Overlaps between Frailty and Sarcopenia Definitions.

Aging is characterized by the catabolism of muscles leading to sarcopenia and frailty. These are two geriatric syndromes with partly overlapping phenotypes. Primary sarcopenia, i.e. loss of muscle mass and function related to aging alone, usually precedes frailty. Thus, robustness passes from sarcopenia over frailty to disability leading eventually to a mortal outcome. Frailty (defined according to the phenotype model) encompasses states as exhaustion, weakness, and slowness, whereas sarcopenia, combining mass and function, is more strictly focused on muscles. Frailty is age related, whereas sarcopenia is also related to disease, starvation, and disuse. In general, the criteria for the two conditions overlap, but frailty requires weight loss, whereas sarcopenia requires muscle loss. Both gait speed and hand grip strength are suggested to be used as diagnostic measures for the two conditions since muscle function is crucial for any of the two syndromes. It is suggested that frailty screening should be part of the geriatric comprehensive assessment starting with measuring walking capacity and complemented by taking a history of fatigue and low activity. For younger adults (i.e. <70 years), sarcopenia screening could first register gait speed or hand grip strength and then body composition measurements. Simple questionnaires are feasible clinical alternatives. Treatment of frailty and sarcopenia overlaps, i.e. provide adequate protein and vitamin D supplementation, and encourage resistance exercise.

Gross motor deficits in children prenatally exposed to alcohol: a meta-analysis.

BACKGROUND AND OBJECTIVES: Gross motor (GM) deficits are often reported in children with prenatal alcohol exposure (PAE), but their prevalence and the domains affected are not clear. The objective of this review was to characterize GM impairment in children with a diagnosis of fetal alcohol spectrum disorder (FASD) or "moderate" to "heavy" maternal alcohol intake. METHODS: A systematic review with meta-analysis was conducted. Medline, Embase, Allied and Complementary Medicine Database, Cumulative Index to Nursing and Allied Health Literature, PsycINFO, PEDro, and Google Scholar databases were searched. Published observational studies including children aged 0 to ≤18 years with (1) an FASD diagnosis or moderate to heavy PAE, or a mother with confirmed alcohol dependency or binge drinking during pregnancy, and (2) GM outcomes obtained by using a standardized assessment tool. Data were extracted regarding participants, exposure, diagnosis, and outcomes by using a standardized protocol. Methodological quality was evaluated by using Strengthening the Reporting of Observational Studies in Epidemiology guidelines. RESULTS: The search recovered 2881 articles of which 14 met the systematic review inclusion criteria. The subjects' mean age ranged from 3 days to 13 years. Study limitations included failure to report cutoffs for impairment, nonstandardized reporting of PAE, and small sample sizes. The meta-analysis pooled results (n = 10) revealed a significant association between a diagnosis of FASD or moderate to heavy PAE and GM impairment (odds ratio: 2.9; 95% confidence interval: 2.1-4.0). GM deficits were found in balance, coordination, and ball skills. There was insufficient data to determine prevalence. CONCLUSIONS: The significant results suggest evaluation of GM proficiency should be a standard component of multidisciplinary FASD diagnostic services.

Rich micronutrient fortification of locally produced infant food does not improve mental and motor development of Zambian infants: a randomised controlled trial.

It is uncertain whether multiple micronutrients benefit the mental and psychomotor development of young children in developing countries. We conducted a randomised double-blind controlled trial to evaluate the effect of a richly micronutrient-fortified v. a basal fortified porridge on mental and psychomotor development in Zambian infants. Infants (n 743) were randomised at age 6 months to receive either the richly fortified or the basal fortified infant food and were followed up until 18 months of age. All the infants were evaluated monthly for achievement of a series of developmental milestones. The Bayley scales of infant development II were administered to a subsample of 502 infants at 6, 12 and 18 months. Rich micronutrient fortification had no significant benefit on the following: (a) number of developmental milestones achieved (rate ratio at 12 months = 1·00; 95 % CI 0·96, 1·05; P = 0·81, adjusted for sex, socio-economic status and maternal education, with similar results at 15 and 18 months); (b) ages of walking unsupported (hazard ratio (HR) 1·04; 95 % CI 0·88, 1·24; P = 0·63, adjusted for the above covariates) and of speaking three or four clear words (HR 1·01; 95 % CI 0·84, 1·20; P = 0·94, adjusted for the above covariates); (c) mental development index (MDI) and psychomotor development index (PDI) of the Bayley scales (scores difference adjusted for baseline scores, age at the assessment, sex, socio-economic status, maternal education, language, age and HIV status: MDI 0·3 (95 % CI - 0·5, 1·1), P = 0·43; PDI - 0·1 (95 % CI - 0·9, 0·7), P = 0·78). In conclusion, the results do not support the hypothesis that rich micronutrient fortification improves Zambian infants' mental and motor development.

Arsenic exposure and motor function among children in Bangladesh.

BACKGROUND: Several reports indicate that drinking water arsenic (WAs) and manganese (WMn) are associated with children's intellectual function. Very little is known, however, about possible associations with other neurologic outcomes such as motor function. METHODS: We investigated the associations of WAs and WMn with motor function in 304 children in Bangladesh, 8-11 years of age. We measured As and Mn concentrations in drinking water, blood, urine, and toenails. We assessed motor function with the Bruininks-Oseretsky test, version 2, in four subscales-fine manual control (FMC), manual coordination (MC), body coordination (BC), and strength and agility-which can be summarized with a total motor composite score (TMC). RESULTS: Log-transformed blood As was associated with decreases in TMC [ß = -3.63; 95% confidence interval (CI): -6.72, -0.54; p < 0.01], FMC (ß = -1.68; 95% CI: -3.19, -0.18; p < 0.05), and BC (ß = -1.61; 95% CI: -2.72, -0.51; p < 0.01), with adjustment for sex, school attendance, head circumference, mother's intelligence, plasma ferritin, and blood Mn, lead, and selenium. Other measures of As exposure (WAs, urinary As, and toenail As) also were inversely associated with motor function scores, particularly TMC and BC. Square-transformed blood selenium was positively associated with TMC (ß = 3.54; 95% CI: 1.10, 6.0; p < 0.01), FMC (ß = 1.55; 95% CI: 0.40, 2.70; p < 0.005), and MC (ß = 1.57; 95% CI: 0.60, 2.75; p < 0.005) in the unadjusted models. Mn exposure was not significantly associated with motor function. CONCLUSION: Our research demonstrates an adverse association of As exposure and a protective association of Se on motor function in children.

Oral-motor dysfunction at 10 months corrected gestational age in infants born less than 37 weeks preterm.

Feeding difficulties are common in preterm infants. These may be associated with inadequate dietary intake, poor growth, and parental anxiety. Oral-motor dysfunction has been observed in preterm infants during sucking and the early stages of weaning but has not been rigorously studied in later infancy when eating a range of food consistencies. We aimed to establish if oral-motor dysfunction during feeding occurs in preterm infants in later infancy and to explore the relationships with specific neonatal risk factors: gestational age at birth, prolonged supplementary oxygen requirement, and delay in establishing full oral feeding. Infants born less than 37 weeks gestational age were evaluated once at 10 months corrected gestational age using a validated feeding assessment (Schedule for Oral Motor Assessment). Fifteen infants were enrolled (9 males, 6 females; median gestational age at birth = 33 weeks, range = 25-36 weeks; median birth weight = 1890 g, range = 710-2950 g). Oral-motor dysfunction was observed in three infants all born after 31 weeks gestation. No relationship was found with the neonatal risk factors. This study indicates that oral-motor dysfunction may occur in later infancy and is not easily predicted from specific neonatal risk factors. Further study is required to evaluate the true prevalence and the health implications of oral-motor dysfunction in this population in later infancy.

Differences in motor imagery between children with developmental coordination disorder with and without the combined type of ADHD.

It has been proposed, and questioned, whether motor impairments in attention-deficit-hyperactivity disorder, combined type (ADHD-C) alone, developmental coordination disorder (DCD) alone, and ADHD-C and comorbid DCD (ADHD-C/DCD) may arise from disruption to a common set of cognitive functions and their related neural substrate. This study examined movement durations for real and imagined movements in a visually guided pointing task in 58 prepubertal children aged 8 to 12 years old with ADHD-C alone (n=14), ADHD-C/DCD (n=14), DCD alone (n=15), and an age-, sex-, and Full-scale IQ-matched healthy comparison group (n=15). There were 10 males and 4 or 5 females in each group. The DCD alone group demonstrated an inability to generate imagined movements that was not present in the ADHD-C group, with or without comorbid DCD, or healthy comparison participants. These findings add to the emerging literature characterizing intended and actual motor impairments associated with DCD alone.

Outcome in patients with profound biotinidase deficiency: relevance of newborn screening.

Profound biotinidase deficiency (PBD) is an autosomal recessively inherited disorder of biotin metabolism, which can be detected by newborn screening and treated with biotin supplementation. Children were investigated in whom PBD was detected by newborn screening and who were treated presymptomatically, or who were not screened but were diagnosed and treated after experiencing initial clinical symptoms (symptomatic children). In a follow-up of our study group, differences in development, social and behavioural adaptation, and signs of residual impairment were examined. Parents and physicians of children with PBD completed questionnaires which included the Child Behavior Checklist and Vineland Adaptive Behavior Scales. Information was obtained for 37 children (24 males, 13 females; median age at recruitment 6 years 8 months, range to 6 months-20 years; median length of follow-up 6 years 6 months, range 5 months to 18 years 3 months). All 11 symptomatic children had residual enzyme activity of <1%, or variants of the Michaelis-Menten constant which were not detected by newborn screening. Some symptomatic children showed residual impairments: hearing impairment (n=2), optic atrophy (n=2), both hearing impairment and optic atrophy (n=2). In addition, symptomatic children had a higher risk of delayed motor and speech development. No child with PBD detected by newborn screening (n=25) had auditory or visual loss; and milestones of speech development and motor skills were reached at an appropriate age. There was no significant difference in social adaptation or behavioural problems between symptomatic and asymptomatic children. Symptomatic children often have developmental delay and are at risk of irreversible damage to auditory, visual, or central nervous functions; whereas children with PBD (established presymptomatically following newborn screening) treated with biotin supplementation, do not experience these effects.