Neuropsychopharmacologia Hungarica最新文献

In their recently published systematic "umbrella" review, Moncrieff and colleagues conclude that there is no consistent evidence that depression is caused by decreased serotonin activity in the central nervous system (CNS). However, this paper - which was extensively publicized and received a lot of attention on the social media - can cause misunderstandings, since the serotonin hypothesis of depression in its original form (i.e. reduced serotonin activity in the CNS = depression) formulated more than 50 years ago has been considered outdated for several decades. It has long been known that depression is a heterogeneous disorder not only genetically, clinically and biologically but also from a pharmacotherapeutic perspective. The decreased activity of serotonin, which undoubtedly plays an essential role in the pathogenesis of depression, is characteristic of only a subgroup of depressed subjects whose clinical picture is mostly dominated by intensified negative emotions, agitation, anxiety, insomnia, decreased appetite, self-blame and suicidality and these individuals are primarily responsive to SSRIs. By contrast, depression cases with reduced positive affects (characterized by anhedonia, anergia, inhibition and reduced cognitive functions) are mainly caused by a disturbance in the metabolism of dopamine and/or noradrenaline. These patients are primarily responsive to dual-action (e.g. SNRI) antidepressants. Results of serotonin and catecholamine (dopamine, noradrenaline) depletion studies also suggest that that the dysregulation of serotonin and dopamine/noradrenaline in the CNS is characteristic of different subgroups of depressed patients. In addition to the serotonergic, dopaminergic and noradrenergic systems, many other neurotransmitter systems (e.g. cholinergic, glutamatergic, GABAergic) and other mechanisms (e.g. neuroinfl ammation) have also been proven to play a role in the development of the disorder. Knowledge of the data presented in our publication is important since the simplistic interpretation by Moncrieffetal. of the role of serotonin in the pathogenesis of depression may undermine confidence in SSRIs in many patients. (Neuropsychopharmacol Hung 2022; 24(3): 120-125).

Positive psychology has fully examined the flourishing among healthy people but neglected to understand how "optimal human functioning" can apply to the life experiences of a vulnerable person. Considering methodological issues, this article gives a brief overview on how the conceptualization of mental health and mental disorders affects the consideration of strengths along with the presence of dysfunction with the emergence of positive psychology. First, we summarize the shortcomings of the applicability of clinical positive psychology, focusing especially on Hungarian clinical practice. Second, we discuss the problems with the conceptualization of mental health in positive psychological framework. Third, we propose a model, the Maintainable Positive Mental Health Theory based on capacities and competences. Finally, we conclude with methodological questions and present a research protocol. The key finding of our review is that the opportunity exists for psychiatrists and psychologists to embrace disability as part of human experiences and to show how people with vulnerabilities can be supported to recover. (Neuropsychopharmacol Hung 2022; 24(3): 113-119).

The incidence of borderline personality disorder (BPD) in psychiatric care has shown growing tendencies. Despite its frequency, it is an underdiagnosed disease. Profound knowledge of etiological factors of BPD is essential for the proper diagnosis and treatment. The present study aims to provide a developmental psychopathological analysis of borderline personality disorder, which includes a thorough review of genetic and environmental etiological factors, an introduction to the functionalist approach of evolutionary perspective, and an overview of age specific characteristics of borderline symptoms. Recent research suggests that in addition to neurobiological and psychosocial factors, genetic vulnerability may be responsible for the development of BPD. Psychosocial background includes childhood trauma, maternal mental illness, maladaptive parenting styles and dysfunctional parent-child relationship, all of which are recognized as contributing factors to the development of insecure or disorganized attachment styles in the infant. Regarding the neurobiological background, changes in the hypothalamic-pituitary-adrenal axis, neurotransmission, endogenous opioid system, and neuroplasticity play a prominent role, the development of which is also affected by childhood traumatic events. Brain imaging studies reveal differences in the limbic system (hippocampus, amygdala) and frontal cortex, which are also involved in stress response, cognition, memory function, and emotion regulation. Early developmental processes may also play an important role in the development of the disorder, as depression during pregnancy or increased stress affects the quality of maternal care and may also affect gene expression through epigenetic mechanisms. With respect to the gene-environment interaction, the interaction of the child's impulsive traits and the invalidating family environment can be highlighted, which can lead to disruption of emotion regulation. The persistence of BPD symptoms is supported by the evolutionary approach concerning several aspects. Fear of abandonment can be explained by the anticipation of exclusion and maladaptive attempts to avoid it. Developmental psychopathological analysis contributes to the development of effective prevention and intervention tools through a better understanding of the background of borderline personality disorder. In terms of prognosis, as a result of effective treatments, symptoms can be reduced, so improvement can be achieved in a large proportion of patients.

This review aims to present social anxiety disorder from a developmental psychopathological perspective. Evolutionary theories share the view that social anxiety might be adaptive in specific contexts, and suggest several mechanisms of dysfunction (adaptive trade-off , mismatch, individual differences). The aetiology of social anxiety disorder is characterized by a complex interplay of genetic and environmental factors including gene-environment interactions,correlations and epigenetic mechanisms. Although the main diagnostic criteria of social anxiety disorder are the same throughout the lifespan, developmental characteristics alter its presentation. In children, behavioural symptoms are common. We can view refusal of speech as a specific manifestation of avoidant behaviour related to young age. Therefore, some researchers suggest that selective mutism is an age-specific subtype of the disorder. Even though the majority of researchers agree that behavioural inhibition is an age-specific temperamental risk factor of social anxiety disorder, it might also be viewed as an early, subclinical form of the disorder. In adolescence, as part of the normal development, there is a temporary increase of social anxiety. In this age group, however, there is also an increase in the prevalence of socialanxiety disorder. Adult-onset social anxiety disorder is rare. In adults, social anxiety disorder has to be diff erentiated from avoidant personality disorder. Social anxiety disorder is characterized by strong homotypic continuity, but evidence for a heterotypic continuity is also available,especially with other anxiety disorders and major depression, probably due to shared genetic factors. The developmental psychopathological approach of social anxiety - developmental paths, age-specific characteristics, etc. - may contribute to an early recognition of the disorder and facilitate more effective therapeutic interventions.

Developmental psychopathology is a relatively new discipline which aims to synthetize theories and empirical results of multiple disciplines focusing on development or psychopathology developmental psychology, psychopathology, neuroscience, genetics, personality psychology, volutionary psychopathology, etc.), in order to uncover mechanisms responsible for normative development and its alterations (psychopathology). We aim to give an introduction into three main themes of developmental psychopathology: models of evolutionary psychopathology mechanisms of the complex interplay of genetic and environmental factors contributing normal and abnormal development, and the age-specific characteristics of mental disorders, as well as their continuities and discontinuities across the lifespan. The perspective of developmental psychopathology adds to our deeper understanding of the aetiology and course of mental disorders, and their recognition and treatment.

According to the currently available research data obsessive-compulsive disorder (OCD)is a disorder of multifactorial etiology, the causes of which include biological, genetic and environmental-social factors alike. Based on an etiology of that kind, it is justifiable to conduct a developmental psychopathological review of OCD, which may lead, through an exploration of the different factors involved, to a deeper understanding of the disorder's overall nature and specific characteristics, as well as to the development of the most efficient therapies possible. The main objective of the present comprehensive study is the developmental psychopathological analysis of the OCD, including the review of the evolutionary approaches and genetic and environmental factors, as well as an exploration of OCD's age-specific forms of manifestation, based on the recent research results and analyses available in the professional literature. According to our present knowledge, the genetic linkage of early-onset OCD is greater than that of the late-onset variant, as the onset of the syndrome can be attributed to genetic factors to the extent of 40-60%, coupled with the contribution of environmental factors like perinatal disorders, reproductive cycle, childhood infections, familial circumstances, age of the parents and traumatic life events. Evolutionary theories address OCD from a functional perspective. They strive to attribute it primarily to individual or group selection theories that a quite heterogeneous OCD syndrome, which is therapeutically difficult to change, remains to present itself with close to identical, invariably high prevalence in all cultures despite the difficulties. Obsessive-compulsive disorder is present in all ages, and it is often difficult to determine whether we are faced with a healthy or a pathological behavior, as certain obsessive phenomena may appear as part of normal development. The analysis of OCD's etiology, a better understanding of the respective function of specific symptoms, a thorough exploration of age-specific variants of the disorder, i.e. a developmental psychopathological analysis of OCD, is of key importance from diagnostic, therapeutic and vocational rehabilitation aspects alike.

The prevalence of bipolar affective disorder is 3% in the general population, with a first occurrence around the age of 20-30. The first symptoms are usually rather mild, thus it is difficult to reach a decision about the diagnosis within the first years. In the past years bipolar affective disorder received increased attention because of the relatively high lifetime prevalence. Nowadays experts in the field try to reach a consensus in understanding the earlier phases of the syndrome, as earlier therapeutic interventions tend to have a better result. General developmental psychopathological factors, and gene-environment interactions or evolutionary theories can greatly contribute to early recognition and understanding of the syndrome. The main aim of our article is to explore the possible developmental psychopathological background of bipolar affective disorder through overview of the literature on general developmental psychopathology factors, gene-environment interaction, and the evolutionary approach, which can contribute to more effective methods of treatment.

The metabolic effect of atypical antipsychotic drugs may manifest itself in weight gain, disturbances in glucose homeostasis and dyslipidemia. One confounding factor is that psychotic disorders themselves make the patients prone to specific metabolic changes. Nevertheless clinical studies have confirmed that atypical anti-psychotic drugs have a different metabolic effect. In the present prospective case-series, four male antipsychotic drug-naive psychiatric patients without any familial history of metabolic disorder were studied. The patients received risperidone or olanzapine monotherapy for 12 weeks; weight, plasma levels of triglyceride, cholesterol, HDL, and fasting glucose were measured in every 4th week. In two patients, oral glucose tolerance test (OGTT) was also performed at days 0 and 56. The average weight gain during the 12-week period was 12%. The cholesterol and triglyceride plasma concentrations were also elevated. The fasting glucose levels did not change during the observation period. In the OGTT performed in two patients, normal fasting glucose and insulin plasma levels were observed after 8 weeks; however, the plasma insulin concentrations were highly elevated after glucose intake, which may suggest the presence of insulin resistance. Our preliminary results confirmed the previous results on the metabolic effect of atypical anti-psychotic drugs, which may lead to metabolic syndrome. The regular control of the metabolic laboratory parameters, early intervention and the modification of the atypical antipsychotic treatment may help to avoid this adverse effect of the drugs.

Gender-specific differences in suicidal behaviour have been analysed in a number of recent studies. According to these, several socioeconomic, demographic, psychiatric, familial, help-seeking differences can be identified in protective and risk factors between males and females. Gender is one of the most replicated predictors for suicide. In the framework of the WHO/EURO Multicentre Study on Suicidal Behaviour, more than fifty thousand suicide attempts have been registered so far. Until now data on more than 1200 monitored suicidal events have been collected in Pecs centre. In most countries male suicid rates are higher. In contrast to suicides, rates of suicide attempts are usually higher in females. Concerning the differences in methods, it is a recognised fact that males use violent methods of both suicide and attempted suicide more often than females. The summarised clinical impression suggests that compliance of male patients is poorer than that of females. According to our data, a typical male attempter is characterised as follows: unemployed, never married, lives alone. He tends to use violent methods; if he takes drugs, it is mostly meprobamate or carbamazepine. A lot of male attempters have alcohol problems or dependence. As for the females, we found high odds ratios in the following cases: divorced or widowed, economically inactive, depressive state in the anamnesis. Female attempters are mainly repeaters using the method of self-poisoning, mostly with benzodiazepines. As suicide is a multicausal phenomenon, its therapy and prevention should also be complex and gender differences should be taken into account in building up our helping strategies.

Unlabelled: Three young people developed psychosis during/ after cannabis intake. The 17-year-old male after only a few marihuana cigarettes, the 22-year-old patient after two years of addiction developed schizoid psychosis; the 20-year-old patient after six years of cannabis addiction had schizoaffective psychosis. The first two patients become symptom-free on the antipsychotics and during the drug-free period. The third patient, who had cannabis during the psychotic symptoms, still has the schizoid psychosis.

Conclusions: The connection between cannabis and psychosis is clear in our three patients. Marihuana is working on the dopamine system and may cause schizoid psychosis, sometimes permanent psychosis. Cannabis, this light drug might not be a "safe" agent.