Facial expression processing in developmental prosopagnosia

<p>Individuals with developmental prosopagnosia experience lifelong deficits recognising facial identity, but whether their ability to process facial expression is also impaired is unclear. Addressing this issue is key for understanding the core deficit in developmental prosopagnosia, and for advancing knowledge about the mechanisms and development of normal face processing. In this thesis, I report two online studies on facial expression processing with large samples of prosopagnosics. In Study 1, I compared facial expression and facial identity perception in 124 prosopagnosics and 133 controls. I used three perceptual tasks including simultaneous matching, sequential matching, and sorting. I also measured inversion effects to examine whether prosopagnosics rely on typical face mechanisms. Prosopagnosics showed subtle deficits with facial expression, but they performed worse with facial identity. Prosopagnosics also showed reduced inversion effects for facial identity but normal inversion effects for facial expression, suggesting they use atypical mechanisms for facial identity but normal mechanisms for facial expression. In Study 2, I extended the findings of Study 1 by assessing facial expression recognition in 78 prosopagnosics and 138 controls. I used four labelling tasks that varied on whether the facial expressions were basic (e.g., happy) or complex (e.g., elated), and whether they were displayed via static (i.e., images) or dynamic (i.e., video clips) stimuli. Prosopagnosics showed subtle deficits with basic expressions but performed normally with complex expressions. Further, prosopagnosics did not show reduced inversion effects for both types of expressions, suggesting they use similar recognition mechanisms as controls. Critically, the subtle expression deficits that prosopagnosics showed in both studies can be accounted for by autism traits, suggesting that expression deficits are not a feature of prosopagnosia per se. I also provide estimates of the prevalence of deficits in facial expression perception (7.70%) and recognition (2.56% - 5.13%) in prosopagnosia, both of which suggest that facial expression processing is normal in the majority of prosopagnosics. Overall, my thesis demonstrates that facial expression processing is not impaired in developmental prosopagnosia, and suggests that facial expression and facial identity processing rely on separate mechanisms that dissociate in development.</p>

Facial expression processing in developmental prosopagnosia

<p>Individuals with developmental prosopagnosia experience lifelong deficits recognising facial identity, but whether their ability to process facial expression is also impaired is unclear. Addressing this issue is key for understanding the core deficit in developmental prosopagnosia, and for advancing knowledge about the mechanisms and development of normal face processing. In this thesis, I report two online studies on facial expression processing with large samples of prosopagnosics. In Study 1, I compared facial expression and facial identity perception in 124 prosopagnosics and 133 controls. I used three perceptual tasks including simultaneous matching, sequential matching, and sorting. I also measured inversion effects to examine whether prosopagnosics rely on typical face mechanisms. Prosopagnosics showed subtle deficits with facial expression, but they performed worse with facial identity. Prosopagnosics also showed reduced inversion effects for facial identity but normal inversion effects for facial expression, suggesting they use atypical mechanisms for facial identity but normal mechanisms for facial expression. In Study 2, I extended the findings of Study 1 by assessing facial expression recognition in 78 prosopagnosics and 138 controls. I used four labelling tasks that varied on whether the facial expressions were basic (e.g., happy) or complex (e.g., elated), and whether they were displayed via static (i.e., images) or dynamic (i.e., video clips) stimuli. Prosopagnosics showed subtle deficits with basic expressions but performed normally with complex expressions. Further, prosopagnosics did not show reduced inversion effects for both types of expressions, suggesting they use similar recognition mechanisms as controls. Critically, the subtle expression deficits that prosopagnosics showed in both studies can be accounted for by autism traits, suggesting that expression deficits are not a feature of prosopagnosia per se. I also provide estimates of the prevalence of deficits in facial expression perception (7.70%) and recognition (2.56% - 5.13%) in prosopagnosia, both of which suggest that facial expression processing is normal in the majority of prosopagnosics. Overall, my thesis demonstrates that facial expression processing is not impaired in developmental prosopagnosia, and suggests that facial expression and facial identity processing rely on separate mechanisms that dissociate in development.</p>

Common Misconceptions about the Phonological Deficit Theory of Dyslexia

In this discussion paper, I review a number of common misconceptions about the phonological deficit theory (PDH) of dyslexia. These include the common but mistaken idea that the PDH is simply about phonemic awareness (PA), and, consequently, is a circular “pseudo”-explanation or epiphenomenon of reading difficulties. I argue that PA is only the “tip of the phonological iceberg” and that “deeper” spoken-language phonological impairments among dyslexics appear well before the onset of reading and even at birth. Furthermore, not even reading-specific expressions of phonological deficits—PA or pseudoword naming, can be considered circular if we clearly distinguish between reading proper—real meaning-bearing words, or real text, and the mechanisms (subskills) of reading development (such as phonological recoding). I also explain why an understanding of what constitutes an efficient writing system explains why phonology is necessarily a major source of variability in reading ability and hence a core deficit (or at least one core deficit) among struggling readers whether dyslexic or non-dyslexic. I also address the misguided notion that the PDH has now fallen out of favor because most dyslexia researchers have (largely) ceased studying phonological processing. I emphasize that acceptance of the PDH does not imply repudiation of other non-phonological hypotheses because the PDH does not claim to account for all the variance in reading ability/disability. Finally, I ask where neurobiology enters the picture and suggest that researchers need to exercise more caution in drawing their conclusions.

EXPLORING THE IMPLEMENTATION OF AN INTERVENTION FOR A PUPIL WITH MATHEMATICAL LEARNING DIFFICULTIES: A CASE STUDY

This study presents a single case study of how a remedial mathematics teacher incorporated an instructional intervention into her teaching practices in order to teach counting to a pupil with mathematical learning difficulties. This new theory-driven intervention was developed by the authors of this study. Dyscalculia is a term which refers to a wide range of mathematical learning difficulties or disabilities. Dyscalculic pupils have a specific mathematics learning disorder with a core deficit in representing and processing of numerosity. They might not be able to recognise numerical quantities, performing counting and so on. Early supports such as interventions have a great potential in helping dyscalculic pupils to improve mathematical skills. However, there remains a lack of appropriate instructional scaffolds to help dyscalculic pupils to organise their learning structures by addressing both cognitive deficits and mathematical skills. The present study involves a primary school remedial teacher, Daisy, and an at-risk dyscalculic pupil, David, both pseudonyms. Data were collected through interviews, lesson observations, and reflective journals. The findings revealed that the proposed intervention improved the counting ability of the pupil.

Dynamic face processing impairments are associated with cognitive and positive psychotic symptoms across psychiatric disorders

Impairments in social cognition—including recognition of facial expressions—are increasingly recognised as a core deficit in schizophrenia. It remains unclear whether other aspects of face processing (such as identity recognition) are also impaired, and whether such deficits can be attributed to more general cognitive difficulties. Moreover, while the majority of past studies have used picture-based tasks to assess face recognition, literature suggests that video-based tasks elicit different neural activations and have greater ecological validity. This study aimed to characterise face processing using video-based stimuli in psychiatric inpatients with and without psychosis. Symptom correlates of face processing impairments were also examined. Eighty-six psychiatric inpatients and twenty healthy controls completed a series of tasks using video-based stimuli. These included two emotion recognition tasks, two non-emotional facial identity recognition tasks, and a non-face control task. Symptoms were assessed using the Positive and Negative Syndrome Scale. Schizophrenia and bipolar disorder groups were significantly impaired on the emotion-processing tasks and the non-face task compared to healthy controls and patients without psychosis. Patients with other forms of psychosis performed intermediately. Groups did not differ in non-emotional face processing. Positive symptoms of psychosis correlated directly with both emotion-processing performance and non-face discrimination across patients. We found that identity processing performance was inversely associated with cognition-related symptoms only. Findings suggest that deficits in emotion-processing reflect symptom pathology independent of diagnosis. Emotion-processing deficits in schizophrenia may be better accounted for by task-relevant factors—such as attention—that are not specific to emotion processing.

A network approach to dyslexia: Mapping the reading network

Research on the etiology of dyslexia typically uses an approach based on a single core deficit, failing to understand how variations in combinations of factors contribute to reading development and how this combination relates to intervention outcome. To fill this gap, this study explored links between 28 cognitive, environmental, and demographic variables related to dyslexia by employing a network analysis using a large clinical database of 1,257 elementary school children. We found two highly connected subparts in the network: one comprising reading fluency and accuracy measures, and one comprising intelligence-related measures. Interestingly, phoneme awareness was functionally related to the controlled and accurate processing of letter–speech sound mappings, whereas rapid automatized naming was more functionally related to the automated convergence of visual and speech information. We found evidence for the contribution of a variety of factors to (a)typical reading development, though associated with different aspects of the reading process. As such, our results contradict prevailing claims that dyslexia is caused by a single core deficit. This study shows how the network approach to psychopathology can be used to study complex interactions within the reading network and discusses future directions for more personalized interventions.

Nonsymbolic-Magnitude Deficit in Adults With Developmental Dyscalculia: Evidence of Impaired Size Discrimination but Intact Size Constancy

Although researchers have debated whether a core deficit of nonsymbolic representation of magnitude underlies developmental dyscalculia (DD), research has mostly focused on numerosity processing. We probed the possibility of a general magnitude deficit in individuals with DD and asked whether sensitivity to size varied in contexts of depth ordering and size constancy. We measured full psychometric functions in size-discrimination tasks in 12 participants with DD and 13 control participants. Results showed that although people with DD exhibited veridical perceived magnitude, their sensitivity to size was clearly impaired. In contrast, when objects were embedded in depth cues allowing size-constancy computations, participants with DD demonstrated typical sensitivity to size. These results demonstrate a deficit in the perceptual resolutions of magnitude in DD. At the same time, the finding of an intact size constancy suggests that when magnitude perception is facilitated by implicit mandatory computations of size constancy, this deficit is no longer evident.

Children With Dyscalculia Show Hippocampal Hyperactivity During Symbolic Number Perception

Dyscalculia is a learning disability affecting the acquisition of arithmetical skills in children with normal intelligence and age-appropriate education. Two hypotheses attempt to explain the main cause of dyscalculia. The first hypothesis suggests that a problem with the core mechanisms of perceiving (non-symbolic) quantities is the cause of dyscalculia (core deficit hypothesis), while the alternative hypothesis suggests that dyscalculics have problems only with the processing of numerical symbols (access deficit hypothesis). In the present study, the symbolic and non-symbolic numerosity processing of typically developing children and children with dyscalculia were examined with functional magnetic resonance imaging (fMRI). Control (n = 15, mean age: 11.26) and dyscalculia (n = 12, mean age: 11.25) groups were determined using a wide-scale screening process. Participants performed a quantity comparison paradigm in the fMRI with two number conditions (dot and symbol comparison) and two difficulty levels (0.5 and 0.7 ratio). The results showed that the bilateral intraparietal sulcus (IPS), left dorsolateral prefrontal cortex (DLPFC) and left fusiform gyrus (so-called “number form area”) were activated for number perception as well as bilateral occipital and supplementary motor areas. The task difficulty engaged bilateral insular cortex, anterior cingulate cortex, IPS, and DLPFC activation. The dyscalculia group showed more activation in the left orbitofrontal cortex, left medial prefrontal cortex, and right anterior cingulate cortex than the control group. The dyscalculia group showed left hippocampus activation specifically for the symbolic condition. Increased left hippocampal and left-lateralized frontal network activation suggest increased executive and memory-based compensation mechanisms during symbolic processing for dyscalculics. Overall, our findings support the access deficit hypothesis as a neural basis for dyscalculia.

Quantfying the disorganization and the core deficit in classical schizophrenia

AimsTo derive scores for mental disorganization and impoverishment from commonly used rating scales, and test the hypothesis that disorganization and impoverishment, along with impaired cognition and role-function reflect a latent variable that is a plausible candidate for the putative core deficit.BackgroundFor more than 100 years, disorganization and impoverishment of mental activity have been recognised as fundamental symptoms of schizophrenia. These symptoms may reflect a core brain process underlying persisting disability. Delusions and hallucinations have been regarded as accessory features. The psychopathological processes predisposing to persisting disability in schizophrenia are poorly understood. The delineation of a core deficit underlying persisting disability would be potentially of great value in predicting outcome and developing improved treatment.MethodPatients aged 18–55 years were included if: they satisfied DSM IV criteria for schizophrenia or schizoaffective disorder. Healthy controls were recruited by public advertisement and selected to match the patient group in age and sex. Study sample included 39 participants with schizophrenia, 1 with schizoaffective disorder and 44 matched healthy controls. We derived disorganization and impoverishment scores from three symptom scales: PANSS, SSPI and CASH. We computed composite scores for disorganization and for impoverishment and employed Confirmatory Factor Analysis to test the hypothesis that a single factor accounts for the relationships between disorganization, impoverishment, cognitive impairment and impaired role function. We assessed the relationship between this latent “core deficit” and diminished Post Movement Beta Rebound (PMBR), an electrophysiological measure from Magnetoencephalography (MEG), associated with persisting brain disorders.ResultFit indices for the single factor model from CFA indicated a good fit: χ2(2) = 1.817, p = .403; RMSEA <.001 GFI = .979. PMBR was significantly reduced in the schizophrenia group compared to healthy controls, t (68) = 3.55, p < .001. Within the patient group, PMBR was significantly and negatively correlated with the CFA factor scores representing the Core Deficit score, r=−.543, p < .01, indicating that high core deficit scores were associated with reduced PMBR. PMBR was significantly correlated with the composite Disorganization score, r=−.521, p < .001.ConclusionOur findings demonstrate that the shared variance between impoverishment (psychomotor poverty); disorganization; cognitive impairment; and impaired role function can be accounted for by a latent variable that can reasonably be described as the core deficit of classical schizophrenia. The demonstration that the severity of the putative core deficit is correlated with the reduction in PMBR provides evidence that the core deficit is associated with an identifiable abnormality of brain dysfunction.

Emotion regulation difficulties in anorexia nervosa: associations with improvements in eating psychopathology

Background Difficulties with emotion regulation have been established as a core deficit in anorexia nervosa (AN). However, limited research has evaluated whether weight gain is associated with improvements in emotion regulation difficulties in AN and whether improvements in emotion regulation are associated with reductions in eating disorder psychopathology. The aims of this study were threefold: 1) to examine the nature and extent of emotion regulation difficulties in AN; 2) to determine whether these difficulties improved during intensive treatment for the eating disorder; and 3) to study whether improvements in emotion regulation were associated with improvements in eating disorder psychopathology. Method The participants were 108 patients who met DSM-IV-TR criteria for AN and were admitted to a specialized intensive treatment program. Self-report measures of eating disorder symptoms and difficulties with emotion regulation were administered at admission to and discharge from the program. Results Patients with the binge-purge subtype of AN reported greater difficulties with impulse control when upset and more limited access to emotion regulation strategies when experiencing negative emotions than those with the restricting subtype. Among those who completed treatment and became weight restored, improvements in emotion regulation difficulties were observed. Greater pre-to-post treatment improvements in emotional clarity and engagement in goal directed behaviours when upset were associated with greater reductions in eating disorder psychopathology during treatment. Conclusions These findings add to growing evidence suggesting that eating disorder symptoms may be related to emotion regulation difficulties in AN and that integrating strategies to address emotion regulation deficits may be important to improving treatment outcome in AN.