The Relationship between History of Traumatic Brain Injury and Longitudinal Changes in Cortical Thickness among Patients with Alzheimer's Disease.

BACKGROUND: There has been little direct examination of how traumatic brain injury (TBI) affects the rate of neurodegeneration for individuals with Alzheimer's disease (AD). METHODS: The study examined 89 cognitively normal adults (65 with and 24 without prior TBI) and 65 with AD (16 with and 49 without prior TBI). Cortical thickness was quantified from T1-weighted MRI scans at baseline and follow-up (mean interval 33.4 months). Partial least squares analysis was used to evaluate the effects of AD and TBI history on the longitudinal change in cortical thickness. RESULTS: Significant group effects were identified throughout the frontal and temporal cortices. Comparison of the AD groups to their control cohorts showed greater relative atrophy for the AD cohort with prior TBI. CONCLUSION: These results indicate that a history of TBI exacerbates longitudinal declines in cortical thickness among AD patients, providing new insights into the shared pathomechanisms between these neurological conditions.

Causal effects of sepsis on structural changes in cerebral cortex: A Mendelian randomization investigation.

Previous research has shown a strong correlation between sepsis and brain structure. However, whether this relationship represents a causality remains elusive. In this study, we employed Mendelian randomization (MR) to probe the associations of genetically predicted sepsis and sepsis-related death with structural changes in specific brain regions. Genome-wide association study (GWAS) data for sepsis phenotypes (sepsis and sepsis-related death) were obtained from the IEU OpenGWAS. Correspondingly, GWAS data for brain structural traits (volume of the subcortical structure, cortical thickness, and surface area) were derived from the ENIGMA consortium. Inverse variance weighted was mainly utilized to assess the causal effects, while weighted median and MR-Egger regression served as complementary methods. Sensitivity analyses were implemented with Cochran Q test, MR-Egger regression, and MR-PRESSO. In addition, a reverse MR analysis was carried out to assess the possibility of reverse causation. We identified that genetic liability to sepsis was normally significantly associated with a reduced surface area of the postcentral gyrus (ß = -35.5280, SE = 13.7465, P = .0096). The genetic liability to sepsis-related death showed a suggestive positive correlation with the surface area of fusiform gyrus (ß = 11.0920, SE = 3.6412, P = .0023) and posterior cingulate gyrus (ß = 3.6530, SE = 1.6684, P = .0286), While it presented a suggestive negative correlation with surface area of the caudal middle frontal gyrus (ß = -11.4586, SE = 5.1501, P = .0261) and frontal pole (ß = -1.0024, SE = 0.4329, P = .0206). We also indicated a possible bidirectional causal association between genetic liability to sepsis-related death and the thickness of the transverse temporal gyrus. Sensitivity analyses verified the robustness of the above associations. These findings suggested that genetically determined liability to sepsis might influence the specific brain structure in a causal way, offering new perspectives to investigate the mechanism of sepsis-related neuropsychiatric disorders.

Causal relationship between primary headache mediated by circulating cytokines and cerebral cortex structure: a mediation Mendelian randomization study.

Inflammation may be related to structural changes in the cerebral cortex. We aimed to explore whether cytokines mediate the link between these changes and primary headache. The summary statistics of genome-wide association study (GWAS) related to migraine and its subtypes, cluster headache were derived from the FinnGen Release 10 database, and tension-type headache data was from the GWAS Catalog. Ninety-one cytokines were obtained from genome-wide pQTL mapping data. GWAS data on cortical surface area (SA) and thickness (TH) came from the ENIGMA Consortium. The methods of Mendelian randomization (MR) analysis included the inverse-variance-weighted (IVW), MR-Egger, and weighted median. Migraine reduces the SA of paracentral[ß = -1.3645, OR = 0.2555, 95%CI (0.0660, 0.9898)] by fibroblast growth factor-23(FGF-23), with an intermediate ratio (IR) of 38.13%. Migraine may reduce the TH of superior parietal[ß = -0.0029, OR = 0.9971, 95%CI (0.9943, 0.9999)] by interleukin (IL)-15RA, with an absolute IR of 11.11%. Migraine without aura may reduce the TH of rostral anterior cingulate[ß = -0.0005, OR = 0.9995, 95%CI (0.9991, 0.9999)] by IL-18R1, with an IR of 11.63%. FGF23 and IL-15RA are associated with reduced SA or TH in migraine, while IL-18R1 is associated with increased TH in migraine without aura.

Sex differences in functional cortical organization reflect differences in network topology rather than cortical morphometry.

Differences in brain size between the sexes are consistently reported. However, the consequences of this anatomical difference on sex differences in intrinsic brain function remain unclear. In the current study, we investigate whether sex differences in intrinsic cortical functional organization may be associated with differences in cortical morphometry, namely different measures of brain size, microstructure, and the geodesic distance of connectivity profiles. For this, we compute a low dimensional representation of functional cortical organization, the sensory-association axis, and identify widespread sex differences. Contrary to our expectations, sex differences in functional organization do not appear to be systematically associated with differences in total surface area, microstructural organization, or geodesic distance, despite these morphometric properties being per se associated with functional organization and differing between sexes. Instead, functional sex differences in the sensory-association axis are associated with differences in functional connectivity profiles and network topology. Collectively, our findings suggest that sex differences in functional cortical organization extend beyond sex differences in cortical morphometry.

Wide-field calcium imaging of cortical activation and functional connectivity in externally- and internally-driven locomotion.

The role of the cerebral cortex in self-initiated versus sensory-driven movements is central to understanding volitional action. Whether the differences in these two movement classes are due to specific cortical areas versus more cortex-wide engagement is debated. Using wide-field Ca2+ imaging, we compared neural dynamics during spontaneous and motorized treadmill locomotion, determining the similarities and differences in cortex-wide activation and functional connectivity (FC). During motorized locomotion, the cortex exhibits greater activation globally prior to and during locomotion starting compared to spontaneous and less during steady-state walking, during stopping, and after termination. Both conditions are characterized by FC increases in anterior secondary motor cortex (M2) nodes and decreases in all other regions. There are also cortex-wide differences; most notably, M2 decreases in FC with all other nodes during motorized stopping and after termination. Therefore, both internally- and externally-generated movements widely engage the cortex, with differences represented in cortex-wide activation and FC patterns.

Repetition dynamically and rapidly increases cortical, but not hippocampal, offline reactivation.

No sooner is an experience over than its neural representation begins to be transformed through memory reactivation during offline periods. The lion's share of prior research has focused on understanding offline reactivation within the hippocampus. However, it is hypothesized that consolidation processes involve offline reactivation in cortical regions as well as coordinated reactivation in the hippocampus and cortex. Using fMRI, we presented novel and repeated paired associates to participants during encoding and measured offline memory reactivation for those events during an immediate post-encoding rest period. post-encoding reactivation frequency of repeated and once-presented events did not differ in the hippocampus. However, offline reactivation in widespread cortical regions and hippocampal-cortical coordinated reactivation were significantly enhanced for repeated events. These results provide evidence that repetition might facilitate the distribution of memory representations across cortical networks, a hallmark of systems-level consolidation. Interestingly, we found that offline reactivation frequency in both hippocampus and cortex explained variance in behavioral success on an immediate associative recognition test for the once-presented information, potentially indicating a role of offline reactivation in maintaining these novel, weaker, memories. Together, our findings highlight that endogenous offline reactivation can be robustly and significantly modulated by study repetition.

Propofol disrupts the functional core-matrix architecture of the thalamus in humans.

Research into the role of thalamocortical circuits in anesthesia-induced unconsciousness is difficult due to anatomical and functional complexity. Prior neuroimaging studies have examined either the thalamus as a whole or focused on specific subregions, overlooking the distinct neuronal subtypes like core and matrix cells. We conducted a study of heathy volunteers and functional magnetic resonance imaging during conscious baseline, deep sedation, and recovery. We advanced the functional gradient mapping technique to delineate the functional geometry of thalamocortical circuits, within a framework of the unimodal-transmodal functional axis of the cortex. Here we show a significant shift in this geometry during deep sedation, marked by a transmodal-deficient geometry. This alteration is closely linked to the spatial variations in the matrix cell composition within the thalamus. This research bridges cellular and systems-level understanding, highlighting the crucial role of thalamic core-matrix functional architecture in understanding the neural mechanisms of states of consciousness.

Dataset factors associated with age-related changes in brain structure and function in neurodevelopmental conditions.

With brain structure and function undergoing complex changes throughout childhood and adolescence, age is a critical consideration in neuroimaging studies, particularly for those of individuals with neurodevelopmental conditions. However, despite the increasing use of large, consortium-based datasets to examine brain structure and function in neurotypical and neurodivergent populations, it is unclear whether age-related changes are consistent between datasets and whether inconsistencies related to differences in sample characteristics, such as demographics and phenotypic features, exist. To address this, we built models of age-related changes of brain structure (regional cortical thickness and regional surface area; N = 1218) and function (resting-state functional connectivity strength; N = 1254) in two neurodiverse datasets: the Province of Ontario Neurodevelopmental Network and the Healthy Brain Network. We examined whether deviations from these models differed between the datasets, and explored whether these deviations were associated with demographic and clinical variables. We found significant differences between the two datasets for measures of cortical surface area and functional connectivity strength throughout the brain. For regional measures of cortical surface area, the patterns of differences were associated with race/ethnicity, while for functional connectivity strength, positive associations were observed with head motion. Our findings highlight that patterns of age-related changes in the brain may be influenced by demographic and phenotypic characteristics, and thus future studies should consider these when examining or controlling for age effects in analyses.

Compressed cerebro-cerebellar functional gradients in children and adolescents with attention-deficit/hyperactivity disorder.

Both cortical and cerebellar developmental differences have been implicated in attention-deficit/hyperactivity disorder (ADHD). Recently accumulating neuroimaging studies have highlighted hierarchies as a fundamental principle of brain organization, suggesting the importance of assessing hierarchy abnormalities in ADHD. A novel gradient-based resting-state functional connectivity analysis was applied to investigate the cerebro-cerebellar disturbed hierarchy in children and adolescents with ADHD. We found that the interaction of functional gradient between diagnosis and age was concentrated in default mode network (DMN) and visual network (VN). At the same time, we also found that the opposite gradient changes of DMN and VN caused the compression of the cortical main gradient in ADHD patients, implicating the co-occurrence of both low- (visual processing) and high-order (self-related thought) cognitive dysfunction manifesting in abnormal cerebro-cerebellar organizational hierarchy in ADHD. Our study provides a neurobiological framework to better understand the co-occurrence and interaction of both low-level and high-level functional abnormalities in the cortex and cerebellum in ADHD.

Segmentation of supragranular and infragranular layers in ultra-high-resolution 7T ex vivo MRI of the human cerebral cortex.

Accurate labeling of specific layers in the human cerebral cortex is crucial for advancing our understanding of neurodevelopmental and neurodegenerative disorders. Building on recent advancements in ultra-high-resolution ex vivo MRI, we present a novel semi-supervised segmentation model capable of identifying supragranular and infragranular layers in ex vivo MRI with unprecedented precision. On a dataset consisting of 17 whole-hemisphere ex vivo scans at 120 $\mu $m, we propose a Multi-resolution U-Nets framework that integrates global and local structural information, achieving reliable segmentation maps of the entire hemisphere, with Dice scores over 0.8 for supra- and infragranular layers. This enables surface modeling, atlas construction, anomaly detection in disease states, and cross-modality validation while also paving the way for finer layer segmentation. Our approach offers a powerful tool for comprehensive neuroanatomical investigations and holds promise for advancing our mechanistic understanding of progression of neurodegenerative diseases.

Regional patterns of human cortex development correlate with underlying neurobiology.

Human brain morphology undergoes complex changes over the lifespan. Despite recent progress in tracking brain development via normative models, current knowledge of underlying biological mechanisms is highly limited. We demonstrate that human cortical thickness development and aging trajectories unfold along patterns of molecular and cellular brain organization, traceable from population-level to individual developmental trajectories. During childhood and adolescence, cortex-wide spatial distributions of dopaminergic receptors, inhibitory neurons, glial cell populations, and brain-metabolic features explain up to 50% of the variance associated with a lifespan model of regional cortical thickness trajectories. In contrast, modeled cortical thickness change patterns during adulthood are best explained by cholinergic and glutamatergic neurotransmitter receptor and transporter distributions. These relationships are supported by developmental gene expression trajectories and translate to individual longitudinal data from over 8000 adolescents, explaining up to 59% of developmental change at cohort- and 18% at single-subject level. Integrating neurobiological brain atlases with normative modeling and population neuroimaging provides a biologically meaningful path to understand brain development and aging in living humans.

The association between adverse childhood experiences and alterations in brain volume and cortical thickness in adults with alcohol use disorder.

BACKGROUND: Previous studies have established a connection between adverse childhood experiences (ACE) and alcohol use disorder (AUD), both of which are associated with alterations in grey matter volume (GMV) and cortical thickness (CT). The current study aimed to assess the neurobiological impact of ACE specifically in the context of AUD, as well as the role of maltreatment type (i.e., abuse or neglect) and timing. METHODS: Structural MRI data were collected from 35 adults with AUD (mean age: 40; 31% female) and 28 healthy controls (mean age: 36; 61% female). ACE were assessed retrospectively using the Childhood Trauma Questionnaire, and the Maltreatment and Abuse Chronology interview. Global and regional GMV and CT were estimated using voxel- and surface-based morphometry. RESULTS: Relative to the healthy controls, the AUD group had significantly reduced CT in the left inferior frontal gyrus, left circular sulcus of the insula and subcentral gyrus and sulci (cluster C1), and in the central sulcus and precentral gyrus (cluster C2). Within the AUD group, a reduction of CT in cluster C1 was significantly associated with higher severity of ACE and AUD. Type and timing analyses revealed a significant association between higher levels of abuse at ages 13 to 15 and reduced CT in cluster C1 within the AUD group. CONCLUSIONS: In adults with AUD, abuse experienced during early adolescence is associated with reduced CT in regions involved in inhibitory control, indicating the potential relevance of cognitive pathways in the association between ACE and AUD. Longitudinal studies are needed to confirm and expand upon current findings.

Changes in the structure of spontaneous speech predict the disruption of hierarchical brain organization in first-episode psychosis.

Psychosis implicates changes across a broad range of cognitive functions. These functions are cortically organized in the form of a hierarchy ranging from primary sensorimotor (unimodal) to higher-order association cortices, which involve functions such as language (transmodal). Language has long been documented as undergoing structural changes in psychosis. We hypothesized that these changes as revealed in spontaneous speech patterns may act as readouts of alterations in the configuration of this unimodal-to-transmodal axis of cortical organization in psychosis. Results from 29 patients with first-episodic psychosis (FEP) and 29 controls scanned with 7 T resting-state fMRI confirmed a compression of the cortical hierarchy in FEP, which affected metrics of the hierarchical distance between the sensorimotor and default mode networks, and of the hierarchical organization within the semantic network. These organizational changes were predicted by graphs representing semantic and syntactic associations between meaningful units in speech produced during picture descriptions. These findings unite psychosis, language, and the cortical hierarchy in a single conceptual scheme, which helps to situate language within the neurocognition of psychosis and opens the clinical prospect for mental dysfunction to become computationally measurable in spontaneous speech.

Surface-Based Morphometry Analysis of the Cerebral Cortex in Patients With Probable Idiopathic Rapid Eye Movement Sleep Behavior Disorder.

INTRODUCTION: Strong indications support the notion that idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) acts as a precursor to multiple α-synucleinopathies, including Parkinson's disease and dementia with Lewy bodies. Despite numerous investigations into the alterations in cortical thickness and the volume of subcortical areas associated with this condition, comprehensive studies on the cortical surface morphology, focusing on gyrification and sulcal depth changes, are scarce. The purpose of this research was to explore the cortical surface morphology in individuals with probable iRBD (piRBD), to pinpoint early-phase diagnostic markers. METHODS: This study included 30 piRBD patients confirmed using the RBD Screening Questionnaire (RBDSQ) and 33 control individuals selected from the Parkinson's Progression Markers Initiative (PPMI) database. They underwent neurophysiological tests and MRI scans. The FreeSurfer software was utilized to estimate cortical thickness (CTH), cortical and subcortical volumetry, local gyrification index (LGI), and sulcus depth (SD). Subsequently, these parameters were compared between the two groups. Additionally, linear correlation analysis was employed to estimate the relationship between brain morphological parameters and clinical parameters. RESULTS: Compared to the healthy control (HC), piRBD patients exhibited a significant reduction in CTH, LGI, and cortical volume in the bilateral superior parietal, lateral occipital, orbitofrontal, temporo-occipital, bilateral rostral middle frontal, inferior parietal, and precentral brain regions. Moreover, a significant and notable correlation was observed between CTH and Geriatric Depression Scale (GDS), letter-number sequencing (LTNS), the Benton Judgment of Line Orientation (BJLO) test, and the symbol digit modalities test (SDMT) in several brain regions encompassing the motor cortex. CONCLUSION: Patients with piRBD displayed widespread atrophy in various brain regions, predominantly covering the motor and sensory cortex. Furthermore, LGI could serve as a prognostic biomarker of disease's progression in piRBD.

Quantitative MRI Measures and Cognitive Function in People With Drug-Resistant Juvenile Myoclonic Epilepsy.

BACKGROUND AND OBJECTIVES: Neuroimaging studies have so far identified structural changes in individuals with juvenile myoclonic epilepsy (JME) when compared with controls. However, the underlying mechanisms of drug-resistant JME remain unknown. In this study, we aimed at characterizing the structural underpinnings of drug-resistant JME using MRI-derived cortical morphologic markers. METHODS: In this prospective cross-sectional 2-center study, T1-weighted MRI and neuropsychological measures of verbal memory and executive function were obtained in individuals with drug-resistant and drug-responsive JME recruited from epilepsy outpatient clinics and healthy controls. We performed vertexwise measurements of cortical thickness, surface area, and local gyrification index (LGI). Vertexwise group comparisons were corrected for multiple comparisons at a familywise error (FWE) of 0.05. The neuropsychological profile of disease subgroups was analyzed through principal component analysis. RESULTS: We studied 42 individuals with drug-resistant JME (mean age 29 ± 11 years, 50% female), 37 with drug-responsive JME (mean age 34 ± 10, years, 59% female), and 71 healthy controls (mean age 21 ± 9 years, 61% female). Surface area was increased in participants with drug-resistant JME in the left temporal lobe (Cohen d = 0.82 [-0.52 to -1.12], pFWE < 0.05) when compared with the drug-responsive group. Although no cortical thickness changes were observed between disease subgroups, drug-resistant and drug-sensitive participants showed discrete cortical thinning against controls (Cohen d = -0.42 [-0.83 to -0.01], pFWE < 0.05; Cohen d = -0.57 [-1.03 to -0.11], pFWE < 0.05, respectively). LGI was increased in the left temporal and occipital lobes in drug-resistant participants (Cohen d = 0.60 [0.34-0.86], pFWE < 0.05) when contrasting against drug-sensitive participants, but not controls. The composite executive function score was reduced in drug-resistant individuals compared with controls and drug-sensitive individuals (-1.74 [-2.58 to -0.90], p < 0.001 and -1.29 [-2.25 to -0.33], p < 0.01, respectively). Significant correlations were observed between executive function impairment and increased surface area in the precuneus and medial prefrontal regions (r = -0.79, pFWE < 0.05) in participants with drug-resistant JME. DISCUSSION: We identified a developmental phenotype in individuals with drug-resistant JME characterized by changes in cortical surface area and folding complexity, the extent of which correlates with executive dysfunction. No association was observed between cortical thickness and disease severity. Our findings support a neurodevelopmental basis for drug resistance and cognitive impairment in JME.

Dynamic transient brain states in preschoolers mirror parental report of behavior and emotion regulation.

The temporal dynamics of resting-state networks may represent an intrinsic functional repertoire supporting cognitive control performance across the lifespan. However, little is known about brain dynamics during the preschool period, which is a sensitive time window for cognitive control development. The fast timescale of synchronization and switching characterizing cortical network functional organization gives rise to quasi-stable patterns (i.e., brain states) that recur over time. These can be inferred at the whole-brain level using hidden Markov models (HMMs), an unsupervised machine learning technique that allows the identification of rapid oscillatory patterns at the macroscale of cortical networks. The present study used an HMM technique to investigate dynamic neural reconfigurations and their associations with behavioral (i.e., parental questionnaires) and cognitive (i.e., neuropsychological tests) measures in typically developing preschoolers (4-6 years old). We used high-density EEG to better capture the fast reconfiguration patterns of the HMM-derived metrics (i.e., switching rates, entropy rates, transition probabilities and fractional occupancies). Our results revealed that the HMM-derived metrics were reliable indices of individual neural variability and differed between boys and girls. However, only brain state transition patterns toward prefrontal and default-mode brain states, predicted differences on parental-report questionnaire scores. Overall, these findings support the importance of resting-state brain dynamics as functional scaffolds for behavior and cognition. Brain state transitions may be crucial markers of individual differences in cognitive control development in preschoolers.

The Combination of Presurgical Cortical Gray Matter Volumetry and Cerebral Perfusion Improves the Efficacy of Predicting Postoperative Cognitive Impairment of Elderly Patients.

BACKGROUND: Postoperative cognitive dysfunction (POCD) is a common complication of the central nervous system in elderly surgical patients. Structural MRI and arterial spin labelling (ASL) techniques found that the grey matter volume and cerebral perfusion in some specific brain areas are associated with the occurrence of POCD, but the results are inconsistent, and the predictive accuracy is low. We hypothesised that the combination of cortical grey matter volumetry and cerebral blood flow yield higher accuracy than either of the methods in discriminating the elderly individuals who are susceptible to POCD after abdominal surgery. MATERIALS AND METHODS: Participants underwent neuropsychological testing before and after surgery. Postoperative cognitive dysfunction (POCD) was defined as a decrease in cognitive score of at least 20%. ASL-MRI and T1-weighted imaging were performed before surgery. We compared differences in cerebral blood flow (CBF) and cortical grey matter characteristics between POCD and non-POCD patients and generated receiver operating characteristic curves. RESULTS: Out of 51 patients, 9 (17%) were diagnosed with POCD. CBF in the inferior frontal gyrus was lower in the POCD group compared to the non-POCD group (p < 0.001), and the volume of cortical grey matter in the anterior cingulate gyrus was higher in the POCD group (p < 0.001). The highest AUC value was 0.973. CONCLUSIONS: The combination of cortical grey matter volumetry and cerebral perfusion based on ASL-MRI has improved efficacy in the early warning of POCD to elderly abdominal surgical patients.

Psychiatric phenotype in neurodevelopmental myoclonus-dystonia is underpinned by abnormality of cerebellar modulation on the cerebral cortex.

Psychiatric symptoms are common in neurodevelopmental movement disorders, including some types of dystonia. However, research has mainly focused on motor manifestations and underlying circuits. Myoclonus-dystonia is a rare and homogeneous neurodevelopmental condition serving as an illustrative paradigm of childhood-onset dystonias, associated with psychiatric symptoms. Here, we assessed the prevalence of psychiatric disorders and the severity of depressive symptoms in patients with myoclonus-dystonia and healthy volunteers (HV). Using resting-state functional neuroimaging, we compared the effective connectivity within and among non-motor and motor brain networks between patients and HV. We further explored the hierarchical organization of these networks and examined the relationship between their connectivity and the depressive symptoms. Comparing 19 patients to 25 HV, we found a higher prevalence of anxiety disorders and more depressive symptoms in the patient group. Patients exhibited abnormal modulation of the cerebellum on the cerebral cortex in the sensorimotor, dorsal attention, salience, and default mode networks. Moreover, the salience network activity was directed by the cerebellum in patients and was related to depressive symptoms. Altogether, our findings highlight the role of the cerebellar drive on both motor and non-motor cortical areas in this disorder, suggesting cerebellar involvement in the complex phenotype of such neurodevelopmental movement disorders.

Cortical activity during online motor control in children with and without developmental coordination disorder: a cross-sectional functional near-infrared spectroscopy study.

BACKGROUND: Children with developmental coordination disorder (DCD) have impaired online motor control. Researchers posit that this impairment could be due to a deficit in utilizing the internal model control process. However, there is little neurological evidence to support this view because few neuroimaging studies have focused specifically on tasks involving online motor control. Therefore, the aim of this study was to investigate the differences in cortical hemodynamic activity during an online movement adjustment task between children with and without DCD. METHODS: Twenty children with DCD (mean age: 9.88 ± 1.67 years; gender: 14M/6F) and twenty age-and-gender matched children with typical development (TD) (mean age: 9.87 ± 1.59 years; gender: 14M/6F) were recruited via convenience sampling. Participants performed a double-step reaching task under two conditions (with and without online adjustment of reaching). Cortical hemodynamic activity during task in ten regions of interest, including bilateral primary somatosensory cortex, primary motor cortex, premotor cortex, superior parietal cortex, and inferior parietal cortex was recorded using functional near-infrared spectroscopy. In the analyses, change in oxyhemoglobin (ΔHbO) concentration was used to characterize hemodynamic response. Two-way analyses of variance were conducted for each region of interest to compare hemodynamic responses between groups and conditions. Additionally, Pearson's r correlations between hemodynamic response and task performance were performed. RESULTS: Outcome showed that children with DCD required significantly more time to correct their reaching movements compared to the control group (t = 3.948, P < 0.001). Furthermore, children with DCD have a significantly lower ΔHbO change in the left superior parietal cortex during movement correction, compared to children with TD (F = 4.482, P = 0.041). Additionally, a significant negative correlation (r = - 0.598, P < 0.001) was observed between the difference in movement time of reaching and the difference in ΔHbO between conditions in the left superior parietal cortex. CONCLUSIONS: The findings of this study suggest that deficiencies in processing real-time sensory feedback, considering the function of the superior parietal cortex, might be related to the impaired online motor control observed in children with DCD. Interventions could target this issue to enhance their performance in online motor control.