Search

Das Lebenszeitrisiko für Suizid wird bei Schizophrenen auf 5% und für Suizidversuche auf 25–50% geschätzt. Suizidalität ist stets im Kontext von depressiven Syndromen oder depressiven Episoden zu sehen und ist assoziiert mit mehr depressiven, komorbiden und schweren Formen von Schizophrenie. Die meisten schizophrenen Patienten suizidieren sich in der aktiven Phase der Erkrankung, gequält von depressiven Symptomen. Suizid bei Schizophrenen erfolgt normalerweise nach. einem Suizidversuch, der ebenso häufig kommuniziert wird wie bei nicht-schizophrenen Patienten. Eine besondere Herausforderung stellen Suizide im psychiatrischen Krankenhaus dar, wo Depressive und Schizophrene einen ganz erheblichen Anteil der suizidgefährdeten Patienten ausmachen. Die schizophrenen suizidgefährdeten Patienten sind charakterisiert durch vermehrte Depressivität und paranoid-halluzinatorische Symptomatik, mehr Leidensdruck und verstärkte Psychopharmakotherapie. Die Schaffung einer »antisuizidalen Mentalität« steht bei der Prävention des Krankenhaussuizides im Vordergrund. Die Etablierung einer Atmosphäre von Vertrauen und Offenheit ist notwendig, in der der Patient über Gefühle von Angst, Orientierungslosigkeit, Insuffizienz und Überforderung bis hin zum Empfinden entstehender Suizidphantasien sprechen kann. Der erste Schritt zur Suizidund Suizidversuchsprävention besteht in einer konsequenten Befunderhebung von Suizidalität. Dies beinhaltet die Anamnese mit dem Erfassen der Symptomatik und ihrer chronologischen Entwicklung, Information über Vorerkrankungen (insbesondere Suizidversuche) und die Lebenssituation. Neben der Suizidintention stehen Suizidarrangement und Ernsthaftigkeit der Suizidmethode sowie die Einschätzung der Wiederholungsgefahr im Vordergrund. Das Vertrauensverhältnis zwischen Patient und Therapeut ist die wichtigste Voraussetzung, um suizidale Patienten zuverlässig erkennen und wirksam behandeln zu können. Deshalb muss von Anfang an ein besonderes Augenmerk auf das Zustandekommen einer tragfähigen therapeutischen Beziehung gerichtet werden. Die Therapie beinhaltet Notfallbehandlung, Krisenintervention, Psychotherapie und Pharmakotherapie. Die Notfallbehandlung hat aufgrund der häufig aggressiven und impulsiven suizidalen Handlungen Schizophrener Vorrang und erfordert sofortiges Eingreifen des Therapeuten bei drohender Lebensgefährdung. Die Krisenintervention bei schizophrenen Patienten unterscheidet sich nicht von Krisenintervention bei anderen psychiatrischen Diagnosen, dasselbe gilt für die Psychotherapie. Auf den Umgang mit suizidalen Patienten, spezifische Interventionsstrategien und auf die häufigsten Fehler und riskanten Interventionen wird ausführlich eingegangen. In der Pharmakotherapie werden Akutund Langzeitbehandlung unterschieden. Als Akutbehandlung kommen Neuroleptika, Benzodiazepine, eventuell auch Ketamine und die Elektrokrampftherapie infrage, in der Langzeittherapie Antidepressiva, Lithium, Moodstabilizer und atypische Neuroleptika. Speziell für schizophrene Patienten ist die Wirksamkeit von Antidepressiva bisher empirisch nicht ausreichend belegt, jedoch für atypische Neuroleptika vor allem für Clozapin, aber auch für Olanzapin bei Suizidversuchen.

The theme ‘suicide’ in paintings mirror social, cultural, religious, and philosophical stances to suicide. However, behind these more public aspects of the artist’s work there is often a personal meaning. The motives and interests of the artists go beyond the theme of suicide. An important factor in suicidal behaviour is a depressive mood or disorder. However, the depressive mood as well as the underlying manic-depressive illness of some artists may be seen as an important prerequisite for their creativity. Despite the importance of suicidality in art and that art therapy is well-established for treating patients in psychiatry and psychotherapy, only a small body of empirical literature about the role of art therapy in depressed and suicidal patients exists. In paintings and sculptures of art therapy, done by patients primarily reflect the inner experiences of their illness and biography. Art therapy can help the patient to alleviate self-destructive ways of acting.

Objectives: The objective of this study was to prove concepts in the characterization of suicidal patients and the possible usefulness of those markers to potentially identify patients with a higher risk for suicidality. Methods: Patients with a recent suicide attempt were compared with patients suffering from depression, adjustment disorder, anxiety, or eating disorders without suicidality, healthy controls and remitted patients with a history of at least 1 suicide attempt (≥1 year). We analyzed impulsivity (Barratt Impulsivity Scale, BIS) and saliva cortisol concentrations. Results: Independently of suicidality and disease state patients display higher BIS scores than healthy controls. Saliva cortisol levels tend to be higher in patients in the acute disease state than in remitted patients and healthy controls. Conclusions: Saliva cortisol may be a useful marker that reveals alterations in nonsuicidal patients suffering from depression, adjustment disorder, anxiety, or eating disorders who might be at risk.

Patients with both major depression and personality disorders have a high risk of suicidal behavior. Lithium is meant to have anti-suicidal properties in patients with affective disorders. The anti-suicidal effect of lithium in patients with affective disorders and comorbid personality disorders has not been investigated yet.A post-hoc analysis of a subsample of patients with depression and comorbid personality disorder (PD) and a recent suicide attempt (n = 19) from the prospective, placebo-controlled lithium intervention study (N = 167), was conducted.Three patients in the lithium group (n = 8) and two patients in the placebo group (n = 11) presented a suicide attempt throughout the course of the study. No differences related to suicidal behavior could be detected between the placebo group and the group with lithium intervention.On the basis of the small sample size, among patients with comorbid PD, lithium does not seem to have an effect on suicidal behavior in contrast to patients with affective disorders without comorbid PD.

Individual characteristics of pathophysiology and course of depressive episodes are at present not considered in diagnostics. There are no biological markers available that can assist in categorizing subtypes of depression and detecting molecular variances related to disease-causing mechanisms between depressed patients. Identification of such differences is important to create patient subgroups, which will benefit from medications that specifically target the pathophysiology underlying their clinical condition. To detect characteristic biological markers for major depression, we analyzed the cerebrospinal fluid (CSF) proteome of depressed vs control persons, using two-dimensional polyacrylamide gel electrophoresis and time-of-flight (TOF) mass spectrometry peptide profiling. Proteins of interest were identified by matrix-assisted laser desorption ionization TOF mass spectrometry (MALDI-TOF-MS). Validation of protein markers was performed by immunoblotting. We found 11 proteins and 144 peptide features that differed significantly between CSF from depressed patients and controls. In addition, we detected differences in the phosphorylation pattern of several CSF proteins. A subset of the differentially expressed proteins implicated in brain metabolism or central nervous system disease was validated by immunoblotting. The identified proteins are involved in neuroprotection and neuronal development, sleep regulation, and amyloid plaque deposition in the aging brain. This is one of the first hypothesis-free studies that identify characteristic protein expression differences in CSF of depressed patients. Proteomic approaches represent a powerful tool for the identification of disease markers for subgroups of patients with major depression.

Objective: Evidence based on controlled studies is still limited for treatment strategies that prevent recurrence of suicide attempts. Findings from observational as well as meta-analytic studies strongly suggest that lithium may have suicide-protective properties. Method: Patients with a recent suicide attempt in the context of an affective spectrum disorder (n = 167) were treated with either lithium or placebo during a 12-month period. Results: Survival analysis showed no significant difference of suicidal acts between lithium and placebo-treated individuals (adjusted hazard ratio 0.517; 95% CI 0.18–1.43). However, post hoc analysis revealed that all completed suicides had occurred in the placebo group accounting for a significant difference in incidence rates (P = 0.049). Conclusion: Results indicate that lithium treatment might be effective in reducing the risk of completed suicide in adult patients with affective disorders. Our findings contribute to the growing body of evidence suggesting a specific antisuicidal effect of lithium.

Various studies provide consistent evidence for a genetic component in suicidal behavior. First molecular genetic studies concentrated on genes of the serotonergic system based on the biochemical evidence that serotonergic neurotransmission is implicated in this behavior. Furthermore, genes of the dopaminergic and noradrenergic neurotransmitter systems have also been the subjects of investigations in this context. Some epidemical and clinical studies showed that low serum cholesterol levels are associated with suicidal behavior and genes involved in these pathways have been investigated. Microarray experiments provide the possibility of genome-wide gene expression analysis and help to investigate associated molecular mechanisms. The aim of this article is to review molecular genetic studies in suicidal behavior and to emphasize findings on new genes.

Objective: This study evaluated the associations between suicidal ideation and suicide attempts in mothers and various aspects of suicidality in their offspring in a representative community sample. Method: Baseline and 4-year follow-up data were used from the Early Developmental Stages of Psychopathology study, a prospective, longitudinal community study of adolescents and young adults. Results are based on 933 adolescents who completed follow-up and for whom direct diagnostic information for the biological mother was available. Suicidal ideation and suicide attempts were assessed in adolescents and mothers with the Munich-Composite International Diagnostic Interview. Results: Compared to offspring of mothers without suicidality, offspring of mothers reporting suicide attempts showed a remarkably higher risk for suicidal thoughts and suicide attempts and a tendency toward suicide attempts at an earlier age. Associations were comparable for male and female offspring. Transmission of maternal suicidality was roughly stable with control for maternal comorbid psychopathology. Conclusions: The offspring of mothers with suicide attempts are at a markedly increased risk for suicidality themselves and tend to manifest suicide attempts earlier than offspring of mothers without suicidality. Suicidality seems to run in families, independent of depression and other psychopathology.

Several studies have shown that there is a significantly increased risk of suicide related mortality in patients with a positive history of suicide attempts. The SUPLI-Study is the first prospective, randomized, double blind, placebo controlled multi-center trial focusing on the proposed suicide preventive effects of lithium in patients with suicidal behavior but not suffering from bipolar disorder or recurrent major depressive disorder. Patients with a recent history of a suicide attempt are treated with lithium versus placebo during a 12 month period. The hypothesis is that lithium treatment will lead to a 50% reduction of suicidal behavior. The protocol of the study and preliminary results are presented.

Functional and structural abnormalities in the thalamus as well as a generalized phospholipid membrane disorder have been implicated in the pathogenesis of schizophrenic psychosis. To determine whether thalamic neuronal abnormalities and altered membrane-associated metabolites can be detected in schizophrenic patients, we used in vivo proton magnetic resonance spectroscopy (1H-MRS) in 32 acutely-ill, medicated schizophrenic patients and 17 age-matched controls. Thalamic and white matter metabolite concentrations (myo-inositol (mI), choline-containing compounds (Cho), total creatine (Cr) and N-acetylaspartate (NAA)) were estimated and corrected for atrophy (CSF) and gray and white matter contributions (GM, WM) by use of image-based voxel segmentation. Thalamic NAA was significantly reduced in schizophrenic patients, whereas Cho and mI were significantly increased in the parietal white matter. White matter Cr was significantly elevated in patients and correlated positively with the brief psychiatric rating scores (BPRS). Regional metabolite levels were inversely associated with GM and WM content reaching significance for mI and Cr in the thalamus and Cho and NAA in the white matter. Reduced NAA in the left thalamus of schizophrenic patients confirms and extends previous spectroscopic data and agrees well with histologic and imaging findings of reduced neuronal density and volume. Elevated Cho in line with 31P-MRS studies suggests increased myelin degradation thus further supporting a generalized membrane disorder in schizophrenic patients. In addition, we demonstrate the need to correct metabolite concentrations for regional tissue composition in studies employing patients with altered brain morphology.

Studies in psychiatric patients described an association between lower serum cholesterol concentrations, suicidality, depression, impulsivity, and aggression which is not entirely attributable to depression-related malnutrition and weight-loss. Several lines of evidence suggest that a serotonergic deficit in the prefrontal cortex may predispose vulnerable subjects to impulsive, autoaggressive, and suicidal behaviour in stressful life-events. In-vitro studies, animal experiments, and human in-vivo studies support the hypothesis that cholesterol reduction may contribute to the serotonergic abnormalities which have been postulated in suicidal subjects. Recently it was hypothesized that decreased consumption of polyunsaturated fatty acids, especially omega-3 fatty acids, may be a risk factor for depression and suicide. Data from human studies in healthy volunteers suggest that increasing the dietary intake of omega-3 fatty acids may increase central serotonergic activity and reduce impulsive and aggressive behaviours. Earlier epidemiological studies showed an association between low cholesterol concentrations and increased suicide risk. Recent epidemiological studies with greater samples and longer follow-up periods, however, even showed a positive correlation between cholesterol concentrations and suicide risk after controlling for potential confounding variables. Large trials of statins (simvastatin, lovastatin, pravastatin) did not show an increase of suicide mortality.

Studies in postmortem brain tissue from suicide victims show a presynaptic serotonergic deficit resulting in compensatory upregulation of postsynaptic 5-HT2 receptors in the prefrontal cortex. Reduced levels of cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid, the major serotonin metabolite, are associated with violent suicide attempts independent of psychiatric diagnosis and predict future suicide attempts and suicide completion, consistent with the notion of a biochemical trait. Neuroendocrine challenge tests, platelet studies and a polymorphism in the gene for tryptophan hydroxylase, the rate-limiting enzyme in the biosynthesis of serotonin, suggest that serotonergic activity may be reduced. This serotonergic abnormality might be related to the vulnerability or diathesis for suicidal behaviour by predisposing individuals to impulsive and autoaggressive behaviour. The hypothesis of hyperactivity of the hypothalamic pituitary adrenal axis (HPA) is supported by the postmortem findings of increased CSF corticotropin releasing hormone (CRH) concentrations and reduced CRH receptor binding sites in the frontal cortex of suicide victims (interpreted as downregulation following CRH hypersecretion) and dexamethasone nonsuppression in suicide attempters. Animal studies and in vitro experiments indicate that the HPA system modulates serotonergic activity. It is hypothesized that the serotonergic alterations potentially result from dysregulation of the HPA system. Data from epidemiological and clinical studies demonstrate that low levels of cholesterol are associated with increased suicide risk. In neuronal membranes cholesterol modulates presynaptic and postsynaptic serotonergic neurotransmission. In monkeys dietary cholesterol lowering inhibits central serotonergic activity and predisposes the animals to impulsive and aggressive behaviour. It is speculated that dysregulation of the HPA system and disordered cholesterol metabolism could enhance the serotonergic deficit, thus contributing to a neurobiological vulnerability or diathesis for impulsive and autoaggressive behaviour.

Although both dimensional and categorical approaches to an assessment of personality disorders (PD) exist, only instruments for a categorical approach to the assessment of PD have been developed. The reliability of the diagnostic assessment of PD could be improved by using questionnaires, checklists, and structured interviews. However, a comparison of structured interviews among themselves and with checklists or self-rating questionnaires showed only insufficient to satisfactory agreement. Therefore, there are no instruments for the assessment of DSM-III/DSM-IV and ICD-10 PD that could be clinically and scientifically interchanged. There is an increasing tendency to a dimensional approach to the assessment of PD.

This article reviews recent research results on posttraumatic stress disorder (PTSD). Epidemiological studies show that PTSD is a common disorder within the normal population with a high degree of chronic courses. Degree of severity as well as dissociative symptoms during the traumatic event seem to have an impact on course and outcome of PTSD. A genetic disposition, familial psychopathology and premorbid personality traits as background variables seem to have an influence on the development of PTSD whereas coping strategies, as well as social support, modify the course of the disease. The investigation of biological parameters refers to the hypothalamic-pituitary-adrenal-axis system, provocation studies, psychophysiological studies, and studies of the endogenous opiate system. In regard to therapy studies only those with a randomised allocation to two different therapies as well as with a control group without therapy or a waiting list group are considered, using the DSM-III or DSM-III-R diagnostic criteria for PtSD. Five pharmacological studies could show a positive effect by antidepressants. Six behaviour therapy studies (two systematic desensitisation and four flioding) produced an improvement of PTSD symptomatology. The pathogenetic models discussed here are memory imprinting, kindling, dysregulation of the opioid neuromodulation, classical conditioning and disturbed cognitive schemas, which reflect as single models only a facet of the pathogenesis.