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Australian Family Physician Sep 2005Developmental delay occurs in up to 5% of children under 5 years of age. This includes delays in speech and language development, motor development, social-emotional... (Review)
Review
BACKGROUND
Developmental delay occurs in up to 5% of children under 5 years of age. This includes delays in speech and language development, motor development, social-emotional development, and cognitive development. General practitioners are in an ideal position to play a central role in the early detection of developmental and behavioural problems in young children.
OBJECTIVE
This article discusses the advantages and disadvantages of various methods health professionals use to assess children's development. It recommends ongoing developmental surveillance (rather than point-in-time assessment) and a multidisciplinary approach.
DISCUSSION
In a busy general practice, obtaining parent reports of development is a good "first line screen", and an efficient and effective way of selecting out children who require a more detailed assessment and/or referral. Early intervention is essential for optimising developmental progress in the delayed child.
Topics: Child Development; Child, Preschool; Developmental Disabilities; Family Practice; Humans; Infant; Mass Screening; Medical History Taking; Parents; Physician's Role; Professional-Family Relations; Referral and Consultation
PubMed: 16184205
DOI: No ID Found -
International Journal of Epidemiology Oct 2022Impaired neurodevelopment is reported among children conceived by assisted reproductive technologies (ART). However, this might be explained by conditions underlying...
BACKGROUND
Impaired neurodevelopment is reported among children conceived by assisted reproductive technologies (ART). However, this might be explained by conditions underlying parental subfecundity, rather than the ART procedure.
METHODS
We examined associations of parental time-to-pregnancy (TTP) and conception by ART with neurodevelopmental traits up to 8 years of age, including motor and language skills, social delays and difficulties, and inattention-hyperactivity, among 92 142 singletons participating in the Norwegian Mother, Father and Child Cohort Study (MoBa). Mothers reported TTP and neurodevelopmental traits through questionnaires. Mean differences in standardized neurodevelopmental traits were estimated using linear regression, adjusting for maternal age, parity, educational level, body mass index and smoking, and paternal age.
RESULTS
A longer TTP was associated with decreased language skills and motor skills at 6, 18 and 36 months (P-values for trend ≤0.01), prosocial skills delay at 36 months (P-values for trend ≤0.001) and increased scores for inattention-hyperactivity traits at all ages up to 8 years (P-values for trend from 0.06 to 0.01). Effect sizes were small, ranging between 0.03 and 0.05 difference in the standardized neurodevelopmental scores. Estimates for ART were imprecise, but there were no differences between children conceived by ART and naturally conceived children of subfecund parents (TTP ≥12 months).
CONCLUSIONS
Longer parental TTP is modestly but robustly associated with offspring neurodevelopmental delays and difficulties, with no added impact of ART. Future studies should investigate the underlying causes of-or aspects related to-parental subfecundity which might explain the association with offspring neurodevelopmental delays and difficulties.
Topics: Child; Cohort Studies; Female; Fertility; Humans; Mothers; Pregnancy; Reproductive Techniques, Assisted
PubMed: 35536321
DOI: 10.1093/ije/dyac094 -
Current Topics in Behavioral... 2012Structural and functional imaging studies in subjects with attention deficit hyperactivity disorder (ADHD) are reviewed with the goal of gleaning information about... (Review)
Review
Structural and functional imaging studies in subjects with attention deficit hyperactivity disorder (ADHD) are reviewed with the goal of gleaning information about neurodevelopmental abnormalities characterizing the disorder. Structural imaging studies, particularly those with longitudinal designs, suggest that brain maturation is delayed by a few years in ADHD. However, a maturational delay model alone is incomplete: alternate courses are suggested by differences associated with phenotypic factors, such as symptom remission/persistence and exposure to stimulant treatment. Findings from functional imaging studies point to multiple loci of abnormalities that are not limited to frontal-striatal circuitry, which is important for executive and motivational function, but also include parietal, temporal and motor cortices, and the cerebellum. However, a definitive conclusion about maturational delays or alternate trajectories cannot be drawn from this work as activation patterns are influenced by task-specific factors that may induce variable performance levels and strategies across development. In addition, no studies have implemented cross-sectional or longitudinal designs, without which the developmental origin of differences in activation cannot be inferred. Thus, current task-evoked functional imaging provides information about dynamic or state-dependent differences rather than fixed or trait-related differences. In the future, task-free functional imaging holds promise for revealing neurodevelopmental information that is minimally influenced by performance/strategic differences. Further, studies using longitudinal designs that identify sources of phenotypic heterogeneity in brain maturation and characterize the relationship between brain function and underlying structural properties are needed to provide a comprehensive view of neurodevelopmental abnormalities in ADHD.
Topics: Attention Deficit Disorder with Hyperactivity; Brain; Cognition Disorders; Developmental Disabilities; Humans; Neuroimaging
PubMed: 21541845
DOI: 10.1007/7854_2011_138 -
Toxicology Nov 2021Phthalates are chemicals widely used in packaging and consumer products, which have been shown to interfere with normal hormonal function and development in some human...
UNLABELLED
Phthalates are chemicals widely used in packaging and consumer products, which have been shown to interfere with normal hormonal function and development in some human and animal studies. In recent decades, pregnant women's exposure to phthalates has been shown to alter the cognitive outcomes of their babies, and some studies have found delays in motor development.
METHODS
electronic databases including PubMed/MEDLINE and Scopus were searched from their inception to March 2021, using the keywords "phthalate", "cognitive" and "motor".
RESULTS
most studies find statistically significant inverse relationships between maternal urinary phthalate concentration during pregnancy and subsequent outcomes in children's cognitive and motor scales, especially in boys rather than girls. However, many associations are not significant, and there were even positive associations, especially in the third trimester.
CONCLUSION
the relationship between exposure to phthalates during pregnancy and low results on neurocognitive scales is sufficiently clear to adopt policies to reduce exposure. Further studies are needed to analyze sex differences, coordination and motor scales, and phthalate levels during breastfeeding.
Topics: Animals; Cognition; Female; Humans; Male; Maternal Exposure; Motor Skills; Phthalic Acids; Pregnancy; Prenatal Exposure Delayed Effects; Sex Factors
PubMed: 34624397
DOI: 10.1016/j.tox.2021.152980 -
International Journal of Molecular... Mar 2023DJ-1 is a redox sensitive protein with a wide range of functions related to oxidative stress protection. Mutations in the gene, which codes for DJ-1 are associated with...
DJ-1 is a redox sensitive protein with a wide range of functions related to oxidative stress protection. Mutations in the gene, which codes for DJ-1 are associated with early onset familial Parkinson's disease and increased astrocytic DJ-1 levels are found in pathologic tissues from idiopathic Parkinson's disease. We have previously established a DJ-1 knockout zebrafish line that developed normally, but with aging the DJ-1 null fish had a lowered level of tyrosine hydroxylase, respiratory mitochondrial failure and a lower body mass. Here we have examined the DJ-1 knockout from the early adult stage and show that loss of DJ-1 results in a progressive, age-dependent increase in both motoric and non-motoric symptoms associated to Parkinson's disease. These changes coincide with changes in mitochondrial and mitochondrial associated proteins. Recent studies have suggested that a decline in NAD+ can contribute to Parkinson's disease and that supplementation of NAD+ precursors may delay disease progression. We found that the brain NAD+/NADH ratio decreased in aging zebrafish but did not correlate with DJ-1 induced altered behavior. Differences were first observed at the late adult stage in which NAD+ and NADPH levels were decreased in DJ-1 knockouts. Considering the experimental power of zebrafish and the development of Parkinson's disease-related symptoms in the DJ-1 null fish, this model can serve as a useful tool both to understand the progression of the disease and the effect of suggested treatments.
Topics: Animals; Parkinson Disease; Zebrafish; NAD; Brain; Protein Deglycase DJ-1
PubMed: 37047429
DOI: 10.3390/ijms24076456 -
Molecular Medicine Reports Oct 2017Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease, which involves the progressive degeneration of motor neurons. ALS has long been considered a... (Review)
Review
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease, which involves the progressive degeneration of motor neurons. ALS has long been considered a disease of the grey matter; however, pathological alterations of the white matter (WM), including axonal loss, axonal demyelination and oligodendrocyte death, have been reported in patients with ALS. The present review examined motor neuron death as the primary cause of ALS and evaluated the associated WM damage that is guided by neuronal‑glial interactions. Previous studies have suggested that WM damage may occur prior to the death of motor neurons, and thus may be considered an early indicator for the diagnosis and prognosis of ALS. However, the exact molecular mechanisms underlying early‑onset WM damage in ALS have yet to be elucidated. The present review explored the detailed anatomy of WM and identified several pathological mechanisms that may be implicated in WM damage in ALS. In addition, it associated the pathophysiological alterations of WM, which may contribute to motor neuron death in ALS, with similar mechanisms of WM damage that are involved in multiple sclerosis (MS). Furthermore, the early detection of WM damage in ALS, using neuroimaging techniques, may lead to earlier therapeutic intervention, using immunomodulatory treatment strategies similar to those used in relapsing‑remitting MS, aimed at delaying WM damage in ALS. Early therapeutic approaches may have the potential to delay motor neuron damage and thus prolong the survival of patients with ALS. The therapeutic interventions that are currently available for ALS are only marginally effective. However, early intervention with immunomodulatory drugs may slow the progression of WM damage in the early stages of ALS, thus delaying motor neuron death and increasing the life expectancy of patients with ALS.
Topics: Amyotrophic Lateral Sclerosis; Animals; Disease Progression; Humans; Models, Biological; White Matter
PubMed: 28791401
DOI: 10.3892/mmr.2017.7186 -
Autism Research : Official Journal of... May 2022Angelman syndrome (AS) is a genetic neurodevelopmental disorder characterized by developmental delay, lack of speech, seizures, intellectual disability, hypotonia, and...
Angelman syndrome (AS) is a genetic neurodevelopmental disorder characterized by developmental delay, lack of speech, seizures, intellectual disability, hypotonia, and motor coordination deficits. Motor abilities are an important outcome measure in AS as they comprise a broad repertoire of metrics including ataxia, hypotonia, delayed ambulation, crouched gait, and poor posture, and motor dysfunction affects nearly every individual with AS. Guided by collaborative work with AS clinicians studying gait, the goal of this study was to perform an in-depth gait analysis using the automated treadmill assay, DigiGait. Our hypothesis is that gait presents a strong opportunity for a reliable, quantitative, and translational metric that can serve to evaluate novel pharmacological, dietary, and genetic therapies. In this study, we used an automated gait analysis system, in addition to standard motor behavioral assays, to evaluate components of motor, exploration, coordination, balance, and gait impairments across the lifespan in an AS mouse model. Our study demonstrated marked global motoric deficits in AS mice, corroborating previous reports. Uniquely, this is the first report of nuanced aberrations in quantitative spatial and temporal components of gait in AS mice compared to sex- and age-matched wildtype littermates followed longitudinally using metrics that are analogous in AS individuals. Our findings contribute evidence toward the use of nuanced motor outcomes (i.e., gait) as valuable and translationally powerful metrics for therapeutic development for AS, as well as other genetic neurodevelopmental syndromes. LAY SUMMARY: Movement disorders affect nearly every individual with Angelman Syndrome (AS). The most common motor problems include spasticity, ataxia of gait (observed in the majority of ambulatory individuals), tremor, and muscle weakness. This report focused on quantifying various spatial and temporal aspects of gait as a reliable, translatable outcome measure in a preclinical AS model longitudinally across development. By increasing the number of translational, reliable, functional outcome measures in our wheelhouse, we will create more opportunities for identifying and advancing successful medical interventions.
Topics: Angelman Syndrome; Animals; Autism Spectrum Disorder; Disease Models, Animal; Gait; Humans; Mice; Movement Disorders; Muscle Hypotonia; Outcome Assessment, Health Care
PubMed: 35274462
DOI: 10.1002/aur.2697 -
BMC Medicine Aug 2023Moderate and late preterm (MLPT) birth accounts for the vast majority of preterm births, which is a global public health problem. The association between MLPT and...
BACKGROUND
Moderate and late preterm (MLPT) birth accounts for the vast majority of preterm births, which is a global public health problem. The association between MLPT and neurobehavioral developmental delays in children and the underlying biological mechanisms need to be further revealed. The "placenta-brain axis" (PBA) provides a new perspective for gene regulation and risk prediction of neurodevelopmental delays in MLPT children.
METHODS
The authors performed multivariate logistic regression models between MLPT and children's neurodevelopmental outcomes, using data from 129 MLPT infants and 3136 full-term controls from the Ma'anshan Birth Cohort (MABC). Furthermore, the authors identified the abnormally regulated PBA-related genes in MLPT placenta by bioinformatics analysis of RNA-seq data and RT-qPCR verification on independent samples. Finally, the authors established the prediction model of neurodevelopmental delay in children with MLPT using multiple machine learning models.
RESULTS
The authors found an increased risk of neurodevelopmental delay in children with MLPT at 6 months, 18 months, and 48 months, especially in boys. Further verification showed that APOE and CST3 genes were significantly correlated with the developmental levels of gross-motor domain, fine-motor domain, and personal social domain in 6-month-old male MLPT children.
CONCLUSIONS
These findings suggested that there was a sex-specific association between MLPT and neurodevelopmental delays. Moreover, APOE and CST3 were identified as placental biomarkers. The results provided guidance for the etiology investigation, risk prediction, and early intervention of neurodevelopmental delays in children with MLPT.
Topics: Pregnancy; Infant; Infant, Newborn; Humans; Child; Female; Male; Premature Birth; Placenta; Brain; Computational Biology; Apolipoproteins E
PubMed: 37633927
DOI: 10.1186/s12916-023-03023-1 -
Clinical Linguistics & Phonetics 2019Speech Motor Delay (SMD) is a recently proposed childhood motor speech disorder characterized by imprecise and unstable speech, prosody, and voice that does not meet...
Speech Motor Delay (SMD) is a recently proposed childhood motor speech disorder characterized by imprecise and unstable speech, prosody, and voice that does not meet criteria for either Childhood Dysarthria or Childhood Apraxia of Speech. The goals of the present research were to obtain information on the phenotype of SMD and initial information on the persistence of SMD in children receiving treatment for idiopathic Speech Delay (SD). Five questions about the phenotype and persistence of SMD were posed using a database of audio-recordings and participant records and longitudinal data from audio-recordings of children with early SMD treated for SD. Three phenotype questions examined associations between participant risk factors and prevalence of SMD, and described the most frequent speech, prosody, and voice signs of early SMD. To provide initial estimates of the persistence of SMD, two questions examined associations between the persistence of SMD and participant risk factors using the audio-recordings of 14 participants with SMD treated for idiopathic SD. Phenotype findings indicated that SMD is characterized by across-the-board delays in the spatiotemporal precision and stability of speech, prosody, and voice production. Persistence findings indicated that although most participants normalized early SMD by 6 years of age, SMD persisted until at least late adolescence in 21.4% of participants. Findings are interpreted to support the construct validity of SMD and the potential for research using additional assessment modalities to explicate its genomic and neuromotor causal pathways. : CAS: Childhood Apraxia of Speech; CD: Childhood Dysarthria; MSD: Motor Speech Disorder; No MSD: No Motor Speech Disorder; PSI: Precision-Stability Index; SD: Speech Delay; SMD: Speech Motor Delay; SSD: Speech Sound Disorders.
Topics: Child, Preschool; Female; Humans; Language Development Disorders; Male; Phenotype; Risk Factors; Speech Disorders; Speech Sound Disorder; Surveys and Questionnaires; Voice
PubMed: 31221011
DOI: 10.1080/02699206.2019.1595733 -
Global Pediatric Health 2021A mere 33% of all children meet the recommended minimum physical activity guidelines for adequate health maintenance. Available literature however suggests children are... (Review)
Review
A mere 33% of all children meet the recommended minimum physical activity guidelines for adequate health maintenance. Available literature however suggests children are more likely to be active when they are competent with their own motor ability. This review aimed to evaluate how several regimented motor skills training courses and interventions improve motor skill competence among children compared with age matched control peers. Electronic databases were searched and included Medline Complete and Psych INFO (both hosted by EBSCO Host). The search syntax examined titles and abstracts. The study aimed to create novelty by examining participants with and without developmental delays simultaneously from studies around the globe. Included interventions were aimed at the most crucial developmental years for children (between 3 and 11 years). Results were found in favor of the motor skill intervention groups (from pre-to post-test). Included interventions involved weekly motor skills exposure of 60 to 120 minutes for periods of between 2 and 6 months. Over 50% of included interventions involved alterations to current school curriculums. The included studies were of moderate to high quality. The findings suggest that for those with and without developmental delays, several interventions can be effectively applied in once weekly 60-minute sessions (over eight or more weeks) to improve children's motor skill abilities. Applying appropriate difficulty to interventions seems equally influential. Implications are discussed.
PubMed: 34841010
DOI: 10.1177/2333794X211057707