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Biomedical subjects

Chris Frith

Publications and source records attributed to Chris Frith.

At least 19 recordsLinked to original sources
PubMed2006

Attention does not modulate neural responses to social stimuli in autism spectrum disorders.

We investigated whether individuals with autism spectrum disorders (ASD) would show attentional modulation for social (face) and non-social (house) stimuli. Sixteen individuals with ASD and 16 matched control participants completed a task in which pairs of face and house stimuli were present on every trial, with one of the pairs randomly assigned to attended locations and the other to unattended locations. Both mass-univariate (SPM) and region of interest analyses suggested that responses to houses were modulated by attention in both groups, but that only the control participants demonstrated attentional modulation of face-selective regions. Thus, the participants with ASD demonstrated a lack of attentional modulation which was particularly evident for the social stimulus. Analyses of effective connectivity indicated that these results were due to a failure of attention to modulate connectivity between extrastriate areas and V1. We discuss how these results may suggest a mechanism to explain the reduced salience of social stimuli in ASD.

Adult↗
PubMed2005

Theory of mind.

Explore the source record for details and available documents.

Brain↗
PubMed2005

The self in action: lessons from delusions of control.

Patients with delusions of control are abnormally aware of the sensory consequences of their actions and have difficulty with on-line corrections of movement. As a result they do not feel in control of their movements. At the same time they are strongly aware of the action being intentional. This leads them to believe that their actions are being controlled by an external agent. In contrast, the normal mark of the self in action is that we have very little experience of it. Most of the time we are not aware of the sensory consequences of our actions or of the various subtle corrections that we make during the course of goal-directed actions. We know that we are agents and that we are successfully causing the world to change. But as actors we move through the world like shadows glimpsed only occasional from the corner of an eye.

Awareness↗
PubMed2005

Two distinct neural effects of blinking on human visual processing.

Humans blink every few seconds, yet the changes in retinal illumination during a blink are rarely noticed, perhaps because visual sensitivity is suppressed. Furthermore, despite the loss of visual input, visual experience remains continuous across blinks. The neural mechanisms in humans underlying these two phenomena of blink suppression and visual continuity are unknown. We investigated the neural basis of these two complementary behavioural effects using functional magnetic resonance imaging to measure how voluntary blinking affected cortical responses to visual stimulation. Two factors were independently manipulated in a blocked design; the presence/absence of voluntary blinking, and the presence/absence of visual stimulation. To control for the simple loss of visual input caused by eyelid closure, we created a fifth condition where external darkenings were dynamically matched to each subjects' own blinks. Areas of lateral occipital cortex, including area V5/MT, showed suppression of responses to visual stimulation during blinking, consistent with the known loss in visual sensitivity. In contrast, a medial parieto-occipital region, homologous to macaque area V6A, showed responses to blinks that increased when visual stimulation was present. Our data are consistent with a role for this region in the active maintenance of visual continuity across blinks. Moreover, both suppression in lateral occipital and activation in medial parieto-occipital cortex were greater during blinks than during matched external darkenings of the visual scene, suggesting that they result from an extra-retinal signal associated with the blink motor command. Our findings therefore suggest two distinct neural correlates of blinking on human visual processing.

Adolescent↗
PubMed2005

Association of symptoms and executive function in schizophrenia and bipolar disorder.

The extent to which cognitive impairment in psychosis is related to the particular disorder or the pattern of symptoms is unclear. We examined executive function in two groups of schizophrenia patients with predominant symptoms of disorganisation (n=15) and psychomotor poverty (n=15), respectively, two groups of bipolar I disorder patients with predominant symptoms of mania (n=15) and depression (n=15), respectively, and 30 healthy controls. We predicted that the pattern of symptoms ('excess' [disorganisation/mania] or 'deficiency' [negative symptoms/depression]) would be more related to executive ability than the underlying disorder. The patient groups showed partially overlapping executive dysfunctions relative to the control group. There were no significant differences between groups with 'excess' symptoms (schizophrenia patients with thought disorder and bipolar patients with mania), or between groups with 'deficiency' symptoms (schizophrenia patients with negative symptoms and bipolar patients with depression). In contrast, differences were noted between groups with the same diagnosis: Schizophrenia patients with disorganisation were less accurate in semantic verbal fluency than those with negative symptoms; and bipolar patients with mania tended to be faster, but less accurate, in sentence completion than those with depression. A statistical comparison of the associations of 'diagnosis' and the 'excess-deficiency' dimension with executive function revealed a trend for a greater association of the latter with two measures of performance accuracy. Executive dysfunction in patients with psychotic disorders may be more related to their symptom profile than their diagnosis.

Adolescent↗
PubMed2005

The role of motor contagion in the prediction of action.

It has been proposed that actions are intrinsically linked to perception. The idea behind these theories is that observing, imagining or in any way representing an action excites the motor programs used to execute that same action. There is neurophysiological evidence that neurons in premotor cortex of monkeys respond both during movement execution and during the observation of goal-directed action ('mirror neurons'). In humans, a proportion of the brain regions involved in executing actions are activated by the mere observation of action (the 'mirror system'). In this paper, we briefly review recent empirical studies of the mirror system, and discuss studies demonstrating interference effects between observed and executed movements. This interference, which might be a form of 'motor contagion', seems to arise specifically from the observation of biological movements, whether or not these movements are goal-directed. We suggest that this crude motor contagion is the first step in a more sophisticated predictive system that allows us to infer goals from the observation of actions.

Humans↗
PubMed2005

The neural basis of hallucinations and delusions.

Schizophrenia is a biologically based disorder characterised by false perceptions (hallucinations) and false beliefs (delusions). The underlying physiological cause of these mental abnormalities remains unknown. There is increasing evidence that one class of symptom, the 'made experiences' including delusions of alien control and thought insertion, is associated with abnormalities in the mechanism that predicts the outcome of intended actions (the forward model). For these patients active movements feel like passive movements. As a result these patients do not feel in control of their actions. However, comparison with various neurological disorders, such as those associated with parietal lobe lesions, suggest that this abnormal experience is not sufficient to explain the feeling that some other agent is controlling is one's actions. Preliminary evidence suggests that patients with schizophrenia have an exaggerated sense of agency. In combination with the feeling of not being in control, this exaggerated sense of agency could explain delusions of alien control in which the patient attributes his own actions to another agent. Little is yet know about the neural basis of the predictive mechanisms that create the feeling that we are in control of our movements. Such prediction requires integration of information about intended movements generated in frontal cortex with sensory processing in posterior regions of the brain. Measures of functional connectivity suggest that long-range interactions between frontal and posterior regions are abnormally reduced in patients with schizophrenia. Further research is needed to explore the precise involvement of long-range connections in the mechanisms of forward modelling.

Animals↗
PubMed2004

Brain mechanisms for inferring deceit in the actions of others.

During social interactions, it is important to judge accurately whether a person is honest or deceitful. We often use nonverbal cues to infer whether others are trying to deceive us. Using functional magnetic resonance imaging, we studied subjects watching videos of actors lifting a box and judged whether or not the actors were trying to deceive them concerning the real weight of the box. When the subjects judged the actions as reflecting deceptive intention, there was activation of the amygdala and rostral anterior cingulate cortex. These areas were not activated when subjects made judgements about the beliefs rather than the intentions of others. We suggest that these activations reflect the observers' judgements of social intentions toward themselves and might reflect an emotional response to being deceived.

Adult↗
PubMed2004

What's at the top in the top-down control of action? Script-sharing and 'top-top' control of action in cognitive experiments.

The distinction between bottom-up and top-down control of action has been central in cognitive psychology, and, subsequently, in functional neuroimaging. While the model has proven successful in describing central mechanisms in cognitive experiments, it has serious shortcomings in explaining how top-down control is established. In particular, questions as to what is at the top in top-down control lead us to a controlling homunculus located in a mythical brain region with outputs and no inputs. Based on a discussion of recent brain imaging experiments, we argue for the need to factor the interaction between the experimenter and the experimental participant into a realistic understanding of top-down control. We suggest these interactions involve a 'sharing of scripts' for perception and action that may be described as 'top-top processes.' We thereby expand the understanding of the homunculus to include elements of social cognition. This conceptual reconfiguration may grant some sort of asylum for a--not very omnipotent--homunculus.

Animals↗
PubMed2004

Comprehension, encoding, and monitoring in the production of confabulation in memory: a study with schizophrenic patients.

INTRODUCTION: The aim of the present study was to test the hypotheses proposed by Nathaniel-James and collaborators (Nathaniel-James & Frith, 1996; Nathaniel-James, Foong, & Frith, 1996) to account for the cognitive deficits involved in the production of confabulations in schizophrenic patients: impairments in comprehension, memory encoding, and memory monitoring. METHOD: Five patients were investigated in this multiple single-case study. Comprehension abilities were investigated in several tests in which a memory bias was avoided. The encoding deficit hypothesis was tested by manipulating cues at encoding and/or retrieval. "Memory monitoring" abilities were examined in two tasks: the Hayling test for all patients and an AB-AC word pairs learning task for two patients. RESULTS: Four of the patients produced an abnormal level of confabulations in story and fable learning tests. All patients exhibited encoding deficits and specific comprehension difficulties. However, some demonstrated preserved memory monitoring abilities. Across different tests, it was observed that the more the confabulations occurred, the more severe were the comprehension difficulties. CONCLUSION: The results are in favour of the hypothesis that verbal comprehension difficulties lead to the production of confabulation. They are inconsistent with the idea that memory monitoring impairment is necessarily involved.

Journal Article↗
PubMed2004

Neural correlates of attentional capture in visual search.

Much behavioral research has shown that the presence of a unique singleton distractor during a task of visual search will typically capture attention and thus disrupt target search. Here we examined the neural correlates of such attentional capture using functional magnetic resonance imaging in human subjects during performance of a visual search task. The presence (vs. absence) of a salient yet irrelevant color singleton distractor was associated with activity in the superior parietal cortex and frontal cortex. These findings imply that the singleton distractor induced spatial shifts of attention despite its irrelevance, as predicted from an AC account. Moreover, behavioral interference by singleton distractors was strongly and negatively correlated with frontal activity. These findings provide direct evidence that the frontal cortex is involved in control of interference from irrelevant but attention-capturing distractors.

Adult↗
PubMed2003

Self-awareness and action.

In this review we discuss how we are aware that actions are self-generated. We review behavioural data that suggest that a prediction of the sensory consequences of movement might be used to label actions and their consequences as self-generated. We also describe recent functional neuroimaging experiments and studies of neurological and psychiatric patients, which suggest that the parietal cortex plays a crucial role in the awareness of action.

Awareness↗
PubMed2003

What do imaging studies tell us about the neural basis of autism?

There is no clear evidence from imaging studies for specific structural abnormalities in the brains of people with autism. The most robust observation is of greater total brain volume. There is evidence that this greater volume is not present at birth, but appears during the first few years. This brain enlargement might be a marker of abnormal connectivity due to lack of pruning. While abnormalities have often been reported in the cerebellum and the amygdala, these are difficult to interpret since both increases and decreases in the size of these structures have been observed. Another way of identifying the neural basis of autism is to investigate brain systems underlying cognitive functions compromised in this disorder such as face perception and 'theory of mind'. Autistic people fail to activate the 'fusiform face area' during face perception tasks and show weak activation of medial frontal cortex and superior temporal gyrus when performing theory of mind tasks. These problems stem from a lack of integration of sensory processing with cognitive evaluation. I speculate that this problem reflects a failure of top-down modulation of early sensory processing. The problem could result from abnormal connectivity and lack of pruning.

Adolescent↗