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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.

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.

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

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.

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.

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.

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.

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.