Biomedical subjects

R J R Blair

Publications and source records attributed to R J R Blair.

At least 19 recordsLinked to original sources

PubMed2007

Dissociable systems for empathy.

Empathy is a lay term that is becoming increasingly used in the field of cognitive neuroscience. In this paper, it is argued that empathy is a loose collection of partially dissociable neurocognitive systems. Two forms of 'emotional' empathy were considered: First, responding to emotional expressions, particularly angry expressions, leading to response reversal. Secondly, responding to emotional expressions, particularly fearful and sad expressions, leading to stimulus-reinforcement learning. The implications of these forms of empathy for understanding specific psychiatric conditions are briefly considered.

Affect↗

PubMed2006

Neural correlates of response reversal: considering acquisition.

Previous work on response reversal has typically used a single pair of stimuli that serially reverse. This conflation of acquisition and reversal processes has prevented an examination of the functional role of neural systems implicated in response reversal during acquisition despite the relevance of such data in evaluating accounts of response reversal. In the current study, participants encountered 16 independent reversing stimulus pairs in the context of a probabilistic response reversal paradigm. Functional regions of interest identified as involved in response reversal through a contrast used in the previous literature (punished errors made in the reversal phase versus rewarded correct responses), were interrogated across conditions. Consistent with suggestions that middle frontal cortex codes reward, this region showed significantly greater responses to rewarded rather than punished trials irrespective of accuracy or learning phase (acquisition or reversal). Consistent with the suggestion that this coding of the expectation of reinforcement is acquired via input from the amygdala, we observed significant positive connectivity between activity within the amygdala and a region of rostral anterior cingulate cortex highly proximal to this region of middle frontal/mesial prefrontal cortex. In contrast, inferior frontal cortex, anterior cingulate cortex and caudate showed greater responses to punished errors than to the rewarded correct responses. These three regions also showed significant activation to rewarded errors during acquisition, in contrast to positions suggesting that inferior frontal cortex represents punishment or suppresses previously rewarded responses. Moreover, a connectivity analysis with an anterior cingulate cortex seed revealed highly significant positive connectivity among them. The implications of these data for recent accounts of response reversal and of response reversal impairments in specific neuropsychiatric populations are discussed.

Adult↗

PubMed2006

The impact of processing load on emotion.

This event-related fMRI study examined the impact of processing load on the BOLD response to emotional expressions. Participants were presented with composite stimuli consisting of neutral and fearful faces upon which semi-transparent words were superimposed. This manipulation held stimulus-driven features constant across multiple levels of processing load. Participants made either (1) gender discriminations based on the face; (2) case judgments based on the words; or (3) syllable number judgments based on the words. A significant main effect for processing load was revealed in prefrontal cortex, parietal cortex, visual processing areas, and amygdala. Critically, enhanced activity in the amygdala and medial prefrontal cortex seen during gender discriminations was significantly reduced during the linguistic task conditions. A connectivity analysis conducted to investigate theories of cognitive modulation of emotion showed that activity in dorsolateral prefrontal cortex was inversely related to activity in the ventromedial prefrontal cortex. Together, the data suggest that the processing of task-irrelevant emotional information, like neutral information, is subject to the effects of processing load and is under top-down control.

Adult↗

PubMed2006

Impaired recognition of fear facial expressions in 5-HTTLPR S-polymorphism carriers following tryptophan depletion.

RATIONALE: Genotype at the 5' promoter region (5-HTTLPR) of the serotonin transporter has been implicated in moderating the effects of acute tryptophan depletion on neurocognitive functioning. Acute tryptophan depletion has been associated with the processing of fear-relevant cues, such as emotional expressions, but the effect of genotype at the 5-HTTLPR has not been assessed. OBJECTIVE: The present study investigated the effects of acute tryptophan depletion on the recognition of standardized facial expressions of emotions in healthy volunteers classified as ll homozygotes or s carriers. MATERIALS AND METHODS: A double-blind between-groups design was used with volunteers randomly selected to ingest capsules containing an amino acid mixture specifically lacking tryptophan, or placebo capsules containing lactose. 5 h after capsule ingestion, subjects were required to identify anger, disgust, fear, happiness, sadness, and surprise expressions that progressed from neutral to each full emotional expression in 5% steps. RESULTS: Tryptophan depletion significantly impaired the recognition of fearful facial expressions in s carriers but not ll homozygotes. This impairment was specific to fear expressions. No significant differences in the recognition of other expressions were found. Free tryptophan levels were correlated with fear recognition in s carriers but not ll homozygotes. CONCLUSIONS: The effects of acute tryptophan depletion on the processing of emotional expressions varies as a function of genotype at the 5-HTTLPR. Depletion impairs the recognition of fear in s carriers but not ll homozygotes. This finding reinforces the importance of considering genotype when assessing the behavioral effects of pharmacologic modulation.

Adult↗

PubMed2006

The emergence of psychopathy: implications for the neuropsychological approach to developmental disorders.

In this paper, I am going to examine the disorder of psychopathy and consider how genetic anomalies could give rise to the relatively specific neuro-cognitive impairments seen in individuals with this disorder. I will argue that genetic anomalies in psychopathy reduce the salience of punishment information (perhaps as a function of noradrenergic disturbance). I will argue that the ability of the amygdala to form the stimulus-punishment associations necessary for successful socialization is disrupted and that because of this, individuals with psychopathy do not learn to avoid actions that will harm others. It is noted that this model follows the neuropsychological approach to the study of developmental disorders, an approach that has been recently criticized. I will argue that these criticisms are less applicable to psychopathy. Indeed, animal work on the development of the neural systems necessary for emotion, does not support a constructivist approach with respect to affect. Importantly, such work indicates that while environmental effects can alter the responsiveness of the basic neural architecture mediating emotion, environmental effects do not construct this architecture. However, caveats to the neuropsychological approach with reference to this disorder are noted.

Amygdala↗

PubMed2006

They know the words, but not the music: affective and semantic priming in individuals with psychopathy.

Previous work has indicated dysfunctional affect-language interactions in individuals with psychopathy through use of the lexical decision task. However, it has been uncertain as to whether these deficits actually reflect impaired affect-language interactions or a more fundamental deficit in general semantic processing. In this study, we examined affective priming and semantic priming (dependent measures were reaction times and error rates) in individuals with psychopathy and comparison individuals, classified according to the psychopathy checklist revised (PCL-R) [Hare, R.D., 1991. The Hare Psychopathy Checklist-Revised. Multi-Health Systems, Toronto, Ont] Individuals with psychopathy showed significantly less affective priming relative to comparison individuals. In contrast, the two groups showed comparable levels of semantic priming. The results are discussed with reference to current models of psychopathy.

Adult↗

PubMed2006

The role of the amygdala and rostral anterior cingulate in encoding expected outcomes during learning.

Successful passive avoidance learning is thought to require the use of learned stimulus-reinforcement associations to guide decision making [Baxter, M.G., Murray, E.A., 2002. The amygdala and reward. Nature Reviews. Neuroscience 3, 563-573]. The current experiment investigated the neural correlates of successful passive avoidance learning in 19 healthy adults. Behaviorally, subjects showed a distinct pattern of performance: early indiscriminate responding to stimuli (pre-criterion performance), followed by relatively rapid learning before a plateau of successful performance (post-criterion performance). Neural responses to post-criterion correct responses were compared with neural responses to both incorrect responses and pre-criterion correct responses. Post-criterion correct responding was associated with increased activation in regions including rostral anterior cingulate, insula, caudate, hippocampal regions, and the amygdala.

Adult↗

PubMed2006

Differentiating among prefrontal substrates in psychopathy: neuropsychological test findings.

Frontal lobe and consequent executive dysfunction have long been related to psychopathy. More recently, there have been suggestions that specific regions of frontal cortex, rather than all of frontal cortex, may be implicated in psychopathy. To examine this issue, the authors presented 25 individuals with psychopathy and 30 comparison individuals with measures preferentially indexing the orbitofrontal cortex (OFC; object alternation task), dorsolateral prefrontal cortex (DLPFC; spatial alternation task), and anterior cingulate cortex (ACC; number-Stroop reading and counting tasks). The individuals with psychopathy showed significant impairment on the measure preferentially sensitive to OFC functioning. In contrast, the 2 groups did not show impairment on the measures preferentially sensitive to the functioning of the DLPFC or ACC. These results are interpreted with reference to executive dysfunction accounts of the disorder.

Antisocial Personality Disorder↗

PubMed2006

Instrumental learning and relearning in individuals with psychopathy and in patients with lesions involving the amygdala or orbitofrontal cortex.

Previous work has shown that individuals with psychopathy are impaired on some forms of associative learning, particularly stimulus-reinforcement learning (Blair et al., 2004; Newman & Kosson, 1986). Animal work suggests that the acquisition of stimulus-reinforcement associations requires the amygdala (Baxter & Murray, 2002). Individuals with psychopathy also show impoverished reversal learning (Mitchell, Colledge, Leonard, & Blair, 2002). Reversal learning is supported by the ventrolateral and orbitofrontal cortex (Rolls, 2004). In this paper we present experiments investigating stimulus-reinforcement learning and relearning in patients with lesions of the orbitofrontal cortex or amygdala, and individuals with developmental psychopathy without known trauma. The results are interpreted with reference to current neurocognitive models of stimulus-reinforcement learning, relearning, and developmental psychopathy.

Adult↗

PubMed2006

Heightened sensitivity to facial expressions of emotion in borderline personality disorder.

Individuals with borderline personality disorder (BPD) have been hypothesized to exhibit significant problems associated with emotional sensitivity. The current study examined emotional sensitivity (i.e., low threshold for recognition of emotional stimuli) in BPD by comparing 20 individuals with BPD and 20 normal controls on their accuracy in identifying emotional expressions. Results demonstrated that, as facial expressions morphed from neutral to maximum intensity, participants with BPD correctly identified facial affect at an earlier stage than did healthy controls. Participants with BPD were more sensitive than healthy controls in identifying emotional expressions in general, regardless of valence. These findings could not be explained by participants with BPD responding faster with more errors. Overall, results appear to support the contention that heightened emotional sensitivity may be a core feature of BPD.

Adult↗

PubMed2006

Divergent patterns of aggressive and neurocognitive characteristics in acquired versus developmental psychopathy.

An analogy is often drawn between patients with personality changes following orbitofrontal cortex lesions and individuals with developmental psychopathy. We present patient CL, who had acquired psychopathy following an orbitofrontal cortex lesion. Unlike previous studies, CL was assessed on a valid and reliable measure of psychopathy and was compared with controls and patients with developmental psychopathy on measures of instrumental (re)learning, extinction, emotional processing, and social cognition. The results provide further support for the notion that acquired and developmental forms of psychopathy are associated with dissociable neurocognitive deficits that leave each at different levels of risk for reactive and instrumental aggression.

Adult↗

PubMed2005

Responding to the emotions of others: dissociating forms of empathy through the study of typical and psychiatric populations.

Empathy is a lay term that is becoming increasingly viewed as a unitary function within the field of cognitive neuroscience. In this paper, a selective review of the empathy literature is provided. It is argued from this literature that empathy is not a unitary system but rather a loose collection of partially dissociable neurocognitive systems. In particular, three main divisions can be made: cognitive empathy (or Theory of Mind), motor empathy, and emotional empathy. The two main psychiatric disorders associated with empathic dysfunction are considered: autism and psychopathy. It is argued that individuals with autism show difficulties with cognitive and motor empathy but less clear difficulties with respect to emotional empathy. In contrast, individuals with psychopathy show clear difficulties with a specific form of emotional empathy but no indications of impairment with cognitive and motor empathy.

Affect↗

PubMed2005

Applying a cognitive neuroscience perspective to the disorder of psychopathy.

Four models of psychopathy (frontal lobe dysfunction, response set modulation, fear dysfunction, and violence inhibition mechanism hypotheses) are reviewed from the perspective of cognitive neuroscience. Each model is considered both with respect to the psychopathy data and, more importantly, for the present purposes, with respect to the broader cognitive neuroscience fields to which the model refers (e.g., models of attention with respect to the response set modulation account and models of emotion with respect to the fear dysfunction and violence inhibition mechanism models). The paper concludes with an articulation of the more recent integrated emotion systems model, an account inspired both by recent findings in affective cognitive neuroscience as well as in the study of psychopathy. Some directions for future work are considered.

Amygdala↗

PubMed2005

Deafness to fear in boys with psychopathic tendencies.

The processing of the emotional signals of others is fundamental for normal socialization and interaction. Reduced responsiveness to the expressions of sadness and fear has been implicated in the development of psychopathy (Blair, 1995). The current study investigates the ability of boys with psychopathic tendencies to process auditory affect information. Boys with psychopathic tendencies and a comparison group, as defined by the Antisocial Process Screening Device (APSD: Frick & Hare, 2001), were presented with neutral words spoken with intonations conveying happiness, disgust, anger, sadness and fear and were asked to identify the emotion of the speaker based on prosody. The boys with psychopathic tendencies presented with a selective impairment for the recognition of fearful vocal affect. These results are interpreted with reference to amygdala dysfunction and components of the Integrated Emotion Systems model.

Affect↗

PubMed2005

Response reversal and children with psychopathic tendencies: success is a function of salience of contingency change.

BACKGROUND: Previous work has inconsistently reported difficulties with response reversal/extinction in children with psychopathic tendencies. METHOD: We tested the hypothesis that the degree of impairment seen in children with psychopathic tendencies is a function of the salience of contingency change. We investigated the performance of children with psychopathic tendencies on a novel probabilistic response reversal task involving four conditions with gradated reward-punishment contingencies (100-0, 90-10, 80-20 and 70-30; i.e., for the 100-0 contingency, responding to one object is always rewarded while responding to the other is always punished). RESULTS: In line with predictions, the impairment seen in the children with psychopathic tendencies was an inverse function of the salience of the contingency change. CONCLUSIONS: We suggest that this data is consistent with suggestions of subtle orbital frontal cortex impairment in children with psychopathic tendencies.

Adolescent↗

PubMed2005

Deficits on a probabilistic response-reversal task in patients with pediatric bipolar disorder.

OBJECTIVE: Patients with bipolar disorder become hyperhedonic when manic and anhedonic when depressed; therefore, it is important to test whether patients with bipolar disorder show deficits on behavioral paradigms exploring reward/punishment mechanisms. METHOD: A probabilistic response-reversal task was administered to 24 bipolar children and 25 comparison subjects. RESULTS: Patients made more errors during probabilistic reversal, took longer to learn the new reward object, and were less likely to meet the learning criterion. CONCLUSIONS: Children with bipolar disorder may have a reversal learning deficit.

Adolescent↗

PubMed2004

The roles of orbital frontal cortex in the modulation of antisocial behavior.

This article considers potential roles of orbital frontal cortex in the modulation of antisocial behavior. Two forms of aggression are distinguished: reactive aggression elicited in response to frustration/threat and goal directed, instrumental aggression. It is suggested that orbital frontal cortex is directly involved in the modulation of reactive aggression. It is argued that orbital frontal cortex does not "inhibit" reactive aggression but rather may both increase or decrease its probability as a function of social cues present in the environment. Early dysfunction in this function of orbital frontal cortex may be linked to the development of Borderline Personality Disorder. Instrumental aggression is linked to a fundamental failure in moral socialization. However, the available data suggest that the amygdala, but not orbital frontal cortex, is required for functions such as aversive conditioning and passive avoidance learning that are necessary for moral socialization. Psychopathic individuals who present with significant instrumental aggression, are impaired in aversive conditioning and passive avoidance learning and show evidence of amygdala dysfunction. Orbital frontal cortex and the amygdala are involved in response reversal where instrumental responses must be reversed following contingency change. Impairments in response reversal are also seen in psychopathic individuals. However, it remains unclear whether impairment in response reversal per se is associated with antisocial behavior.

Adult↗

PubMed2003

Facial expressions, their communicatory functions and neuro-cognitive substrates.

Human emotional expressions serve a crucial communicatory role allowing the rapid transmission of valence information from one individual to another. This paper will review the literature on the neural mechanisms necessary for this communication: both the mechanisms involved in the production of emotional expressions and those involved in the interpretation of the emotional expressions of others. Finally, reference to the neuro-psychiatric disorders of autism, psychopathy and acquired sociopathy will be made. In these conditions, the appropriate processing of emotional expressions is impaired. In autism, it is argued that the basic response to emotional expressions remains intact but that there is impaired ability to represent the referent of the individual displaying the emotion. In psychopathy, the response to fearful and sad expressions is attenuated and this interferes with socialization resulting in an individual who fails to learn to avoid actions that result in harm to others. In acquired sociopathy, the response to angry expressions in particular is attenuated resulting in reduced regulation of social behaviour.

Affect↗