Cortex最新文献

Background

The Frontal Aslant Tract (FAT) has been associated with executive functions (EF), but it remains unclear what role the FAT plays in EF, and whether preoperative dysfunction of the FAT is associated to long-lasting postsurgical executive impairments.

Methods

In this study, we examined the course of EF from pre-surgery (n = 75) to 3 (n = 61) and 12 (n = 25) months after surgery in patients with frontal and parietal low-grade gliomas (LGGs), to establish the degree to which long-term EF deficits exist. Secondly, we used patient-specific tractography to investigate the extent to which overlap of the tumor with the FAT, as well as integrity of the FAT, presurgery were related to EF on the short and longer term after surgery.

Results

LGG patients performed worse than healthy controls on all EF tests before and 3 months postsurgery. Whereas performances on three out of the four tests had normalized 1 year postsurgery (n = 26), performance on the cognitive flexibility test remained significantly worse than in healthy controls. Patients in whom the tumor overlapped with the core of the right FAT performed worse presurgery on three of the EF tests compared to those in whom the tumor did not overlap with the right FAT. Presurgical right FAT integrity was not related to presurgical EF, but only to postsurgical EF (from pre-to 3 months postsurgery). Longitudinal analyses demonstrated that patients with right (but not left) FAT core overlap performed on average worse over the pre- and postsurgical timepoints on the cognitive flexibility test.

Conclusions

We emphasized that LGG patients perform worse than healthy controls on the EF tests, which normalizes 1-year postsurgery except for cognitive flexibility. Importantly, in patients with right hemispheric tumors, tumor involvement of the FAT was associated with worse pre- and 3- months postsurgical performance, specifically concerning cognitive flexibility.

Humans rely heavily on facial expressions for social communication to convey their thoughts and emotions and to understand them in others. One prominent but controversial view is that humans learn to recognize the significance of facial expressions by mimicking the expressions of others. This view predicts that an inability to make facial expressions (e.g., facial paralysis) would result in reduced perceptual sensitivity to others' facial expressions. To test this hypothesis, we developed a diverse battery of sensitive emotion recognition tasks to characterize expression perception in individuals with Moebius Syndrome (MBS), a congenital neurological disorder that causes facial palsy. Using computer-based detection tasks we systematically assessed expression perception thresholds for static and dynamic face and body expressions. We found that while MBS individuals were able to perform challenging perceptual control tasks and body expression tasks, they were less efficient at extracting emotion from facial expressions, compared to matched controls. Exploratory analyses of fMRI data from a small group of MBS participants suggested potentially reduced engagement of the amygdala in MBS participants during expression processing relative to matched controls. Collectively, these results suggest a role for facial mimicry and consequent facial feedback and motor experience in the perception of others' facial expressions.

Previous research has demonstrated that humans combine multiple sources of spatial information such as self-motion and landmark cues while navigating through an environment. However, it is unclear whether this involves comparing multiple representations obtained from different sources during navigation (parallel hypothesis) or building a representation first based on self-motion cues and then combining with landmarks later (serial hypothesis). We tested these two hypotheses (parallel vs serial) in an active navigation task using wireless mobile scalp EEG recordings. Participants walked through an immersive virtual hallway with or without conflicts between self-motion and landmarks (i.e., intersections) and pointed toward the starting position of the hallway. We employed the oscillatory signals recorded during mobile wireless scalp EEG as a means of identifying when participant representations based on self-motion versus landmark cues might have first emerged. We found that path segments, including intersections present early during navigation, were more strongly associated with later pointing error, regardless of when they appeared during encoding. We also found that there was sufficient information contained within the frontal-midline theta and posterior alpha oscillatory signals in the earliest segments of navigation involving intersections to decode condition (i.e., conflicting vs not conflicting). Together, these findings suggest that intersections play a pivotal role in the early development of spatial representations, suggesting that memory representations for the geometry of walked paths likely develop early during navigation, in support of the parallel hypothesis.

Converging evidence recently put forward the notion that dedicated neurocognitive mechanisms do exist for the suppression of salient, but irrelevant distractors. Along this line, it is plausible to hypothesize that, in appropriate contexts, experience-dependent forms of attentional learning might selectively induce plastic changes within this dedicated circuitry, thus allowing an independent shaping of priorities at the service of attentional filtering. Conversely, previous work suggested that statistical learning (SL) of both target and distractor spatial probability distributions converge in adjusting only the overall attentional priority of locations: in fact, in the presence of an independent manipulation, either related to the target or to the distractor only, SL induces indirect effects (e.g., changes in filtering efficiency due to an uneven distribution of targets), suggesting that SL-induced plastic changes affect a shared neural substrate. Here we tested whether, when (conflicting) target- and distractor-related manipulations are concurrently applied to the very same locations, dedicated mechanisms might support the selective encoding of spatial priority in relation to the specific attentional operation involved. In three related experiments, human healthy participants discriminated the direction of a target arrow, while ignoring a salient distractor, if present; both target and distractor spatial probability distributions were concurrently manipulated in relation to each single location. Critically, the selection bias produced by the target-related SL was marginally reduced by an adverse distractor contingency, and the suppression bias generated by the distractor-related SL was erased, or even reversed, by an adverse target contingency. Our results suggest that even conflicting target- and distractor-related SL manipulations result in the adjustment of a unique spatial priority computation, likely because the process directly relies on direct plastic alterations of shared spatial priority map(s).

Autism spectrum disorders (ASD) and attention-deficit hyperactivity disorder (ADHD) are highly prevalent neurodevelopmental conditions that often co-occur and present both common and distinct neurodevelopmental profiles. Studying the developmental pathways leading to the emergence of ASD and/or ADHD symptomatology is crucial in understanding neurodiversity and discovering the mechanisms that underpin it. This study used functional near-infrared spectroscopy (fNIRS) to investigate differences in cortical specialization to social stimuli between 4- to 6-month-old infants at typical and elevated likelihood of ASD and/or ADHD. Results showed that infants at both elevated likelihood of ASD and ADHD had reduced selectivity to vocal sounds in left middle and superior temporal gyrus. Furthermore, infants at elevated likelihood of ASD showed attenuated responses to visual social stimuli in several cortical regions compared to infants at typical likelihood. Individual brain responses to visual social stimuli were associated with later autism traits, but not ADHD traits. These outcomes support our previous observations showing atypical social brain responses in infants at elevated likelihood of ASD and align with later atypical brain responses to social stimuli observed in children and adults with ASD. These findings highlight the importance of characterizing antecedent biomarkers of atypicalities in processing socially relevant information that might contribute to both phenotypic overlap and divergence across ASD and ADHD conditions and their association with the later emergence of behavioural symptoms.

Pseudoneglect is a set of visuospatial biases that entails a behavioral advantage for stimuli appearing in the left hemifield compared to the right one. Although right hemisphere dominance for visuospatial processing has been invoked to explain this phenomenon, its neurophysiological mechanisms are still debated, and the role of intra- and inter-hemispheric connectivity is yet to be defined. The present study explored the possibility of modulating pseudoneglect in healthy participants through a cortico-cortical paired associative stimulation protocol (ccPAS): a non-invasive brain stimulation protocol that manipulates the interplay between brain regions through the repeated, time-locked coupling of two transcranial magnetic stimulation (TMS) pulses. In the first experiment, healthy participants underwent a frontal-to-parietal (FP) and a parietal-to-frontal (PF) ccPAS. In the FP protocol, the first TMS pulse targeted the right frontal eye field (FEF), and the second pulse the right inferior parietal lobule (IPL), two critical areas for visuospatial and attentional processing. In the PF condition, the order of the pulses was reversed. In both protocols, the inter-stimulus interval (ISI) was 10 ms. Before and after stimulation, pseudoneglect was assessed with a landmark task and a manual line bisection task. A second experiment controlled for ccPAS timing dependency by testing FP-ccPAS with a longer ISI of 100 ms. Results showed that after administering the FP-ccPAS with the ISI of 10 ms, participants’ leftward bias in the landmark task increased significantly, with no effects in the manual line bisection task. The other two protocols tested were ineffective. Our findings showed that ccPAS could be used to modulate pseudoneglect by exploiting frontal-to-parietal connectivity, possibly through increased top-down attentional control. FP-ccPAS could represent a promising tool to investigate connectivity properties within visuospatial and attentional networks in the healthy and as a potential rehabilitation protocol in patients suffering from severe visuospatial pathologies.

Developmental regression describes when a child loses previously established skills, such as the ability to speak words and is most recognised in neurodevelopmental conditions including Autism; Developmental Epileptic Encephalopathies, such as Landau Kleffner syndrome, and genetic conditions such as Rett syndrome and Phelan McDermid syndrome. Although studies have reported developmental regression for over 100 years, there remain significant knowledge gaps within and between conditions that feature developmental regression. The certainty of evidence from earlier work has been limited by condition-specific studies, retrospective methodology, and inconsistency in the definitions and measures used for classification. Given prior limitations in the field, there is a paucity of knowledge about neurocognitive mechanisms, trajectories and outcomes for children with developmental regression, and their families. Here we provide a comprehensive overview, synthesise key definitions, clinical measures, and aetiological clues associated with developmental regression and discuss impacts on caregiver physical and mental health to clarify challenges and highlight future directions in the field.

This article tackles the theoretical thinking behind PPI and inclusion, input from people with neurodiverse conditions. By providing a perspective on how the prefix “Neuro” is positioned in a neutral and authoritative way (exemplified through our brief review of articles within Cortex), we explore how “epistemic injustice” (a concept used frequently in law, politics, philosophy and social science) can potentially arise. Epistemic injustice typically refers to a pernicious power dynamic whereby oppressed groups are silenced (Fricker 2007), either because certain voices are not given weight (“testimonial injustice”), or the ways in which they are allowed to speak (e.g., interpret their own experiences) are limited (“hermeneutical injustice”) (Kidd and Carel 2016). We show how, for “neurodiversity”, the mainstream “neuro” narratives are often positively felt by those deemed to be neurodiverse, and the lines between oppressor and oppressed break down, as both neuroscientists and people with neurodiverse conditions co-opt and influence each other’s positions.

As first described by Francis Galton, some persons perceive vividly and automatically in their mind's eye the written form of words that they are hearing. This phenomenon, labeled ticker-tape synesthesia (TTS), is thought to reflect an abnormally strong influence of speech processing in language areas on to orthographic representations in the visual cortex. Considering the relevance of TTS for the study of reading acquisition, we looked for objective behavioral advantages or impairments in 22 synesthetes, as compared to 22 matched control participants. In three auditory tasks relying on orthographic working memory (letters counting, backward spelling, and letter shape decision), we predicted and observed better performance in synesthetes than in controls. In two visual tasks (lexical decision and letter decision) with a concurrent auditory stimulation, we predicted that synesthetes should suffer from a larger interference by irrelevant speech than controls, but eventually found no difference between the groups. Those results, which we discuss in relation to orthographic processing, mental imagery, and working memory, promote TTS from pure subjectivity to an experimentally measurable phenomenon.

Introduction

Myotonic dystrophy type 1 (DM1) is associated with motor dysfunction as well as psychological and cognitive impairments, including altered social cognition. Theory of mind (ToM) impairments have been reported in this disease but their nature and their cognitive/cerebral correlates have yet to be determined.

Methods

Fifty DM1 patients and 50 healthy controls were assessed using the Movie for the Assessment of Social Cognition, which quantifies impairments in affective and cognitive components of ToM through the depiction of everyday situations. We also measured the study participants' cognitive, behavioral and social abilities, quality of life, and brain MRI characteristics.

Results

DM1 patients presented a significant impairment in ToM performance compared to controls (p < .001). The patients' errors were related to hypomentalizations (p < .001 vs controls) but not to hypermentalizations (p = .95). The affective component was affected (p < .001 vs controls) but not the cognitive component (p = .09). The ToM impairment was associated with demographic variables (older age and a lower educational level), genetic findings (a larger CTG triplets repeat expansion) and cognitive scores (slower information processing speed). Associations were also found with brain MRI variables (lower white matter and supratentorial volumes) but not with behavioral or social variables.

Discussion

DM1 patients display a ToM impairment, characterized by predominant hypomentalizations concerning the affective component. This impairment might result from structural brain abnormalities observed in DM1.