2. Kapfhammer HP. Perso¨nlichkeitssto¨rungen – Diagnostische Konzepte, Neurobiologie, Pharmakotherapie. Psychiatrie Psychotherapie 2008;4:37–57 3. Rinne T, Ingenhoven T. Pharmacotherapy of severe personality disorders: A critical review. In: van Luyn B, Akhtar S, Livesley WJ (eds.) Severe personality disorders. Cambridge University Press, Cambridge, 2007, pp. 137–163. 4. Siever LJ. Endophenotypes in the personality disorders. Dialogues Clin Neurosci 2005;7:139–151 5. Whittle S, Allen NB, Lubman DI, Yu¨cel M. The neurobiological basis of temperament: Towards a better understanding of psychopathology. Neurosci Biobehav Rev 2006;30:511–525
Causes, diagnoses and treatment of post-traumatic stress disorder Dragica Kozaric´-Kovacˇic´ Department of Psychiatry, Dubrava University Hospital, Referral Center for Stress-related Disorders of the Croatian Ministry of Health and Social Welfare, Regional Center for Psychotrauma, Zagreb, Croatia Post-traumatic stress disorder (PTSD) is an anxiety disorder that can develop after experiencing or witnessing a life-threatening event, such as accident, disaster, war trauma, violence or abuse (family, sexual, physical, and/or psychological), or any situation that seriously threatens the integrity of a person. The disorder, however, does not develop in every person exposed to traumatic experience. Stress results from an interaction between the mind and the body. The brain is the organ that determines reaction to stress as it decides on what is stressful and controls biological and physiological responses to stress. These responses vary from one person to another due to differences in their biological, genetic, environmental, and psychological characteristics, as well as their personal history. Stress causes neuroanatomical and neurochemical changes in the brain. Early traumatic experience (eg, abuse or severe neglect in childhood) may affect the brain structures and functions so as to make a person vulnerable to negative stressful events and more prone to later development of PTSD or other anxiety-related disorders. A particular genetic profile also plays a role in vulnerability or resilience to stress. For example, individuals with a short ss allele of serotonin transporter are more vulnerable to depression and PTSD, especially if they had early traumatic experience. A long-term dysregulation of cortisol and noradrenalin, the main stress mediators, favors the development of different anxiety disorders, including PTSD. Stress-induced changes in hippocampus (atrophy), amygdales (volume reduction), and prefrontal cortex are also frequent findings in patients with these disorders. The neurobiological changes in the brain, which result from dysregulation of noradrenergic, serotoninergic, dopaminergic, and other neurotransmitter systems, provide the basis for psychopharmacologic treatment of patients with PTSD. The evaluation of different biomarkers might facilitate a goal of the modern medicine, a proper treatment for an individual patient at a given stage of disease. This is especially important in PTSD, a disorder with complex clinical picture, diverse symptoms, and different comorbidities. PTSD was officially proposed as separate diagnosis in DSM-III, although the clinical consequences of trauma were recognized since ancient times. After its identification in DSM-III, the neurobiology of chronic PTSD has been area of increasing investigation. Earlier the psychoanalytic model of explanation and treatment mostly prevailed. Epidemiological studies show high prevalence of PTSD in general population and specific groups exposed to the traumatic events (survivors of war trauma, natural disasters, terrorist attacks, etc.). Trauma and its consequences affect significantly individual health and functioning, and whole society. The diagnosis of PTSD
may have several subtypes, including psychotic symptoms, depending upon pre-existing psychiatric disorder, trauma severity and duration, comorbidity, post-trauma social environment, etc. The role of trauma as an etiological factor in other psychiatric disorders and symptoms remains to be clarified. Complex neurobiological changes triggered by such a traumatic and stressful experience may explain a wide range of PTSD symptoms and provide the rationale for psychopharmacological treatment. Selective serotonin-reuptake inhibitors make the firstline treatment of PTSD. Clinical experience has shown that they are more effective than noradrenalin-reuptake inhibitors or tricyclic antidepressants. Antipsychotic drugs, especially atypical ones, have been shown effective in PTSD patients with psychotic characteristics or refractoriness to other treatments. Mood stabilizers seem to reduce mostly autonomous overreactions to stress, whereas the evidence for effectiveness of monoamine oxidase inhibitors is largely inconclusive. Other groups of medications, such as serotonin agonists and antagonists, new antidepressants, dual inhibitors of serotonin- and noradrenalin-reuptake, anticonvulsants, and opiate antagonists are also sometimes used in PTSD treatment. However, as shown in the present article, most clinical studies performed to date to investigate the effectiveness of different psychopharmacological agents in the therapy of PTSD have serious limitations in terms of small sample size, lack of blinding and randomization, and small effect size. More rigorously designed, comparative studies are needed to determine the usefulness, efficacy, tolerability, and safety of particular psychopharmaceutical drugs in the treatment of this therapeutically and functionally challenging disorder. One group of medications is often not enough for the treatment of all the PTSD symptoms, especially in cases where PTSD is comorbid with depression, alcoholism, borderline personality disorder, or psychotic, panic, or other disorders. Irrespective of the different mechanisms of action of drugs used in the treatment of PTSD, the final goal is always the same – to reduce distress, reinforce the psychological defense system, and restore the functioning of the person. However, evidence from controlled clinical trials showing the effectiveness of pharmacotherapy in PTSD is still unsatisfactory.
Anxiety disorders: causes, diagnosis and treatment Jrgen Deckert Department of Psychiatry, Psychosomatics and Psychotherapy, University of Wrzburg, Germany Causes: Anxiety disorders are complex disorders. Environmental and genetic factors equally contribute to their pathogenesis. In the first half of the last century, on the basis of Freud’s concept of anxiety neurosis, environmental factors such as life events in childhood and adolescence have been stressed as pathogenetic factors. They include separation from parents or spouses by death or divorce, experiences of physical or sexual violence and physical illness. Based on Klein’s observation that some forms of anxiety neurosis can be successfully treated by antidepressants, biological factors have been given more attention in the second half of the last century. Twin and family studies provide evidence for a major contribution of genetic factors. Linkage and association studies point to candidate loci such as chromosomes 13q and 22q as well as candidate genes such as serotonergic and noradrenergic genes. Genomewide association studies, due to their hypothesis-free approach, will help to identify new genes and new pathophysiological pathways. The contribution of each factor, however, will be minor and explain only a few percent of the variance. Research efforts such as the DFG-funded special research network TRR58 on ’’Fear, Anxiety and Anxiety Disorders’’ utilizing endophenotypes (imag-
2009 The Authors Journal Compilation 2009 John Wiley & Sons A/S Acta Neuropsychiatrica 2009: 21 (Supplement 2): 1–72 Downloaded from https://www.cambridge.org/core. RMIT University Library, on 22 Dec 2017 at 00:31:48, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0924270800032592
9
ing genomics, pharmacogenomics) as well as animal models (knockout mice) will enhance our understanding of the complex interplay between environmental and genetic factors in the context of fear and anxiety networks including among others the amygdale and the prefrontal cortex. Diagnosis: Anxiety disorders like other mental disorders are defined as categories. IDC-10 and DSM-IV differentiate panic disorder with and without agoraphobia, generalized anxiety disorder, social phobia and specific phobia. Sometimes and in particular in the American literature post-traumatic stress disorder and obsessive-compulsive disorder are also added to the anxiety disorders although they show clearly distinct features from the other core anxiety disorders. Diagnosing an anxiety disorder warrants careful exclusion of somatic disorders imitating anxiety disorders. These include hyperthyreosis, certain arrhythmias, epilepsies and vestibular disorders among others. In addition to a careful physical examination therefore an electrocardiogram, an electroencephalogramm and a routine blood test including thyroid parameters should be performed. Depending on the results further tests such as a 24hour electrocardiogram, a 24 hour electroencephalogram, a cCT and/or a cMRT and a drug screening may become necessary. Occasionally, a real comorbidity may exist between anxiety disorders and certain somatic disorders such as arrythmias and asthma bronchiale. As anxiety may be a symptom also in other mental disorders, unias well as bipolar depressive disorders and somatoform disorders in particular have to be considered as alternative diagnoses. As with somatic disorders there may be true comorbidity with these disorders and also secondary substance abuse disorders which will effect treatment strategies. Structured interviews such as the SCID or the CIDI may be helpful in differentiating them. Rating scales such as the HAMAS or the PAS allow to semiquantitatively define the severity of the anxiety disorder. In addition to establishing the categorical diagnosis it is important to define personality, cognitive and coping features of the individual patient as they will be important in designing an individually tailored therapy. Equally important are informations on the present life situation and the personal history (life events) in particular with regard to the nature of relations to family members as they are also important for designing the therapy. Treatment: As in some anxiety disorders such as panic disorder the patient has a somatic concept of the disorder based on its predominantly somatic symptoms, the first and most important treatment step is to develop a common psychosomatic concept of the etiopathogenesis of the disorder. Helpful models are the stressvulnerability and the anxiety circle models. The need to spend enough time for this step cannot be overstressed. Once this has been achieved, the therapy of choice in the treatment of anxiety disorders today is cognitive behavioural therapy. Numerous studies have proven its efficacy and numerous manuals for the individual anxiety disorders have been developed. The core element seems to be exposure to the fear inducing subject, object or situation. Research efforts such as the BMBF-funded PanicNet focus on the question if this is indeed so, and if yes, which form of exposure is more effective. Exposure in sense in generalized anxiety disorder or in sensu in agoraphobia. Modifications with a greater focus on cognitive strategies and a gradual exposure have to be applied in the elderly and the case of true comorbidity with certain somatic disorders. Cognitive behavioural therapy may be administered as more intensive individual therapy or as less intensive group therapy. The latter may be a good complement in particular in the case of social phobia. In some instances, e.g. blood-injury phobia additional treatment elements may be necessary. Psychodynamic therapy elements may be helpful in secondary prevention. Among pharmacological approaches, treatment with selective serotonergic antidepressants is considered the treatment of choice. As, however, they may cause a worsening of symptoms prior to
10
symptom reduction, their medication must be preceded by a careful information of the patient of their undesired effects. In general, in comparison with the treatment of depressions, uptitration should be slower and the maintenance dose lower. In particular in the case of comorbidity with depression, sedating antidepressants may be helpful. The use of benzodiazepines should be restricted to emergency situations because of their liability to the development of abuse and dependence. High-potency typical antipsychotics should not be administered because of the risk of tardive dyskinesia. A matter of controversy over the years has been the comparative efficacy and the combination of cognitive behavioural psychotherapy and pharmacotherapy with antidepressants. While convictions are strong, data are few. Those which exist seem to indicate that while pharmacotherapy has a faster, psychotherapy has a longerlasting effect. The combination, if necessary in severe cases, seems to have advantages by combining a faster effect without compromising a long-lasting effect. Questions like these are topics of discussion of committees for treatment guidelines such as the S3guideline currently being developed in Germany. Nevertheless, there seems to be emerging a consensus that while effective in many cases, cognitive behavioural therapy with exposure as core element may have to be complemented in severe cases by other therapy elements individually tailored to the individual patient. References: 1. Zwanzger P, Deckert J Angsterkrankungen – Ursachen, Klinik, Therapie. Nervenarzt 2007;78:349–360. 2. Domschke K, Deckert J Genetik der Angsterkrankungen, Nervenarzt 2007;78:825–35.
On psychodynamics of personal value-judgements – Nietzsche¢s theory of resentment and its reception by Karl Jaspers and Kurt Schneider Matthias Bormuth Institute of Medical Ethics and History of Medicine, University of Tbingen, Tbingen, Germany Abstract: A hundred years ago when Karl Jaspers was introducing psychological understanding to psychiatry the founder of the school of Heidelberg spoke of Friedrich Nietzsche as one of the ’’greatest’’ psychologists. Especially his theory of resentment with its core thesis unconscious prejudices were influencing our behaviour was able to illuminate the complex structure of human will. Taking into account this horizon of psychiatric history of ideas the presentation wants to persecute the following three questions: 1) Why the postulate which Nietzsche was giving on cultural prejudices of our thoughts, feelings and acts was so provocative so that many of the classical thinkers of psychological understanding were taking it up according to the needs of their disciplines sociology, psychology, psychiatry and philosophy? 2) What were the results of this inspiring theory which could be especially seen in the works of Karl Jaspers and Kurt Schneider? In other words: What were the aspects in which they agreed in their reception of Nietzsche and what were the points in which the two psychiatrists of the school of Heidelberg differed in the way they took the theory of resentment into account for their psychological understanding? 3) What could be the actual significance of the historical fact that Nietzsche and in his footsteps Max Weber were taking deep influence on psychiatric thinking around 1900? Introduction: A hundred years ago when Karl Jaspers was introducing psychological understanding to psychiatry the founder of the school of Heidelberg spoke of Friedrich Nietzsche as one of the ’’greatest’’ psychologists (1,2). Especially his theory of resentment with its core thesis unconscious prejudices were influencing our thoughts, feelings and acts was able to illuminate the complex structure of human will. The freedom was not only dependent on natural reasons but had also to be thought as
2009 The Authors Journal Compilation 2009 John Wiley & Sons A/S Acta Neuropsychiatrica 2009: 21 (Supplement 2): 1–72
Downloaded from https://www.cambridge.org/core. RMIT University Library, on 22 Dec 2017 at 00:31:48, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0924270800032592
Causes, diagnoses and treatment of post-traumatic stress disorder Dragica Kozaric´-Kovacˇic´ Department of Psychiatry, Dubrava University Hospital, Referral Center for Stress-related Disorders of the Croatian Ministry of Health and Social Welfare, Regional Center for Psychotrauma, Zagreb, Croatia Post-traumatic stress disorder (PTSD) is an anxiety disorder that can develop after experiencing or witnessing a life-threatening event, such as accident, disaster, war trauma, violence or abuse (family, sexual, physical, and/or psychological), or any situation that seriously threatens the integrity of a person. The disorder, however, does not develop in every person exposed to traumatic experience. Stress results from an interaction between the mind and the body. The brain is the organ that determines reaction to stress as it decides on what is stressful and controls biological and physiological responses to stress. These responses vary from one person to another due to differences in their biological, genetic, environmental, and psychological characteristics, as well as their personal history. Stress causes neuroanatomical and neurochemical changes in the brain. Early traumatic experience (eg, abuse or severe neglect in childhood) may affect the brain structures and functions so as to make a person vulnerable to negative stressful events and more prone to later development of PTSD or other anxiety-related disorders. A particular genetic profile also plays a role in vulnerability or resilience to stress. For example, individuals with a short ss allele of serotonin transporter are more vulnerable to depression and PTSD, especially if they had early traumatic experience. A long-term dysregulation of cortisol and noradrenalin, the main stress mediators, favors the development of different anxiety disorders, including PTSD. Stress-induced changes in hippocampus (atrophy), amygdales (volume reduction), and prefrontal cortex are also frequent findings in patients with these disorders. The neurobiological changes in the brain, which result from dysregulation of noradrenergic, serotoninergic, dopaminergic, and other neurotransmitter systems, provide the basis for psychopharmacologic treatment of patients with PTSD. The evaluation of different biomarkers might facilitate a goal of the modern medicine, a proper treatment for an individual patient at a given stage of disease. This is especially important in PTSD, a disorder with complex clinical picture, diverse symptoms, and different comorbidities. PTSD was officially proposed as separate diagnosis in DSM-III, although the clinical consequences of trauma were recognized since ancient times. After its identification in DSM-III, the neurobiology of chronic PTSD has been area of increasing investigation. Earlier the psychoanalytic model of explanation and treatment mostly prevailed. Epidemiological studies show high prevalence of PTSD in general population and specific groups exposed to the traumatic events (survivors of war trauma, natural disasters, terrorist attacks, etc.). Trauma and its consequences affect significantly individual health and functioning, and whole society. The diagnosis of PTSD
may have several subtypes, including psychotic symptoms, depending upon pre-existing psychiatric disorder, trauma severity and duration, comorbidity, post-trauma social environment, etc. The role of trauma as an etiological factor in other psychiatric disorders and symptoms remains to be clarified. Complex neurobiological changes triggered by such a traumatic and stressful experience may explain a wide range of PTSD symptoms and provide the rationale for psychopharmacological treatment. Selective serotonin-reuptake inhibitors make the firstline treatment of PTSD. Clinical experience has shown that they are more effective than noradrenalin-reuptake inhibitors or tricyclic antidepressants. Antipsychotic drugs, especially atypical ones, have been shown effective in PTSD patients with psychotic characteristics or refractoriness to other treatments. Mood stabilizers seem to reduce mostly autonomous overreactions to stress, whereas the evidence for effectiveness of monoamine oxidase inhibitors is largely inconclusive. Other groups of medications, such as serotonin agonists and antagonists, new antidepressants, dual inhibitors of serotonin- and noradrenalin-reuptake, anticonvulsants, and opiate antagonists are also sometimes used in PTSD treatment. However, as shown in the present article, most clinical studies performed to date to investigate the effectiveness of different psychopharmacological agents in the therapy of PTSD have serious limitations in terms of small sample size, lack of blinding and randomization, and small effect size. More rigorously designed, comparative studies are needed to determine the usefulness, efficacy, tolerability, and safety of particular psychopharmaceutical drugs in the treatment of this therapeutically and functionally challenging disorder. One group of medications is often not enough for the treatment of all the PTSD symptoms, especially in cases where PTSD is comorbid with depression, alcoholism, borderline personality disorder, or psychotic, panic, or other disorders. Irrespective of the different mechanisms of action of drugs used in the treatment of PTSD, the final goal is always the same – to reduce distress, reinforce the psychological defense system, and restore the functioning of the person. However, evidence from controlled clinical trials showing the effectiveness of pharmacotherapy in PTSD is still unsatisfactory.
Anxiety disorders: causes, diagnosis and treatment Jrgen Deckert Department of Psychiatry, Psychosomatics and Psychotherapy, University of Wrzburg, Germany Causes: Anxiety disorders are complex disorders. Environmental and genetic factors equally contribute to their pathogenesis. In the first half of the last century, on the basis of Freud’s concept of anxiety neurosis, environmental factors such as life events in childhood and adolescence have been stressed as pathogenetic factors. They include separation from parents or spouses by death or divorce, experiences of physical or sexual violence and physical illness. Based on Klein’s observation that some forms of anxiety neurosis can be successfully treated by antidepressants, biological factors have been given more attention in the second half of the last century. Twin and family studies provide evidence for a major contribution of genetic factors. Linkage and association studies point to candidate loci such as chromosomes 13q and 22q as well as candidate genes such as serotonergic and noradrenergic genes. Genomewide association studies, due to their hypothesis-free approach, will help to identify new genes and new pathophysiological pathways. The contribution of each factor, however, will be minor and explain only a few percent of the variance. Research efforts such as the DFG-funded special research network TRR58 on ’’Fear, Anxiety and Anxiety Disorders’’ utilizing endophenotypes (imag-
2009 The Authors Journal Compilation 2009 John Wiley & Sons A/S Acta Neuropsychiatrica 2009: 21 (Supplement 2): 1–72 Downloaded from https://www.cambridge.org/core. RMIT University Library, on 22 Dec 2017 at 00:31:48, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0924270800032592
9
ing genomics, pharmacogenomics) as well as animal models (knockout mice) will enhance our understanding of the complex interplay between environmental and genetic factors in the context of fear and anxiety networks including among others the amygdale and the prefrontal cortex. Diagnosis: Anxiety disorders like other mental disorders are defined as categories. IDC-10 and DSM-IV differentiate panic disorder with and without agoraphobia, generalized anxiety disorder, social phobia and specific phobia. Sometimes and in particular in the American literature post-traumatic stress disorder and obsessive-compulsive disorder are also added to the anxiety disorders although they show clearly distinct features from the other core anxiety disorders. Diagnosing an anxiety disorder warrants careful exclusion of somatic disorders imitating anxiety disorders. These include hyperthyreosis, certain arrhythmias, epilepsies and vestibular disorders among others. In addition to a careful physical examination therefore an electrocardiogram, an electroencephalogramm and a routine blood test including thyroid parameters should be performed. Depending on the results further tests such as a 24hour electrocardiogram, a 24 hour electroencephalogram, a cCT and/or a cMRT and a drug screening may become necessary. Occasionally, a real comorbidity may exist between anxiety disorders and certain somatic disorders such as arrythmias and asthma bronchiale. As anxiety may be a symptom also in other mental disorders, unias well as bipolar depressive disorders and somatoform disorders in particular have to be considered as alternative diagnoses. As with somatic disorders there may be true comorbidity with these disorders and also secondary substance abuse disorders which will effect treatment strategies. Structured interviews such as the SCID or the CIDI may be helpful in differentiating them. Rating scales such as the HAMAS or the PAS allow to semiquantitatively define the severity of the anxiety disorder. In addition to establishing the categorical diagnosis it is important to define personality, cognitive and coping features of the individual patient as they will be important in designing an individually tailored therapy. Equally important are informations on the present life situation and the personal history (life events) in particular with regard to the nature of relations to family members as they are also important for designing the therapy. Treatment: As in some anxiety disorders such as panic disorder the patient has a somatic concept of the disorder based on its predominantly somatic symptoms, the first and most important treatment step is to develop a common psychosomatic concept of the etiopathogenesis of the disorder. Helpful models are the stressvulnerability and the anxiety circle models. The need to spend enough time for this step cannot be overstressed. Once this has been achieved, the therapy of choice in the treatment of anxiety disorders today is cognitive behavioural therapy. Numerous studies have proven its efficacy and numerous manuals for the individual anxiety disorders have been developed. The core element seems to be exposure to the fear inducing subject, object or situation. Research efforts such as the BMBF-funded PanicNet focus on the question if this is indeed so, and if yes, which form of exposure is more effective. Exposure in sense in generalized anxiety disorder or in sensu in agoraphobia. Modifications with a greater focus on cognitive strategies and a gradual exposure have to be applied in the elderly and the case of true comorbidity with certain somatic disorders. Cognitive behavioural therapy may be administered as more intensive individual therapy or as less intensive group therapy. The latter may be a good complement in particular in the case of social phobia. In some instances, e.g. blood-injury phobia additional treatment elements may be necessary. Psychodynamic therapy elements may be helpful in secondary prevention. Among pharmacological approaches, treatment with selective serotonergic antidepressants is considered the treatment of choice. As, however, they may cause a worsening of symptoms prior to
10
symptom reduction, their medication must be preceded by a careful information of the patient of their undesired effects. In general, in comparison with the treatment of depressions, uptitration should be slower and the maintenance dose lower. In particular in the case of comorbidity with depression, sedating antidepressants may be helpful. The use of benzodiazepines should be restricted to emergency situations because of their liability to the development of abuse and dependence. High-potency typical antipsychotics should not be administered because of the risk of tardive dyskinesia. A matter of controversy over the years has been the comparative efficacy and the combination of cognitive behavioural psychotherapy and pharmacotherapy with antidepressants. While convictions are strong, data are few. Those which exist seem to indicate that while pharmacotherapy has a faster, psychotherapy has a longerlasting effect. The combination, if necessary in severe cases, seems to have advantages by combining a faster effect without compromising a long-lasting effect. Questions like these are topics of discussion of committees for treatment guidelines such as the S3guideline currently being developed in Germany. Nevertheless, there seems to be emerging a consensus that while effective in many cases, cognitive behavioural therapy with exposure as core element may have to be complemented in severe cases by other therapy elements individually tailored to the individual patient. References: 1. Zwanzger P, Deckert J Angsterkrankungen – Ursachen, Klinik, Therapie. Nervenarzt 2007;78:349–360. 2. Domschke K, Deckert J Genetik der Angsterkrankungen, Nervenarzt 2007;78:825–35.
On psychodynamics of personal value-judgements – Nietzsche¢s theory of resentment and its reception by Karl Jaspers and Kurt Schneider Matthias Bormuth Institute of Medical Ethics and History of Medicine, University of Tbingen, Tbingen, Germany Abstract: A hundred years ago when Karl Jaspers was introducing psychological understanding to psychiatry the founder of the school of Heidelberg spoke of Friedrich Nietzsche as one of the ’’greatest’’ psychologists. Especially his theory of resentment with its core thesis unconscious prejudices were influencing our behaviour was able to illuminate the complex structure of human will. Taking into account this horizon of psychiatric history of ideas the presentation wants to persecute the following three questions: 1) Why the postulate which Nietzsche was giving on cultural prejudices of our thoughts, feelings and acts was so provocative so that many of the classical thinkers of psychological understanding were taking it up according to the needs of their disciplines sociology, psychology, psychiatry and philosophy? 2) What were the results of this inspiring theory which could be especially seen in the works of Karl Jaspers and Kurt Schneider? In other words: What were the aspects in which they agreed in their reception of Nietzsche and what were the points in which the two psychiatrists of the school of Heidelberg differed in the way they took the theory of resentment into account for their psychological understanding? 3) What could be the actual significance of the historical fact that Nietzsche and in his footsteps Max Weber were taking deep influence on psychiatric thinking around 1900? Introduction: A hundred years ago when Karl Jaspers was introducing psychological understanding to psychiatry the founder of the school of Heidelberg spoke of Friedrich Nietzsche as one of the ’’greatest’’ psychologists (1,2). Especially his theory of resentment with its core thesis unconscious prejudices were influencing our thoughts, feelings and acts was able to illuminate the complex structure of human will. The freedom was not only dependent on natural reasons but had also to be thought as
2009 The Authors Journal Compilation 2009 John Wiley & Sons A/S Acta Neuropsychiatrica 2009: 21 (Supplement 2): 1–72
Downloaded from https://www.cambridge.org/core. RMIT University Library, on 22 Dec 2017 at 00:31:48, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0924270800032592
