Cortex最新文献

Knowing when confidence computations take place is critical for building a mechanistic understanding of the neural and computational bases of metacognition. Yet, even though a substantial amount of research has focused on revealing the neural correlates and computations underlying human confidence judgments, very little is known about the timing of confidence computations. To understand when confidence is computed, we delivered single pulses of transcranial magnetic stimulation (TMS) at different times after stimulus presentation while subjects judged the orientation of a briefly presented visual stimulus and provided a confidence rating. TMS was delivered to either the right dorsolateral prefrontal cortex (DLPFC) in the experimental group or to vertex in the control group. We found that TMS to right DLPFC, but not to vertex, led to increased confidence in the absence of changes to accuracy or metacognitive efficiency. Critically, equivalent levels of confidence increase occurred for TMS delivered between 200 and 500 msec after stimulus presentation. These results suggest that confidence computations occur during a broad window that begins before the perceptual decision has been fully made and thus provide important constraints for theories of confidence generation.

Inner speech refers to the experience of talking to oneself in one's head. While notoriously challenging to investigate, it has also been central to a range of questions concerning mind, brain, and behaviour. Posited as a key component in executive function and self-regulation, inner speech has been claimed to be crucial in higher cognitive operations, self-knowledge and self-awareness. Such arguments have traditionally been supported with examples of atypical development. But variations in inner speech – and in some cases, significant diversity – in fact pose several key challenges to such claims, and raises many more questions for, language, thought and mental health more generally.

In this review, we will summarise evidence on the experience and operation of inner speech in child and adult neurotypical populations, autistic people and other neurodivergent groups, and people with diverse experiences of linguistic and sensory development, including deafness. We will demonstrate that the relationship between inner speech and cognitive operations may be more complex than first assumed when explored through the lens of cognitive and neurological diversity, and the implications of that for understanding the developing brain in all populations. We discuss why and how the experience of inner speech in neurodivergent groups has often been assumed rather than investigated, making it an important opportunity for researchers to develop innovative future work that integrates participatory insights with cognitive methodology. Finally, we will outline why variations in inner speech – in neurotypical and neurodivergent populations alike – nevertheless have a range of important implications for mental health vulnerability and unmet need. In this sense, the example of inner speech offers us both a way of looking back at the logic of developmental psychology and neuropsychology, and a clue to its future in a neurodiverse world.

Autism spectrum disorder (ASD) is a neurodevelopmental condition with a highly heterogeneous adult phenotype that includes social and non-social behavioral characteristics. The link between the characteristics assignable to the different domains remains unresolved. One possibility is that social and non-social behaviors in autism are modulated by a common underlying deficit. However, here we report evidence supporting an alternative concept that is individual-centered rather than deficit-centered. Individuals are assumed to have a distinctive style in the strategies they adopt to perform social and non-social tasks with these styles presumably being structured differently between autistic individuals and typically-developed (TD) individuals. We tested this hypothesis for the execution of time-coordinated (synchronized) actions. Participants performed (i) a social task that required synchronized gaze and pointing actions to interact with another person, and (ii) a non-social task that required finger-tapping actions synchronized to periodic stimuli at different time-scales and sensory modalities. In both tasks, synchronization behavior differed between ASD and TD groups. However, a principal component analysis of individual behaviors across tasks revealed associations between social and non-social features for the TD persons but such cross–domain associations were strikingly absent for autistic individuals. The highly differentiated strategies between domains in ASD are inconsistent with a general synchronization deficit and instead highlight the individualized developmental heterogeneity in the acquisition of domain-specific behaviors. We propose a cognitive model to help disentangle individual-centered from deficit-centered effects in other domains. Our findings reinforce the importance to identify individually differentiated phenotypes to personalize autism therapies.

Neuroimaging can capture brain restructuring after anterior temporal lobe resection (ATLR), a surgical procedure to treat drug-resistant temporal lobe epilepsy (TLE). Here, we examine the effects of this surgery on brain morphology measured in recently-proposed independent variables.

We studied 101 individuals with TLE (55 left, 46 right onset) who underwent ATLR. For each individual we considered one pre-surgical MRI and one follow-up MRI 2–13 months after surgery. We used a surface-based method to locally compute traditional morphological variables, and the independent measures K, I, and S, where K measures white matter tension, I captures isometric scaling, and S contains the remaining information about cortical shape. A normative model trained on data from 924 healthy controls was used to debias the data and account for healthy ageing effects occurring during scans. A SurfStat random field theory clustering approach assessed changes across the cortex caused by ATLR.

Compared to preoperative data, surgery had marked effects on all morphological measures. Ipsilateral effects were located in the orbitofrontal and inferior frontal gyri, the pre- and postcentral gyri and supramarginal gyrus, and the lateral occipital gyrus and lingual cortex. Contralateral effects were in the lateral occipital gyrus, and inferior frontal gyrus and frontal pole.

The restructuring following ATLR is reflected in widespread morphological changes, mainly in regions near the resection, but also remotely in regions that are structurally connected to the anterior temporal lobe. The causes could include mechanical effects, Wallerian degeneration, or compensatory plasticity. The study of independent measures revealed additional effects compared to traditional measures.

The oscillatory brain activities reflect neuro-computational processes that are critical for speech production and sensorimotor control. In the present study, we used neural oscillations in left-hemisphere stroke survivors with aphasia as a model to investigate network-level functional connectivity deficits associated with disrupted speech auditory feedback control. Electroencephalography signals were recorded from 40 post-stroke aphasia and 39 neurologically intact control participants while they performed speech vowel production and listening tasks under pitch-shifted altered auditory feedback (AAF) conditions. Using weighted phase-lag index, we calculated broadband (1–70 Hz) functional neural connectivity between electrode pairs covering the frontal, pre- and post-central, and parietal regions. Results revealed reduced fronto-central delta and theta band and centro-parietal low-beta band connectivity in left-hemisphere electrodes associated with diminished speech AAF compensation responses in post-stroke aphasia compared with controls. Lesion-mapping analysis demonstrated that stroke-induced damage to multi-modal brain networks within the inferior frontal gyrus, Rolandic operculum, inferior parietal lobule, angular gyrus, and supramarginal gyrus predicted the reduced functional neural connectivity within the delta and low-beta bands during both tasks in aphasia. These results provide evidence that disrupted neural connectivity due to left-hemisphere brain damage can result in network-wide dysfunctions associated with impaired sensorimotor integration mechanisms for speech auditory feedback control.

Pain is strongly modulated by expectations and beliefs. Across species, subregions of ventromedial prefrontal cortex (VMPFC) are implicated in a variety of functions germane to pain, predictions, and learning. Human fMRI studies show that VMPFC activity tracks expectations about pain and mediates expectancy effects on pain-related activity in other brain regions. Prior lesion studies suggest that VMPFC may instead play a more general role in generating affective responses to painful stimuli. To test whether VMPFC is required to generate affective responses to pain or is more specifically involved in expectancy-based pain modulation, we studied responses to heat stimuli in five adults with bilateral surgical lesions of VMPFC and twenty healthy adults without brain damage. All participants underwent a quantitative sensory testing procedure followed by a pain expectancy task in which cues predicting either low or high pain were followed by intermittent medium intensity heat stimuli. Compared to adults without brain damage, individuals with VMPFC lesions reported larger differences in expected pain based on predictive cues and failed to update expectations following the covert introduction of unexpected medium temperature stimuli. Consistent with observed expectancy differences, subjective pain unpleasantness ratings in the VMPFC lesion group were more strongly modulated by cue during thermal stimulation. We found no group differences in overall pain sensitivity, nor in relationships between pain and autonomic arousal, suggesting that VMPFC damage specifically enhances the effect of expectations on pain processing, likely driven by impaired integration of new sensory feedback to update expectations about pain. These results provide essential new data regarding the specific functional contribution of VMPFC to pain modulation.

Unawareness of memory deficits is an early manifestation in patients with Alzheimer’s disease (AD), which often delays diagnosis. This intriguing behavior constitutes a form of anosognosia, whose neural mechanisms remain largely unknown. We hypothesized that anosognosia may depend on a critical synaptic failure in the error-monitoring system, which would prevent AD patients from being aware of their own memory impairment. To investigate, we measured event-related potentials (ERPs) evoked by erroneous responses during a word memory recognition task in two groups of amyloid positive individuals with only subjective memory complaints at study entry: those who progressed to AD within the five-year study period (PROG group), and those who remained cognitively normal (CTRL group). A significant reduction in the amplitude of the positivity error (Pe), an ERP related to error awareness, was observed in the PROG group at the time of AD diagnosis (vs study entry) in intra-group analysis, as well as when compared with the CTRL group in inter-group analysis, based on the last EEG acquisition for all subjects. Importantly, at the time of AD diagnosis, the PROG group exhibited clinical signs of anosognosia, overestimating their cognitive abilities, as evidenced by the discrepancy scores obtained from caregiver/informant vs participant reports on the cognitive subscale of the Healthy Aging Brain Care Monitor. To our knowledge, this is the first study to reveal the emergence of a failure in the error-monitoring system during a word memory recognition task at the early stages of AD. This finding, along with the decline of awareness for cognitive impairment observed in the PROG group, strongly suggests that a synaptic dysfunction in the error-monitoring system may be the critical neural mechanism at the origin of unawareness of deficits in AD.

Different individuals experience varying degrees of vividness in their visual mental images. The distribution of these variations across different imagery domains, such as object shape, color, written words, faces, and spatial relationships, remains unknown. To address this issue, we conducted a study with 117 healthy participants who reported different levels of imagery vividness. Of these participants, 44 reported experiencing absent or nearly absent visual imagery, a condition known as “aphantasia”. These individuals were compared to those with typical (N = 42) or unusually vivid (N = 31) imagery ability. We used an online version of the French-language Battérie Imagination-Perception (eBIP), which consists of tasks tapping each of the above-mentioned domains, both in visual imagery and in visual perception. We recorded the accuracy and response times (RTs) of participants' responses. Aphantasic participants reached similar levels of accuracy on all tasks compared to the other groups (Bayesian repeated measures ANOVA, BF = .02). However, their RTs were slower in both imagery and perceptual tasks (BF = 266), and they had lower confidence in their responses on perceptual tasks (BF = 7.78e5). A Bayesian regression analysis revealed that there was an inverse correlation between subjective vividness and RTs for the entire participant group: higher levels of vividness were associated with faster RTs. The pattern was similar in all the explored domains. The findings suggest that individuals with congenital aphantasia experience a slowing in processing visual information in both imagery and perception, but the precision of their processing remains unaffected. The observed performance pattern lends support to the hypotheses that congenital aphantasia is primarily a deficit of phenomenal consciousness, or that it employs alternative strategies other than visualization to access preserved visual information.

Introduction

Attention Deficit/Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder with many functional impairments thought to be underpinned by difficulties in executive function domains such as working memory. The superior longitudinal fasciculus (SLF) plays an integral role in the development of working memory in neurotypical children. Neuroimaging research suggests reduced white matter organization of the SLF may contribute to working memory difficulties commonly seen in ADHD. This study aimed to examine the relationship between white matter organization of the SLF and working memory in children with ADHD.

Methods

We examined the association of tract volume and apparent fibre density (AFD) of the SLF with working memory in children with ADHD (n = 64) and controls (n = 58) aged 9–11years. Children completed a computerized spatial n-back task and underwent diffusion magnetic resonance imaging (dMRI). Constrained spherical deconvolution-based tractography was used to construct the three branches of the SLF bilaterally and examine volume and AFD of the SLF.

Results

Regression analyses revealed children with ADHD exhibited poorer working memory, and lower volume and AFD of the left SLF-II compared to healthy controls. There was also an association between reaction time and variability (RT and RT-V) and the left SLF-II. Further analyses revealed volume of the left SLF-II mediated the relationship between ADHD and working memory performance (RT and RT-V).

Discussion

These findings add to the current body of ADHD literature, revealing the potential role of frontoparietal white matter in working memory difficulties in ADHD.