Search

Psychopathy; Fear conditioning; Children Psicopatía; Condicionamiento del miedo; Niños Psicopatia; Condicionament de la por; Nens Deficits in fear conditioning related to psychopathy have been widely studied in adults. However, evidence in children and adolescents is scarce and inconsistent. This research aimed to expand knowledge about fear conditioning in psychopathy and its dimensions in child and early adolescent clinical populations. Participants were 45 boys (outpatients) aged 6–14 years (M = 10.59, SD = 2.04). They were assessed with the parents’ and teachers’ versions of the Child Problematic Traits Inventory (CPTI). A fear conditioning paradigm (Neumann et al., in Biological Psychology, 79(3), 337–342, 2008) for children and adolescents was used. Conditioned stimuli (CS+ and CS-) were geometric shapes and the unconditioned stimulus (US) was an unpleasant sound of metal scraping on slate (83 dB). Difference scores (CS+ minus CS-) in skin conductance responses (SCR) and self-reported cognitive and affective measures were considered as indices of fear conditioning. Results showed that: a) deficits in fear conditioning were related to some psychopathy dimensions but not to psychopathy as a unitary construct; b) the Impulsivity-Need for Stimulation dimension was a predictor of impaired fear conditioning at a cognitive level; c) the interaction of Callous-Unemotional and Impulsivity-Need for Stimulation dimensions was a significant predictor of impaired electrodermal fear conditioning; d) by contrast, the Grandiose-Deceitful dimension, was marginally associated with a greater electrodermal fear conditioning. In conclusion, psychopathy dimensions and their interactions, but not psychopathy as a whole, predicted deficits in fear conditioning as measured by SCR and cognitive indices. These findings confirm the notion that psychopathic traits are associated with deficits in fear conditioning in child and adolescent clinical populations and provide support for a multidimensional approach to youth psychopathy. Open Access Funding provided by Universitat Autonoma de Barcelona. This research was financially supported by the Ministerio de Economía y Competitividad, Spanish Government (MINECO/FEDER, UE), reference: PSI2015-67441-R and by the AGAUR, Generalitat de Catalunya (2017 SGR1586). A.I. is recipient of a Ph.D. fellowship by the Secretaria d’Universitats i Recerca of Generalitat de Catalunya and European Social Fund (FI-DGR 2017).

We sought to provide evidence for a combined effect of two attentional mechanisms during associative learning. Participants’ eye movements were recorded as they predicted the outcomes following different pairs of cues. Across the trials of an initial stage, a relevant cue in each pair was consistently followed by one of two outcomes, while an irrelevant cue was equally followed by either of them. Thus, the relevant cue should have been associated with small relative prediction errors, compared to the irrelevant cue. In a later stage, each pair came to be followed by one outcome on a random half of the trials and by the other outcome on the remaining half, and thus there should have been a rise in the overall prediction error. Consistent with an attentional mechanism based on relative prediction error, an attentional advantage for the relevant cue was evident in the first stage. However, in accordance with a mechanism linked to overall prediction error, the attention paid to both types of cues increased at the beginning of the second stage. These results showed up in both dwell times and within-trial patterns of fixations, and they were predicted by a hybrid model of attention.

Objective:To explore motor praxis in adults with Prader–Willi syndrome (PWS) in comparison with a control group of people with intellectual disability (ID) and to examine the relationship with brain structural measurements.Method:Thirty adult participants with PWS and 132 with ID of nongenetic etiology (matched by age, sex, and ID level) were assessed using a comprehensive evaluation of the praxis function, which included pantomime of tool use, imitation of meaningful and meaningless gestures, motor sequencing, and constructional praxis.Results:Results support specific praxis difficulties in PWS, with worse performance in the imitation of motor actions and better performance in constructional praxis than ID peers. Compared with both control groups, PWS showed increased gray matter volume in sensorimotor and subcortical regions. However, we found no obvious association between these alterations and praxis performance. Instead, praxis scores correlated with regional volume measures in distributed apparently normal brain areas.Conclusions:Our findings are consistent in showing significant impairment in gesture imitation abilities in PWS and, otherwise, further indicate that the visuospatial praxis domain is relatively preserved. Praxis disability in PWS was not associated with a specific, focal alteration of brain anatomy. Altered imitation gestures could, therefore, be a consequence of widespread brain dysfunction. However, the specific contribution of key brain structures (e.g., areas containing mirror neurons) should be more finely tested in future research.

Hyperphagia is one of the main problems of patients with Prader-Willi syndrome (PWS) to cope with everyday life. The underlying mechanisms are not yet well understood. Gut-brain hormones are an interrelated network that may be at least partially involved. We aimed to study the hormonal profile of PWS patients in comparison with obese and healthy controls. Thirty adult PWS patients (15 men, age 27.5 ± 8.02 years, BMI 32.4 ± 8.14 kg/m2), 30 obese and 30 healthy controls were studied before and after eating a hypercaloric liquid diet. Plasma brain-derived neurotrophic factor (BDNF), leptin, total and active ghrelin, peptide YY (PYY), pancreatic polypeptide (PP), Glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and amylin were determined at times 0′, 30′, 60′ and 120′. Cluster analysis was used. When considering all peptides together, two clusters were established according to fasting hormonal standardized concentrations. Cluster 1 encompassed most of obese (25/30) and healthy controls (28/30). By contrast, the majority of patients with PWS were located in Cluster 2 (23/27) and presented a similar fasting profile with hyperghrelinemia, high levels of leptin, PYY, GIP and GLP-1, compared to Cluster 1, that may reflect a dysfunction of these hunger/satiety hormones. When peptide behavior over the time was considered, PP concentrations were not sustained postprandially from 60 min onwards in Cluster 2. BDNF and amylin did not help to differentiate the two clusters. Thus, cluster analysis could be a good tool to distinguish and characterize the differences in hormone responses between PWS and obese or healthy controls.

Recent neurobiological models of obsessive-compulsive disorder (OCD) have highlighted the potential role of abnormalities in fear learning processes. We compared brain activation -as assessed with whole-brain functional magnetic resonance imaging- during fear conditioning, fear extinction learning, and fear extinction recall in patients with OCD (n = 18) and healthy controls (n = 18). We also investigated whether brain activation during any of these processes was associated with exposure-based cognitive-behavioral therapy (CBT) outcome in patients. Patients with OCD showed significantly lower brain activation in the right insulo-opercular region and the dorsal anterior cingulate cortex during fear conditioning in comparison to healthy controls. Moreover, brain activation in the right insula predicted CBT outcome, with lower activation predicting a better outcome. Brain activation during extinction learning or recall did not differ between patients and controls or predicted CBT outcome in patients. Our results suggest that neural activations during fear conditioning in patients with OCD are abnormal and predict CBT outcome.

Resumen Introduccion La escala Health of the Nation Outcome Scales for People with Learning Disabilities (HoNOS-LD) fue creada para evaluar de forma breve el funcionamiento de las personas con trastorno de desarrollo intelectual y problemas de salud mental/trastornos de conducta. El objetivo del presente trabajo fue estudiar las evidencias sobre la validez de las puntuaciones obtenidas con la escala HoNOS-LD traducida al castellano. Material y metodos La muestra estaba formada por 111 participantes que fueron evaluados con la HoNOS-LD traducida al castellano y otros cuestionarios relacionados. Para estudiar la fiabilidad entre examinadores y la fiabilidad test-retest, 33 participantes fueron evaluados por 2 examinadores y reevaluados al cabo de 7 dias. Resultados De acuerdo con criterios clinicos y conceptuales, y con el resultado del analisis paralelo, se selecciono una solucion factorial con unico factor. La consistencia interna fue buena (coeficiente omega de 0,87). Las fiabilidades entre examinadores y test-retest fueron excelentes (coeficientes de correlacion intraclase de 0,95 y 0,98, respectivamente). Las correlaciones entre secciones de la HoNOS-LD y los instrumentos relacionados fueron en el sentido esperado y altamente significativas ( p Conclusiones La version en castellano de la HoNOS-LD representa un instrumento breve, valido y fiable, que permitira la evaluacion rutinaria del funcionamiento con distintas finalidades, incluyendo el diagnostico y la intervencion.

A genetic analysis of unexplained mild-moderate intellectual disability and co-morbid psychiatric or behavioural disorders is not systematically conducted in adults. A cohort of 100 adult patients affected by both phenotypes were analysed in order to identify the presence of copy number variants (CNVs) responsible for their condition identifying a yield of 12.8% of pathogenic CNVs (19% when including clinically recognizable microdeletion syndromes). Moreover, there is a detailed clinical description of an additional 11% of the patients harbouring possible pathogenic CNVs—including a 7q31 deletion (IMMP2L) in two unrelated patients and duplications in 3q29, 9p24.2p24.1 and 15q14q15.1—providing new evidence of its contribution to the phenotype. This study adds further proof of including chromosomal microarray analysis (CMA) as a mandatory test to improve the diagnosis in the adult patients in psychiatric services. Electronic supplementary material The online version of this article (10.1007/s10519-018-9902-6) contains supplementary material, which is available to authorized users.

Fear extinction models have a key role in our understanding of anxiety disorders and their treatment with exposure therapy. Here, we tested whether individual differences in fear extinction learning and fear extinction recall in the laboratory were associated with the outcomes of an exposure therapy analog (ETA). Fifty adults with fear of spiders participated in a two-day fear-learning paradigm assessing fear extinction learning and fear extinction recall, and then underwent a brief ETA. Correlational analyses indicated that enhanced extinction learning was associated with better ETA outcome. Our results partially support the idea that individual differences in fear extinction learning may be associated with exposure therapy outcome, but suggest that further research in this area is needed. This work was supported by an ANPIR grant to E. F. (grant numberBA-3/2016); a KU Leuven program funding grant (grant number PF/10/005) and FP7 Marie Curie International Outgoing Fellowship (grantnumber 627743) to B. V.; PROMOSAM Investigación en procesos, me-canismos y tratamientos psicológicos para la promoción de la saludmental grant to M. T-F. (grant number PSI2014-56303-RED); Carlos IIIHealth Institute/FEDER grant to M. A. F. (grant number PI16/00144).

Compulsions are among the most typical behaviors in Prader-Willi syndrome (PWS). The most frequent causes of PWS are deletion of the genes located in the segment 15q11-q13 of the paternal allele and maternal uniparental disomy of cromosome 15. The aim of the present work was to study compulsive behavior in a sample of adults with PWS and analyze potential differences as a function of the genetic cause/subtype.In the 27 study participants, existence of type I deletion (n=7), type II deletion (n=13), and maternal disomy (n=7) was determined by means of genetic tests. The Yale-Brown Obsessive Compulsive Scale, the Compulsive Behavior Checklist, and the Repetitive Behavior Questionnaire were used to assess occurrence and severity of compulsions.Most of the participants showed compulsive behavior, the most frequent compulsions were those of inappropriate grooming (skin picking) and order (hoarding). The occurrence of compulsions was less frequent in the maternal disomy group than in the deletion groups. Severe compulsions were more frequent in those participants with type II deletion than in the other groups.Differences in occurrence and severity of compulsions exist as a function of PWS genetic subtype. Our results support the idea that individuals with maternal disomy are less affected by compulsive behavior. More research on the severity of compulsions as a function of deletion type should be done, as the studies conducted so far have shown contradictory results.

We investigated whether a sudden rise in prediction error widens an individual’s focus of attention by increasing ocular fixations on cues that otherwise tend to be ignored. To this end, we used a discrimination learning task including cues that were either relevant or irrelevant for predicting the outcomes. Half of participants experienced contingency reversal once they had learned to predict the outcomes (reversal group, n = 30). The other half experienced the same contingencies throughout the task (control group, n = 30). As participants’ prediction accuracy increased, they showed a decrease in the number of fixations directed to the irrelevant cues. Following contingency reversal, participants in the reversal group showed a drop in accuracy, indicating a rise in prediction error, and fixated on the irrelevant cues more often than participants in the control group. We discuss the results in the context of attentional theories of associative learning.

Abnormal fear conditioning processes (including fear acquisition and conditioned fear-generalization) have been implicated in the pathogenesis of anxiety disorders. Previous research has shown that individuals with panic disorder present enhanced conditioned fear-generalization in comparison to healthy controls. Enhanced conditioned fear-generalization could also characterize generalized anxiety disorder (GAD), but research so far is inconclusive. An important confounding factor in previous research is comorbidity. The present study examined conditioned fear-acquisition and fear-generalization in 28 patients with GAD and 30 healthy controls using a recently developed fear acquisition and generalization paradigm assessing fear-potentiated startle and online expectancies of the unconditioned stimulus. Analyses focused on GAD patients without comorbidity but included also patients with comorbid anxiety disorders. Patients and controls did not differ as regards fear acquisition. However, contrary to our hypothesis, both groups did not differ either in most indexes of conditioned fear-generalization. Moreover, dimensional measures of GAD symptoms were not correlated with conditioned fear-generalization indexes. Comorbidity did not have a significant impact on the results. Our data suggest that conditioned fear-generalization is not enhanced in GAD. Results are discussed with special attention to the possible effects of comorbidity on fear learning abnormalities. ispartof: BEHAVIOR THERAPY vol:46 issue:5 pages:627-639 ispartof: location:England status: published

We studied the temporal stability of individual differences in the acquisition and generalization of fear. Seventy-one participants were tested in two almost identical fear-acquisition and fear-generalization sessions (separated by 8 months). Acquisition and generalization were measured by the fear-potentiated startle, the skin conductance response, and online expectancies of the unconditioned stimulus. To control for the effects of previous experience, different stimuli were used for half of the participants in Session 2. Acquisition and generalization did not differ across sessions or as a function of the stimuli used in Session 2, and a significant proportion of individual differences in these processes was stable over time (generalizability coefficients ranged from 0.17 to 0.38). When the same stimuli were used, acquisition measures showed compromised stability. The results are discussed in terms of their theoretical and applied implications.

Although enhanced fear conditioning has been implicated in the origins of social anxiety disorder (SAD), laboratory evidence in support of this association is limited. Using a paradigm employing socially relevant unconditioned stimuli, we conducted two separate studies to asses fear conditioning in individuals with SAD and non-clinical individuals with high social anxiety (subclinical social anxiety [SSA]). They were compared with age-matched and gender-matched individuals with another anxiety disorder (panic disorder with agoraphobia) and healthy controls (Study 1) and with individuals with low social anxiety (Study 2). Contrary to our expectations, in both studies, self-report measures (ratings of anxiety, unpleasantness and arousal to the conditioned stimuli) of fear conditioning failed to discriminate between SAD or SSA and the other participant groups. Our results suggest that enhanced fear conditioning does not play a major role in pathological social anxiety. Copyright © 2014 John Wiley & Sons, Ltd. Key Practitioner Message  We used a social conditioning paradigm to study fear conditioning in clinical and subclinical social anxiety.  We found no evidence of enhanced fear conditioning in social anxiety individuals.  Enhanced fear conditioning may not be a hallmark of pathological social anxiety.

Previous studies have shown that individuals with anxiety disorders exhibit deficits in fear inhibition and excessive generalization of fear, but little data exist on individuals at risk from these disorders. The present study examined the role of trait anxiety in the acquisition and generalization of fear in 126 healthy participants selected on the basis of their trait-anxiety scores. Measures of conditioning included fear-potentiated startle, skin conductance response and online risk ratings for the unconditioned stimulus. Contrary to our hypotheses, trait anxiety did not have any effect either on the acquisition or the generalization of fear. Our results suggest that these fear conditioning processes are not impaired in individuals at risk from anxiety.

Few studies have investigated the role of the BDNF-val66met polymorphism in fear conditioning in humans, and previous results have been inconsistent. In the present study, we examined whether the BDNF-val66met was associated with differences in the acquisition and generalization of fear during a differential conditioning paradigm in a large sample of participants (N = 141). Using three different indexes of fear learning (fear-potentiated startle, skin conductance response, and online risk ratings) no effects of the BDNF-val66met were found either on the acquisition or the generalization of conditioned fear. Taken together with previous data, our study suggests that the BDNF-val66met polymorphism has no effect on the acquisition or generalization of fear.

Based on Lazarus’ transactional model of stress, this study examined how the information provided in a medical diagnosis (the severity of the illness, the effectiveness of the treatment and the self-efficacy to follow this treatment) are combined to generate perception of stress. Twenty-seven scenarios were presented to 152 volunteer students and their level of perceived stress was recorded. Results revealed that the lack of efficacy of the treatment raises the perception of stress proportionally to the different degrees of illness severity, but having a low perceived ability to follow the treatment triggers high levels of stress, particularly when the diagnosis is serious.

Context: Prader-Willi syndrome (PWS) is characterized by severe hyperphagia. Brain-derived neurotrophic factor (BDNF) and leptin are reciprocally involved in energy homeostasis. Objectives: To analyze the role of BDNF and leptin in satiety in genetic subtypes of PWS. Design: Experimental study. Setting: University hospital. Subjects: 90 adults: 30 PWS patients; 30 age-sex-BMI-matched obese controls; and 30 age-sex-matched lean controls. Interventions: Subjects ingested a liquid meal after fasting ≥10 hours. Main Outcome Measures: Leptin and BDNF levels in plasma extracted before ingestion and 30’, 60’, and 120’ after ingestion. Hunger, measured on a 100-point visual analogue scale before ingestion and 60’ and 120’ after ingestion. Results: Fasting BDNF levels were lower in PWS than in controls (p = 0.05). Postprandially, PWS patients showed only a truncated early peak in BDNF, and their BDNF levels at 60' and 120' were lower compared with lean controls (p

The Trail Making Test (TMT) is used as an indicator of visual scanning, graphomotor speed, and executive function. The aim of this study was to examine the TMT relationships with several neuropsychological measures and to provide normative data in community-dwelling participants of 55 years and older. A population-based Spanish-speaking sample of 2,564 participants was used. The TMT, Symbol Digit Test, Stroop Color-Word Test, Digit Span Test, Verbal Fluency tests, and the MacQuarrie Test for Mechanical Ability tapping subtest were administered. Exploratory factor analyses and regression lineal models were used. Normative data for the TMT scores were obtained. A total of 1,923 participants (76.3%) participated, 52.4% were women, and the mean age was 66.5 years (Digit Span = 8.0). The Symbol Digit Test, MacQuarrie Test for Mechanical Ability tapping subtest, Stroop Color-Word Test, and Digit Span Test scores were associated in the performance of most TMT scores, but the contribution of each measure was different depending on the TMT score. Normative tables according to significant factors such as age, education level, and sex were created. Measures of visual scanning, graphomotor speed, and visuomotor processing speed were more related to the performance of the TMT-A score, while working memory and inhibition control were mainly associated with the TMT-B and derived TMT scores.

Despite the effectiveness of exposure therapy for treating anxiety disorders, a number of patients fail to benefi t or experience a return of fear after treatment. Research suggests that anxious individuals show defi cits in the mechanisms believed to underlie exposure therapy, such as inhibitory learning. Targeting these processes may help improve the effi cacy of expo- sure-based procedures. The primary aim of this paper is to provide examples to clinicians for how to apply this model to optimize exposure therapy with anxious clients, in ways that distinguish it from a "fear habituation" approach and "belief disconfi rma- tion" approach within standard cognitive-behavior therapy. Exposure optimization strategies include 1) expectancy violation, 2) deepened extinction, 3) occasional reinforced extinction, 4) removal of safety signals, 5) variability, 6) retrieval cues, 7) multiple contexts, and 8) affect labeling. Case studies illustrate methods of applying these techniques with a variety of anxiety disorders.

Although enhanced fear conditioning has been implicated in the origins of social anxiety disorder (SAD), laboratory evidence in support of this association is limited. Using a paradigm employing socially relevant unconditioned stimuli, we conducted two separate studies to asses fear conditioning in individuals with SAD and non-clinical individuals with high social anxiety (subclinical social anxiety [SSA]). They were compared with age-matched and gender-matched individuals with another anxiety disorder (panic disorder with agoraphobia) and healthy controls (Study 1) and with individuals with low social anxiety (Study 2). Contrary to our expectations, in both studies, self-report measures (ratings of anxiety, unpleasantness and arousal to the conditioned stimuli) of fear conditioning failed to discriminate between SAD or SSA and the other participant groups. Our results suggest that enhanced fear conditioning does not play a major role in pathological social anxiety.We used a social conditioning paradigm to study fear conditioning in clinical and subclinical social anxiety. We found no evidence of enhanced fear conditioning in social anxiety individuals. Enhanced fear conditioning may not be a hallmark of pathological social anxiety.

Introduccion. La evaluacion neuropsicologica en las personas con discapacidad intelectual es importante para determinar los deficits cognitivos especificos que subyacen a la afectacion cerebral, limitan el funcionamiento intelectual y afectan al comportamiento adaptativo. A pesar de ello, no existen baterias neuropsicologicas en castellano adaptadas y validadas para esta poblacion. Objetivo. Adaptar el programa integrado de exploracion neuropsicologica-test Barcelona y validar la nueva version, el test Barcelona para discapacidad intelectual (TB-DI), estableciendo datos normativos para el empleo clinico. Sujetos y metodos. A partir de los datos obtenidos en una muestra piloto de 65 personas con discapacidad intelectual, se realizaron cambios en el test original. Para estudiar las propiedades psicometricas del TB-DI, se administro a una muestra de 170 personas con discapacidad intelectual y a un grupo de 60 personas sin ella. Mediante modelos de regresion, se determino que variables eran importantes para la estratificacion de los datos normativos. Resultados. El TB-DI, compuesto de 67 subtests agrupados en ocho dominios cognitivos, muestra unas buenas propiedades psicometricas. Se crean datos normativos para cinco grupos en funcion del nivel de discapacidad intelectual, la edad y la competencia curricular. Estos datos se organizan en percentiles, lo que permite trazar perfiles cognitivos en el ambito clinico y experimental. Conclusion. El TB-DI es un instrumento de alta aplicabilidad para la poblacion con discapacidad intelectual, y muestra una validez y una fiabilidad adecuadas, y con buenas propiedades psicometricas. Los perfiles cognitivos determinados mediante el TB-DI proporcionaran informacion valiosa para el tratamiento integral de las personas adultas con discapacidad intelectual leve y moderada.

Few studies have investigated the role of the BDNF-val66met polymorphism in fear conditioning in humans, and previous results have been inconsistent. In the present study, we examined whether the BDNF-val66met was associated with differences in the acquisition and generalization of fear during a differential conditioning paradigm in a large sample of participants (N = 141). Using three different indexes of fear learning (fear-potentiated startle, skin conductance response, and online risk ratings) no effects of the BDNF-val66met were found either on the acquisition or the generalization of conditioned fear. Taken together with previous data, our study suggests that the BDNF-val66met polymorphism has no effect on the acquisition or generalization of fear.

An important number of studies suggest that individual differences in acquisition and generalization of fear may be implicated the etiology of anxiety disorders. A prerequisite of this idea is that measures of these processes should show individual stability over time. However, this prerequisite has rarely been tested. In order to investigate this question, seventy-five healthy individuals participated in a two-session fear-conditioning and fear-generalization paradigm. Measures of conditioning included fear-potentiated startle, skin conductance response and online risk ratings for the unconditioned stimulus. Time between sessions spanned approximately 8 months. ANOVAs showed that for the whole sample the acquisition and generalization of fear did not differ across sessions. On the other hand, generalizability coefficients showed that individual differences in the acquisition of fear were moderately stable over time, whereas idiosyncratic generalization patterns were less stable.

The Trail Making Test (TMT) is used as an indicator of visual scanning, graphomotor speed, and executive function. The aim of this study was to examine the TMT relationships with several neuropsychological measures and to provide normative data in community-dwelling participants of 55 years and older. A population-based Spanish-speaking sample of 2,564 participants was used. The TMT, Symbol Digit Test, Stroop Color–Word Test, Digit Span Test, Verbal Fluency tests, and the MacQuarrie Test for Mechanical Ability tapping subtest were administered. Exploratory factor analyses and regression lineal models were used. Normative data for the TMT scores were obtained. A total of 1,923 participants (76.3%) participated, 52.4% were women, and the mean age was 66.5 years (Digit Span = 8.0). The Symbol Digit Test, MacQuarrie Test for Mechanical Ability tapping subtest, Stroop Color–Word Test, and Digit Span Test scores were associated in the performance of most TMT scores, but the contribution of each measure was different depending on the TMT score. Normative tables according to significant factors such as age, education level, and sex were created. Measures of visual scanning, graphomotor speed, and visuomotor processing speed were more related to the performance of the TMT-A score, while working memory and inhibition control were mainly associated with the TMT-B and derived TMT scores.