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Background: Epicardial adipose tissue (EAT) has been recently identified as a major player in the development of the atherosclerotic process. This study aimed to investigate the role of EAT as a marker associated with a higher vulnerability of atheromatous coronary plaques in patients with acute myocardial infarction (AMI) as compared to patients with stable angina.

Family studies can provide a wealth of information regarding risk factors in psychological disorders. No studies have compared the trauma experiences and coping strategies of problem gamblers with those of their first-degree relatives. Therefore, in this study, childhood trauma and coping strategies were investigated among participants with gambling disorder, their first-degree biological relatives, and community controls. Participants completed diagnostic interviews and symptom severity assessments. Participants also completed the Childhood Trauma Questionnaire (CTQ) which assesses history of abuse and neglect, and the Coping Inventory for Stressful Situations (CISS) which assesses task, emotion, and avoidance oriented coping strategies. Analysis of variance showed that there was a significant effect for group, but not gender, on the CTQ. Multivariate analysis of variance revealed a significant effect for group on coping style. Post-hoc tests showed that probands and relatives were less likely to use task-oriented coping compared to controls, but probands and relatives did not differ from each other on task-oriented coping. Mediation analysis showed that task-oriented coping did not mediate the relation between childhood trauma and gambling severity. By using a family study design, this study was able for the first time to delineate familial and disease-specific effects associated with childhood trauma and coping strategies in gambling disorder. [ABSTRACT FROM AUTHOR]

ABSTRACT Objective Intelligence is a known vulnerability marker in various psychiatric disorders. In eating disorders (ED) intelligence has not been studied thoroughly. Small-scale studies indicate that intelligence levels might be above general population norms, but larger scale studies are lacking. The aim of this study was to determine intellectual functioning in ED patients and associations with severity of the disorder. Methods: Wechsler's Full scale IQ (FSIQ), Verbal IQ (VIQ) and Performance IQ (PIQ) of 703 adolescent and adult ED patients were compared with population norms. Exploratory analyzes were performed on associations between IQ and both somatic severity (BMI and duration of the disorder) and psychological/behavioral severity (Eating Disorder Inventory [EDI-II] ratings) of the ED. Results: Mean IQ's were significantly higher than population means and effect-sizes were small-to-medium ( d = .28, .16 and .23 for VIQ, PIQ, and FSIQ). No linear associations between IQ and BMI were found, but the most severely underweight adult anorexia nervosa (AN) patients (BMI ≤ 15) had higher VIQ (107.7) than the other adult AN patients (VIQ 102.1). In adult AN patients PIQ was associated with psychological/behavioral severity of the ED. Discussion: Our findings suggest that, in contrast with other severe mental disorders where low intelligence is a risk factor, higher than average intelligence might increase the vulnerability to develop an ED. © 2016 Wiley Periodicals, Inc.(Int J Eat Disord 2017; 50:481-489) [ABSTRACT FROM AUTHOR]

Studies have demonstrated that personality traits differ in schizophrenia patients and family members compared to controls, suggesting familial risk. This study evaluated personality traits in a family study of schizophrenia, as well as the relationship between personality traits and symptoms and social functioning in schizophrenia patients. Thirty-two schizophrenia patients, 28 adult non-psychotic relatives, and 27 community controls completed the Dimensional Assessment of Personality Pathology–Basic Questionnaire (DAPP-BQ). Schizophrenia patients differed on many dimensions of the DAPP-BQ compared to controls and/or relatives: affective lability, anxiousness, callousness, conduct problems, cognitive dysregulation, identity problem, intimacy, insecure attachment, low affiliation, narcissism, oppositionality, restricted expression, self-harm, submissiveness, and suspiciousness. No differences were found between relatives and controls. Furthermore, in schizophrenia patients, associations were found between personality and particularly general symptoms, as well as social functioning. Personality traits can be conceptualized as an extended phenotype in schizophrenia patients. [ABSTRACT FROM AUTHOR]

Schizophrenia patients have impaired performance and abnormal brain activation during facial emotion recognition, which may represent a marker of genetic liability to schizophrenia. However, it remains unclear whether the impairment is specific to recognizing emotion from faces or is instead attributable to more generalized dysfunction. The current study aimed to distinguish between specific and generalized neural dysfunction underlying impaired facial emotion recognition in schizophrenia and examine associations with genetic liability. Twenty-eight schizophrenia patients, 27 nonpsychotic first-degree relatives, and 27 community controls underwent functional magnetic resonance imaging while making judgments about either the emotion or age of emotional faces. Patients had performance deficits during the emotion and age discrimination conditions compared to relatives and controls, while relatives had intact performance. Patients had hypoactivation compared to controls across conditions, mainly in medial prefrontal cortex. Unlike controls, patients demonstrated a failure to recruit the dorsomedial prefrontal cortex, a region involved in social cognition and decision-making, and relatives had a pattern of recruitment intermediate between patients and controls. Compared to controls, relatives had greater deactivation of regions associated with the default mode network, and patients had similar findings during age discrimination. The common patterns of performance deficits and activation abnormalities during emotion and age discrimination in schizophrenia suggest that generalized cognitive impairment, notably in social cognition and decision-making, contributes to impaired facial emotion recognition. Similar functional activation patterns in relatives, despite intact performance, suggest that brain activation may represent a more sensitive marker of genetic liability than behaviour. Hyperdeactivation of default mode network regions in relatives may represent cognitive inefficiency, or compensatory mechanisms that help maintain intact performance. [ABSTRACT FROM AUTHOR]

In response to the review article written by Pavuluri and May [1] and to the original article by Tomasino et al [2] we will comment the recent neuroimaging findings of insular dysfunctions in Schizophrenia and Bipolar Disorders, focusing on people at genetic risk for developing psychotic symptoms. A disrupted insular functioning was reported in several studies, even though the results were not univocal with respect to the direction of the effect (some studies reported a reduced activation, other an augmented activation) and the lateralization of the observed alterations (left, right or bilateral). We will conclude that an altered function of the insula during both cognitive and emotional task may be a candidate vulnerability marker for psychotic disorders. [ABSTRACT FROM AUTHOR]

Abstract: Background: Research in cognitive processes and attitudes in bipolar disorder is scarce and has provided mixed findings, possibly due to differences in current mood state. It is unclear whether alterations in cognitive processes and attitudes are only related to the depressive mood states of bipolar patients or also represent a vulnerability marker for the development of future (depressive) episodes. This was investigated in the current study. Methods: Both implicit (attentional bias for emotional words) and explicit (dysfunctional attitudes and personality characteristics) measures of cognitive processes and attitudes were assessed in 77 bipolar patients with varying levels of depressive symptoms (depressed=17, euthymic n=60), their healthy first-degree relatives (n=39) and a healthy control group (n=61). Analyses of variance were used to investigate differences between groups. Results: Mildly depressed patients with bipolar disorder demonstrated an attentional bias away from positive emotional words and showed increased dysfunctional attitudes and higher levels of neuroticism. Euthymic patients were largely comparable to healthy controls and only differed from controls in higher levels of neuroticism. Relatives were similar to controls on all measures, although they significantly differed from bipolar patients in displaying less neuroticism and more extraversion. Limitations: No firm conclusions regarding causality can be drawn from the associations that were found between cognitive processes and attitudes and the evolution of mood symptoms in bipolar disorder. Conclusion: Alterations in cognitive processes and attitudes in bipolar patients appear to be mostly related to the expression of mood symptomatology rather than to the vulnerability for bipolar disorder. [Copyright &y& Elsevier]

Background: Genetic factors have been implicated in the development of substance abuse disorders, but the role of pre-existing vulnerability in addiction is still poorly understood. Personality traits of impulsivity and sensation-seeking are highly prevalent in chronic drug users and have been linked with an increased risk for substance abuse. However, it has not been clear whether these personality traits are a cause or an effect of stimulant drug dependence. Method: We compared self-reported levels of impulsivity and sensation-seeking between 30 sibling pairs of stimulant-dependent individuals and their biological brothers/sisters who did not have a significant drug-taking history and 30 unrelated, nondrug-taking control volunteers. Results: Siblings of chronic stimulant users reported significantly higher levels of trait-impulsivity than control volunteers but did not differ from control volunteers with regard to sensation-seeking traits. Stimulant-dependent individuals reported significantly higher levels of impulsivity and sensation-seeking compared with both their siblings and control volunteers. Conclusions: These data indicate that impulsivity is a behavioral endophenotype mediating risk for stimulant dependence that may be exacerbated by chronic drug exposure, whereas abnormal sensation-seeking is more likely to be an effect of stimulant drug abuse. [ABSTRACT FROM AUTHOR]

Objective: Impairment in social functioning is a central feature of schizophrenia and is known to be evident before the onset of psychosis, acting as a potential vulnerability marker. The aim of the present study was to test the hypothesis that social impairment is simultaneously a state and trait marker of risk for schizophrenia and schizophrenia-related disorder. Method: Social functioning was examined in three groups: ultra-high-risk subjects (UHR, n =32), genetic high-risk subjects (GHR, n =32), and age- and IQ-matched healthy controls (HC, n =30). Social functioning was assessed using the Social Functioning Scale (SFS), and prodromal symptoms were assessed in high-risk subjects using the Comprehensive Assessment of At-Risk Mental States (CAARMS). Results: Both the UHR and GHR groups exhibited significantly impaired social functioning compared with the HC group, and the UHR group was more impaired than the GHR group. In the UHR group, duration of prodromal symptoms was related to impaired 'interpersonal behaviour'. Positive and negative symptoms were not significantly associated with social functioning, whereas disorganized and general symptoms were significantly correlated with poor 'independence-competence' in UHR individuals. Conclusion: The findings support the hypothesis that impairment in social functioning is both a trait and state marker of risk for schizophrenia and other psychotic disorders, implying that social impairment constitutes a mediating vulnerability indicator of psychotic disorders including schizophrenia. [ABSTRACT FROM AUTHOR]

Abstract: Many factors have been associated with the development of schizophrenia, yet few studies have looked at these same factors in individuals considered at risk for schizophrenia, but who have not yet reached diagnostic threshold. The rate of obstetrical complications was assessed as part of a comprehensive battery in subjects at risk (N =52), or in the first episode of schizophrenia (N =18), and in normal comparison subjects (N =43). The rate of obstetrical complications was increased in the at risk (46%) and first episode (39%) samples compared to the normal comparison (19%) group, however, follow-up analyses were only significant between the at risk and normal comparison subjects. Obstetrical complications may be an important risk factor in identifying vulnerable subjects and ultimately may, along with other risk factors, be part of an algorithm for determining likelihood of developing schizophrenia. [Copyright &y& Elsevier]

Abstract: Objective: Recently, in a post-mortem and a subsequent structural MR study, a significantly increased gyrification index (GI) was demonstrated in the frontal lobe in individuals with schizophrenia. To examine whether frontal lobe hypergyria is region-specific and whether this might be a suitable endophenotype in the search for the genetic basis of schizophrenia, the frontal as well as parieto-occipital GI were determined in MRI scans of families affected with schizophrenia. Method: In the MRI scans of 48 subjects suffering from schizophrenia, in 82 of their first-degree relatives and in 41 control subjects, the GI was determined in three sections anterior to the genu of the corpus callosum and three sections posterior to the splenium, thus allowing for a selective determination of this measure in the frontal as well as the parietal lobe. Outer and inner contours constituting the GI was determined in each section by manual tracing. Statistical analysis was performed using MANOVA with factors diagnostic group and intervening factors from preliminary analyses. Results: The frontal, but not parieto-occipital GI was significantly higher in schizophrenic patients as well as unaffected relatives compared with control subjects (right: 7%, F =13.24, df=3, 155, p <0.0005, left: 6%, F =8.92, df=3, 155, p <0.0005). There was no overall difference between affected and unaffected family members. On the left side however, there was a significant interaction between diagnostic group and genetic loading (F =4.68, df=2, 101, p =0.01): significantly higher GI was found in affected compared with unaffected family members only in uniaffected and not multiaffected families. Conclusions: These results support our primary finding of hypergyria in the frontal lobe in schizophrenic patients. Compared to the parietal lobe, hypergyria seems to affect the frontal lobe selectively and serves as a suitable neurodevelopmental, possibly even an endophenotypic marker. [Copyright &y& Elsevier]

Hyperechogenicity of the substantia nigra (SN) has been proposed to be a typical finding in Parkinson’s disease (PD) and a marker of vulnerability to nigrostriatal dysfunction in healthy subjects. This large cross-sectional study including 1120 subjects older than 50 years without any signs of PD was performed to evaluate the association of SN hyperechogenicity and other proposed epidemiological risk factors for PD. Among all variables assessed only family history of PD and male gender proved to be significantly associated with SN hyperechogenicity, indicating a genetic predisposition for the ultrasound marker. [ABSTRACT FROM AUTHOR]

Objective: Complex genetic mechanisms are involved in the vulnerability to depressive disorders and cognitive dysfunctions found in depression. This study was performed to explore the effect of the familial risk for depression on electrophysiological correlates of attentional functions as demonstrated by an event-related potential (ERP) go/no-go experiment. Methods: The component P3b as an indicator of target detection processing was investigated in two groups of healthy subjects with or without a family history of depression (n = 14 each). An electrophysiological source localization method (LORETA) was employed to allow a neuro-anatomical interpretation for the ERP data. Results: The group with a familial risk for depression showed a reduced P3b amplitude over left temporal areas in contrast to the control group. This two-dimensional effect was associated with a significantly reduced activation of the left middle temporal gyrus. Conclusions: The P3b amplitude decrement might represent a neurocognitive vulnerability marker for the development of depression. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Abstract: Previous studies on spatial orienting of attention in schizophrenia demonstrated a deficit of Inhibition of Return (IOR). However, other studies reported a delay in the manifestation, but an overall normal amount of IOR in patients with schizophrenia. However, the latter studies used a cue-back manipulation which is known to reinstate or speed up IOR. Hence, it is not clear whether even very long cue target intervals would allow IOR to develop in patients with schizophrenia in the absence of a cue-back manipulation. The aim of the present study was to study IOR in patients with schizophrenia using a single cue paradigm and a very long cue target interval of >1 s in order to differentiate between blunted and delayed IOR. We examined 32 inpatients with schizophrenia and 16 healthy controls with a covert orienting of attention task (COVAT) with non-predictive peripheral cues and three stimulus onset asynchronies (SOA: 100 ms, 800 ms and 1050 ms). We found a lack of Inhibition of Return (IOR) in patients with schizophrenia with both long SOAs of 800 and 1050 ms. As in a previous study of our group, the IOR deficit was unrelated to psychopathology, length of illness, number of previous psychotic episodes and type of neuroleptic medication. In summary, our study confirms and extends previous reports of deficient IOR in patients with schizophrenia. IOR seems to be not just delayed, but rather profoundly disturbed in schizophrenia. Deficient IOR in patients with schizophrenia might be viewed as a trait or alternatively as a vulnerability marker of the disorder. [Copyright &y& Elsevier]

Previous cross-sectional studies on covert orienting of visual attention in schizophrenia have been inconsistent. In the present longitudinal study, we examined 40 medicated acutely ill inpatients with a covert orienting of attention task (COVAT) shortly after admission, and again 12–16 weeks after the initial examination, while most patients were in (partial) remission. We administered a COVAT with nonpredictive peripheral cues and two stimulus-onset asynchronies (SOA; 100 and 800 ms). In addition, we examined 34 healthy control subjects twice (2 weeks apart). The most important finding was a lack of inhibition of return (IOR) in patients with schizophrenia, both at the first examination in an acute psychotic state and at the follow-up examination after considerable clinical improvement. The IOR deficit was unrelated to psychopathology, length of illness, number of previous psychotic episodes, and type of neuroleptic (NL) medication. Deficient IOR in patients with schizophrenia appears to be state-independent and might be viewed as a trait or vulnerability marker of the disorder. Subsequent studies with never-medicated populations and with schizotypal or high-risk subjects are needed in order to further analyze the possible role of NL medications and to clarify whether blunted IOR might represent a vulnerability marker of schizophrenia. [Copyright &y& Elsevier]

Enhanced semantic priming (SP) has been reported in individuals with schizophrenia who exhibit positive formal thought disorder (TD) and it has been linked to heightened automatic spreading activation in semantic networks of these patients. However, the state or trait nature of semantic hyperpriming in schizophrenia and its relation to clinical features (e.g., length of illness, symptom shifts) is not clear. To explore these issues, we administered a lexical decision task with semantically related, indirectly related or unrelated prime-target pairs to acutely ill inpatients with schizophrenia shortly after admission and again after 12–16 weeks, while most patients were already in (partial) remission (n=33). In addition, we examined 20 healthy control subjects twice (2 weeks apart). Relative to control subjects, TD patients with schizophrenia exhibited hyperpriming only in the acute psychotic state, but not during the follow-up examination, when TD and other positive symptoms had resolved. There were no associations between priming effects and length of illness or number of previous psychotic episodes. In conclusion, semantic hyperpriming in TD patients with schizophrenia appears to be clearly state-dependent and might be viewed as an episode marker of psychosis with TD. [Copyright &y& Elsevier]

Increased echogenicity of the substantia nigra (SN) on ultrasound is a typical sonographic finding in Parkinson’s disease (PD). Sonographic signal intensity of the SN is related to tissue iron content with higher iron level being associated with increased echogenicity. Recent findings indicate that hyperechogenicity of the SN represents an important susceptibility factor for nigrostriatal degeneration. In this study we determined the prevalence of a characteristic ultrasound sign of Parkinson’s disease in first-degree relatives of PD patients. Fourteen patients with sporadic PD and 58 of their relatives underwent neurological, neuropsychological, and ultrasound examination. In addition, four pairs of relatives (one member of each pair exhibiting increased echogenicity of the SN and the other with regular SN echogenicity) underwent 18F-Dopa PET examination. On transcranial sonography, 26 of the 58 relatives exhibited SN hyperechogenicity. Twenty-four relatives showed minor signs of motor slowing. Relatives with SN hyperechogenicity more often showed signs of hypokinesia (16 v 8 relatives; U test, P = 0.01) and impaired executive functions (Tower of London task, problems solved with the minimum number of moves; U test, P = 0.012) than relatives without this echo pattern. In addition, 18F-Dopa uptake (influx constants) at the putamen was reduced in subjects with SN hyperechogenicity compared to their relatives without this ultrasound sign (Wilcoxon, P = 0.03). In conclusion, approximately 45% of relatives of PD patients exhibited an increased echogenicity of the SN. This sign is associated with clinical findings and objective measurements, indicating some degree of impaired nigrostriatal function. [Copyright &y& Elsevier]

Recently an increased echogenicity of the substantia nigra (SN) in patients with Parkinson's disease (PD) was demonstrated by transcranial ultrasound (TCS). In this study we set out to compare SN echogenicitiy with disease characteristics (time of onset, duration, toxin exposure) in a large patients sample. Patients' history and exposure to toxins were recorded from 112 PD patients who underwent a thorough neurological examination including assessment of disease stage according to Hoehn and Yahr and CURS (Columbia University Rating Scale). Personality was assessed according to the Freiburg Personality Inventory. In all patients the area of SN echogenicity was encircled and measured by TCS. All except 9 patients had hyperechogenic SN areas exceeding the mean plus standard deviation values of an age matched control group (0.19cm2). The age of disease onset was lower in patients who displayed an area of SN echogenicity above this value. The area of SN echogenicity was larger contralateral to the side with more severe symptoms. None of the other characteristics correlated with ultrasound findings. We conclude that SN hyperechogenicity is a typical finding in PD. The cause of hyperechogenicity is so far unknown. Investigation of the underlying reason might disclose a pathogenic factor in PD. [ABSTRACT FROM AUTHOR]

Abstract: Hyperechogenicity of the substantia nigra (SN) detected by transcranial sonography is a typical finding in more than 90% of patients with Parkinson''s disease (PD) but may also be visible in about 9% of healthy adults. In this study, we found a correlation between SN hyperechogenicity and subtle motor dysfunction in otherwise healthy young tap dancers. In accordance with former findings, results of the present study confirm the hypothesis that SN hyperechogenicity is a marker for a possible functional impairment of the nigrostriatal system, that may become evident under challenging conditions. [Copyright &y& Elsevier]