Evoked potentials provide noninvasive measures of nerve transmission and CNS functioning. Auditory brainstem responses (ABR) and visual evoked potentials (VEP) show dramatic changes in infancy, largely as a result of progressive myelination. Because iron is required for normal myelination, pathway transmission in these sensory systems might be affected by early iron deficiency. We previously reported evidence to that effect: infants with iron-deficiency anemia (IDA) had slower transmission through the auditory brainstem pathway, uncorrected by iron therapy. To determine long-term effects, ABR and/or VEP of healthy Chilean children who were treated for IDA or were nonanemic in infancy were compared at approximately 4 y of age. Absolute latencies for all ABR waves and interpeak latencies (except I-III interval) were significantly longer in former IDA children. Longer latency was also observed for the P100 wave on VEP. The magnitude of differences was large-about 1 SD. These findings, with differences in latencies but not amplitudes, further support the hypothesis that IDA in infancy alters myelination and provide evidence that effects on transmission through the auditory and visual systems can be long lasting. Subtle changes in sensory pathway transmission might be an underlying mechanism for the derailment of other developmental aspects in early IDA. Neurophysiologic methodologies are noninvasive approaches that can provide information about the functional integration of the CNS. For example, dramatic decreases in latencies in auditory and visual evoked potentials in infancy are often used to index the overall intactness and maturation of the CNS. Progressively shorter latencies until adult levels are achieved are thought to reflect the increasing speed of transmission through sensory pathways, resulting in large part from increased myelination of the auditory and optic nerves and at the intracerebral level (1-5).ABR represent the progressive activation of different levels of the auditory pathway: wave I is generated peripherally in the auditory nerve, wave III reflects the firing of axons exiting the cochlear nuclear complex, and wave V reflects an action potential generated by axons from the lateral lemniscus (6, 7). We recently reported the use of ABR to determine the effects of early IDA on the functional development of the auditory system (8). Six-month-old Chilean infants with IDA tended to show longer latencies than controls, indicating slower transmission through the brainstem portion of the auditory pathway. Differences became pronounced at 12 and 18 mo, despite iron therapy. Because iron is required for the functioning of several neurotransmission systems, myelination, and neuronal metabolic activity, different processes may relate to these lasting ABR abnormalities. However, the findings of differences in latency but not amplitude and more effects on the central (versus peripheral) portion of the auditory pathway appeared to be strong support for the hypothesis that impaired myelination was the explana...
Objective To determine the long-term effects of iron deficiency on the neural correlates of recognition memory. Study design Non-anemic control participants (n=93) and 116 otherwise healthy formerly iron-deficient anemic (FIDA) Chilean children were selected from a larger longitudinal study. Participants were identified at 6, 12, or 18 months as iron-deficient anemic or non-anemic and subsequently received oral iron treatment. This follow-up was conducted when participants were 10 years old. Behavioral measures and event-related potentials from 28 scalp electrodes were measured during an old/new word recognition memory task. Results The new/old effect of the FN400 amplitude, where new words are associated with greater amplitude than old words, was present within the control group only. The control group also showed faster FN400 latency than the FIDA group and larger mean amplitude for the P300 component. Conclusions Although overall behavioral performance is comparable between groups, the results show that group differences in cognitive function have not been resolved ten years after iron treatment. Long-lasting changes in myelination and energy metabolism, perhaps especially in the hippocampus, may account for these long-term effects on an important aspect of human cognitive development.
Aim The aim of this study was to assess the effects of iron-deficiency anemia (IDA) in infancy on executive functioning at age 10 years, specifically inhibitory control on the Go/No-Go task. We predicted that children who had IDA in infancy would show poorer inhibitory control. Method We assessed cognitive inhibitory control in 132 Chilean children (mean [SD] age 10y 0mo [1mo]): 69 children had IDA in infancy (45 males, 24 females) and 63 comparison children who did not have IDA (26 males, 37 females). Participants performed the Go/No-Go task with event-related potentials. Group differences in behavioral (accuracy, reaction time) and electrophysiological outcomes (N2 and P300 components) were analyzed using repeated-measures analyses of variance. N2 and P300 are interpreted to reflect attention and resource allocation respectively. Results Relative to comparison participants, children who had IDA in infancy showed slower reaction time (mean [SE], 528.7ms [14.2] vs 485.0ms [15.0], 95% confidence interval [CI] for difference between groups 0.9–86.5); lower accuracy (95.4% [0.5] vs 96.9% [0.6], 95% CI −3.0 to −0.1); longer latency to N2 peak (378.9ms [4.9] vs 356.9ms [5.0], 95% CI 7.5–36.6); and smaller P300 amplitude (4.5μV [0.8] vs 7.6μV [0.9], 95% CI–5.5 to −0.5). Interpretation IDA in infancy was associated with slower reaction times and poorer inhibitory control 8 to 9 years after iron therapy. These findings are consistent with the long-lasting effects of early IDA on myelination and/or prefrontal–striatal circuits where dopamine is the major neurotransmitter.
BACKGROUND Preventing obesity is a worldwide public health priority. In vulnerable children living in obesogenic environments, with easy access to high-caloric food, alterations in inhibitory control functions might favor excessive food intake and affect energy regulation. We hypothesized that overweight/obese children would present lower inhibitory control in comparison to normal weight children. METHODS We measured inhibitory control functions in 93 otherwise healthy overweight/obese and 92 normal weight 10-year-old children using the Stroop test and the Go/No-Go task. Event-related potentials were recorded during the Go/No-Go task. RESULTS Overweight/obese children showed slower reaction times (1248.6 ms (95% confidence interval (CI): 1182.9–1314.3) vs 1149.0 ms (95% CI: 1083.0–1215.1)) on the Stroop test, higher reaction time variability (0.25 (95% CI: 0.22–0.27) vs 0.21 (95% CI: 0.19–0.24)) on the Go/No-Go task and decreased P300 amplitude (4.1 µV (95% CI: 3.0–5.2) vs 6.4 µV (95% CI: 5.2–7.6)) on event-related potentials compared with normal weight children. CONCLUSIONS Our results indicate altered inhibitory control functions in otherwise healthy overweight/obese children, which might contribute to their excessive food consumption.
With the discovery of rapid eye movement (REM) sleep, sleep was no longer considered a homogeneous state of passive rest for the brain. On the contrary, sleep, and especially REM sleep, appeared as an active condition of intense cerebral activity. The fact that we get large amounts of sleep in early life suggested that sleep may play a role in brain maturation. This idea has been investigated for many years through a large number of animal and human studies, but evidence remains fragmented. The hypothesis proposed was that REM sleep would provide an endogenous source of activation, possibly critical for structural maturation of the central nervous system. This proposal led to a series of experiments looking at the role of REM sleep in brain development. In particular, the influence of sleep in developing the visual system has been highlighted. More recently, non-REM (NREM) sleep state has become a major focus of attention. The current data underscore the importance of both REM sleep and NREM sleep states in normal synaptic development and lend support to their functional roles in brain maturation. Both sleep states appear to be important for neuronal development, but the corresponding contribution is likely to be different.
We present a new methodology to detect and characterize sleep spindles (SSs), based on the nonlinear algorithms, empirical-mode decomposition, and Hilbert-Huang transform, which provide adequate temporal and frequency resolutions in the electroencephalographic analysis. In addition, the application of fuzzy logic allows to emulate expert's procedures. Additionally, we built a database of 56 all-night polysomnographic recordings from children for training and testing, which is among the largest annotated databases published on the subject. The database was split into training (27 recordings), validation (10 recordings), and testing (19 recordings) datasets. The SS events were marked by sleep experts using visual inspection, and these marks were used as golden standard. The overall SS detection performance on the testing dataset of continuous all-night sleep recordings was 88.2% sensitivity, 89.7% specificity, and 11.9% false-positive (FP) rate. Considering only non-REM sleep stage 2, the results showed 92.2% sensitivity, 90.1% specificity, and 8.9% FP rate. In general, our system presents enhanced results when compared with most systems found in the literature, thus improving SS detection precision significantly without the need of hypnogram information.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.