Immature Central Nervous System Research Articles

Assessing Postural Control From Birth to Adulthood Among Individuals Born Preterm: A Systematic Review.

Premature life exposure, meaning an immature central nervous system, presents a significant challenge for the development of postural control and, in turn, overall motor development. Preventing motor delay thus requires identifying, characterizing, and quantifying deficit in postural control as early as possible. In our study, we reviewed the procedures used in past studies to assess postural control among individuals born preterm, specifically the characterization of participants, the instruments and motor tasks involved, the types of data collected and analyzed, and the outcomes. To that end, we performed a literature search on PubMed, Wiley Online Library, Web of Science, and Scopus using Boolean logic and assessed the quality of the studies with a standardized assessment based on the Strengthening the Reporting of Observational Studies in Epidemiology guidelines and the Cochrane Handbook for Systematic Reviews of Interventions. Of 35 potential studies, 24 were included; all evaluated infants born preterm, but six did not include a control group of full-term infants. Although the heterogeneity of measurements, variability of instruments, and divergence in motor tasks examined limit definitive conclusions based on quantitative synthesis and the generalization of the results, most studies revealed dysfunctional postural control among individuals born preterm.

Recovery of walking in nonambulatory children with chronic spinal cord injuries: Case series.

The immature central nervous system is recognized as having substantial neuroplastic capacity. In this study, we explored the hypothesis that rehabilitation can exploit that potential and elicit reciprocal walking in nonambulatory children with chronic, severe (i.e., lower extremity motor score < 10/50) spinal cord injuries (SCIs). Seven male subjects (3-12 years of age) who were at least 1-year post-SCI and incapable of discrete leg movements believed to be required for walking, enrolled in activity-based locomotor training (ABLT; clinicaltrials.gov NCT00488280). Six children completed the study. Following a minimum of 49 sessions of ABLT, three of the six children achieved walking with reverse rolling walkers. Stepping development, however, was not accompanied by improvement in discrete leg movements as underscored by the persistence of synergistic movements and little change in lower extremity motor scores. Interestingly, acoustic startle responses exhibited by the three responding children suggested preserved reticulospinal inputs to circuitry below the level of injury capable of mediating leg movements. On the other hand, no indication of corticospinal integrity was obtained with transcranial magnetic stimulation evoked responses in the same individuals. These findings suggest some children who are not predicted to improve motor and locomotor function may have a reserve of adaptive plasticity that can emerge in response to rehabilitative strategies such as ABLT. Further studies are warranted to determine whether a critical need exists to re-examine rehabilitation approaches for pediatric SCI with poor prognosis for any ambulatory recovery.

Postoperative neurocognitive dysfunction in children

The Pediatric Society of Anesthesia in partnership with the FDA (Food and Drug Administration) and IARS (International Anesthesiology Research Society) have set up a Safe Kids organization, which studies the safety and anesthetic effects on the immature central nervous system. 2018).In recent years, the Food and Drug Administration (FDA) has shown a growing interest in the neurological changes that can occur in young children after exposure to intravenous and volatile anesthetics.These organizations have provided conclusive data on the safety and effects of anesthetics on the nervous system in children, as well as the ongoing concern of pediatric anesthetists for the long-term safety of the anesthetic.

Pharmacological evidence that GABA-induced relaxation of rat proximal duodenum longitudinal muscle depends on NKCC cotransporter activity and Ca2+ influx.

γ-Aminobutyric acid (GABA) is the main inhibitory neurotransmitter in adult central nervous system (CNS) synapses, but it excites immature CNS neurons as well as neurons in the myenteric plexus. The present work aimed to determine whether GABA-induced nonadrenergic, noncholinergic (NANC) neuronal-mediated relaxation of the rat duodenum is dependent on the activity of Na+ K+ Cl- cotransporters (NKCC) and requires calcium influx. In the presence of guanethidine (3µmol/L), atropine (3µmol/L), and indomethacin (1µmol/L), relaxations induced by GABA (100µmol/L), KCl (5-10mmol/L) and electrical field stimulation (1-8Hz, 2ms, 60V), but not those induced by bradykinin (10-100nmol/L) were abolished by lidocaine (300µmol/L). However, only GABA-induced relaxations were reduced in a concentration-dependent manner by the NKCC1/2 inhibitors bumetanide (0.1-1µmol/L) and furosemide (1-10µmol/L). GABA-induced NANC neuronal relaxation was abolished by bicuculline (30µmol/L) and inhibited by N-nitroarginine methyl ester (l-NAME, 300µmol/L). The ω-conotoxin GVIA (1µmol/L), which acts exclusively on neuronal CaV2 channels, but not on smooth muscle voltage-gated Ca2+ CaV1 channels, and nonselective blockers of these channels (verapamil 100nmol/L and ruthenium red 10µmol/L), reduced GABA-induced relaxations. These results showed that the activation of GABAA receptors induces NANC nitrergic neuronal relaxations in the rat duodenum, which depend on NKCC activity and CaV2 channel activation, suggesting that this phenomenon results from neuronal depolarization promoted by Cl- efflux through GABAA receptors, with subsequent Ca2+ influx and nitric oxide release.

Effects of application of Kinesio Taping on the Tibialis Anterior muscle in Cerebral Palsy: case series

Justification: Cerebral palsy (CP) caused by injury to the immature Central Nervous System and causes repercussions as serious as the extent of the lesion. Equine foot is common in children with spastic CP, due to hyperactivity of the plantar flexors in relation to the main dorsoflexor, tibialis anterior. Treatment based on adaptations made to improve patients' quality of life. The Kinesio Taping® (KT®) method aims to maintain therapeutic results, being the functional correction technique widely used in neurological patients to limit unwanted or pathological movements. Objective: To observe the effects of KT® application on the tibialis anterior on spasticity levels and tibio-tarsal range of motion in CP. Methods: The descriptive observational study of the case series type, carried out from October 24th to November 31th 2014. Which seven children underwent assessment of spasticity of the right lower limb and of the right tibio-tarsal joint range of motion and intervention using the KT® method. Results: The final sample consisted of seven children aged between 7 and 14 years, one of which was female. Most children reduced or maintained the degree of spasticity, and increased plantar flexion at rest and ranges in dorsiflexion and plantar flexion. Conclusion: The results suggest that, although the participants did not demonstrate affinity with the technique, there was some interference of the Kinésio Taping® method in their spasticity and in their tibio-tarsal joint mobility.

Technical and practical tips for performing brain magnetic resonance imaging in premature neonates

MR imaging of premature neonates is challenging due to their small size, need for temperature support and monitoring, and immature central nervous system. Use of MR compatible incubators and MR compatible monitoring apparatus, careful selection of imaging protocols, and real time review of images by a radiologist can streamline the imaging process and improve image quality. Imaging should be focused upon (1) the child's biorhythms (imaging during sleep cycles), (2) minimizing delays during transport and (3) delaying noisy MR sequences until the end of an examination. Successful imaging of premature neonates requires teamwork: advanced planning, careful communication among neonatologists, nurses, and radiologists, established imaging protocols, and coordination among team members during all aspects of the process.

Assessment and Management of Delirium in the Pediatric Intensive Care Unit: A Review.

Many critically ill patients suffer from delirium which is associated with significant morbidity and mortality. There is a paucity of data about the incidence, symptoms, or treatment of delirium in the pediatric intensive care unit (PICU). Risk factors for delirium are common in the PICU including central nervous system immaturity, developmental delay, mechanical ventilation, and use of anticholinergic agents, corticosteroids, vasopressors, opioids, or benzodiazepines. Hypoactive delirium is the most common subtype in pediatric patients; however, hyperactive delirium has also been reported. Various screening tools are validated in the pediatric population, with the Cornell Assessment of Pediatric Delirium (CAPD) applicable to the largest age range and able to detect signs and symptoms consistent with both hypo- and hyperactive delirium. Treatment of delirium should always include identification and reversal of the underlying etiology, reserving pharmacologic management for those patients without symptom resolution, or with significant impact to medical care. Atypical antipsychotics (olanzapine, quetiapine, and risperidone) should be used first-line in patients requiring pharmacologic treatment owing to their apparent efficacy and low incidence of reported adverse effects. The choice of atypical antipsychotic should be based on adverse effect profile, available dosage forms, and consideration of medication interactions. Intravenous haloperidol may be a potential treatment option in patients unable to tolerate oral medications and with significant symptoms. However, given the high incidence of serious adverse effects with intravenous haloperidol, routine use should be avoided. Dexmedetomidine should be used when sedation is needed and when clinically appropriate, given the positive impact on delirium. Additional well-designed trials assessing screening and treatment of PICU delirium are needed.

Effects of urethane and isoflurane on the sensory evoked response and local blood flow in the early postnatal rat somatosensory cortex

Functional studies in the central nervous system are often conducted using anesthesia. While the dose-dependent effects of anesthesia on neuronal activity have been extensively characterized in adults, little is known about the effects of anesthesia on cortical activity and cerebral blood flow in the immature central nervous system. Substitution of electrophysiological recordings with the less-invasive technique of optical intrinsic signal imaging (OIS) in vivo allowed simultaneous recordings of sensory-evoked functional response and local blood flow changes in the neonatal rat barrel cortex. Using OIS we characterize the effects of two widely used anesthetics—urethane and isoflurane. We found that both anesthetics suppressed the sensory-evoked optical intrinsic signal in a dose-dependent manner. Dependence of the cortical response suppression matched the exponential decay model. At experimental levels of anesthesia, urethane affected the evoked cortical response less than isoflurane, which is in agreement with the results of electrophysiological recordings demonstrated by other authors. Changes in oxygenation and local blood flow also showed negative correlation with both anesthetics. The high similarity in immature patterns of activity recorded in different regions of the developing cortex suggested similar principles of development regardless of the cortical region. Therefore the indicated results should be taken into account during functional explorations in the entire developing cortex. Our results also point to urethane as the anesthetic of choice in non-survival experimental recordings in the developing brain as it produces less prominent impairment of cortical neuronal activity in neonatal animals.

Prospects for the Use of Cannabinoids in Psychiatric Disorders.

Increasing evidence suggests an essential role of the endocannabinoid system in modulating cognitive abilities, mood, stress, and sleep. The psychoactive effects of cannabis are described as euphoric, calming, anxiolytic, and sleep-inducing and positively affect the mood, but can also adversely affect therapy. The responses to cannabinoid medications depend on the patient's endocannabinoid system activity, the proportion of phytocannabinoids, the terpenoid composition, and the dose used. There is some evidence for a therapeutic use of phytocannabinoids in psychiatric conditions. THC and CBD may have opposing effects on anxiety. Current guidelines recommend caution in using THC in patients with anxiety or mood disorders. In a small number of clinical trials, cannabinoids used to treat cancer, HIV, multiple sclerosis, hepatitis C, Crohn's disease, and chronic neuropathic pain report decreases in anxiety or depression symptoms and presented sedative and anxiolytic effects. Several studies have investigated the influence of potential genetic factors on psychosis and schizophrenia development after cannabis use. THC may increase the risk of psychosis, especially in young patients with an immature central nervous system. There is limited evidence from clinical trials that cannabinoids are effective therapy for sleep disorders associated with concomitant conditions. There is evidence for a possible role of cannabis as a substitute for alcohol and drugs, also in the context of the risks of opioid use (e.g., opioid-related mortality). In this narrative review of the recent evidence, we discuss the prospects of using the psychoactive effects of cannabinoids in treating mental and psychiatric disorders. However, this evidence is weak for some clinical conditions and well-designed randomized controlled trials are currently lacking. Furthermore, some disorders may be worsened by cannabis use.

Whole-Head Magnetoencephalogram and Its Application in Developmental Communication Disorders Research: A Review

The human brain undergoes tremendous changes during the first decade of life. The susceptibility of the immature central nervous system to factors such as adverse environments and genetic factors is attributed to its plasticity. Neurodevelopmental disorders (NDDs) occur once the immature brain veers off the typical developmental trajectory. However, little is known about the neurophysiological traits of atypically developing children because it is challenging for them to remain still during recording. Magnetoencephalography (MEG) is a noninvasive neuroimaging technique with high-spatiotemporal resolution. An ultralow magnetic field produced by neural electrical activity can be detected using a highly sensitive whole-head magnetometer array. Current cryogenic SQUID-MEG combined with individual MRI has shown great potential in reflecting neural activity under resting states and during tasks. MEG instrumentation for children is expected to be an effective tool for investigating brain dynamics, which provides neuropsychological evidence for atypical development in communication ability. In this paper, the advantages of pediatric MEG in neurodevelopmental disorder studies are discussed first and compared with those of several noninvasive functional imaging modalities. Existing commercial pediatric MEG systems are summarized based on their respective characteristics and parameters. State-of-the-art newly emerging sensing techniques based on spin-exchange relaxation-free (SERF) along with their application in detecting infants' brain responses are introduced. Recent discoveries on MEG biomarkers in children with NDDs are then summarized concerning disorders that have comorbidities in communication, such as specific language impairment (SLI), autism spectrum disorders (ASD), dyslexia and stuttering. Progress on multimodality research and total-field wearable SERF magnetometers offers insight into the neuropsychological substrates of communication disorders.

Postnatal Maturation of Amplitude Integrated Electroencephalogram in Preterm SGA and Preterm AGA Neonates: A Prospective Observational Study

Introduction: Maturation of the brain is affected by various biological and environmental factors encountered by the infant during the intensive care period in Neonatal Intensive Care Unit (NICU) due to the medical treatments, procedures, and the noisy environment that disrupts the normal brain development process. Severe neurological sequelae of preterm infants are common because of the immature central nervous system. Cerebral Function Monitor (CFM) or Amplitude integrated Electroencephalogram (a-EEG) is a device for monitoring the background neurological activity. Aim: To assess postnatal maturation of a-EEG in clinically stable and neurologically normal preterm Small for Gestational Age (SGA) and preterm Appropriate for Gestational Age (AGA) neonates from 30 weeks 0/7 days to 34 weeks 6/7 days of gestation admitted in a tertiary care NICU at J. K. Lon Mother and Child Hospital, attached to Government Medical College, Kota. Materials and Methods: This prospective observational study was conducted over a one year duration, from January 2020 to December 2020 on 60 preterm neonates that were admitted in NICU of a tertiary care hospital. The serial a-EEG recording was done on haemodynamically stable, included preterm neonates after taking consent, on 3rd, 7th, and 14th postnatal day of life during the course of admission. The postnatal maturation of amplitude integrated EEG of Preterm Small for Gestational Age (PSGA) neonates was compared with their Preterm Appropriate for Gestational Age (PAGA) neonates based on a validated a-EEG scoring. The analysis was done by using Statistical Package for Social Sciences (SPSS) version 21.0. Student t-test was applied. Results: The total a-EEG scores for 3rd, 7th, and 14th day of SGA group neonates were 7.55±1.45, 7.25±1.02 and 10.22±1.05 and were delayed from the AGA group of neonates with 7.86±1.55, 8.68±1.00 and 10.62±1.01, with mean difference (95% CI), 0.30 (-0.49 to 1.13), 1.43 (0.88 to 1.97) and 0.39 (-0.15 to 0.95) respectively. Only the total a-EEG scores for day 7 were significantly delayed in SGA group. Conclusion: All the maturation a-EEG scores of clinically stable and neurologically normal PSGA neonates was found to be significantly delayed at any point of life on postnatal day 7th of life.

Faktor Risiko Prenatal Perinatal Dan Postnatal Pada Kejadian Cerebral Palsy

Background: Cerebral Palsy (CP) is a disability disorder motor motorization is most common in children with a prevalence of 2-3 per 1000 live births. The term CP is explained as a group of movement and posture disorders that are often accompanied by impaired sensation, perception, cognition, communication, behavior, epilepsy, and secondary disorders of the musculoskeletal system. Disorders of CP occur in the immature central nervous system with non-progressive traits occurring in the prenatal, perinatal, and postnatal period. Methods: The purpose of this study is to determine how much prenatal risk factors, perinatal, and postnatal events in CP at the Kitty Center Clinic in Jakarta for 5 year (2013 - 2017). Result: An observational descriptive study, which described prenatal perinatal, and postnatal risk factors for CP events at the Kitty Center Clinic in Jakarta for a period of 5 years (2013-2017) with a total of 523 study subjects. Based on the analysis of data obtained, based on the type of CP 35% quadripelgia spastic, 36% spastic diplegia, 6% spastic hemiplegia, 9% athetosis, and 14% hypotonia. Based on sex 62% are men, and 38% are women with a ratio of 1.6: 1.0. Based on the age of the child 11% &lt;2 years, 34% 3-6 years, 33% 7-12 years, and 22%13-18 years. Conclusion: Based on risk factors of 62% prenatal, 25% perinatal, and 12% postnatal. Prenatal risk factor is the biggest risk factor as much as 62% which causes Cerebral Palsy at the Kitty Center Clinic in Jakarta.

Minocycline attenuates ethanol-induced cell death and microglial activation in the developing spinal cord.

Developmental exposure to ethanol may cause fetal alcohol spectrum disorders (FASD), and the immature central nervous system (CNS) is particularly vulnerable to ethanol. In addition to vulnerability in the developing brain, we previously showed that ethanol also caused neuroapoptosis, microglial activation, and neuroinflammation in the spinal cord. Minocycline is an antibiotic that inhibits microglial activation and alleviates neuroinflammation. We sought to determine whether minocycline could protect spinal cord neurons against ethanol-induced damage. In this study, we showed that minocycline significantly inhibited ethanol-induced caspase-3 activation, microglial activation, and the expression of pro-inflammatory cytokines in the developing spinal cord. Moreover, minocycline blocked ethanol-induced activation of glycogen synthase kinase 3 beta (GSK3β), a key regulator of microglial activation. Meanwhile, minocycline significantly restored ethanol-induced inhibition of protein kinase B (AKT), mammalian target of the rapamycin (mTOR), and ERK1/2 signaling pathways, which were important pro-survival signaling pathways for neurons. Together, minocycline may attenuate ethanol-induced damage to the developing spinal cord by inhibiting microglial activation/neuroinflammation and by restoring the pro-survival signaling.

Early movement restriction leads to enduring disorders in muscle and locomotion

Motor control and body representation in the central nervous system (CNS) as well as musculoskeletal architecture and physiology are shaped during development by sensorimotor experience and feedback, but the emergence of locomotor disorders during maturation and their persistence over time remain a matter of debate in the absence of brain damage. By using transient immobilization of the hind limbs, we investigated the enduring impact of postnatal sensorimotor restriction (SMR) on gait and posture on treadmill, age-related changes in locomotion, musculoskeletal histopathology and Hoffmann reflex in adult rats without brain damage. SMR degrades most gait parameters and induces overextended knees and ankles, leading to digitigrade locomotion that resembles equinus. Based on variations in gait parameters, SMR appears to alter age-dependent plasticity of treadmill locomotion. SMR also leads to small but significantly decreased tibial bone length, chondromalacia, degenerative changes in the knee joint, gastrocnemius myofiber atrophy and muscle hyperreflexia, suggestive of spasticity. We showed that reduced and atypical patterns of motor outputs, and somatosensory inputs and feedback to the immature CNS, even in the absence of perinatal brain damage, play a pivotal role in the emergence of movement disorders and musculoskeletal pathologies, and in their persistence over time. Understanding how atypical sensorimotor development likely contributes to these degradations may guide effective rehabilitation treatments in children with either acquired (ie, with brain damage) or developmental (ie, without brain injury) motor disabilities.

Sensory integration intervention and the development of the premature infant: A controlled trial.

Premature infants are at risk of sensory processing difficulties and developmental delays due to an immature central nervous system and possible episodes of medical instability, discomfort, pain and stress during the first weeks or months after birth. To investigate the effect of Ayres Sensory Integration (ASI) on the development of premature infants in the first 12 months of life. A pre-/post-test experimental design was used to randomly divide 24 premature infants from a low socioeconomic setting in Bloemfontein, South Africa, into experimental and control groups after being matched by corrected age and gender. Developmental status was determined with the Bayley III Scales of Infant and Toddler Development, the Test of Sensory Functions in Infants and the Infant/Toddler Sensory Profile. The experimental group received 10 weeks of ASI intervention. ASI intervention had a positive effect on the sensory processing and development of premature infants, especially in terms of cognitive, language and motor development. ASI intervention at an early age enhances the developmental progress of premature infants.

Taurine as an Essential Neuromodulator during Perinatal Cortical Development.

A variety of experimental studies demonstrated that neurotransmitters are an important factor for the development of the central nervous system, affecting neurodevelopmental events like neurogenesis, neuronal migration, programmed cell death, and differentiation. While the role of the classical neurotransmitters glutamate and gamma-aminobutyric acid (GABA) on neuronal development is well established, the aminosulfonic acid taurine has also been considered as possible neuromodulator during early neuronal development. The purpose of the present review article is to summarize the properties of taurine as neuromodulator in detail, focusing on the direct involvement of taurine on various neurodevelopmental events and the regulation of neuronal activity during early developmental epochs. The current knowledge is that taurine lacks a synaptic release mechanism but is released by volume-sensitive organic anion channels and/or a reversal of the taurine transporter. Extracellular taurine affects neurons and neuronal progenitor cells mainly via glycine, GABA(A), and GABA(B) receptors with considerable receptor and subtype-specific affinities. Taurine has been shown to directly influence neurogenesis in vitro as well as neuronal migration in vitro and in vivo. It provides a depolarizing signal for a variety of neuronal population in the immature central nervous system, thereby directly influencing neuronal activity. While in the neocortex, taurine probably enhance neuronal activity, in the immature hippocampus, a tonic taurinergic tone might be necessary to attenuate activity. In summary, taurine must be considered as an essential modulator of neurodevelopmental events, and possible adverse consequences on fetal and/or early postnatal development should be evaluated for pharmacological therapies affecting taurinergic functions.

The spectrum of neuropathological changes associated with congenital Zika virus infection.

A major concern associated with ZIKV infection is the increased incidence of microcephaly with frequent calcifications in infants born from infected mothers. To date, postmortem analysis of the central nervous system (CNS) in congenital infection is limited to individual reports or small series. We report a comprehensive neuropathological study in ten newborn babies infected with ZIKV during pregnancy, including the spinal cords and dorsal root ganglia (DRG), and also muscle, pituitaries, eye, systemic organs, and placentas. Using in situ hybridization(ISH) and electron microscopy, we investigated the role of direct viral infection in the pathogenesis of the lesions. Nine women had Zika symptoms between the 4th and 18th and one in the 28th gestational week. Two babies were born at 32, one at34 and 36weeks eachand six at term. The cephalic perimeter was reduced in four, and normal or enlarged in six patients, although the brain weights were lower than expected. All had arthrogryposis, except the patient infected at 28weeks gestation. We defined three patterns of CNS lesions, with different patterns of destructive, calcification, hypoplasia, and migration disturbances. Ventriculomegaly was severe in the first pattern due to midbrain damage with aqueduct stenosis/distortion. The second pattern had small brains and mild/moderate (ex-vacuo) ventriculomegaly. The third pattern, a well-formed brain with mild calcification, coincided with late infection. The absence of descending fibres resulted in hypoplastic basis pontis, pyramids, and cortico-spinal tracts. Spinal motor cell loss explained the intrauterine akinesia, arthrogryposis, and neurogenic muscle atrophy. DRG, dorsal nerve roots, and columns were normal. Lympho-histiocytic inflammation was mild. ISH showed meningeal, germinal matrix, and neocortical infection, consistent with neural progenitors death leading to proliferation and migration disorders. A secondary ischemic process may explain the destructive lesions. In conclusion, we characterized the destructive and malformative consequences of ZIKV in the nervous system, as reflected in the topography and severity of lesions, anatomic localization of the virus, and timing of infection during gestation. Our findings indicate a developmental vulnerability of the immature CNS, and shed light on possible mechanisms of brain injury of this newly recognized public health threat.

Monosialoganglioside 1 may alleviate neurotoxicity induced by propofol combined with remifentanil in neural stem cells.

Monosialoganglioside 1 (GM1) is the main ganglioside subtype and has neuroprotective properties in the central nervous system. In this study, we aimed to determine whether GM1 alleviates neurotoxicity induced by moderate and high concentrations of propofol combined with remifentanil in the immature central nervous system. Hippocampal neural stem cells were isolated from newborn Sprague-Dawley rats and treated with remifentanil (5, 10, 20 ng/mL) and propofol (1.0, 2.5, 5.0 μg/mL), and/or GM1 (12.5, 25, 50 μg/mL). GM1 reversed combined propofol and remifentanil-induced decreases in the percentage of 5-bromodeoxyuridine(+) cells and also reversed the increase in apoptotic cell percentage during neural stem cell proliferation and differentiation. However, GM1 with combined propofol and remifentanil did not affect β-tubulin(+) or glial fibrillary acidic protein(+) cell percentage during neural stem cell differentiation. In conclusion, we show that GM1 alleviates the damaging effects of propofol combined with remifentanil at moderate and high exposure concentrations in neural stem cells in vitro, and exerts protective effects on the immature central nervous system.

Sleep architecture in children with arousal disorders

IntroductionArousal disorders (AD) are sleep disorders that primarily involve behaviour typical of being awake (e.g. talking, walking, handling objects, yelling or crying). They present during partial arousal typically during slow wave sleep (SWS). By definition it has been suggested that parasomnias do not cause changes in sleep architecture or insomnia symptoms or daytime drowsiness. MethodA comparative and retrospective study was conducted to study the sleep architecture of a group of paediatric patients with clinical and polysomnographic diagnosis of arousal disorders (ADG), paired by age and gender with a group of healthy children (HCG). The research was conducted at the Sleep Disorders Clinic of the Faculty of Medicine of the Universidad Nacional Autónoma de Mexico. The Student's t test for independent samples was used to compare sleep architecture and a value of p<0.05 was used to determine significance. ResultsThere was a significant increase in rapid eye movement sleep (REM) and REM sleep latency and a significant reduction in light sleep (stages N1 and N2) in the ADG compared to the (HCG). ConclusionsIt has been reported that AD first manifests during the pre-school years and that the frequency of events gradually decreases and abate completely during adolescence, which is why AD is believed to be the manifestation of an immature central nervous system (CNS). It may be that the sleep architecture characteristics shown by patients in the ADG would correspond to CNS immaturity in healthy but younger children.

Excessive crying in infants

ObjectiveReview the literature on excessive crying in young infants, also known as infantile colic, and its effects on family dynamics, its pathophysiology, and new treatment interventions. Data sourceThe literature review was carried out in the Medline, PsycINFO, LILACS, SciELO, and Cochrane Library databases, using the terms “excessive crying,” and “infantile colic,” as well technical books and technical reports on child development, selecting the most relevant articles on the subject, with emphasis on recent literature published in the last five years. Summary of the findingsExcessive crying is a common symptom in the first 3 months of life and leads to approximately 20% of pediatric consultations. Different prevalence rates of excessive crying have been reported, ranging from 14% to approximately 30% in infants up to 3 months of age. There is evidence linking excessive crying early in life with adaptive problems in the preschool period, as well as with early weaning, maternal anxiety and depression, attention deficit hyperactivity disorder, and other behavioral problems. Several pathophysiological mechanisms can explain these symptoms, such as circadian rhythm alterations, central nervous system immaturity, and alterations in the intestinal microbiota. Several treatment alternatives have been described, including behavioral measures, manipulation techniques, use of medication, and acupuncture, with controversial results and effectiveness. ConclusionExcessive crying in the early months is a prevalent symptom; the pediatrician's attention is necessary to understand and adequately manage the problem and offer support to exhausted parents. The prescription of drugs of questionable action and with potential side effects is not a recommended treatment, except in extreme situations. The effectiveness of dietary treatments and use of probiotics still require confirmation. There is incomplete evidence regarding alternative treatments such as manipulation techniques, acupuncture, and use of the herbal supplements and behavioral interventions.