Specifically, combined treatment showed significant superiority for ADHD with learning disorders (ES 0.66) and ODD (ES 0.98), lower for ADHD with sleep or anxiety disorders.
Noonan syndrome is a heterogenous rasopathy typically presenting with short stature, characteristic facial features, cardiac abnormalities including pulmonic valve stenosis, ASD and hypertrophic cardiomyopathy (HCM), cryptorchidism, ectodermal abnormalities, and learning differences.
A surprising number of variants have been found in the N-methyl-d-aspartate receptor (NMDAR) gene family, with the GRIN2B gene encoding the GluN2B subunit being implicated in many cases of neurodevelopmental disorders, which are psychiatric conditions originating in childhood and include language, motor, and learning disorders, autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), developmental delay, epilepsy, and schizophrenia.
Developmental dyslexia, the most common childhood learning disorder, is highly heritable, and recent studies have identified KIAA0319-Like (KIAA0319L) as a candidate dyslexia susceptibility gene at the 1p36-34 (DYX8) locus.
This study examined the test-retest reliability of the four- and two-factor structures (i.e., Memory and Speed) of ImPACT over a 2-year interval across multiple groups with premorbid conditions, including those with a history of special education or learning disorders (LD; n = 114), treatment history for headache/migraine (n = 81), and a control group (n = 792).
Developmental dyslexia, the most common childhood learning disorder, is highly heritable, and recent studies have identified KIAA0319-Like (KIAA0319L) as a candidate dyslexia susceptibility gene at the 1p36-34 (DYX8) locus.
Here we related mutations in EPM2A with phenotypes of 22 patients (14 families) and identified two subsyndromes: (i) classical LD with adolescent-onset stimulus-sensitive grand mal, absence and myoclonic seizures followed by dementia and neurologic deterioration, and associated mainly with mutations in exon 4 (P = 0.0007); (ii) atypical LD with childhood-onset dyslexia and learning disorder followed by epilepsy and neurologic deterioration, and associated mainly with mutations in exon 1 (P = 0.0015).
Taken together, these results show that reduced expression of KCC2, lumbar hyperreflexia, spasticity, altered properties of the soleus muscle, as well as cortical hyperexcitability may likely interplay into a self-perpetuating cycle, leading to the emergence, and persistence of neurodevelopmental disorders (NDD) in EP and CP, such as sensorimotor impairments, and probably hyperactivity, attention, and learning disorders.
The EEG analysis showed that the non-LD children displayed significant interference effects both in the ERP components, with N2, N450 and SP exhibiting a larger activation in incongruent condition than the congruent condition, and brain oscillation, with early and late alpha demonstrating a larger desynchronization in the incongruent condition compared to the congruent condition.
This expression pattern is consistent with GSCL having either an indirect role in the development of neural crest-derived structures or a direct role in a subset of the phenotype observed in DGS/VCFS, such as learning disorders or psychiatric disease.
The EEG analysis showed that the non-LD children displayed significant interference effects both in the ERP components, with N2, N450 and SP exhibiting a larger activation in incongruent condition than the congruent condition, and brain oscillation, with early and late alpha demonstrating a larger desynchronization in the incongruent condition compared to the congruent condition.
After CAT, children diagnosed with ADHD-LD showed 1) improvements in trained skills, measured directly within the software and indirectly by external psychometric tests; 2) improvements in attention, memory, and some executive functioning; 3) improvements in academic performance, particularly in mathematics; and 4) reductions in maladaptive behavioral features.
Protective effects of astragalosides on dexamethasone and Aβ25-35 induced learning and memory impairments due to decrease amyloid precursor protein expression in 12-month male rats.
Ethosuximide Induces Hippocampal Neurogenesis and Reverses Cognitive Deficits in an Amyloid-β Toxin-induced Alzheimer Rat Model via the Phosphatidylinositol 3-Kinase (PI3K)/Akt/Wnt/β-Catenin Pathway.