PubMed Health⌕ Search

PubMed · 14624832

Static balance and developmental coordination disorder.

Abstract

The development of static balance is a basic characteristic of normal motor development. Most of the developmental motor tests include a measure of static balance. Children with a developmental coordination disorder (DCD) often fail this item. Twenty-four children at risk for DCD with balance problems (DCD-BP) and 24 matched control children in the age range of 6-12 years participated in a detailed study of balance control. Additional groups of children (6-7 years, N=25; 10-11 years, n=16; with M-ABC scores >15th percentile) were selected randomly to study developmental changes in balance control in the age range of interest. Three experiments were conducted to examine developmental and clinical differences in the control of static balance. In the first, we measured the excursion of the centre of pressure (force-plate) in conditions with and without vision while standing still on one or two legs for 20 s. In the second experiment, EMGs were measured while standing on one leg. In the third experiment, in which only a subgroup of the DCD-BP and matched control children participated, a short unexpected force in the back lightly perturbed normal standing and EMG and force-plate responses were measured during balance recovery. In conditions of one-leg stance, children were not always able to maintain balance. Only epochs of stable postural control (7.5-20 s) were analysed. The results showed improvement of static balance with age, but only subtle differences between the DCD and control groups. Centre of pressure measures differed in the more difficult conditions. DCD-BP children had more difficulty standing on one leg with eyes closed. While standing on the non-preferred leg the EMGs of the DCD-BP children showed slightly more co-activation of the muscles of lower and upper leg. Perturbation of standing resulted in longer duration of recovery in the first trial in this group. Apparently DCD children learn to compensate for the perturbation within a few trials as well as control children do. The clear improvement with age shows that our measures of balance control are sensitive to detect changes. The general conclusion that may be drawn from this study is that under normal conditions static balance control is not a problem for children with DCD. Only in difficult or novel situations they seem to suffer from increased postural sway as a result of non-optimal balance control.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Reint H Geuze. 2003. Static balance and developmental coordination disorder.. https://doi.org/10.1016/j.humov.2003.09.008

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Prevalence and risk factors for persistent faecal carriage of extended spectrum beta-lactamase producing Escherichia coli in a paediatric community population.

OBJECTIVE: To investigate clinical and microbiological factors associated with persistent faecal carriage of extended spectrum beta-lactamase (ESBL) producing Escherichia coli in infants. METHODS: Between 2010 and 2022, children aged 3 months to 2 years old were sampled in a community setting in France, at two visits, V1 and V2, 3-24 months apart, to screen for prolonged faecal carriage of ESBL-producing E. coli. Patient clinical information and whole genome sequence of each isolate were used for association studies. RESULTS: A total of 4641 children were sampled. 375 (8%) carried an ESBL-producing Enterobacterales, among which 142 of ESBL-producing E. coli carriers were once again sampled at V2 and included in this study. 21.8% (n = 31/142) and 18.4% (n = 16/99) carried the same ESBL-producing E. coli clone for at least 3 and 6 months, respectively. B2 phylogroup, and among which ST131 clones were associated with an increased risk of persistent carriage. Multivariate analysis identified virulence associated genes involved in adhesion (papC/papGII allele and a tia-like gene) and encoding toxin (senB) as major risk factors for persistence. A genome wide association study highlighted the potential role of the frz metabolic operon, known to be involved in enterocytes adhesion/internalisation. CONCLUSION: Main extraintestinal pathogenic E. coli genomic features (phylogenetic background, adhesion properties) are associated with ESBL-producing E. coli gut colonisation persistence in infants, which could potentially lead to an increased risk of febrile urinary tract infection in these patients.

Child↗

Extensive and differential platinum chemotherapy mutagenesis in livers of children.

Childhood cancer survivors often experience late adverse effects that may be linked to chemotherapy mutagenesis. We studied chemotherapy mutagenesis in normal pediatric tissues using duplex sequencing (NanoSeq) to enable the detection of mutations from single DNA molecules. We found that platinum chemotherapeutics increased the mutation burdens of normal pediatric tissues to levels seen in adults. In the liver, platinum agents imparted a tissue-specific mutational signature that was absent from other tissues. Gene-focused duplex sequencing revealed that chemotherapy mutagenesis generates a great diversity of nonsynonymous variants, some of which may have functional potential, such as leukemogenic variants in blood. Our findings demonstrate extensive chemotherapy mutagenesis in normal tissues of children, which may provide a plausible link between chemotherapy exposure and adverse effects in later life.

Child↗

Clinical and immunological characterization of a child with a homozygous TBK1 kinase-domain truncation.

TBK1 is a serine-tyrosine kinase protein that transmits signals from pattern recognition receptors to the NF-κB pathway leading to production of Type 1 Interferons. Mutations in this protein have been associated with arthritis, vasculitis, herpes simplex encephalitis and amyotrophic lateral sclerosis. In the current study, we characterized the functional consequences of a TBK1-variant bearing a truncation in exon 4 and 5 in a patient with poly arthritis resembling juvenile idiopathic arthritis and necrotizing encephalitis. The truncation was associated with reduced TBK1 protein abundance and altered phosphorylation. The variant was associated with increased basal/and or Poly-I: C induced IL-6, TNFα, IL-1β and IL-18 and type 1 Interferon ex vivo. Our findings expand the phenotypic spectrum of TBK1 loss-of-function variants and may provide insight into the management of immune dysregulation in affected patients.

Child↗