Monica Dhar

Cascade of Neural Events Leading from Error Commission to Subsequent Awareness Revealed Using EEG Source Imaging

The goal of the present study was to shed light on the respective contributions of three important action monitoring brain regions (i.e. cingulate cortex, insula, and orbitofrontal cortex) during the conscious detection of response errors. To this end, fourteen healthy adults performed a speeded Go/Nogo task comprising Nogo trials of varying levels of difficulty, designed to elicit aware and unaware errors. Error awareness was indicated by participants with a second key press after the target key press. Meanwhile, electromyogram (EMG) from the response hand was recorded in addition to high-density scalp electroencephalogram (EEG). In the EMG-locked grand averages, aware errors clearly elicited an error-related negativity (ERN) reflecting error detection, and a later error positivity (Pe) reflecting conscious error awareness. However, no Pe was recorded after unaware errors or hits. These results are in line with previous studies suggesting that error awareness is associated with generation of the Pe. Source localisation results confirmed that the posterior cingulate motor area was the main generator of the ERN. However, inverse solution results also point to the involvement of the left posterior insula during the time interval of the Pe, and hence error awareness. Moreover, consecutive to this insular activity, the right orbitofrontal cortex (OFC) was activated in response to aware and unaware errors but not in response to hits, consistent with the implication of this area in the evaluation of the value of an error. These results reveal a precise sequence of activations in these three non-overlapping brain regions following error commission, enabling a progressive differentiation between aware and unaware errors as a function of time elapsed, thanks to the involvement first of interoceptive or proprioceptive processes (left insula), later leading to the detection of a breach in the prepotent response mode (right OFC).

Information Processing Differences and Similarities in Adults with Dyslexia and Adults with Attention Deficit Hyperactivity Disorder during a Continuous Performance Test: A Study of Cortical Potentials.

Twenty male adults with ADHD, 16 dyslexic adults, 15 comorbid adults, and 16 normal controls were compared on performance and underlying brain responses, during a cued Continuous Performance Test (O-X CPT), with the aim of discovering features of information processing differentiating between the groups. The study evaluated both cue- and target-related processes by analysing performance measures (errors, reaction time, and variability of reaction time), and event-related potentials (ERPs). Cue-related ERP components included the Cue-N2, Cue-P3, contingent negative variation (CNV) consisting of the CNV1, related to cue orienting, and the CNV2, related to response preparation. For targets, a distinction was made between response-related (Go), and inhibitory (Nogo) processing. Target-related components included the Go-P3, Nogo-N2, and Nogo-P3. Performance deficits were found only for the ADHD group, who demonstrated a faster decline in response speed with time-on-task and greater overall within-subject variability. No group differences were found for cue-related ERP components. Yet, controlling for group differences in internalising problems, inhibitory control was reduced in all clinical groups compared to controls, as demonstrated by an absence of frontal amplification of P3 in the Nogo condition, relative to the Go condition. For the ADHD group, in contrast to the comorbid and the dyslexic group, this effect remained after controlling for externalising symptoms, indicating that only for the ADHD group deficiencies in inhibitory control were not explained by externalising behaviour.

Early error detection is generic, but subsequent adaption to errors is not: evidence from ERPs

The aim of the present study was to investigate whether error detection and subsequent regulatory processes could be influenced by pre-familiarisation with task-relevant stimulus features. To this end, 19 healthy adults performed a speeded Go/NoGo task with compound targets, involving two concurrent stimulus attributes, which were either pre-familiarised or not, while high-density EEG was recorded. During the speeded Go/NoGo task, response errors clearly elicited an error-related negativity (ERN) and error positivity (Pe), but these error-related components were not modulated by familiarisation. By comparison, post-error adaptive processes were found to depend on familiarisation, as distinct topographic ERP effects were evidenced for familiarised vs. non-familiarised stimuli. Moreover, post-error slowing was abolished in the condition comprising familiarised attributes. These results suggest that pre-familiarisation with a stimulus property leaves unaffected error detection mechanisms, while altering subsequent adaptive processes. Whereas error detection mechanisms may be generic, the automatic adaptive processes consecutive to error detection may be malleable, and influenced by pre-familiarisation of stimulus features.

Integration of Face and Voice During Emotion Perception: Is There Anything Gained for the Perceptual System Beyond Stimulus Modality Redundancy?

In this chapter, we review empirical data and theoretical models which have been put forward in the affective science literature to account for the perception of emotions, when this process is simultaneously accomplished by sight and hearing. The visual component is provided by the face configuration that undergoes some geometric changes, which in turn lead to different and discrete emotion facial expressions. The auditory component is provided by the voice and its changes in pitch, duration, and/or intensity leading to different affective tones of voice. Face–voice integration during emotion perception occurs when affective information conveyed by the two sensory modalities is integrated into a unified percept, or multisensory object. Although one may assume that the rapid and mandatory combination of multiple or complementary affective cues is adaptive (i.e., it likely reduces the effects of adverse factors like drifts or intrinsic noise), the central nervous system must however show some selectivity regarding which inputs from separate senses may eventually combine, as compared with merely redundant emotion signals. Indeed, not all spatial or temporal coincidences or co-occurrences lead to the perception of unified objects. Interestingly, results of behavioral studies confirm this conjecture, and indicate that the combination of emotional facial expressions with affective prosody leads to the creation of genuinely multisensory emotional objects, which show different properties compared to the combination of an emotional facial expression with another redundant or distracting emotional facial expression, or an emotion written word. Hence, the findings and models reviewed in this chapter suggest that some selectivity can be found in the way visual and auditory information is actually combined during emotion perception. The rapid and automatic pairing of an emotional face with an affective voice might present a naturalistic situation in the sense that there is no need for mediation by higher-level cognitive, attentional or linguistic processes, which may be necessary for the efficient decoding of other stimulus categories or multisensory objects.

Of rats and men: A reply to Skottun

In a letter to Cortex, Skottun (2010, this issue) commented on the use of an animal model that was referred to in our paper (Dhar et al., 2010, this issue) to generate a hypothesis on how the neural development in dyslexia may lead to deficits in visual processing. Here we present a response to this letter. Animal models are taken very seriously in the field of medicine and a point was intended to be made by including a rat modelof dyslexia. Toclarify this point, two findings inparticular appear to have lead to the use of a rodent model to study dyslexia. First, there was the finding that language impaired individuals show deviances in rapid auditory processing (Tallal, 1980). The second was the discovery of minute malformations in autopsied brains in dyslexics (Galaburda et al., 1985; Humphreys et al., 1990). The authors hypothesised that the two findings may be related and that there may even be a causal connection. To investigate this, they made focal cortical lesions in rodent brains and found that these lesions ultimately led to subcortical damage. Moreover, it was found that lesions in rats were related to reduced ability to discriminate rapid auditory stimuli, parallel to the auditory processing deficits observed in dyslexics (Clark et al., 2000; Fitch et al., 1994). The model therefore suggested a developmental trajectory for impaired magnocellular auditory processing in dyslexia. It was hypothesised that through structural abnormalities in early development, possibly mediated by testosterone levels, changes may occur in connectivity and in thalamic nuclei. Analogously, and due to the fact that deficits in visual processing have been found in dyslexics (Dhar et al., 2008; Eden et al., 1996; Facoetti et al., 2006; Livingstone et al., 1991; Lovegrove, 1996; Stein and Walsh, 1997), it was considered that deficient visual magnocellular processing may arise from a similar mechanism in humans, namely aberrant early development of magnocellular pathways. The fact that in dyslexics abnormalities in magnocellular layers of lateral geniculate nuclei (LGN) were found (Livingstone et al., 1991) supports this notion. Although our paper may have erroneously suggested that in rats malformations were found in the magnocellular layers of not only the medial geniculate nuclei (MGN) involved in transient auditory perception but also in the magnocellular layers of the LGN, involved in transient visual perception, we do not think that the absence of a magnocellular visual system in rats can be taken as evidence against a magnocellular theory of dyslexia. Herman et al. (1997) studied the MGN and LGN in rats that had received cortical injuries and found thalamic abnormalities in LGN (reduced cell number and volume of LGN) that were distinct from those seen in MGN (cell distribution and mean cell size). However, the LGN in rats, which is somewhat homogenous, cannot be compared to LGN in primates, so the problem with our paper might be the use of the phrase ‘magnocellular visual system’ in relation to rats. We hypothesise that if cortical malformations could affect MGN in rats, leading to the deficient processing of specifically rapid auditory stimuli, it is possible that a similar mechanism would apply to dyslexic individuals in whom visual processing deficits occur. Moreover, evidence showing deficits in rapid sensory processing both in the visual and auditory domain in dyslexics is simply too abundant to dismiss (e.g., Farmer and Klein, 1995; Habib, 2000; Hari and Renvall, 2001).

Medical Art Therapy of the Future: Building an Interactive Virtual Underwater World in a Children’s Hospital

We are developing an interactive virtual underwater world with the aim to reduce stress and boredom in hospitalised children, to improve their quality of life, by employing an evidence-based design process and by using techniques from Artificial Life and Human-Computer Interaction. A 3D motion sensing camera tracks the activity of children in front of a wall projection. As they wave their hands, colorful sea creatures paddle closer to say hi and interact with the children.

Atypical neural responding to hearing one’s own name in adults with ASD.

Diminished responding to hearing one’s own name is one of the earliest and strongest predictors of autism spectrum disorder (ASD). Here, we studied, for the first time, the neural correlates of hearing one’s own name in ASD. Based on existing research, we hypothesized enhancement of late parietal positive activity specifically for the own name in neurotypicals, and for this effect to be reduced in adults with ASD. Source localization analyses were conducted to estimate group differences in brain regions underlying this effect. Twenty-one adults with ASD, and 21 age- and gender-matched neurotypicals were presented with 3 categories of names (own name, close other, unknown other) as task-irrelevant deviant stimuli in an auditory oddball paradigm while electroencephalogram was recorded. As expected, late parietal positivity was observed specifically for own names in neurotypicals, indicating enhanced attention to the own name. This preferential effect was absent in the ASD group. This group difference was associated with diminished activation in the right temporoparietal junction (rTPJ) in adults with ASD. Further, a familiarity effect was found for N1 amplitude, with larger amplitudes for familiar names (own name and close other). However, groups did not differ for this effect. These findings provide evidence of atypical neural responding to hearing one’s own name in adults with ASD, suggesting a deficit in self–other distinction associated with rTPJ dysfunction.