Abnormal Neural Connectivity Research Articles

Treatment effects of N-acetyl cysteine on resting-state functional MRI and cognitive performance in patients with chronic mild traumatic brain injury: a longitudinal study.

Mild traumatic brain injury (mTBI) is a significant public health concern, specially characterized by a complex pattern of abnormal neural activity and functional connectivity. It is often associated with a broad spectrum of short-term and long-term cognitive and behavioral symptoms including memory dysfunction, headache, and balance difficulties. Furthermore, there is evidence that oxidative stress significantly contributes to these symptoms and neurophysiological changes. The purpose of this study was to assess the effect of N-acetylcysteine (NAC) on brain function and chronic symptoms in mTBI patients. Fifty patients diagnosed with chronic mTBI participated in this study. They were categorized into two groups including controls (CN, n = 25), and patients receiving treatment with N-acetyl cysteine (NAC, n = 25). NAC group received 50 mg/kg intravenous (IV) medication once a day per week. In the rest of the week, they took one 500 mg NAC tablet twice per day. Each patient underwent rs-fMRI scanning at two timepoints including the baseline and 3 months later at follow-up, while the NAC group received a combination of oral and IV NAC over that time. Three rs-fMRI metrics were measured including fractional amplitude of low frequency fluctuations (fALFF), degree centrality (DC), and functional connectivity strength (FCS). Neuropsychological tests were also assessed at the same day of scanning for each patient. The alteration of rs-fMRI metrics and cognitive scores were measured over 3 months treatment with NAC. Then, the correlation analysis was executed to estimate the association of rs-fMRI measurements and cognitive performance over 3 months (p < 0.05). Two significant group-by-time effects demonstrated the changes of rs-fMRI metrics particularly in the regions located in the default mode network (DMN), sensorimotor network, and emotional circuits that were significantly correlated with cognitive function recovery over 3 months treatment with NAC (p < 0.05). NAC appears to modulate neural activity and functional connectivity in specific brain networks, and these changes could account for clinical improvement. This study confirmed the short-term therapeutic efficacy of NAC in chronic mTBI patients that may contribute to understanding of neurophysiological effects of NAC in mTBI. These findings encourage further research on long-term neurobehavioral assessment of NAC assisting development of therapeutic plans in mTBI.

Serine Proteases and Their Inhibitors Affect the Rate of GnRH Neuronal Migration in the Embryonic Chick Model: A Thesis Proposal

Development in an organism is a highly complex task that requires a specific sequence for proper function. One of these tasks is neuronal migration and the extracellular cues that help to guide neurons to their appropriate locations. If neurons do not migrate to their appropriate locations, then there are abnormal neural connections, which can result in neuronal migration disorders (NMD). It has been shown that the inhibition and stimulation of migration may be balanced due to effects of serine protease inhibitors and serine proteases. Serine proteases and their inhibitors can alter the various chemoattraction-signaling cues and thereby modulate neuronal migratory processes. Furthermore, there exists a delicate balance between serine proteases and their inhibitors to modulate migration of neurons within development. Thus, by understanding how the balance of serine protease and serine protease inhibitor activity works, one can further understand how these changes affect neuronal migration in development. Experiments to test in vivo neuronal migration of chick GnRH neurons during embryogenesis were investigated to elucidate the role these proteins play in migration. Protein coated beads were inserted and GnRH levels measured to control. Such experimentation is crucial, as these studies are the first to explore the role of proteases in neural migration in an in vivo model. These findings indicate that the ability to initiate migration lies inherently within the neuron itself such that changes of the extracellular matrix composition are irrelevant in the initial timing. Neurons entering the CNS earlier in trypsin-treated embryos indicates continuous movement may be a cell autonomous event with trypsin-induced proteolysis. In other words, the ability of GnRH neurons to migrate across glial boundaries and through the brain to its target site is independent of further maturation of the neuron or the brain. Taken together, this study can provide knowledge regarding these proteins and their relation to development. This knowledge can potentially lead to therapies that can provide ameliorative care for patients suffering with NMD.

Functional connectivity density alterations in children with strabismus and amblyopia based on resting-state functional magnetic resonance imaging (fMRI)

PurposeTo explore functional connectivity density (FCD) values of brain areas in children with strabismus and amblyopia (SA) based on blood oxygen level-dependent (BOLD) signals.MethodsThis study recruited 26 children (14 male, 12 females) with SA and 26 healthy children (14 male, 12 female) as healthy controls (HCs). Both groups matched in age, gender, educational level and socioeconomic background. While resting, all participants underwent fMRI scanning and global FCD (gFCD) and local FCD (lFCD) values were calculated. Receiver operating characteristic (ROC) curves were created to investigate whether there was a significant difference between children with SA and healthy controls.ResultsWhen compared with healthy controls, children with SA had significantly lower gFCD values in the right cerebellum, left putamen, and right superior frontal gyrus; however, the same metrics showed opposite changes in the right angular gyrus, left middle cingulate gyrus, left angular gyrus, right superior parietal gyrus, and right middle frontal gyrus. In children with SA, lFCD values were found to be remarkably decreased in regions of the middle right temporal pole, right cerebellum, left putamen, left hippocampus, right hippocampus, left thalamus, left cerebellum; values were increased in the right superior parietal gyrus as compared with healthy controls.ConclusionWe noted abnormal neural connectivity in some brain areas of children with SA; detailing such connectivity aberrations is useful in exploring the pathophysiology of SA and providing useful information for future clinical management.

Abnormalities in electroencephalographic microstates are state and trait markers of major depressive disorder.

Neuroimaging studies have shown that major depressive disorder (MDD) is characterized by abnormal neural activity and connectivity. However, hemodynamic imaging techniques lack the temporal resolution needed to resolve the dynamics of brain mechanisms underlying MDD. Moreover, it is unclear whether putative abnormalities persist after remission. To address these gaps, we used microstate analysis to study resting-state brain activity in major depressive disorder (MDD). Electroencephalographic (EEG) "microstates" are canonical voltage topographies that reflect brief activations of components of resting-state brain networks. We used polarity-insensitive k-means clustering to segment resting-state high-density (128-channel) EEG data into microstates. Data from 79 healthy controls (HC), 63 individuals with MDD, and 30 individuals with remitted MDD (rMDD) were included. The groups produced similar sets of five microstates, including four widely-reported canonical microstates (A-D). The proportion of microstate D was decreased in MDD and rMDD compared to the HC group (Cohen's d = 0.63 and 0.72, respectively) and the duration and occurrence of microstate D was reduced in the MDD group compared to the HC group (Cohen's d = 0.43 and 0.58, respectively). Among the MDD group, proportion and duration of microstate D were negatively correlated with symptom severity (Spearman's rho = -0.34 and -0.46, respectively). Finally, microstate transition probabilities were nonrandom and the MDD group, relative to the HC and the rMDD groups, exhibited multiple distinct transition probabilities, primarily involving microstates A and C. Our findings highlight both state and trait abnormalities in resting-state brain activity in MDD.

Modulation of frontal gamma oscillations improves working memory in schizophrenia

Schizophrenia is a debilitating mental disorder that is associated with cognitive deficits. Impairments in cognition occur early in the course of illness and are associated with poor functional outcome, but have been difficult to treat with conventional treatments. Recent studies have implicated abnormal neural network dynamics and impaired connectivity in frontal brain regions as possible causes of cognitive deficits. For example, high-frequency, dorsal-lateral prefrontal oscillatory activity in the gamma range (30–50 Hz) is associated with impaired working memory in individuals with schizophrenia.In light of these findings, it may be possible to use EEG neurofeedback (EEG-NFB) to train individuals with schizophrenia to enhance frontal gamma activity to improve working memory and cognition. In a single-group, proof-of-concept study, 31 individuals with schizophrenia received 12 weeks of twice weekly EEG-NFB to enhance frontal gamma band response. EEG-NFB was well-tolerated, associated with increased gamma training threshold, and significant increases in frontal gamma power during an n-back working memory task. Additionally, EEG-NFB was associated with significant improvements in n-back performance and working memory, speed of processing, and reasoning and problem solving on neuropsychological tests. Change in gamma power was associated with change in cognition. Significant improvements in psychiatric symptoms were also found. These encouraging findings suggest EEG-NFB targeting frontal gamma activity may provide a novel effective approach to cognitive remediation in schizophrenia, although placebo-controlled trials are needed to assess the effects of non-treatment related factors.

Disruption of Regional Brain Activity and Functional Connectivity in Patients with Asymptomatic Vulnerable Carotid Plaque

Background & aimsStudies have shown that moderate to severe stenosis of the carotid was associated with abnormal neural activity and functional connectivity (FC). However, whether there is a change of neuronal activity in individuals with asymptomatic vulnerable carotid plaque but mild stenosis (VCP) remains unknown. MethodsFrom December 2015 to December 2017, a total of 31 patients with VCP and 31 no carotid plaque (NCP) controls were performed multi-modal state functional magnetic resonance imaging and investigated the regional brain activity and FC. Two basic algorithms of rs-fMRI, arterial spin labeling, and inflammatory biomarkers were comprehensively evaluated. The time series of aberrant ReHo and FC were also extracted and correlated with other clinical imaging features. ResultsAs compared with NCP group, decreased regional brain activity was found mainly in left middle occipital gyrus (MOG) in the VCP group, but there was no significant difference in cerebral blood flow between the two groups. With the left MOG as seed, decreased FC was found between left MOG and right MOG and frontoparietal network in VCP group. Carotid intima-media thickness but not inflammatory biomarkers including high sensitivity c-reactive protein and interleukin-6 was significantly correlated with aberrant ReHo and FC in left MOG and right MOG. Conclusionsregional brain activity and FC may serve as early imaging markers for vascular-related brain dysfunctions and clinical indicators for early intervention of both atherosclerotic cerebral infarction and vascular cognitive impairments.

Inducing synesthesia in non-synesthetes: Short-term visual deprivation facilitates auditory-evoked visual percepts.

Sounds can modulate activity in visual cortex, facilitating the detection of visual targets. However, these sound-driven modulations are not thought to evoke conscious visual percepts in the general population. In individuals with synesthesia, however, multisensory interactions do lead to qualitatively different experiences such as sounds evoking flashes of light. Why, if multisensory interactions are present in all individuals, do only synesthetes experience abnormal qualia? Competing models differ in the time required for synesthetic experiences to emerge. The cross-activation model suggests synesthesia arises over months or years from the development of abnormal neural connections. Here we demonstrate that after ∼5 min of visual deprivation, sounds can evoke synesthesia-like percepts (vivid colors and Klüver form-constants) in ∼50% of non-synesthetes. These results challenge aspects of the cross-activation model and suggest that synesthesia exists as a latent feature in all individuals, manifesting when the balance of activity across the senses has been altered.

1.3 Abnormal Neural Connectivity in Girls but Not Boys with Autism: A Group-Matched, Quality-Controlled, Diffusion Tensor Imaging Study

1.3 Abnormal Neural Connectivity in Girls but Not Boys with Autism: A Group-Matched, Quality-Controlled, Diffusion Tensor Imaging Study

How Useful Is Electroencephalography in the Diagnosis of Autism Spectrum Disorders and the Delineation of Subtypes: A Systematic Review.

Autism spectrum disorders (ASD) are thought to be associated with abnormal neural connectivity. Presently, neural connectivity is a theoretical construct that cannot be easily measured. Research in network science and time series analysis suggests that neural network structure, a marker of neural activity, can be measured with electroencephalography (EEG). EEG can be quantified by different methods of analysis to potentially detect brain abnormalities. The aim of this review is to examine evidence for the utility of three methods of EEG signal analysis in the ASD diagnosis and subtype delineation. We conducted a review of literature in which 40 studies were identified and classified according to the principal method of EEG analysis in three categories: functional connectivity analysis, spectral power analysis, and information dynamics. All studies identified significant differences between ASD patients and non-ASD subjects. However, due to high heterogeneity in the results, generalizations could not be inferred and none of the methods alone are currently useful as a new diagnostic tool. The lack of studies prevented the analysis of these methods as tools for ASD subtypes delineation. These results confirm EEG abnormalities in ASD, but as yet not sufficient to help in the diagnosis. Future research with larger samples and more robust study designs could allow for higher sensitivity and consistency in characterizing ASD, paving the way for developing new means of diagnosis.

Sublethal Dosage of Imidacloprid Reduces the Microglomerular Density of Honey Bee Mushroom Bodies.

The dramatic loss of honey bees is a major concern worldwide. Previous studies have indicated that neonicotinoid insecticides cause behavioural abnormalities and have proven that exposure to sublethal doses of imidacloprid during the larval stage decreases the olfactory learning ability of adults. The present study shows the effect of sublethal doses of imidacloprid on the neural development of the honey bee brain by immunolabelling synaptic units in the calyces of mushroom bodies. We found that the density of the synaptic units in the region of the calyces, which are responsible for olfactory and visual functions, decreased after being exposed to a sublethal dose of imidacloprid. This not only links a decrease in olfactory learning ability to abnormal neural connectivity but also provides evidence that imidacloprid damages the development of the nervous system in regions responsible for both olfaction and vision during the larval stage of the honey bee.

A Diffusion MRI Tractography Connectome of the Mouse Brain and Comparison with Neuronal Tracer Data.

Interest in structural brain connectivity has grown with the understanding that abnormal neural connections may play a role in neurologic and psychiatric diseases. Small animal connectivity mapping techniques are particularly important for identifying aberrant connectivity in disease models. Diffusion magnetic resonance imaging tractography can provide nondestructive, 3D, brain-wide connectivity maps, but has historically been limited by low spatial resolution, low signal-to-noise ratio, and the difficulty in estimating multiple fiber orientations within a single image voxel. Small animal diffusion tractography can be substantially improved through the combination of ex vivo MRI with exogenous contrast agents, advanced diffusion acquisition and reconstruction techniques, and probabilistic fiber tracking. Here, we present a comprehensive, probabilistic tractography connectome of the mouse brain at microscopic resolution, and a comparison of these data with a neuronal tracer-based connectivity data from the Allen Brain Atlas. This work serves as a reference database for future tractography studies in the mouse brain, and demonstrates the fundamental differences between tractography and neuronal tracer data.

Altered Structural Brain Networks in Tuberous Sclerosis Complex

Tuberous sclerosis complex (TSC) is characterized by benign hamartomas in multiple organs including the brain and its clinical phenotypes may be associated with abnormal neural connections. We aimed to provide the first detailed findings on disrupted structural brain networks in TSC patients. Structural whole-brain connectivity maps were constructed using structural and diffusion MRI in 20 TSC (age range: 3-24 years) and 20 typically developing (TD; 3-23 years) subjects. We assessed global (short- and long-association and interhemispheric fibers) and regional white matter connectivity, and performed graph theoretical analysis using gyral pattern- and atlas-based node parcellations. Significantly higher mean diffusivity (MD) was shown in TSC patients than in TD controls throughout the whole brain and positively correlated with tuber load severity. A significant increase in MD was mainly influenced by an increase in radial diffusivity. Furthermore, interhemispheric connectivity was particularly reduced in TSC, which leads to increased network segregation within hemispheres. TSC patients with developmental delay (DD) showed significantly higher MD than those without DD primarily in intrahemispheric connections. Our analysis allows non-biased determination of differential white matter involvement, which may provide better measures of "lesion load" and lead to a better understanding of disease mechanisms.

Quantitative EEG in autistic children

Background Autism spectrum disorder is a neurodevelopmental disorder that is characterized mainly by difficulties in social interaction and communication. Studies have suggested abnormal neural connectivity patterns in the brains of patients with autism. Objective The current work aimed to study the quantitative electroencephalography (EEG) findings in autistic children and compare it with those of normal controls. Methods The EEG recordings of 21 autistic children between 4 and 12 years of age were compared with those of 21 age-matched and sex-matched controls under an eyes-opened condition. Differences in cerebral functioning were examined using measurements of absolute and relative power and intrahemispheric and interhemispheric coherence. Results There were statistically significant differences in EEG power between the autistic and control groups, with greater absolute of delta and theta power especially at the frontal region in autistic children. There was also global reduction in relative alpha and beta power especially in the frontal, central, and posterior regions in autistic children. In addition, there was a pattern of underconnectivity and overconnectivity when measuring the intrahemispheric and interhemispheric coherence in the autistic compared with the control group. Conclusion These results suggested regional dysfunction of the brain in autistic children, along with a pattern of abnormal neural connectivity, which could explain the autistic symptomatology.

Neurobiology of psychiatric disorders

Neurobiologically spoken, the supstrate of the mind is formed by neuronal networks, and dysregulated neurocircuitry can cause psychiatric disorders. Psychiatric disorders are diagnosed by symptom clusters that are the result of abnormal brain tissue, and/or activity in specialized areas of the brain. Dysregulated circuitry results from abnormal neural function, or abnormal neural connections from one brain area to another, which leads to neurotransmitter imbalances. Each psychiatric disorder has uniquely dysregulated circuitry and thereby unique neurotransmitter imbalance, such as: prefrontal cortical-limbic pathways in depression or prefrontal cortical-striatal pathways in schizophrenia ie. serotonin-norepinephrin-dopamin imbalance in depression, or dopamine hyperactivity in schizophrenia. Biological psychiatry has completely changed the farmacological treatment of psychiatric disorders, and new foundings in that field are supportive to futher more neuropsychopharmacological and nonpharmacological therapy studies, whish has as a result more safe and effective therapy for psychiatric disorders.

Global Resting-State Functional Magnetic Resonance Imaging Analysis Identifies Frontal Cortex, Striatal, and Cerebellar Dysconnectivity in Obsessive-Compulsive Disorder

Obsessive-compulsive disorder (OCD) is associated with regional hyperactivity in cortico-striatal circuits. However, the large-scale patterns of abnormal neural connectivity remain uncharacterized. Resting-state functional connectivity studies have shown altered connectivity within the implicated circuitry, but they have used seed-driven approaches wherein a circuit of interest is defined a priori. This limits their ability to identify network abnormalities beyond the prevailing framework. This limitation is particularly problematic within the prefrontal cortex (PFC), which is large and heterogeneous and where a priori specification of seeds is therefore difficult. A hypothesis-neutral, data-driven approach to the analysis of connectivity is vital. We analyzed resting-state functional connectivity data collected at 3T in 27 OCD patients and 66 matched control subjects with a recently developed data-driven global brain connectivity (GBC) method, both within the PFC and across the whole brain. We found clusters of decreased connectivity in the left lateral PFC in both whole-brain and PFC-restricted analyses. Increased GBC was found in the right putamen and left cerebellar cortex. Within regions of interest in the basal ganglia and thalamus, we identified increased GBC in dorsal striatum and anterior thalamus, which was reduced in patients on medication. The ventral striatum/nucleus accumbens exhibited decreased global connectivity but increased connectivity specifically with the ventral anterior cingulate cortex in subjects with OCD. These findings identify previously uncharacterized PFC and basal ganglia dysconnectivity in OCD and reveal differentially altered GBC in dorsal and ventral striatum. Results highlight complex disturbances in PFC networks, which could contribute to disrupted cortical-striatal-cerebellar circuits in OCD.

Segmentation of the mouse fourth deep lumbrical muscle connectome reveals concentric organisation of motor units

Connectomic analysis of the nervous system aims to discover and establish principles that underpin normal and abnormal neural connectivity and function. Here we performed image analysis of motor unit connectivity in the fourth deep lumbrical muscle (4DL) of mice, using transgenic expression of fluorescent protein in motor neurones as a morphological reporter. We developed a method that accelerated segmentation of confocal image projections of 4DL motor units, by applying high resolution (63×, 1.4 NA objective) imaging or deconvolution only where either proved necessary, in order to resolve axon crossings that produced ambiguities in the correct assignment of axon terminals to identified motor units imaged at lower optical resolution (40×, 1.3 NA). The 4DL muscles contained between 4 and 9 motor units and motor unit sizes ranged in distribution from 3 to 111 motor nerve terminals per unit. Several structural properties of the motor units were consistent with those reported in other muscles, including suboptimal wiring length and distribution of motor unit size. Surprisingly, however, small motor units were confined to a region of the muscle near the nerve entry point, whereas their larger counterparts were progressively more widely dispersed, suggesting a previously unrecognised form of segregated motor innervation in this muscle. We also found small but significant differences in variance of motor endplate length in motor units, which correlated weakly with their motor unit size. Thus, our connectomic analysis has revealed a pattern of concentric innervation that may perhaps also exist in other, cylindrical muscles that have not previously been thought to show segregated motor unit organisation. This organisation may be the outcome of competition during postnatal development based on intrinsic neuronal differences in synaptic size or synaptic strength that generates a territorial hierarchy in motor unit size and disposition.

Is macrocephaly a neural marker of a local bias in autism?

Previous research has suggested that the local processing bias often reported in studies of Autism Spectrum Condition may only be typical of a subgroup of individuals with autism also presenting with macrocephaly. The current study examined a group of children with autism, with and without macrocephaly, on the Children's Embedded Figures Test (CEFT), a well-established measure of local processing bias. The results demonstrated that the children with autism and macrocephaly performed significantly better on the CEFT than children with autism without macrocephaly, indicative of a local bias. These results lend support to the proposal that both macrocephaly in autism and a local processing bias may arise from the same underlying neural processes and these characteristics represent an endophenotype in a subgroup of individuals with ASC worthy of further investigation.

Pattern Strabismus: Where Does the Brain's Role End and the Muscle's Begin?

Vertically incomitant pattern strabismus comprises 50% of infantile horizontal strabismus. The oblique muscle dysfunction has been associated with pattern strabismus. High-resolution orbit imaging and contemporary neurophysiology studies in non-human primate models of strabismus have shed light into the mechanisms of pattern strabismus. In this review, we will examine our current understanding of etiologies of pattern strabismus. Speculated pathophysiology includes oblique muscle dysfunction, loss of fusion with altered recti muscle pull, displacements and instability in connective tissue pulleys of the recti muscles, vestibular hypofunction, and abnormal neural connections. Orbital mechanical factors, such as abnormal pulleys, were reported as a cause of pattern strabismus in patients with craniofacial anomalies, connective tissue disorders, and late-onset strabismus. In contrast, abnormal neural connections could be responsible for the development of a pattern in infantile-onset strabismus. Pattern strabismus is likely multifactorial. Understanding the mechanisms of pattern strabismus is pivotal to determine an appropriate surgical treatment strategy for these patients.

Abnormal Neural Connectivity in Schizophrenia and fMRI-Brain-Computer Interface as a Potential Therapeutic Approach

Considering that single locations of structural and functional abnormalities are insufficient to explain the diverse psychopathology of schizophrenia, new models have postulated that the impairments associated with the disease arise from a failure to integrate the activity of local and distributed neural circuits: the “abnormal neural connectivity hypothesis.” In the last years, new evidence coming from neuroimaging have supported and expanded this theory. However, despite the increasing evidence that schizophrenia is a disorder of neural connectivity, so far there are no treatments that have shown to produce a significant change in brain connectivity, or that have been specifically designed to alleviate this problem. Brain-Computer Interfaces based on real-time functional Magnetic Resonance Imaging (fMRI-BCI) are novel techniques that have allowed subjects to achieve self-regulation of circumscribed brain regions. In recent studies, experiments with this technology have resulted in new findings suggesting that this methodology could be used to train subjects to enhance brain connectivity, and therefore could potentially be used as a therapeutic tool in mental disorders including schizophrenia. The present article summarizes the findings coming from hemodynamics-based neuroimaging that support the abnormal connectivity hypothesis in schizophrenia, and discusses a new approach that could address this problem.

Task-related functional connectivity in autism spectrum conditions: an EEG study using wavelet transform coherence

BackgroundAutism Spectrum Conditions (ASC) are a set of pervasive neurodevelopmental conditions characterized by a wide range of lifelong signs and symptoms. Recent explanatory models of autism propose abnormal neural connectivity and are supported by studies showing decreased interhemispheric coherence in individuals with ASC. The first aim of this study was to test the hypothesis of reduced interhemispheric coherence in ASC, and secondly to investigate specific effects of task performance on interhemispheric coherence in ASC.MethodsWe analyzed electroencephalography (EEG) data from 15 participants with ASC and 15 typical controls, using Wavelet Transform Coherence (WTC) to calculate interhemispheric coherence during face and chair matching tasks, for EEG frequencies from 5 to 40 Hz and during the first 400 ms post-stimulus onset.ResultsResults demonstrate a reduction of interhemispheric coherence in the ASC group, relative to the control group, in both tasks and for all electrode pairs studied. For both tasks, group differences were generally observed after around 150 ms and at frequencies lower than 13 Hz. Regarding within-group task comparisons, while the control group presented differences in interhemispheric coherence between faces and chairs tasks at various electrode pairs (FT7-FT8, TP7-TP8, P7-P8), such differences were only seen for one electrode pair in the ASC group (T7-T8). No significant differences in EEG power spectra were observed between groups.ConclusionsInterhemispheric coherence is reduced in people with ASC, in a time and frequency specific manner, during visual perception and categorization of both social and inanimate stimuli and this reduction in coherence is widely dispersed across the brain.Results of within-group task comparisons may reflect an impairment in task differentiation in people with ASC relative to typically developing individuals.Overall, the results of this research support the value of WTC in examining the time-frequency microstructure of task-related interhemispheric EEG coherence in people with ASC.