Assessing the agency of potential actors in the visual world is a critically important aspect of social cognition. Adult observers are generally capable of distinguishing real faces from artificial faces (even allowing for recent advances in graphics technology and motion capture); even small deviations from real facial appearance can lead to profound effects on face recognition. Presently, we examined how early components ofvisual event-related potentials (ERPs) are affected by the “life” in human faces and animal faces. We presented participants with real and artificial faces of humans and dogs, and analyzed the response properties of the P100 and the N170 as a function of stimulus appearance and task (species categorization vs. animacy categorization). The P100 exhibited sensitivity to face species and animacy. We found that the N170's differential responses to human faces vs. dog faces depended on the task participants’ performed. Also, the effect of species was only evident for real faces of humans and dogs, failing to obtain with artificial faces. These results suggest that face animacy does modulate early components of visual ERPs – the N170 is not merely a crude face detector, but reflects the tuning of the visual system to natural face appearance.
Face perception; event-related potentials; social cognition
It is widely suggested that ASD is characterized by atypical local/global processing, but the published findings are contradictory. In an effort to resolve this question, we tested a large group of children on both a free-choice task and an instructed task using hierarchical local-global stimuli. We find that although children with autism showed a reduced preference to report global properties of a stimulus when given a choice, their ability to process global properties when instructed to do so is unimpaired. These findings support prior claims that people with ASD show a disinclination, not a disability, in global processing, and highlight the broader question of whether other characteristics of autism may also reflect disinclinations rather than disabilities.
Autism Spectrum Disorder; Global/Local Processing; Global Attention; Cognitive Development
Difficulties in visual attention are often implicated in autism spectrum disorders (ASD) but it remains unclear which aspects of attention are affected. Here, we used a multiple object tracking (MOT) task to quantitatively characterize dynamic attentional function in children with ASD aged 5–12. While the ASD group performed significantly worse overall, the group difference did not increase with increased object speed. This finding suggests that decreased MOT performance is not due to deficits in dynamic attention but instead to a diminished capacity to select and maintain attention on multiple targets. Further, MOT performance improved from 5–10 years in both typical and ASD groups with similar developmental trajectories. These results argue against a specific deficit in dynamic attention in ASD.
Autism Spectrum Disorder; Multiple Object Tracking; Dynamic Attention; Spatial Attention; Cognitive Development
Premutation fragile X carriers have a CGG repeat expansion (55 to 200 repeats) in the promoter region of the fragile X mental retardation 1 (FMR1) gene. Amygdala dysfunction has been observed in premutation symptomatology, and recent research has suggested the amygdala as an area susceptible to the molecular effects of the premutation. The current study utilizes structural magnetic resonance imaging (MRI) to examine the relationship between amygdala volume, CGG expansion size, FMR1 mRNA, and psychological symptoms in male premutation carriers without FXTAS compared with age and IQ matched controls. No significant between group differences in amygdala volume were found. However, a significant negative correlation between amygdala volume and CGG was found in the lower range of CGG repeat expansions, but not in the higher range of CGG repeat expansions.
Fragile X premutation; Amygdala; FMR1; mRNA; Structural MRI
Despite several Findings of perceptual asynchronies between object features, it remains unclear whether independent neuronal populations necessarily code these perceptually unbound properties. To examine this, we investigated the binding between an object’s spatial frequency and its rotational motion using contingent motion aftereffects (MAE). Subjects adapted to an oscillating grating whose direction of rotation was paired with a high or low spatial frequency pattern. In separate adaptation conditions, we varied the moment when the spatial frequency change occurred relative to the direction reversal. After adapting to one stimulus, subjects made judgments of either the perceived MAE (rotational movement) or the position shift (instantaneous phase rotation) that accompanied the MAE. To null the spatial frequency-contingent MAE, motion reversals had to physically lag changes in spatial frequency during adaptation. To null the position shift that accompanied the MAE, however, no temporal lag between the attributes was required. This demonstrates that perceived motion and position can be perceptually misbound. Indeed, in certain conditions, subjects perceived the test pattern to drift in one direction while its position appeared shifted in the opposite direction. The dissociation between perceived motion and position of the same test pattern, following identical adaptation, demonstrates that distinguishable neural populations code for these object properties.
Vision; Perception; Motion; Color-motion asynchrony; Binding; Spatial frequency; Texture; Contingent aftereffect; Motion aftereffect; MAE; Localization; Differential latency
Recent evidence suggests those with autism may be generally impaired in visual motion perception. To examine this, we investigated both coherent and biological motion processing in adolescents with autism employing both psychophysical and fMRI methods. Those with autism performed as well as matched controls during coherent motion perception but had significantly higher thresholds for biological motion perception. The autism group showed reduced posterior Superior Temporal Sulcus (pSTS), parietal and frontal activity during a biological motion task while showing similar levels of activity in MT+/V5 during both coherent and biological motion trials. Activity in MT+/V5 was predictive of individual coherent motion thresholds in both groups. Activity in dorsolateral prefrontal cortex (DLPFC) and pSTS was predictive of biological motion thresholds in control participants but not in those with autism. Notably, however, activity in DLPFC was negatively related to autism symptom severity. These results suggest that impairments in higher-order social or attentional networks may underlie visual motion deficits observed in autism.
Although many studies have reported face identity recognition deficits in autism spectrum disorders (ASD), two fundamental question remains: 1) Is this deficit “process specific” for face memory in particular, or does it extend to perceptual discrimination of faces as well? And 2) Is the deficit “domain specific” for faces, or is it found more generally for other social or even nonsocial stimuli? The answers to these questions are important both for understanding the nature of autism and its developmental etiology, and for understanding the functional architecture of face processing in the typical brain. Here we show that children with ASD are impaired (compared to age and IQ-matched typical children) in face memory, but not face perception, demonstrating process specificity. Further, we find no deficit for either memory or perception of places or cars, indicating domain specificity. Importantly, we further showed deficits in both the perception and memory of bodies, suggesting that the relevant domain of deficit may be social rather than specifically facial. These results provide a more precise characterization of the cognitive phenotype of autism and further indicate a functional dissociation between face memory and face perception.
The fragile X premutation provides a unique opportunity for the study of genetic and brain mechanisms of behavior and cognition in the context of neurodevelopment and neurodegeneration. Although the neurodegenerative phenotype, fragile X-associated tremor/ataxia syndrome (FXTAS), is well described, evidence of a causal link between the premutation and psychiatric disorder earlier in life, clear delineation of a behavioral/cognitive phenotype, and characterization of the physiological basis of observed symptoms have been elusive.
We completed functional magnetic resonance imaging (fMRI) targeting the amygdala with an emotion-matching task and concurrent infra-red eyetracking, FMR1 molecular genetic testing, and neuropsychological assessment in 23 men with the premutation (mean age = 32.9 years) and 25 male controls (mean age = 30.1).
Premutation carriers had significantly smaller left and right amygdala volume and reduced right amygdala activation during the task relative to controls. Although both elevated FMR1 mRNA and reduced FMR1 protein (FMRP) were associated with the reduced activation, multiple regression analysis suggested that reduced FMRP is the primary factor. Premutation carriers also had higher ratings of autism spectrum symptoms than controls that were associated with the reduced amygdala response.
Although prior studies have emphasized a toxic gain-of-function effect of elevated mRNA associated with the premutation, the current results point to the role of reduced FMRP in alterations of brain activity and behavior.
FMR1; fragile X; premutation; amygdala; insula; FXTAS
A fundamental assumption in neuroscience is that brain structure determines function. Accordingly, functionally distinct regions of cortex should be structurally distinct in their connections to other areas. We tested this hypothesis in relation to face selectivity in the fusiform gyrus. By using only structural connectivity, as measured through diffusion weighted imaging, we are able to predict functional activation to faces in the fusiform gyrus. These predictions outperformed two control models and a standard group-average benchmark. The structure-function relationship discovered from these participants was highly robust in predicting activation in a second group of participants, despite differences in acquisition parameters and stimuli. This approach can thus reliably estimate activation in participants who cannot perform functional imaging tasks, and is an alternative to group-activation maps. Additionally, we identified cortical regions whose connectivity is highly influential in predicting face-selectivity within the fusiform, suggesting a possible mechanistic architecture underlying face processing in humans.
Diffusion imaging; DTI; DWI; tractography; fusiform; structural connectivity; FFA
Previous functional MRI (fMRI) studies have shown that fragile X mental retardation 1 (FMR1) fragile X premutation allele carriers (FXPCs) exhibit decreased hippocampal activation during a recall task and lower inferior frontal activation during a working memory task compared to matched controls. The molecular characteristics of FXPCs includes 55–200 CGG trinucleotide expansions, increased FMR1 mRNA levels, and decreased FMRP levels especially at higher repeat sizes. In the current study, we utilized MRI to examine differences in hippocampal volume and function during an encoding task in young male FXPCs. While no decreases in either hippocampal volume or hippocampal activity were observed during the encoding task in FXPCs, FMRP level (measured in blood) correlated with decreases in parahippocampal activation. In addition, activity in the right dorsolateral prefrontal cortex during correctly encoded trials correlated negatively with mRNA levels. These results, as well as the established biological effects associated with elevated mRNA levels and decreased FMRP levels on dendritic maturation and axonal growth, prompted us to explore functional connectivity between the hippocampus, prefrontal cortex, and parahippocampal gyrus using a psychophysiological interaction analysis. In FXPCs, the right hippocampus evinced significantly lower connectivity with right ventrolateral prefrontal cortex (VLPFC) and right parahippocampal gyrus. Furthermore, the weaker connectivity between the right hippocampus and VLPFC was associated with reduced FMRP in the FXPC group. These results suggest that while FXPCs show relatively typical brain response during encoding, faulty connectivity between frontal and hippocampal regions may have subsequent effects on recall and working memory.
fragile X premutation; memory; prefrontal cortex; psychophysiological interaction analysis
Several groups have recently reported that people with autism may suffer from a deficit in visual motion processing and proposed that these deficits may be related to a general dorsal stream dysfunction. In order to test the dorsal stream deficit hypothesis, we investigated coherent and biological motion perception as well as coherent form perception in a group of adolescents with autism and a group of age-matched typically developing controls. If the dorsal stream hypothesis were true, we would expect to document deficits in both coherent and biological motion processing in this group but find no deficit in coherent form perception. Using the method of constant stimuli and standard psychophysical analysis techniques, we measured thresholds for coherent motion, biological motion and coherent form. We found that adolescents with autism showed reduced sensitivity to both coherent and biological motion but performed as well as age-matched controls during coherent form perception. Correlations between intelligence quotient and task performance, however, appear to drive much of the group difference in coherent motion perception. Differences between groups on coherent motion perception did not remain significant when intelligence quotient was controlled for, but group differences in biological motion perception were more robust, remaining significant even when intelligence quotient differences were accounted for. Additionally, aspects of task performance on the biological motion perception task were related to autism symptomatology. These results do not support a general dorsal stream dysfunction in adolescents with autism but provide evidence of a more complex impairment in higher-level dynamic attentional processes.
autism; visual motion; biological motion; coherent motion; dorsal stream
Recent studies reveal that young carriers of the fragile X premutation are at increased risk for psychiatric conditions, memory problems and executive deficits. Post mortem and structural MRI studies suggest the hippocampus is preferentially affected by the premutation. The current study utilized magnetic resonance imaging (MRI) to explore the relationship between hippocampal structure and function as well as molecular/genetic and psychiatric measures in men with the fragile X premutation. Although the groups did not differ in hippocampal volume, the premutation group showed reduced left hippocampal activation and increased right parietal activation during a recall task relative to controls. These results suggest that brain function underlying memory recall is affected by premutation status. Left hippocampal activation was negatively correlated with both FMR1 mRNA level and psychiatric symptomology in the premutation group. These associations support the theory that increased levels of FMR1 mRNA affect brain function and contribute to psychiatric symptoms.
Fragile X premutation; FMR1 mRNA; Hippocampus; fMRI; Recall; Memory