The influential factors and non-pharmacological interventions of cognitive impairment in children with ischemic stroke

Hypoxic-ischemic and traumatic brain injuries are leading causes of long-term mortality and disability in infants and children. Although several preclinical models using rodents of different ages have been developed, species differences in the timing of key brain maturation events can render comparisons of vulnerability and regenerative capacities difficult to interpret. Traditional models of developmental brain injury have utilized rodents at postnatal day 7-10 as being roughly equivalent to a term human infant, based historically on the measurement of post-mortem brain weights during the 1970s. Here we will examine fundamental brain development processes that occur in both rodents and humans, to delineate a comparable time course of postnatal brain development across species. We consider the timing of neurogenesis, synaptogenesis, gliogenesis, oligodendrocyte maturation and age-dependent behaviors that coincide with developmentally regulated molecular and biochemical changes. In general, while the time scale is considerably different, the sequence of key events in brain maturation is largely consistent between humans and rodents. Further, there are distinct parallels in regional vulnerability as well as functional consequences in response to brain injuries. With a focus on developmental hypoxic-ischemic encephalopathy and traumatic brain injury, this review offers guidelines for researchers when considering the most appropriate rodent age for the developmental stage or process of interest to approximate human brain development. Copyright © 2013 Elsevier Ltd. All rights reserved.

Human and other animal studies demonstrate that exercise targets many aspects of brain function and has broad effects on overall brain health. The benefits of exercise have been best defined for learning and memory, protection from neurodegeneration and alleviation of depression, particularly in elderly populations. Exercise increases synaptic plasticity by directly affecting synaptic structure and potentiating synaptic strength, and by strengthening the underlying systems that support plasticity including neurogenesis, metabolism and vascular function. Such exercise-induced structural and functional change has been documented in various brain regions but has been best-studied in the hippocampus - the focus of this review. A key mechanism mediating these broad benefits of exercise on the brain is induction of central and peripheral growth factors and growth factor cascades, which instruct downstream structural and functional change. In addition, exercise reduces peripheral risk factors such as diabetes, hypertension and cardiovascular disease, which converge to cause brain dysfunction and neurodegeneration. A common mechanism underlying the central and peripheral effects of exercise might be related to inflammation, which can impair growth factor signaling both systemically and in the brain. Thus, through regulation of growth factors and reduction of peripheral and central risk factors, exercise ensures successful brain function.

Transcranial magnetic stimulation (TMS) and repetitive TMS (rTMS) are indirect and non-invasive methods used to induce excitability changes in the motor cortex via a wire coil generating a magnetic field that passes through the scalp. Today, TMS has become a key method to investigate brain functioning in humans. Moreover, because rTMS can lead to long-lasting after-effects in the brain, it is thought to be able to induce plasticity. This tool appears to be a potential therapy for neurological and psychiatric diseases. However, the physiological mechanisms underlying the effects induced by TMS and rTMS have not yet been clearly identified. The purpose of the present review is to summarize the main knowledge available for TMS and rTMS to allow for understanding their mode of action and to specify the different parameters that influence their effects. This review takes an inventory of the most-used rTMS paradigms in clinical research and exhibits the hypotheses commonly assumed to explain rTMS after-effects.