Central Nervous System Impairment Research Articles

Iodine fortification of foods and condiments, other than salt, for preventing iodine deficiency disorders

Iodine fortification of foods and condiments, other than salt, for preventing iodine deficiency disorders

HIF-1α Involves in Neuronal Apoptosis after Traumatic Brain Injury in Adult Rats

Hypoxia-inducible factor-1α (HIF-1α), a well-identified hypoxia-related protein, is involved in regulating the biological functions of various cell types including neurons. The traditional biological function of HIF-1α is promoting the transcription of some pro-survival genes when exposing to low oxygen conditions. Meanwhile, some studies also point out that HIF-1α shows the detrimental role in several central nervous system (CNS) disorders. Up to now, the knowledge of HIF-1α function in CNS is still limited. To investigate whether HIF-1α is involved in CNS impairment and repair, we employed a traumatic brain injury model in adult rats. Upregulation of HIF-1α was observed in the injured brain cortex by western blot analysis and immunohistochemistry staining. Terminal deoxynucleotidyl transferase deoxy-UTP nick-end labeling (TUNEL) and 4',6-diamidino-2-phenylindole (DAPI) staining suggested that HIF-1α was relevant to neuronal apoptosis after brain injury. In addition, glutamate excitotoxic model of primary cortex neurons was introduced to further investigate the role of HIF-1α in neuronal apoptosis; the result implied HIF-1α was associated with the regulation of p53 and BNIP3 in the apoptotic neurons. Based on our data, we suggested that HIF-1α might play an important role in neuronal apoptosis after traumatic brain injury in rat, which might also provide a basis for the further study on its role in regulating the transcription of target genes in apoptotic neurons, and might gain a novel strategy for the clinical therapy for traumatic brain injury.

Brain magnetic resonance imaging pattern and outcome in children with haemolytic‐uraemic syndrome and neurological impairment treated with eculizumab

The aim of this study was to describe the magnetic resonance imaging (MRI) findings and the neurological and neuropsychological outcomes in paediatric, diarrhoea-associated haemolytic-uraemic syndrome (D+HUS) with central nervous system impairment treated with eculizumab, a monoclonal antibody. The 14-month single-centre prospective study included seven children (three males, four females; age range 16 mo-7 y 8 mo; median age 3 y 7 mo) with typical D+HUS and acute neurological impairment. In the acute phase of the disease, neurological assessment and brain magnetic resonance imaging (MRI), including measurement of the apparent diffusion coefficient (ADC), were performed, and neuropsychological evaluation and brain MRI were also carried out 6 months after disease onset. In the acute phase, basal ganglia and white matter abnormalities with ADC restriction were a common and reversible MRI finding. In all the surviving patients (5/7), follow-up MRI after 6 months was normal, indicating reversible lesions. Clinical and neuropsychological evaluations after 6 months were also normal. This specific brain MRI pattern consisting of an ADC decrease in basal ganglia and white matter without major T2/fluid-attenuated inversion recovery (FLAIR) injury may be a key finding in the acute phase of the disease in favour of a vasculitis hypothesis. These reversible lesions were associated with a good neurological outcome. These results call for further evaluation of the potential role of eculizumab in the choice of treatment for severe D+HUS, particularly in the case of early neurological signs.

Morphometric studies of thyroid gland of Wistar rats exposed to alcohol during pregnancy and/or lactation

Maternal alcohol consumption during pregnancy and lactation results to some developmental defects such as microcephaly, impairment of central nervous system and mental retardation in the offspring. However,information is limited on the effects of alcohol on the organs of dams being exposed during pregnancy and/or lactation including the thyroid gland. Rat model was employed to investigate the morphometric effects ofalcohol on the thyroid gland in dams. 75 female Wistar rats assigned to 3 groups of 25 each were used. Group 1 served as control (C), group 2 and 3 were exposed to alcohol during pregnancy and lactation (APL) and duringlactation only (AL) respectively. At Day (D)7, D14, D21, D35 and D49 postpartum, 5 lactating rats were randomly selected from the three groups and sacrificed. After the sacrifice, the thyroids were dissected out andtheir weights determined. Thereafter, thyroid tissues were fixed in Bouin’s fluid and prepared for routine histological examination. The results of the investigation showed significant reduction (p<0.05) in the weightsof the thyroid glands. Histological evaluation showed reduced diameter of thyroid follicles, disorganization of follicular cells and desquamation of follicular cells of thyroid glands in alcohol-exposed rats. Our findingssuggest that alcohol intake during pregnancy and/or lactation could be injurious to the thyroid glands.Keywords: Alcohol, pregnancy, lactation, thyroids, Wistar rats.

Central nervous system vasculitis secondary to systemic sclerosis

Systemic sclerosis (SSc) or scleroderma is a connective tissue disease with a diverse array of clinical manifestations secondary to underlying fibrosis and autoimmunity. Central nervous system (CNS) impairment is uncommon in SSc. Here we report the fourth known patient with CNS vasculitis caused by SSc. In each previous report, the patient was a middle-aged to elderly female. Our patient was 24years old at the time of presentation, significantly younger than the other reported patients. Importantly, our patient’s rapidly progressive clinical course and poor response to immunosuppression have not been reported in patients with CNS vasculitis secondary to scleroderma. Although CNS vasculitis is extremely rare in SSc, our report suggests that clinicians should consider this diagnosis in the differential of SSc patients with neurologic impairment.

Genetic Variants in the Host Restriction Factor APOBEC3G are Associated With HIV-1–Related Disease Progression and Central Nervous System Impairment in Children

Apolipoprotein B mRNA editing catalytic polypeptide 3G (APOBEC3G) protein is incorporated into nascent virus particles and mediates cytidine deamination (C-to-U) of first-strand reverse transcripts of HIV-1 in target cells resulting in G-to-A hypermutation of the coding strand and premature degradation. We investigated the effects of APOBEC3G genetic variants on HIV-1-related disease in children. APOBEC3G variants were detected using real-time polymerase chain reaction in HIV-1-infected children from Pediatric AIDS Clinical Trials Group (PACTG) protocols P152 and P300 that evaluated the effectiveness of 3 mono- or dual-nucleoside reverse transcriptase inhibitor treatments. Of the 1049 children evaluated, 60% were non-Hispanic black, 26% Hispanic, 13% non-Hispanic white, and 1% other or unknown race/ethnicity. Age ranged from 42 days to 18 years; 45% were males. APOBEC3G-H186R homozygous G/G genotype was associated with more rapid HIV-1 disease progression [hazard ratio (HR): 1.69; P = 0.01] and central nervous system (CNS) impairment (HR: 2.00; P = 0.02) compared with the wild-type A/A or heterozygous A/G genotype in a recessive model. In both additive and dominant models, APOBEC3G-F119F-C allele was associated with protection against disease progression (HR [additive]: 0.69; P = 0.002 and HR [dominant]: 0.60; P = 0.001, respectively) and CNS impairment (HR [additive]: 0.65; P = 0.02 and HR [dominant]: 0.54; P = 0.007, respectively). These associations remained significant in multivariate analyses controlling for baseline characteristics or previously identified genetic variants known to alter HIV-1-related disease in this cohort of children. APOBEC3G-H186R and F119F variants are associated with altered HIV-1-related disease progression and CNS impairment in children.

Intermittent hypoxia from obstructive sleep apnea may cause neuronal impairment and dysfunction in central nervous system: the potential roles played by microglia

Obstructive sleep apnea (OSA) is a common condition characterized by repetitive episodes of complete (apnea) or partial (hypopnea) obstruction of the upper airway during sleep, resulting in oxygen desaturation and arousal from sleep. Intermittent hypoxia (IH) resulting from OSA may cause structural neuron damage and dysfunction in the central nervous system (CNS). Clinically, it manifests as neurocognitive and behavioral deficits with oxidative stress and inflammatory impairment as its pathophysiological basis, which are mediated by microglia at the cellular level. Microglia are dominant proinflammatory cells in the CNS. They induce CNS oxidative stress and inflammation, mainly through mitochondria, reduced nicotinamide adenine dinucleotide phosphate oxidase, and the release of excitatory toxic neurotransmitters. The balance between neurotoxic versus protective and anti- versus proinflammatory microglial factors might determine the final roles of microglia after IH exposure from OSA. Microglia inflammatory impairments will continue and cascade persistently upon activation, ultimately resulting in clinically significant neuron damage and dysfunction in the CNS. In this review article, we summarize the mechanisms of structural neuron damage in the CNS and its concomitant dysfunction due to IH from OSA, and the potential roles played by microglia in this process.

A Novel Approach to Obesity from Mental Function

Obesity is well recognized as serious problem in the world. Regular exercise and modest food intake are the basic strategies for healthy body weight. Although, it is very difficult to lose weight and it is much more difficult to avoid weight regain. Recently, from basic and clinical studies, some part of this difficulty might be explained by impairment of central nervous system due to obesity. Indeed, mental function, such as cognitive impairment, depression, vulnerability to stress, wrong body image, low self-esteem and disregulation of hedonic hunger contribute to development of obesity. The link between such mental disorders and obesity is likely to be bidirectional. Brain inflammation and imbalance of neuronal plasticity caused by disregulation of metabolic signals are candidates which cause mental disorders associated with obesity.

Coefficient of Energy Balance: Effective Tool for Early Differential Diagnosis of CNS Diseases

Urgent examination of cerebrospinal fluid (CSF) provides immediate important information about the character of central nervous system (CNS) impairment. Although this examination includes energy parameters such as glucose and lactate concentrations, it does not commonly use Coefficient of Energy Balance (CEB). In this study, we focused on CEB because it enables more exact assessment of actual energy state in the CSF compartment than glucose and lactate alone. CEB informs about the actual functioning condition of present cells, and it does not require any other analysis or costs. Using Kruskal-Wallis ANOVA, we examined a large CSF sample (n = 8183) and we compared CEB values among groups with different cytological syndromes. We found a statistically significant difference of CEB between the group with granulocyte pleocytosis and the control group. These results indicate a high degree of anaerobic metabolism caused by the oxidative burst of neutrophils. Similarly, we found a statistically significant difference of CEB between the control group and groups with tumorous oligocytosis plus pleocytosis and monocyte pleocytosis. This difference can be attributed to the oxidative burst of macrophages. Our findings suggest that CEB combined with CSF cytology has a great importance for diagnosis, differential diagnosis, and early therapy of CNS diseases.

Triple A (Allgrove) syndrome: an unusual association with syringomyelia

Triple A (Allgrove) syndrome was first described by Allgrove in 1978 in two pairs of siblings. Since then, about 100 cases have been reported, all of them displaying an autosomal recessive pattern of inheritance. Clinical picture is characterized by achalasia, alacrimia and ACTH-resistant adrenal failure. A progressive neurological syndrome including central, peripheral and autonomic nervous system impairment, and mild mental retardation is often associated. The triple A syndrome gene, designated AAAS, is localized on chromosome 12q13. It consists of 16 exons, encoding for a 546 aminoacid protein called ALADIN (Alacrimia-Achalasia-aDrenal Insufficiency Neurologic disorder).We report on a 13 year-old boy presenting with Addison’s disease, dysphagia, muscle weakness, excessive fatigue and recent onset gait ataxia. The analysis of the AAAS gene revealed a homozygous missense mutation in exon 12. It was a T > G transversion at nucleotide position 1224, resulting in a change of leucine at amino acid position 381 into arginine (Leu381Arg or L381R). Brain appearance was found normal at magnetic resonance imaging (MRI) and functional spectroscopy analysis showed normal levels of the main metabolites. Spine MRI showed a cystic cavity within the spinal cord (syringomyelia), localized between the sixth cervical vertebra and the first thoracic vertebra. Cerebellar tonsils descended 7 mm caudal to foramen magnum, consistently with a mild type 1 Chiari malformation. Mild posterior inter-vertebral disk protrusions were evident between T9 and T10 and between L4 and L5.To our knowledge, this is the first report describing type 1 Chiari malformation and multiple spinal cord abnormalities in a patient with Allgrove syndrome.

Mannose-binding Lectin and the Risk of HIV Transmission and Disease Progression in Children

Mannose-binding lectin (MBL) can activate the complement system by binding to carbohydrates, such as those presented on the HIV virion surface. It is unclear whether genetically determined MBL deficiency is related to vertical HIV transmission and disease progression in HIV-infected children. A literature search of Medline, Embase and Cochrane Central Register identified all relevant studies on MBL and HIV infection in children. We extracted information on the characteristics of the study group, method of MBL analysis, outcome definitions, follow-up and the risk estimates. The validity of each study was assessed. Nine studies were retrieved. Most were of good validity, but risk adjustment for confounders was missing in 6 studies. Age, treatment and outcome definitions differed between the study groups. In most of the studies, MBL deficiency was associated with an increased frequency of vertical HIV transmission and an increased speed of disease progression. In the 2 most valid studies, carriers of variant genes had an increased odds ratio for transmission and an increased relative hazard for disease progression and central nervous system impairment, especially in children <2 years of age. MBL deficiency is associated with an increased risk of vertical HIV transmission. How this risk relates to other factors that influence transmission is unclear. The association between HIV disease progression and MBL deficiency is most pronounced in children <2 years of age, probably due to immaturity of their adaptive immunity.

Editor’s Choice

Editor’s Choice

Complex Trauma and Prenatal Alcohol Exposure: Clinical Implications

Abstract Complex trauma resulting from chronic maltreatment and prenatal alcohol exposure can significantly affect child development and academic outcomes. Children with histories of maltreatment and those with prenatal alcohol exposure exhibit remarkably similar central nervous system impairments. In this article, I will review the effects of each on the brain and discuss clinical implications for these populations of children.

Physical therapies as an adjunct to Botulinum toxin-A injection of the upper or lower limb in adults following neurological impairment

BackgroundSpasticity of muscles is a common consequence of central nervous system impairment. Traditionally, neurological rehabilitation for spasticity has involved occupational and physical therapy; however, increasingly Botulinum toxin–A injections may be provided. Injection effects are temporary. Consequently, understanding the effect of adjunct physical therapies will help inform multimodal rehabilitation decisions. Presently, these effects are not known. This systematic review will identify and summarize evidence on physical therapies used after Botulinum toxin-A injection to improve motor function in adults with neurological impairments.MethodSystematic searching of seven electronic databases will occur to identify relevant randomized trials. Available trial data will be extracted into a list of pre-defined primary outcomes, including range of movement, spasticity and functional limb use. Pre-defined secondary outcomes will also be reviewed where trials have these data available for reporting. Effects will be expressed as mean differences or standardized mean differences with 95% confidence intervals (CI). Where possible, comparable results will be meta-analyzed, and a summary of the available pool of evidence produced.All randomized controlled trials will be rated using the PEDro methodological quality scale. Where possible, study data will be meta-analyzed using RevMan 5 Software. The protocol was registered in PROSPERO international prosepective register of systematic reviews (PROSPERO 2011:CRD42011001491).DiscussionReview results will be the most comprehensive answer available to the following question: Are physical therapies clinically effective after Botulinum toxin-A injections in adults with neurological spasticity? Results will inform healthcare providers and managers who determine who gets access to and provision of Botulinum toxin-A injection and whether this is done with or without physical therapies. Results will inform the clinicians who conduct physical therapy following injection. This protocol provides readers with the scope and depth of a search that will ultimately answer a complex and pressing treatment question. The variability of current practice and high level of expense associated with multimodal rehabilitation means review results will be more useful and less contestable if the protocol is revealed in full through advance publication.

The genetics of multiple sclerosis: an up-to-date review.

Multiple sclerosis (MS) is a prevalent inflammatory disease of the central nervous system that often leads to disability in young adults. Treatment options are limited and often only partly effective. The disease is likely caused by a complex interaction between multiple genes and environmental factors, leading to inflammatory-mediated central nervous system deterioration. A series of genomic studies have confirmed a central role for the immune system in the development of MS, including genetic association studies that have now dramatically expanded the roster of MS susceptibility genes beyond the longstanding human leukocyte antigen (HLA) association in MS first identified nearly 40 years ago. Advances in technology together with novel models for collaboration across research groups have enabled the discovery of more than 50 non-HLA genetic risk factors associated with MS. However, with a large proportion of the disease heritability still unaccounted for, current studies are now geared towards identification of causal alleles, associated pathways, epigenetic mechanisms, and gene-environment interactions. This article reviews recent efforts in addressing the genetics of MS and the challenges posed by an ever increasing amount of analyzable data, which is spearheading development of novel statistical methods necessary to cope with such complexity.

Carbamazepine treatment of bipolar disorder: a retrospective evaluation of naturalistic long-term outcomes

BackgroundCarbamazepine (CBZ) has been used in the treatment of bipolar disorder, both in acute mania and maintenance therapy, since the early 1970s. Here, we report a follow-up study of CBZ-treated bipolar patients in the Taipei City Psychiatric Centre.MethodsBipolar patients diagnosed according to the DSM-IV system and treated with CBZ at the Taipei City Psychiatric Centre had their charts reviewed to evaluate the efficacy and side effects of this medication during an average follow-up period of 10 years.ResultsA total of 129 bipolar patients (45 males, mean age: 45.7 ± 10.9 year) were included in the analysis of CBZ efficacy used alone (n = 63) or as an add-on after lithium (n = 50) or valproic acid (n = 11), or the both of them (n = 5). The mean age of disease onset was 24.6 ± 9.5 years. The mean duration of CBZ use was 10.4 ± 5.2 year. The mean dose used was 571.3 ± 212.6 mg/day with a mean plasma level of 7.8 ± 5.9 μg/mL. Mean body weight increased from 62.0 ± 13.4 kg to 66.7 ± 13.1 kg during treatment. The frequencies of admission per year before and after CBZ treatment were 0.33 ± 0.46 and 0.14 ± 0.30, respectively. The most common side effects targeted the central nervous system (24%), including dizziness, ataxia and cognitive impairment. Other common side effects were gastrointestinal disturbances (3.6%), tremor (3.6%), skin rash (2.9%), and blurred vision (2.9%). Eighty-eight patients (68.2%) were taking antipsychotics concomitantly. Ninety-six patients (74.4%) needed to use benzodiazepines concomitantly. Sixty-three (48.8%) patients had zero episodes in a 10-year follow-up period, compared to all patients having episodes prior to treatment. Using variable analysis, we found better response to CBZ in males than in females.ConclusionsCBZ is efficacious in the maintenance treatment of bipolar disorder in naturalistic clinical practice, either as monotherapy or in combination with other medications. CBZ is well tolerated by most patients in this patient group.

Infrasonic noise induces axonal degeneration of cultured neurons via a Ca2+ influx pathway

Infrasound is a kind of environmental noise. It can evoke biological resonance in organismic tissues including the central nervous system (CNS), causing displacement and distortion of cellular architectures. Several studies have revealed that certain intensity infrasound can impair normal functions of the brain, but the underlying mechanisms still remain largely unknown. Growing evidence has demonstrated that axonal degeneration is responsible for a variety of CNS dysfunctions. To explore whether neuronal axons are affected under infrasonic insults, we exposed cultured hippocampal neurons to infrasound with a frequency of 16Hz and a pressure level of 130dB for 1h, and examined the morphological and molecular changes of neuronal axons by immunocytochemistry and Western blotting, respectively. Our results showed that infrasound exposure significantly resulted in axonal degeneration of cultured hippocampal neurons, which was relatively independent of neuronal cell death. This infrasound-induced axonal degeneration can be significantly blocked by Ca2+ chelator EGTA and Rho kinase inhibitor Fasudil, but not by proteasome inhibitor MG132. Moreover, calcium imaging and RhoA activation assays revealed a great enhancement of Ca2+ influx within axons and RhoA activation after infrasound exposure, respectively. Depletion of Ca2+ by EGTA markedly inhibited this Ca2+ influx and attenuated RhoA activation as well. Thus, our findings revealed that axonal degeneration may be one of the important mechanisms underlying infrasound-induced CNS impairment, and Ca2+ influx pathway is likely implicated in the process.

Quercetin and Sesamin Protect Neuronal PC12 Cells from High-Glucose-Induced Oxidation, Nitrosative Stress, and Apoptosis

Complications of diabetes are now well-known to affect sensory, motor, and autonomic nerves. Diabetes is also thought to be involved in neurodegenerative processes characteristic of several neurodegenerative diseases. Indeed, it has been acknowledged recently that hyperglycemia-induced oxidative stress contributes to numerous cellular reactions typical of central nervous system deterioration. The goal of the present study was to evaluate the effects of the polyphenol quercetin and the lignan sesamin on high-glucose (HG)-induced oxidative damage in an in vitro model of dopaminergic neurons, neuronal PC12 cells. When incubated with HG (13.5 mg/mL), neuronal PC12 cells showed a significant increase of cellular death. Our results revealed that quercetin and sesamin defend neuronal PC12 cells from HG-induced cellular demise. An elevated level of reactive oxygen and nitrogen species is a consequence of improved oxidative stress after HG administration, and we demonstrated that this production diminishes with quercetin and sesamin treatment. We also found that quercetin and sesamin elicited an increment of superoxide dismutase activity. DNA fragmentation, Bax/Bcl-2 ratio, nuclear translocation of apoptosis-inducing factor, as well as poly(adenosine diphosphate [ADP]-ribose) polymerase cleavage were significantly reduced by quercetin and sesamin administration, affirming their antiapoptotic features. Also, HG treatment impacted caspase-3 cleavage, supporting caspase-3-dependent pathways as mechanisms of apoptotic death. Our results indicate a powerful role for these natural dietary compounds and emphasize preventive or complementary nutritional strategies for diabetes control.

Relation Over Time Between Facial Measurements and Cognitive Outcomes in Fetal Alcohol‐Exposed Children

The identification of individuals exposed prenatally to alcohol can be challenging, with only those having the characteristic pattern of facial features, central nervous system abnormality, and growth retardation receiving a clinical diagnosis of fetal alcohol syndrome (FAS). Seventeen anthropometric measurements were obtained at 5 and 9 years from 125 Cape Town, South African children, studied since birth. The children were divided into 3 groups: FAS or partial FAS (PFAS), heavily exposed nonsyndromal (HE), and non-alcohol-exposed controls (C). Anthropometric measurements were evaluated for mean group differences. Logistic regression models were used to identify the subset of anthropometric measures that best predicted group membership. Anthropometric measurements were examined at the 2 ages in relation to prenatal alcohol exposure obtained prospectively from the mothers during pregnancy. Correlation of these facial measurements with key neurobehavioral outcomes including Wechsler Intelligence Scales for Children-IV IQ and eyeblink conditioning was used to assess their utility as indicators of alcohol-related central nervous system impairment. Significant group differences were found for the majority of the anthropometric measures, with means of these measures smaller in the FAS/PFAS compared with HE or C. Upper facial widths, ear length, lower facial depth, and eye widths were consistent predictors distinguishing those exposed to alcohol from those who were not. Using longitudinal data, unique measures were identified that predicted facial anomalies at one age but not the other, suggesting the face changes as the individual matures. And 41% of the FAS/PFAS group met criteria for microtia at both ages. Three of the predictive anthropometric measures were negatively related to measures of prenatal alcohol consumption, and all were positively related to at least 1 neurobehavioral outcome. The analysis of longitudinal data identified a common set of predictors, as well as some that are unique at each age. Prenatal alcohol exposure appears to have its primary effect on brain growth, reflected by smaller forehead widths, and may suppress neural crest migration to the branchial arches, reflected by deficits in ear length and mandibular dimensions. These results may improve diagnostic resolution and enhance our understanding of the relation between the face and the neuropsychological deficits that occur.

Rozwój ślimaka u niemowląt ze zmianami w obrębie ośrodkowego układu nerwowego powstałymi w następstwie asfiksji okołoporodowej

Asphyxia in neonates with inadequate blood-inner ear barrier function causes damage to the inner ear included the degeneration of outer hair cells of the organ of Corti and oedematous changes in stria vascularis. The major consequences in the central nervous system (CNS) are found to be hypoxic-ischemic encephalopathy (HIE) in term newborns, peri- (PVH) or intraventricular hemorrhages (IVH) and periventricular leucomalacia (PVL) in preterm neonates. was to carry out the objective assessment of the cochlea development using CEOAEs in infants with CNS impairment occurring as an effect of perinatal asphyxia, imaged during trans-fontanel ultrasonography. To the investigation 36 infants with HIE, IVH or PVL were included, the control group encompassed 32 born at term, health children. In all children three times otoscopic examination and CEOAEs recordings were performed: after birth, in 3rd and in 6th month of life using Otodynamics Otoacoustic Analyser ILO-88 in Quick Screen version. Perinatal anamnesis, general pediatric status, results of trans-fontanel ultrasonography and biochemical test results were taken into account in statistical analyses. The mean amplitudes of CEOAEs in the first days of life were significantly reduced in InvG comparing to control babies. In half-octave frequency bandwidth analysis significant reduction of S/N Ratio at 1,5–4 kHz in InvG was observed. 3 and 6 months later the recorded responses significantly increased, they didn’t reach values of CG but no statistical differences between groups were observed. In conclusion, the outer hair cells activity in first days of life is reduced in newborns with CNS impairment and perinatal asphyxia in anamnesis comparing to health children. The maturation of the cochlea is intensive during first 3 months of life, later only subtle changes in CEOAEs are observed.