scholarly journals Early executive function deficit in preterm children and its association with neurodevelopmental disorders in childhood: a literature review

2012 ◽  
Vol 24 (4) ◽  
pp. 291-299 ◽  
Author(s):  
Jing Sun ◽  
Nicholas Buys

Abstract The purpose of this study is to examine the association of deficits of executive function (EF) and neurodevelopmental disorders in preterm children and the potential of assessing EF in infants as means of early identification. EF refers to a collection of related but somewhat discrete abilities, the main ones being working memory, inhibition, and planning. There is a general consensus that EF governs goal-directed behavior that requires holding those plans or programs on-line until executed, inhibiting irrelevant action and planning a sequence of actions. EF plays an essential role in cognitive development and is vital to individual social and intellectual success. Most researchers believe in the coordination and integrate cognitive–perceptual processes in relation to time and space, thus regulating higher-order cognitive processes, such as problem solving, reasoning, logical and flexible thinking, and decision-making. The importance of the maturation of the frontal lobe, particularly the prefrontal cortex, to the development of EF in childhood has been emphasized. Therefore, any abnormal development in the prefrontal lobes of infants and children could be expected to result in significant deficits in cognitive functioning. As this is a late-maturing part of the brain, various neurodevelopmental disorders, such as autism spectrum disorders, attention deficit hyperactivity disorder, language disorders, and schizophrenia, as well as acquired disorders of the right brain (and traumatic brain injury) impair EF, and the prefrontal cortex may be particularly susceptible to delayed development in these populations. The deficits of EF in infants are persistent into childhood and related to neurodevelopmental disorders in childhood and adolescence.

Author(s):  
Ashwini Deshpande Nagarhalli

Attention deficit hyperactivity disorder (ADHD) is one of the widely prevalent externalizing disorders from the category of neurodevelopmental disorders. With the constant rise in the diagnosis of a number of cases presenting ADHD or ADHD-like symptoms, the need to understand issues as experienced by the student requires the right interventions for effective management. The core challenges in the area of academics and overall presentation lie with the executive function deficits that the child has. Hence, addressing those and working on skills like attention, working memory, response inhibition, goal setting, planning, problem solving, and organization has to be considered as part of the management plan. The current chapter explores evidence-based issues and strategies to be targeted in the classroom set up for students with ADHD. It also highlights some classroom-specific strategies, which can be focused by the teachers and remedial therapists.


2021 ◽  
Vol 12 ◽  
Author(s):  
Wenbin Pang ◽  
Xinan Yi ◽  
Ling Li ◽  
Liyan Liu ◽  
Wei Xiang ◽  
...  

Neurodevelopmental disorders are psychiatric diseases that are usually first diagnosed in infancy, childhood and adolescence. Autism spectrum disorder (ASD) is a neurodevelopmental disorder, characterized by core symptoms including impaired social communication, cognitive rigidity and repetitive behavior, accompanied by a wide range of comorbidities such as intellectual disability (ID) and dysmorphisms. While the cause remains largely unknown, genetic, epigenetic, and environmental factors are believed to contribute toward the onset of the disease. Autism Susceptibility Candidate 2 (Auts2) is a gene highly associated with ID and ASD. Therefore, understanding the function of Auts2 gene can provide a unique entry point to untangle the complex neuronal phenotypes of neurodevelpmental disorders. In this review, we discuss the recent discoveries regarding the molecular and cellular functions of Auts2. Auts2 was shown to be a key-regulator of transcriptional network and a mediator of epigenetic regulation in neurodevelopment, the latter potentially providing a link for the neuronal changes of ASD upon environmental risk-factor exposure. In addition, Auts2 could synchronize the balance between excitation and inhibition through regulating the number of excitatory synapses. Cytoplasmic Auts2 could join the fine-tuning of actin dynamics during neuronal migration and neuritogenesis. Furthermore, Auts2 was expressed in developing mouse and human brain regions such as the frontal cortex, dorsal thalamus, and hippocampus, which have been implicated in the impaired cognitive and social function of ASD. Taken together, a comprehensive understanding of Auts2 functions can give deep insights into the cause of the heterogenous manifestation of neurodevelopmental disorders such as ASD.


2021 ◽  
Vol 13 ◽  
Author(s):  
Qing Ye ◽  
Haifeng Chen ◽  
Renyuan Liu ◽  
Ruomeng Qin ◽  
Caimei Luo ◽  
...  

Both episodic memory and executive function are impaired in amnestic mild cognitive impairment (aMCI) subjects, but it is unclear if these impairments are independent or interactive. The present study aimed to explore the relationship between episodic memory deficits and executive function deficits, and the underlying functional mechanisms in aMCI subjects. Thirty-one aMCI subjects and 27 healthy subjects underwent neuropsychological tests and multimodal magnetic resonance imaging (MRI) scans. Hippocampal networks and medial prefrontal cortex (MPFC) networks were identified based on resting-sate functional MRI (fMRI) data. AMCI subjects displayed lower episodic memory scores and executive function scores than control subjects, and the episodic memory scores were positively correlated with the executive function scores in aMCI subjects. Brain network analyses showed an interaction between the hippocampal networks and the MPFC networks, and the interaction was significantly associated with the episodic memory scores and the executive function scores. Notably, aMCI subjects displayed higher functional connectivity (FC) of the right hippocampal network with the right prefrontal cortex than did control subjects, but this difference disappeared when controlling for the MPFC networks. Furthermore, the effects of the MPFC networks on the hippocampal networks were significantly associated with the episodic memory scores in aMCI subjects. The present findings suggested that the episodic memory deficits in aMCI subjects could be partially underpinned by the modulation of the MPFC networks on the hippocampal networks.


Author(s):  
Christen M. Holder ◽  
Nicole Shay

This chapter examines the different theoretical conceptualizations of executive functions and how neuroimaging can reveal their neuroanatomical mechanisms. After briefly considering various definitions and descriptions of executive function, it discusses the results of lesion studies that look into specific executive functions; namely, attention, working memory, inhibition, decision-making, planning and organization, processing speed, and cognitive flexibility or shifting. It also evaluates measures that are used to capture the executive functions just cited, along with the advances that have been achieved with the help of neuroimaging studies. On the basis of neuroimaging evidence, the authors show that the right prefrontal cortex, as well as the parietal and temporal lobes, plays an important role in executive function.


2016 ◽  
Vol 41 (8) ◽  
pp. 2171-2177 ◽  
Author(s):  
Robin J Borchert ◽  
Timothy Rittman ◽  
Luca Passamonti ◽  
Zheng Ye ◽  
Saber Sami ◽  
...  

Abstract Cognitive impairment is common in Parkinson’s disease (PD), but often not improved by dopaminergic treatment. New treatment strategies targeting other neurotransmitter deficits are therefore of growing interest. Imaging the brain at rest (‘task-free’) provides the opportunity to examine the impact of a candidate drug on many of the brain networks that underpin cognition, while minimizing task-related performance confounds. We test this approach using atomoxetine, a selective noradrenaline reuptake inhibitor that modulates the prefrontal cortical activity and can facilitate some executive functions and response inhibition. Thirty-three patients with idiopathic PD underwent task-free fMRI. Patients were scanned twice in a double-blind, placebo-controlled crossover design, following either placebo or 40-mg oral atomoxetine. Seventy-six controls were scanned once without medication to provide normative data. Seed-based correlation analyses were used to measure changes in functional connectivity, with the right inferior frontal gyrus (IFG) a critical region for executive function. Patients on placebo had reduced connectivity relative to controls from right IFG to dorsal anterior cingulate cortex and to left IFG and dorsolateral prefrontal cortex. Atomoxetine increased connectivity from the right IFG to the dorsal anterior cingulate. In addition, the atomoxetine-induced change in connectivity from right IFG to dorsolateral prefrontal cortex was proportional to the change in verbal fluency, a simple index of executive function. The results support the hypothesis that atomoxetine may restore prefrontal networks related to executive functions. We suggest that task-free imaging can support translational pharmacological studies of new drug therapies and provide evidence for engagement of the relevant neurocognitive systems.


2019 ◽  
Vol 116 (14) ◽  
pp. 7083-7088 ◽  
Author(s):  
Min Ma ◽  
Qian Ren ◽  
Jun Yang ◽  
Kai Zhang ◽  
Zhongwei Xiong ◽  
...  

Maternal infection during pregnancy increases risk of neurodevelopmental disorders such as schizophrenia and autism spectrum disorder (ASD) in offspring. In rodents, maternal immune activation (MIA) yields offspring with schizophrenia- and ASD-like behavioral abnormalities. Soluble epoxide hydrolase (sEH) plays a key role in inflammation associated with neurodevelopmental disorders. Here we found higher levels of sEH in the prefrontal cortex (PFC) of juvenile offspring after MIA. Oxylipin analysis showed decreased levels of epoxy fatty acids in the PFC of juvenile offspring after MIA, supporting increased activity of sEH in the PFC of juvenile offspring. Furthermore, expression of sEH (orEPHX2) mRNA in induced pluripotent stem cell-derived neurospheres from schizophrenia patients with the 22q11.2 deletion was higher than that of healthy controls. Moreover, the expression ofEPHX2mRNA in postmortem brain samples (Brodmann area 9 and 40) from ASD patients was higher than that of controls. Treatment with 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl)urea (TPPU), a potent sEH inhibitor, in juvenile offspring from prenatal day (P) 28 to P56 could prevent cognitive deficits and loss of parvalbumin (PV) immunoreactivity in the medial PFC of adult offspring after MIA. In addition, dosing of TPPU to pregnant mothers from E5 to P21 could prevent cognitive deficits, and social interaction deficits and PV immunoreactivity in the medial prefrontal cortex of juvenile offspring after MIA. These findings suggest that increased activity of sEH in the PFC plays a key role in the etiology of neurodevelopmental disorders in offspring after MIA. Therefore, sEH represents a promising prophylactic or therapeutic target for neurodevelopmental disorders in offspring after MIA.


2018 ◽  
Author(s):  
Dina R. Dajani ◽  
Catherine A. Burrows ◽  
Paola Odriozola ◽  
Adriana Baez ◽  
Mary Beth Nebel ◽  
...  

AbstractBackgroundCurrent diagnostic systems for neurodevelopmental disorders do not have clear links to underlying neurobiology, limiting their utility in identifying targeted treatments for individuals. Several factors contribute to this issue, including the use of small samples in neuroimaging research and heterogeneity within diagnostic categories. Here, we aimed to investigate differences in functional brain network integrity between traditional diagnostic categories (autism spectrum disorder [ASD], attention-deficit/hyperactivity disorder [ADHD], typically developing [TD]) and carefully consider the impact of comorbid ASD and ADHD on functional brain network integrity in a large sample. We also assess the neurobiological validity of a novel, potential alternative nosology based on behavioral measures of executive function.MethodFive-minute resting-state fMRI data were obtained from 168 children (128 boys, 40 girls) with ASD, ADHD, comorbid ASD and ADHD, and TD children. Independent component analysis and dual regression were used to compute within- and between-network functional connectivity metrics at the individual level.ResultsNo significant group differences in within- nor between-network functional connectivity were observed between traditional diagnostic categories (ASD, ADHD, TD) even when stratified by comorbidity (ASD+ADHD, ASD, ADHD, TD). Similarly, subgroups classified by executive functioning levels showed no group differences.ConclusionsUsing clinical diagnosis and behavioral measures of executive function, no group differences were observed among the categories examined. Therefore, we suggest that brain imaging metrics may more effectively define clinical subgroups than behavioral metrics, and may contribute to the establishment of a neurobiologically valid nosology for neurodevelopmental disorders.


2020 ◽  
Author(s):  
Sayali Gore ◽  
Eric J. James ◽  
Lin-Chien Huang ◽  
Jenn J. Park ◽  
Andrea Berghella ◽  
...  

AbstractMatrix metalloproteinase-9 (MMP-9) is a secreted endopeptidase targeting extracellular matrix proteins, creating permissive environments for neuronal development and plasticity. Developmental dysregulation of MMP-9 is also associated with neurodevelopmental disorders (ND). Here we test the hypothesis that chronically elevated MMP-9 activity during early neurodevelopment is responsible for neural circuit hyperconnectivity observed after early exposure to valproic acid (VPA), a known teratogen associated with autism spectrum disorder in humans. In Xenopus tadpoles, VPA exposure results in excess local synaptic connectivity, disrupted social behavior and increased seizure susceptibility. We found that overexpressing MMP-9 in the brain copies effects of VPA on synaptic connectivity, and blocking MMP-9 activity pharmacologically or genetically reverses effects of VPA on physiology and behavior. We further show that during normal neurodevelopment MMP-9 levels are tightly regulated by neuronal activity and required for structural plasticity. These studies show a critical role for MMP-9 in both normal and abnormal development.


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