormal experiences in theoretical constructs whose guide-line is the meaning-structures of such experiences. These meaning-organizers - i.e. psychopathological organizers - are synthesizing schemes of comprehension, conferring a unitary meaningfulness to different declinations of pathological phenomena. These constructs are descriptions of the mode of being-in-the-world of a given patient, i.e. his embeddedness in mundane, everyday activities. They are based on a holistic approach, advocating the importance of the global grasping of a phenomenon as an organising and meaningful Gestalt over a particularistic focus of attention.

The establishment of criteriological and manualized systems of diagnosis since the 1980ies has lead to a valuable increase in the precision and reliability of psychiatric diagnosis. On the other hand, the limits of this approach for clinicians and researchers are increasingly becoming apparent. In particular, the assessment of subjective experience is nearly excluded on the theoretical level and downplayed on the pragmatic level, with serious consequences for the validity of psychiatric diagnosis, for empirical research and, above all, for therapeutic purposes.

In my paper, I will argue that a thorough assessment and inclusion of subjective experience in our diagnostic systems will be indispensable for clinical, therapeutic as well as research purposes. To this purpose, I will distinguish three major approaches to the assessment of mental illness:

1. 1. The positivistic, objectifying or 3rd person approach as endorsed by DSM IV and ICD 10, focusing mainly on observable behavioural symptoms.

2. 2. The phenomenological, subject-oriented or 1st person approach, focusing on the patient's self-experience and exploring its basic, often implicit structures.

3. 3. The hermeneutic, intersubjective or 2nd person approach, mainly aiming at the co-construction of shared narratives or interpretations regarding the patient's self-concept, conflicts and relationships, as e.g. in psychodynamic approaches.

These three approaches will be compared regarding their respective values for psychopathological description, diagnosis, research and therapeutic purposes.

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.

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.

Receptor-binding profiles of antipsychotics differ, with important implications for treatment efficacy and tolerability. Receptors implicated in clinical response and adverse effects include dopamine D2, serotonin 5HT1A and 5HT2A, as well as H1 histamine, M1 muscarinic and alpha1 adrenergic receptors. Varying receptor affinities can explain the clinical profile specific to each compound, including adverse events such as weight gain, metabolic disturbance, hypotension, hyperprolactinaemia and extrapyramidal symptoms.

Receptor profiles also play a role when switching between antipsychotics. Consideration of the differences between agents being withdrawn and introduced can minimise adverse events and ensure efficacy is maintained. Using strategies such as cross-titration, the consequences of receptor upregulation, and amplified or muted treatment effects can be minimised. Pharmacokinetic profiles of the agents should also be considered, as withdrawing an agent with a long half-life may lead to hangover effects.

In all patients, a pharmacological basis should be used to select agents with minimal drug-related adverse events. Patients at risk of metabolic syndrome, for example, may benefit from an agent with a low risk of weight gain, such as aripiprazole or ziprasidone, while agents associated with hypotension, such as clozapine, risperidone or quetiapine, should be avoided in elderly patients to reduce the risk of falls. The route of administration also impacts treatment decisions and appropriate use of co-medications needs to be considered carefully.

By paying attention to the pharmacology of antipsychotic agents, physicians can balance good efficacy and a low incidence of adverse events, thereby optimising treatment for their patients with schizophrenia and bipolar disorder.

Multiple neurochemical pathways have been identified to be involved in mediating craving and relapse to alcohol and, further, animal models greatly assist in investigating pharmacological interventions of relapse behaviour. Opioidergic and glutamatergic systems play a key role in alcoholism as demonstrated by the clinically effective compounds naltrexone and acamprosate acting through these systems. Although the dopaminergic system has been in the focus of alcohol research for many years, clinical trials interfering with several components of this system displayed rather disappointing results. This situation, however, could change in light of the discovery that dopamine D3 receptor antagonism produces very consistent and robust results in preclinical studies. Corticotropin-releasing factor signalling and the endocannabinoid system integrate stress-related events and thereby mediate relapse behaviour. Thus, many new targets have been identified and several new compounds are currently undergoing clinical testing. However, given the heterogeneity in treatment response, genetic and protein markers as well as endophenotypes are currently characterised for individualised pharmacotherapy.

Opiate dependence is a serious psychiatric disorder with substantial suffering for the patient, his environment and society as a whole. Currently available treatments include abstinence oriented treatment with naltrexone and substitutian treatments with methadone and buprenorphine. However, treatment compliance with naltrexone is very low resulting in low effectiveness. In addition, existing substituation treatments only show moderate effectiveness resulting in a large number of patients showing continued drug use and serious psychological, somatic and functional impairment.

New treatment strategies involve:

1. a. the development of long acting opiate antagonists (naltrexone) and partial agonist (buprenorphine) to improve treatment compliance and treatment retention,

2. b. new substitution options such as slow release oral morphine (SROM), oral diacetylmorphine (heroin) and inhalable and injectable diacetyl morphine (heroin assisted treatment: HAT).

Recently, a new approach using neurosurgical and neuromodulatory techniques has been advocated to help treatment refractory opiate dependent patients. Finally, certain combinations of farmacotherapy and psychosocial interventions have shown promise for future improvements.

This presentation reviews the evidence of existing treatments for opiate dependence and explores the new treatment options for patients not fully responsive to the existing treatment modalities.

Treatment of cocaine dependence focuses on achieving abstinence and reducing problems associated to cocaine use. Despite extensive research and clinical experience, no “gold standard” has emerged from the different treatment options that have been researched. In general, research has shown that the evidence level for the efficacy of psychosocial interventions is higher than for pharmacologic interventions. With respect to psychosocial interventions, the evidence shows that all those interventions studied show efficacy to some extent, without greater differences in efficacy.

With respect to the pharmacologic options, none of the tested drugs have shown sufficient evidence to clearly be indicated in the treatment of cocaine dependence. Several substances have so far only been tested in smaller descriptive studies or pilot trials and will have to be studied in larger controlled trials. The substance presently with the highest level of evidence is disulfiram, and its effect has been shown to be independent of concomitant alcohol use. Of the substances that find themselves in the pilot stage and need to be confirmed by larger trials, the antidepressant reboxetine and the antiepileptic topiramate can be considered as two very promising ones. Of great interest has been the development of a cocaine vaccine. This vaccine leads to the production of cocaine antibodies, which in turn make cocaine metabolites inactive. A randomised controlled study showed the vaccine to produce cocaine antibodies in humans. A recent open-label study resulted in a significantly higher likelihood for cocaine free urines among vaccinated subjects, so that results are encouraging.