Risk Factor For Psychiatric Disorders Research Articles

Depression and sterile inflammation: Essential role of danger associated molecular patterns

Stress is a major risk factor for psychiatric disorder including major depressive disorder (MDD) and can induce inflammation, which is known to be dysregulated in depression. Several clinical and pre-clinical studies have demonstrated a strong association between depressive symptoms and the expression of factors that increase inflammation. Conversely, administration of anti-inflammatory agents has been shown to ameliorate depressive symptoms, demonstrating the importance of inflammation as a mediator of depression. Although it is clear that inflammation plays a role in the pathophysiology of depression, the mechanism by which inflammation is activated in mood disorders remains unclear. To address this issue, studies have investigated the role of pattern recognition receptor (PRR) activation in stress-induced inflammation and mood disorders. However, the identification of the endogenous factors, referred to as danger-associated molecular patterns (DAMP) that activate these receptors remains understudied. Here we review the role of DAMPs in depression and highlight the clinical evidence for elevation of DAMP signaling in MDD patients and in pre-clinical animal stress models of depression.

Adolescents hospitalisés dans les services de psychiatrie adulte : une étude descriptive à la lumière des problématiques relevant de la protection de l’enfance

BackgroundAdolescents hospitalized in adult mental health departments are many, and an important part of them benefit from a child welfare system. Many teenagers hospitalized at the adult psychiatric services have symptoms of auto- or hetero-aggressive behaviours. The aim of our study was to describe the population of adolescents supported by these services by analyzing their demographic and psychiatric characteristics and their links with the areas of child protection and disability. MethodsWe performed a retrospective descriptive study based on the analysis of hospital records of teenagers supported by the adult psychiatric services. Criteria for the analysis include sociodemographic, psychiatric morbidity and schooling data, data on the terrain, and those related to child protection or disability. Then subpopulations were analyzed in order to compare the different criteria whether or not within the child welfare system. ResultsSixty teenagers were included in our study. An analysis of the total population shows that these adolescents wer exposed to risk factors for psychiatric disorders: lower socioeconomic conditions, psychiatric family history and traumatic life events. Many were also school-leavers compared to the general population. Furthermore, a majority of the teenagers benefited from a child protection measure (n=33) and were institutionalized. The subpopulation analysis helped realize the particular vulnerability of adolescents under the care of child protection. Indeed, we significantly emphasized among them an increased prevalence of parental isolation (P=0.001), of psychiatric family history (P=0.001) and of having experienced traumatic events (P<0.0001). Concerning psychiatric disorders, we also found by the child welfare system that mild to moderate mental retardation was significantly more frequent among teens (P=0.003). In addition, our results show that these adolescents were significantly more often hospitalized (P=0.013). Finally, still in comparison with the other adolescents, these teens were significantly more school-leavers (P=0.032), mostly in specialized or adapted course of study (P<0.001), and more subject to disability (P<0.001), implying a double care. ConclusionThis study has allowed us to better know the youth population supported by adult psychiatric services. It has also enlightened the specific vulnerability of the teenagers under the child protection care who need psychiatric treatment. It offers interesting discussion topics to develop new modalities of care for these young people.

Bumetanide treatment during early development rescues maternal separation-induced susceptibility to stress

Stress is a major risk factor for psychiatric disorders, such as depression, posttraumatic stress disorder, and schizophrenia. Early life stress, such as maternal separation, can have long-term effects on the development of the central nervous system and pathogenesis of psychiatric disorders. In the present study, we found that maternal separation increased the susceptibility to stress in adolescent rats, increased the expression of Na+/K+/2Cl− cotransporter 1 (NKCC1) on postnatal day 14, and increased the expression of K+/2Cl− cotransporter 2 (KCC2) and γ-aminobutyric acid A (GABAA) receptor subunits on postnatal day 40 in the hippocampus. NKCC1 inhibition by the U.S. Food and Drug Administration-approved drug bumetanide during the first two postnatal weeks rescued the depressive- and anxiety-like behavior that was induced by maternal separation and decreased the expression of NKCC1, KCC2 and GABAA receptor α1 and β2,3 subunits in the hippocampus. Bumetanide treatment during early development did not adversely affect body weight or normal behaviors in naive rats, or affect serum osmolality in adult rats. These results suggest that bumetanide treatment during early development may prevent the maternal separation-induced susceptibility to stress and impairments in GABAergic transmission in the hippocampus.

Lack of Social Support Raises Stress Vulnerability in Rats with a History of Ancestral Stress

Stress is a primary risk factor for psychiatric disorders. However, it is not fully understood why some stressed individuals are more vulnerable to psychiatric disorders than others. Here, we investigated whether multigenerational ancestral stress produces phenotypes that are sensitive to depression-like symptoms in rats. We also examined whether social isolation reveals potentially latent sensitivity to depression-like behaviours. F4 female rats born to a lineage of stressed mothers (F0-F3) received stress in adulthood while housed in pairs or alone. Social isolation during stress induced cognitive and psychomotor retardation only in rats exposed to ancestral stress. Social isolation also hampered the resilience of the hypothalamic-pituitary-adrenal axis to chronic stress and reduced hippocampal volume and brain-derived neurotrophic factor (BDNF) expression. Thus, synergy between social isolation and stress may unmask a latent history of ancestral stress, and raises vulnerability to mental health conditions. The findings support the notion that social support critically promotes stress coping and resilience.

Intestinal microbial dysbiosis aggravates the progression of Alzheimer\u2019s disease in Drosophila

Neuroinflammation caused by local deposits of Aβ42 in the brain is key for the pathogenesis and progression of Alzheimer’s disease. However, inflammation in the brain is not always a response to local primary insults. Gut microbiota dysbiosis, which is recently emerging as a risk factor for psychiatric disorders, can also initiate a brain inflammatory response. It still remains unclear however, whether enteric dysbiosis also contributes to Alzheimer’s disease. Here we show that in a Drosophila Alzheimer’s disease model, enterobacteria infection exacerbated progression of Alzheimer’s disease by promoting immune hemocyte recruitment to the brain, thereby provoking TNF-JNK mediated neurodegeneration. Genetic depletion of hemocytes attenuates neuroinflammation and alleviated neurodegeneration. We further found that enteric infection increases the motility of the hemocytes, making them more readily attracted to the brain with an elevated oxidative stress status. This work highlights the importance of gut–brain crosstalk as a fundamental regulatory system in modulating Alzheimer’s disease neurodegeneration.

Poverty hits children first?

SummaryPoverty is a risk factor for mental health problems during childhood and adolescence in general. The economic crisis (2007–2013) seemed to have intensified poverty in families within the most affected countries, esp. in the southern countries of Europe. Within a selective literature review, existing data on the risk of poverty, mental disorders in parents and further risk factors on mental health of children are analyzed. Direct effects like limited access to mental health care system may exist, but are not proved in general. From a developmental perspective, effects of the crisis seem more indirectly mediated by well-known risk factors for psychiatric disorders of children and adolescents: substance abuse in families, mental disorders of parents and loss of perspectives within families are risk factors both on mental health of a child but also for a low educational level which would be a resilience factor. There is evidence that an increase of child abuse and neglect (adverse childhood experiences, ACE) was linked to the economic crisis. Long-term effects e.g. due to ACE may be observed in later times, when children are grown-up.

Is early life environment a risk factor for psychiatric disorder?

IntroductionSeason of birth, an exogenous indicator of early life environment, has been related to higher risk of adverse psychiatric outcomes. According to literature, an excess of 5–8% of winter-spring births is found in individuals who later develop schizophrenia and bipolar disorder; this seasonal birth excess is also found in schizoaffective disorder (winter), major depression (March–May), and autism (March).ObjectivesThe objective of this study was to analyze the seasonal birth patterns of in-patients with psychiatric disorders.AimsUnderstand the relation between psychiatric disorders and season of birth during a 10 year period in a Portuguese University Hospital.MethodsAnalyze the birth date distribution of 2202 in-patients between 2007 and 2016 and compare with the psychiatric diagnosis.ResultsPatients’ diseases analyzed by birthday season: 60% of patients with schizoaffective disorder were born in winter-spring, 48.4% of mental retarded patients were born in autumn, 37% of dementia patients in winter, 77% of patients with delusional disorder in winter-spring, 78% of patients with Cluster A personality disorder in spring-summer and 71% of patients with substance abuse conditions in autumn-winter. No seasonal birth excess was found for bipolar affective disorder, schizophrenia, alcohol abuse, major depressive disorder or Cluster B personality disorder.ConclusionsOur sample data shows evidence for a potential link between season of birth and risk for schizoaffective disorder, dementia, mental retardation, Cluster A personality disorder, delusional disorder and substance abuse. The attempt to explain seasonal birth patterns in psychiatric illnesses could serve to clarify the etiological bases of such disorders.Disclosure of InterestThe authors have not supplied their declaration of competing interest.

Effect of self-esteem on social interactions during the Ultimatum Game

Self-esteem is an attitude formed by self-evaluation based on positive and negative aspects of oneself. Low self-esteem is a risk factor for psychiatric disorders and is especially associated with social difficulties. Recently, behavioral economics has allowed the quantitative study of social interactions. We investigated the association between self-esteem and interpersonal problems and whether self-esteem modulates behavior and emotions during an economic task, the Ultimatum Game (UG). In this task participants accept or reject fair/unfair monetary offers from others. Low (LSE, n=40) and high (HSE, n=45) self-esteem participants were assessed in their interpersonal problems and psychiatric symptoms using self-reported questionnaires, and were compared on their decision making and emotional response during the UG. LSE was associated with depression and anxiety symptoms. In addition, LSE was associated with interpersonal problems, especially in the domains of socially inhibited, nonassertive, overly accommodating, self-sacrificing and cold/distant. During the UG, LSE women reported more anger towards unfair offers than HSE women. Our findings suggest that low self-esteem individuals experience high distress by interpersonal problems in several domains. Importantly, low self-esteem in women seems to be associated with an accentuated emotional response to unfair social exchanges. These results may contribute to treat social difficulties in this population.

P300 Repetitive magnetic stimulation reverses the synaptic phenotype of cultured rat CA1 pyramidal neurons in a maternal immune activation model of schizophrenia

Question Gestational infection is a risk factor for psychiatric disorders. Accordingly, preclinical models of maternal immune activation (MIA) have been developed to study effects of gestational infection on neural and behavioral dysfunction in the offspring. Considering that early pre-symptomatic stages of schizophrenia may affect hippocampal circuits, we here established a hippocampal ‘organotypic in vitro MIA model’ based on the well-established polyinosinic-polycytidylic acid [Poly(I:C)] model of schizophrenia. We studied alterations in synaptic neurotransmission and tested whether repetitive magnetic stimulation (rMS) influences alterations in synaptic excitation/inhibition-balance in this model. Methods Entorhino-hippocampal slice cultures were prepared from litters of Poly(I:C) or vehicle-only injected pregnant dams. The effects of 10 Hz rMS on MIA associated alterations in synaptic properties were assessed in CA1 pyramidal neurons using whole-cell patch clamp recordings. Results Our experiments disclose an increase in inhibitory synaptic strength, while excitatory synapses on CA1 neurons are not changed in slice cultures prepared from Poly(I:C) offspring. This difference is also observed in cultures prepared from cross-fostered animals, thus confirming that gestational infection triggers the synaptic phenotype. Since our recent work has demonstrated that 10 Hz rMS can shift synaptic excitation/inhibition-balance toward excitation, we employed this rMS protocol to test whether we can influence the synaptic phenotype in the Poly(I:C) group. Indeed, 10 Hz rMS reversed the increased inhibitory synaptic strength without affecting excitatory synapses in MIA slice cultures. Conclusion These results suggest that rMS may exert positive effects under pathological conditions by restoring physiological synaptic excitation/inhibition-balance. We propose that ‘organotypic in vitro MIA models’ may serve as preclinical drug and intervention screening assays to evaluate and learn more about rTMS-based treatment strategies in psychiatric diseases associated with gestational infection. (Supported by Federal Ministry of Education and Research, Germany (BMBF, GCBS-WP1: 01EE1403B).).

Investigation of Mental Disorders in Lung Cancer Outpatients: A Retrospective Analysis.

Cancer patients often develop mental conditions, including anxiety and depressive disorder. And, patients with chemotherapy often exhibit mental changes including anxiety and depressive disorder. Furthermore, it is well known that the frequency of delirium is increased in cancer patients receiving terminal care. Thus, the psychiatric and cognitive functions of cancer survivors are significantly influenced by their quality of life. In this study, we performed a retrospective analysis to identify the risk factors for psychiatric disorders in lung cancer survivors. Most lung cancer survivors that were diagnosed with psychiatric disorders had stage 4 disease. In addition, it was found that an increase in disease stage and high doses of opioids are associated with an increased risk of psychiatric disorders in lung cancer survivors. These findings suggest that it is necessary to consider the mental changes experienced by lung cancer patients during disease progression.

Prenatal maternal immune activation and brain development with relevance to psychiatric disorders

Growing evidence from epidemiological studies strongly suggests maternal infection as a risk factor for psychiatric disorders including bipolar disorder, schizophrenia, and autism. Animal studies support this association and demonstrate that maternal immune activation (MIA) changes brain morphology and inflammatory cytokines in the adult offspring. Evidence for changes in inflammatory cytokines is also demonstrated in human post-mortem brain and peripheral blood studies from subjects with psychiatric disorders. This perspective briefly highlights convincing evidence from epidemiological, preclinical and human pathological studies to support the role of MIA in major psychiatric disorders. A better understanding of the link between MIA and brain development in psychiatric disorders will lead to the development of novel immunomodulatory interventions for individuals at risk for psychiatric disorders.

Evolution of structural abnormalities in the rat brain following in utero exposure to maternal immune activation: A longitudinal in vivo MRI study

Genetic and environmental risk factors for psychiatric disorders are suggested to disrupt the trajectory of brain maturation during adolescence, leading to the development of psychopathology in adulthood. Rodent models are powerful tools to dissect the specific effects of such risk factors on brain maturational profiles, particularly when combined with Magnetic Resonance Imaging (MRI; clinically comparable technology). We therefore investigated the effect of maternal immune activation (MIA), an epidemiological risk factor for adult-onset psychiatric disorders, on rat brain maturation using atlas and tensor-based morphometry analysis of longitudinal in vivo MR images. Exposure to MIA resulted in decreases in the volume of several cortical regions, the hippocampus, amygdala, striatum, nucleus accumbens and unexpectedly, the lateral ventricles, relative to controls. In contrast, the volumes of the thalamus, ventral mesencephalon, brain stem and major white matter tracts were larger, relative to controls. These volumetric changes were maximal between post-natal day 50 and 100 with no differences between the groups thereafter. These data are consistent with and extend prior studies of brain structure in MIA-exposed rodents. Apart from the ventricular findings, these data have robust face validity to clinical imaging findings reported in studies of individuals at high clinical risk for a psychiatric disorder. Further work is now required to address the relationship of these MRI changes to behavioral dysfunction and to establish thier cellular correlates.

Psychiatric disorders during early adulthood in those with childhood onset type 1 diabetes: Rates and clinical risk factors from population-based follow-up.

To determine the incidence of and risk factors for psychiatric disorders in early adulthood in patients with childhood onset type 1 diabetes (T1D). In this retrospective-cohort study, we identified a population-based childhood onset T1D cohort and an age and sex matched (5:1) non-diabetic comparison cohort. Data linkage was used to access inpatient hospitalization data, mental health support service data, and mortality data to follow-up both cohorts into early adulthood. The mean age of T1D diagnosis was 9.5 years (SD 4.1), with a mean age at end of follow-up of 26.4 years (SD 5.2, max 37.7). The diagnosis of any psychiatric disorder was observed for 187 of 1302 (14.3%) in the T1D cohort and 400 of 6422 (6.2%) in the comparison cohort [adjusted hazard ratio (HR) 2.3; 95% CI 1.9, 2.7]. Anxiety, eating, mood, and personality and behaviour disorders were observed at higher rates within the T1D cohort. Comorbid psychiatric disorders were more frequent, at the cohort level, within the T1D cohort (2-3 disorders 3.76% vs 1.56%) and service utilization was higher (15+ contacts 6.8% vs 2.8%); though these differences did not remain when restricted to only those individuals diagnosed during follow-up. A history of poor glycaemic control was associated with an increased risk of anxiety, mood, and 'any' disorder (HR ranging from 1.35 to 1.42 for each 1% increase in mean paediatric HbA1c). Our findings highlight the need for access to mental health support services as part of routine patient care for young adults with T1D, and for better predictive tools to facilitate targeting at-risk patients with early intervention programs.

Relationship between perceived parenting style with anxiety levels and loneliness in visually impaired children and adolescents

Background Visual impairment is a risk factor for psychiatric disorders in the affected children and adolescents, but there are only a limited number of studies concerning the mental health characteristics of visually impaired children and adolescents. Objective The aim of this study was to determine levels of loneliness and anxiety in visually impaired children and adolescents, to analyze parenting style perceived by visually impaired children and adolescents, to compare those with typically controls. Methods The study included 40 children and adolescents with visually impairment and 34 control group without visual impairment. Sociodemographic data form, the UCLA loneliness scale, and the State-Trait Anxiety Inventory for Children were used in both groups. The parenting Style Scale was used to determine perceived parental attitudes. Results This study found more loneliness and trait anxiety levels in visually impaired children and adolescents compared to the control group. Authoritative parenting style was the most frequent type of parental attitude in the visually impaired group. In visual impairment group, loneliness level was higher in subgroups of authoritative and permissive-indulgent parenting style. However, level of trait anxiety was higher in authoritative parenting style subgroup compared to the control group. Discussion The results of this study showed higher loneliness and anxiety levels in visually impaired children and adolescents. Further studies are needed to determine psychopathological risks in this population.

Transgenerational disruption of functional 5-HT1AR-induced connectivity in the adult mouse brain by traumatic stress in early life.

Traumatic stress in early life is a strong risk factor for psychiatric disorders that can affect individuals across several generations. Although the underlying mechanisms have been proposed to implicate serotonergic transmission in the brain, the neural circuits involved remain poorly delineated. Using pharmacological functional magnetic resonance imaging in mice, we demonstrate that traumatic stress in postnatal life alters 5-HT1A receptor-evoked local and global functions in both, the exposed animals and their progeny when adult. Disrupted functional connectivity is consistent across generations and match limbic circuits implicated in mood disorders, but also networks not previously linked to traumatic stress. These findings underscore the neurobiology and functional mapping of transgenerational effects of early life experiences.

Western High-Fat Diet Consumption during Adolescence Increases Susceptibility to Traumatic Stress while Selectively Disrupting Hippocampal and Ventricular Volumes.

Psychological trauma and obesity co-occur frequently and have been identified as major risk factors for psychiatric disorders. Surprisingly, preclinical studies examining how obesity disrupts the ability of the brain to cope with psychological trauma are lacking. The objective of this study was to determine whether an obesogenic Western-like high-fat diet (WD) predisposes rats to post-traumatic stress responsivity. Adolescent Lewis rats (postnatal day 28) were fed ad libitum for 8 weeks with either the experimental WD diet (41.4% kcal from fat) or the control diet (16.5% kcal from fat). We modeled psychological trauma by exposing young adult rats to a cat odor threat. The elevated plus maze and the open field test revealed increased psychological trauma-induced anxiety-like behaviors in the rats that consumed the WD when compared with control animals 1 week after undergoing traumatic stress (p < 0.05). Magnetic resonance imaging showed significant hippocampal atrophy (20% reduction) and lateral ventricular enlargement (50% increase) in the animals fed the WD when compared with controls. These volumetric abnormalities were associated with behavioral indices of anxiety, increased leptin and FK506-binding protein 51 (FKBP51) levels, and reduced hippocampal blood vessel density. We found asymmetric structural vulnerabilities to the WD, particularly the ventral and left hippocampus and lateral ventricle. This study highlights how WD consumption during adolescence impacts key substrates implicated in post-traumatic stress disorder. Understanding how consumption of a WD affects the developmental trajectories of the stress neurocircuitry is critical, as stress susceptibility imposes a marked vulnerability to neuropsychiatric disorders.

The protective effects of resveratrol on social stress-induced cytokine release and depressive-like behavior

Social stress is a risk factor for psychiatric disorders, however only a subset of the population is susceptible while others remain resilient. Inflammation has been linked to the pathogenesis of psychosocial disorders in humans and may underlie these individual differences. Using a resident-intruder paradigm capable of revealing individual differences in coping behavior and inflammatory responses, the present study determined if resveratrol (RSV; 0, 10, 30mg/kg/day) protected against persistent stress-induced inflammation in socially defeated rats. Furthermore, the antidepressant efficacy of RSV was evaluated using the sucrose preference test. Active coping rats were characterized by more time spent in upright postures and increased defeat latencies versus passive coping rats. Five days after defeat, flow cytometry revealed enhanced stimulation of proinflammatory proteins (IL-β, TNF-α) in spleen cells of passive rats as compared to active coping and controls, an effect that was blocked by both doses of RSV. Furthermore, only passive coping rats exhibited increased proinflammatory proteins (IL-1β, TNF-α, GM-CSF) in the locus coeruleus (LC), a noradrenergic brain region implicated in depression. Notably, only 30mg/kg RSV blocked LC neuroinflammation and importantly, was the only dose that blocked anhedonia. Alternatively, while stress had minimal impact on resting cytokines in the dorsal raphe (DR), RSV dose-dependently reduced DR cytokine expression. However, this did not result in changes in indoleamine 2,3-dioxygenase activity or serotonin levels. Taken together, these data suggest that social stress-induced depressive-like behavior evident in passive coping rats may be driven by stress-induced neuroinflammation and highlight natural anti-inflammatory agents to protect against social stress-related consequences.

Hair Cortisol and Its Association With Psychological Risk Factors for Psychiatric Disorders: A Pilot Study in Adolescent Twins.

Measuring cortisol in hair is a promising method to assess long-term alterations of the biological stress response system, and hair cortisol concentrations (HCC) may be altered in psychiatric disorders and in subjects suffering from chronic stress. However, the pattern of associations between HCC, chronic stress and mental health require clarification. Our exploratory study: (1) assessed the association between HCC and perceived stress, symptoms of depression and neuroticism, and the trait extraversion (as a control variable); and (2) made use of the twin design to estimate the genetic and environmental covariance between the variables of interest. Hair samples from 109 (74 female) subjects (age range 12-21 years, mean 15.1) including 8 monozygotic (MZ) and 21 dizygotic (DZ) twin pairs were analyzed. Perceived stress was measured with the Perceived Stress Scale and/or the Daily Life and Stressors Scale, neuroticism, and extraversion with the NEO-Five Factor Inventory or the Junior Eysenck Personality Questionnaire, and depressive symptoms with the Somatic and Psychological Health Report. We found a modest positive association between HCC and the three risk factors - perceived stress, symptoms of depression, and neuroticism (r = 0.22-0.33) - but no correlation with extraversion (-0.06). A median split revealed that the associations between HCC and risk factors were stronger (0.47-0.60) in those subjects with HCC >11.36 pg/mg. Furthermore, our results suggest that the genetic effects underlying HCC are largely shared with those that influence perceived stress, depressive symptoms, and neuroticism. These results of our proof of principle study warrant replication in a bigger sample but raise the interesting question of the direction of causation between these variables.

Psychiatric and Behavioural Disorders in Children with Epilepsy: an ILAE Task Force Report.

CONTENTS S1 PrefaceFrank Besag, Albert Aldenkamp, Rochelle Caplan, David W. Dunn, Giuseppe Gobbi, Matti Sillanpaa S2 Epidemiology of psychiatric/behavioural disorder in children with epilepsyMatti Sillanpaa, Frank Besag, Albert Aldenkamp, Rochelle Caplan, David W. Dunn, Giuseppe Gobbi S8 Epilepsy and ADHDFrank Besag, Giuseppe Gobbi, Rochelle Caplan, Matti Sillanpaa, Albert Aldenkamp, David W. Dunn S16 Epilepsy and AutismFrank Besag, Albert Aldenkamp, Rochelle Caplan, David W. Dunn, Giuseppe Gobbi, Matti Sillanpaa S24 Anxiety, depression and childhood epilepsyDavid W. Dunn, Frank Besag, Rochelle Caplan, Albert Aldenkamp, Giuseppe Gobbi, Matti Sillanpaa S31 Epilepsy and psychosis in children and teenagersFrank Besag, Rochelle Caplan, Albert Aldenkamp, David W. Dunn, Giuseppe Gobbi, Matti Sillanpaa S37 Behavioural and psychiatric disorders associated with epilepsy syndromesFrank Besag, Giuseppe Gobbi, Albert Aldenkamp, Rochelle Caplan, David W. Dunn, Matti Sillanpaa S49 Subtle behavioural and cognitive manifestations of epilepsyFrank Besag, Giuseppe Gobbi, Albert Aldenkamp, Rochelle Caplan, David W. Dunn, Matti Sillanpaa S55 Adverse cognitive and behavioural effects of antiepileptic drugsAlbert Aldenkamp, Frank Besag, Giuseppe Gobbi, Rochelle Caplan, David W. Dunn, Matti Sillanpaa S68 Behavioural effects of epilepsy surgeryFrank Besag, Rochelle Caplan, Albert Aldenkamp, David W. Dunn, Giuseppe Gobbi, Matti Sillanpaa S77 When should pharmacotherapy for psychiatric/behavioural disorders in children with epilepsy be prescribed?Frank Besag, Albert Aldenkamp, Rochelle Caplan, David W. Dunn, Giuseppe Gobbi, Matti Sillanpaa PREFACE Psychiatric/behavioural problems are common in children with epilepsy, typically occurring in around 35-50% in epidemiological studies. They can affect the quality of life of the children and their families to a major degree. In many cases these problems create more of a challenge than the epilepsy itself. However, there are relatively few high-quality studies in this area. This collection of papers is intended to represent one step in a long journey towards addressing the lack of information by drawing together the available data on a number of key topics including epidemiology, the relationships between epilepsy and several psychiatric disorders, the role of the epilepsy itself, the effects of antiepileptic drugs and surgery and the place of pharmacotherapy. Although there is relatively good information on epidemiology there is very little information on the causes of and risk factors for psychiatric disorders in childhood epilepsy that might give insight into early diagnosis and prevention. Despite the growing amount of research in genetics, the impact on management has been minimal so far. There is also very sparse high-quality randomised controlled trial data on treatment of psychiatric disorders in childhood epilepsy. Furthermore, with a few exceptions, there is a striking lack of neuroimaging studies in this field. These are areas that would benefit from further attention and research. The information in this report has been put together by the members of the immediate past Child Neuropsychiatry Taskforce of the Neuropsychology Commission of the International League Against Epilepsy, guided by the then chairpersons of the commission: Andres Kanner and Marco Mula. The immediate past Task Force was officially in place from July 2009 to June 2013, although their work has continued since then, in relation to this publication and updating all the papers.

Cryptococcal meningitis in acute onset psychosis: A case-study

IntroductionCryptococcal meningitis is a frequently observed opportunistic infection in patients with late-stage HIV-infection, especially among people living in South-East Asia and Central Africa. The worldwide incidence is estimated at one million cases. The worldwide mortality of HIV-associated cryptococcal meningitis remains high (10–30%), due to the inadequacy of antifungal treatments and complications of increased intracranial pressure. Clinical symptoms of cryptococcal meningitis are fever, headache, vomiting, and altered mental status. Neck stiffness, papiledema, and focal neurological symptoms are sometimes present.ObjectivesWe describe the case of a patient who first developed a delirium, and a few months later an acute-onset psychosis, after a past cryptococcal infection.AimsTo report a case-study describing acute-onset psychosis as a neuropsychiatric consequence of HIV-infection.MethodsA case-study is presented and discussed, followed by a literature review.ResultsA 49-year-old African-born male was admitted to hospital with an acute psychosis. He had been treated by an internist after being found to have HIV. As a result of non-compliance over a period of about four months, his cd4-count had dropped to 40. Six months earlier he had developed cryptococcal meningitis, which left him a number of neurological and psychiatric symptoms. During his stay in hospital, there had to be good collaboration with the specialist in internal medicine whose dual task was to manage the patient's dramatically low cd4-count as well as his psychosis.ConclusionCryptococcal meningitis is a risk factor for psychiatric disorders and mortality in HIV-infected persons.Disclosure of interestThe authors have not supplied their declaration of competing interest.