Neuropsychomotor Developmental Delay Research Articles

Identification of a novel nonsense SLC16A2 gene mutation in an infant with severe neurologic phenotype: A case report.

Allan-Herndon-Dudley syndrome (AHDS) results from a pathogenic variant in the hemizygous subunit of the SLC16A2 gene, which encodes monocarboxylate transporter 8 and follows an X-linked recessive pattern. AHDS manifests as neuropsychomotor developmental delay, intellectual disability, movement disorders, and thyroid hormone abnormalities. It is frequently misdiagnosed as cerebral palsy or hypothyroidism. A 9-month-old male infant exhibited poor head control, hypodynamia, motor retardation, hypertonic limbs, and thyroid abnormalities. Despite levothyroxine supplementation and rehabilitation therapy, no improvements were observed. Whole-exome sequencing identified a novel nonsense mutation in SLC16A2 (c.124G > T, p.E42X), which unequivocally established the diagnosis. AHDS was confirmed. Levothyroxine treatment commenced early in infancy, followed by 3 months of rehabilitation therapy, starting at 5 months of age. The combined administration of levothyroxine and methimazole was initiated at 1 year and 10 months of age, respectively. While improvements were noted in thyroid hormone levels, neurological developmental delays persisted. AHDS should be considered in patients presenting with atypical neurological features and thyroid hormone abnormalities such as elevated triiodothyronine and decreased thyroxine levels. The early utilization of exome sequencing aids in prompt diagnosis. The identified SLC16A2 nonsense mutation correlates with severe neurological phenotypes and adds to the spectrum of genetic variations associated with AHDS.

Caracterização fenotípica de um menino com duplicação 4q associada à anomalia anorretal: relato de caso.

Duplicações de 4q representam anormalidades cromossômicas raras de características clínicas variáveis, estan-do estas relacionadas diretamente ao tamanho do segmento duplicado, e se a alteração foi isolada ou com translocação de outro cromossomo. Anomalias anorretais apresentam-se em um amplo espectro de defeitos congênitos, podendo ser isoladas ou sindrômicas, com cerca de 60% dos pacientes afetados apresentando também outras anomalias. Apresentamos neste relato um caso de anomalia anorretal diagnosticada ao nasci-mento associada à microcefalia, dismorfismos faciais e atraso de desenvolvimento neuropsicomotor. Tem carió-tipo normal e com o auxílio da técnica de CGH-array foi possível o diagnóstico deste caso e a expansão do fenó-tipo clínico da dup4q para incluir a associação com anomalia anorretal.

AN UNUSUAL CASE OF NEUTROPENIA

To describe a child with neutropenia and carrying inborn error of metabolism (IEM). A 10 months-old boy, fist child of non-consanguineous parents, presented severe neutropenia (0.02 × 10 9 /L) with fever, feeding problems, hypertonia and seizures. The frequency of fever and oscillating neutropenia is raised beyond use of antibiotics and granulocyte colony-stimulating factors. Some facial features present during physical examinations (hypertelorism, coarse face and skin dyspigmentation). He has failure to thrive and neuropsychomotor developmental delay. Viral diseases, organic acid in urine and mass spectrometry in tandem was normal. Abdominal ultrasound showed right hydronephrosis. Other image exams not detected alterations. The bone marrow aspirate analysis with karyotype resulted normal, with mild maturation arrest of granulocytic series. He did not have monocytosis or other hematologic disorders. Serum immunoglobulins were normal for the age group. Viral chronic diseases were negative, and she had no other autoimmune disorders. His mother had a first trimester spontaneous abortion, his father has no illnesses, and he has no siblings. A whole exome NGS sequencing showed compound heterozygous: one missense pathogenic CLPB variant (p. Arg408Gly) and other VUS c.1770+2T>A, splicing site. Hospitalizations is still frequent, and neutropenia did not remit to date. This patient presents neutropenia and neurologic involvement, characteristics of caseinolytic peptidase B (CLPB) deficiency, which can range from severe to mild. In this reported case, a severe CLPB deficiency, death usually occurs at a few months of age due to neonatal neurologic involvement (hypotonia or hypertonia, respiratory insufficiency, swallowing problems, absence of voluntary movements, and epilepsy) and severe neutropenia associated with life-threatening infections. A multidisciplinary team is necessary, and no specific dietary or metabolic treatment is available. Hematopoietic stem cell transplant is not indicated in this case. Granulocyte-colony stimulating factor to increase neutrophil counts to reduce the frequency of infections should be used. Neutropenia associated with CLPB disease is present from birth and may be chronic or intermittent with absolute neutrophil counts ranging from severe (< 0.5 per mm 3 ) to mild (< 1.5 per mm 3 ). Elevated urinary excretion of 3-methylglutaconic acid (3-MGA) (typically 2x-10x higher than the reference range) has been observed in most of affected individuals to date. This case may be useful to understand the neutropenia in inborn error of metabolism and clinical signs and symptoms of the disease. The molecular evaluation is fundamental to elucidate diagnostic of neutropenia in newborns.

Interstitial duplication syndrome in the chromosomic region 15q11q13: a case report

Introduction: The chromosomal region 15q11-13 contains a group of genes essential for normal neurodevelopment and alterations in this region result in different syndromes. Among the most frequent alterations, there are chromosomal deletions and duplications. Duplications of chromosome region 15q11q13 occur as a supernumerary chromosome 15, and may occur as interstitial duplications. The main clinical manifestations are intellectual impairment, problems with vision, hearing, teething and in bones and joints. Currently, there are few cases reported in the literature about this genetic condition, which justifies the relevance of this study. Objective: To report a case of duplication in the chromosomal region 15q11q13 and describe the clinical manifestations. Methodology: This is a case report of a qualitative nature. Case report: J.V.A.S., male, eight years old, attended at the Associação de Pais e Amigos dos Excepcionais (APAE), in Anápolis, Goiás, Brazil, in 2017, diagnosed with neuropsychomotor developmental delay (ADNPM) and macrocrania. No complications during childbirth. The patient had head support at six months, sat up at nine months, walked and talked at one year and ten months. He attends school and has good interaction, but has learning difficulties. In 2018, the CGH – ARRAY (aCGH) revealed the presence of a duplication in 15q11.2q13.1 of approximately 6.1Mb classified as pathogenic. Results and discussion: Due to the rarity of this syndrome, we did not find a satisfactory number of articles that specifically addressed this duplication. Conclusion: It is necessary to carry out more studies, in the long term and through satisfactory samples, in order to elucidate the main aspects involved in this pathology.

Suspected neuropsychomotor developmental delay in the first 2 years of life in a birth cohort in the Brazilian Amazon: Incidence, persistence and risk factors

AbstractWe estimated risk factors associated with suspected neuropsychomotor developmental delay at age 2 years, in a birth cohort in the Brazilian Amazon. The Maternal and Child Health and Nutrition in Acre (MINA‐Brasil) study is a population‐based birth cohort involving children born between July 2015 and June 2016 in the municipality of Cruzeiro do Sul, in the Brazilian state of Acre. We assessed neuropsychomotor development in 735 and 819 children at one and 2 years of age, respectively, using the Denver II screening test. Multivariate Poisson regression models were used to investigate the factors associated with suspected developmental delay at age 2 years. The frequency of suspected developmental delay was 29.5 and 51.0% at one and 2 years of age, respectively, with a cumulative incidence of 41.6% and a persistence of 60.6% between the first and second years of life. After adjustment, the risk of developmental delay at 2 years of age was found to be higher for children born to women with fewer years of education and whose mothers had urinary tract infection during pregnancy. Other risk factors included male sex, low height for age at 2 years, malaria at childhood, pacifier use and limited child stimulation at age 2 years.

Neuropsychomotor development in children born preterm at 6 and 12 months of corrected gestational age.

ABSTRACTObjective:To assess the incidence of neuropsychomotor developmental delay at 6 and 12 months of corrected gestational age in children born at 32 gestational weeks or less.Methods:A descriptive and prospective study was carried out at two public maternity hospitals. Between April 2017 and January 2019, we assessed 133 children without any known risk factors for neuropsychomotor developmental delay. The Bayley III scale was used to evaluate cognitive and motor development. The p value of the numerical variables was calculated using the Mann-Whitney test, whereas proportions of categorical variables were compared using the Z-test.Results:The mean maternal age was 26±6.9 years,78.8% were from middle and lower economic classes, and 57.1% of the analyzed children were female. Children presented with a higher incidence of delay at 12 months than at 6 months (10.3 and 2.3% at 12 and 6 months, respectively, for the cognitive score; 22.7 and 12% at 12 and 6 months, respectively, for the composite motor score; and 24.7 and 8.4% at 12 and 6 months, respectively, for the fine motor score).Conclusions:Cognitive and motor developmental delays were significant, with the highest incidence at 12 months. The results of this study encourage further research on this topic, since the exclusion criteria were comprehensive and the delays in neuropsychomotor development were significant.

Identificação de doenças genéticas na Atenção Primária à Saúde

Problema: Embora individualmente raras, somadas, as doenças genéticas têm prevalência global estimada de 31,5 a 73,0 por 1.000 indivíduos. Além disto, doenças genéticas e defeitos congênitos representam a segunda causa de mortalidade infantil no Brasil. Diante deste cenário, foi instituída a Política Nacional de Atenção Integral às Pessoas com Doenças Raras no Sistema Único de Saúde. Esta política prevê funções específicas para Atenção Primária à Saúde (APS) que incluem diagnóstico precoce e mapeamento de pessoas com ou sob-risco de desenvolver doenças genéticas raras e/ou defeitos congênitos para encaminhamento regulado. Essa experiência objetivou colaborar com o desenvolvimento de métodos para o reconhecimento de indivíduos com ou sob-risco de desenvolver doenças genéticas na APS. Métodos: Através de visitas domiciliares e por meio do preenchimento de uma ficha específica, realizou-se busca ativa de casos de doença genética e/ou defeito congênito em uma amostra probabilística aleatória, representativa de uma Unidade de Saúde da Família de um município brasileiro de porte médio. Resultados: Foram investigados 295 domicílios, totalizando 1.160 indivíduos e 238 casais. A média de filhos por casal foi de 2,7, a frequência de consanguinidade foi 3,8% e de abortamento espontâneo foi 8,7%. Foram identificadas 29 pessoas (2,5%) com doenças congênitas, 11 (0,9%) com deficiências auditivas, 10 (0,9%) com deficiência mental e 6 (0,5%) com déficits visuais importantes. Atraso no desenvolvimento neuropsicomotor foi relatado em 8,8% das crianças e adolescentes. Doze indivíduos (1%) possuíam câncer e 9,6% relataram história familiar positiva para câncer. Conclusão: Os profissionais da APS estão em posição privilegiada para identificar e organizar uma rede de cuidados para indivíduos com doenças genéticas e/ou defeitos congênitos. A utilização sistemática de instrumentos que facilitem o reconhecimento de fatores de risco e de situações suspeitas pode ser uma estratégia útil a ser incorporada pela APS.

Caracterização do Processamento Sensorial de Crianças Assistidas em um Programa de Estimulação Precoce

Objetivos: Caracterizar o processamento sensorial de crianças com atraso do desenvolvimento neuropsicomotor assistidas em um Programa de Estimulação Precoce. Metodologia: Estudo quantitativo, descritivo, analítico e transversal realizado em um hospital de referência de Pernambuco. Participaram deste estudo 24 responsáveis de crianças com faixa etária de 0 a 35 meses que estavam sendo atendidas pelo serviço. Para o grupo até 6 meses, foi utilizado o instrumento Perfil Sensorial 2 do Bebê e para o grupo acima de 7 meses, o Perfil Sensorial 2 da Criança Pequena, de prática aplicabilidade. Resultados: A maioria das crianças do grupo de até 6 meses apresentaram desempenho não esperado (hiperresponsividade) para os padrões de processamento sensorial. No grupo de crianças acima de 7 meses, foi observado um desempenho esperado para a maioria nos quadrantes e nas seções sensoriais (geral, auditivo, tato e oral) com exceção das seções sensoriais visual, movimento e comportamental (hiperresponsividade e hiporresponsividade). Conclusão: As crianças com atrasos no desenvolvimento neuropsicomotor apresentaram respostas diferentes para os padrões de processamento sensorial, seja para mais (hiperresponsividade) ou menos (hiporresponsividade), sendo recomendado o acompanhamento com a equipe multidisciplinar para o planejamento de estratégias direcionadas as respostas que mais afetam a sua participação.

Intervenção psicomotora no desenvolvimento infantil: uma revisão integrativa

Objective: Understand the effects of psychomotor intervention in children with neuropsychomotor developmental delay. Methods: This study is an integrative review of the scientific literature. For the research, articles were searched in the following databases: PubMed, PEDro (Physiotherapy Evidence Database), VHL (Virtual Health Library). CAPES Journals Portal and Web of Science, from December 2018 to January 2019, and the Research gate were consulted in January 2019. Results: A total of 867 articles were found, of which 142 were excluded due to non-compliance with the inclusion criteria and 33 were read in full. The study consisted of 7 articles selected according to the criteria, which showed that psychomotricity contributes positively to child development. Conclusion: The contribution of structured psychomotor intervention, despite the heterogeneity of protocols adopted, has positive results in the neuropsychomotor development process in childhood, being a usable resource to recover or prevent delays in child development.

Genetic architecture of retinoic-acid signaling-associated ocular developmental defects.

Ocular developmental anomalies are among the most common causes of severe visual impairment in newborns (combined incidence 1-2:10,000). They comprise a wide range of inborn errors of eye development with a spectrum of overlapping phenotypes and they are frequently associated with extraocular malformations, neuropsychomotor developmental delay and/or intellectual disabilities. Many studies from model organisms have demonstrated the role of retinoic acid (RA) during organogenesis, including eye development, and have revealed the wide spectrum of malformations that can arise from defective RA signaling. However, genes coding for homeobox proteins and morphogenetic factors were implicated in anomalies of ocular development long before genes coding for RA-signaling proteins. The purpose of this review is to discuss current knowledge about the highly complex genetic architecture of RA-signaling-associated ocular developmental anomalies in humans. Despite less than a dozen genes identified thus far, all steps of RA-signaling, from vitamin A transport to target cells to transcriptional activation of RA targets, have been implicated. Furthermore, the majority of these genetic disorders are associated with both dominant and recessive inheritance patterns and a wide spectrum of ocular malformations, which can dominate the phenotype or represent one of many features. Although some genotype-phenotype correlations are described, in many cases, the variability of clinical expression cannot be accounted for by the genotype alone. This observation and the large number of unsolved cases suggest that the relationship between RA signaling and eye development deserves further investigation.

Clinical and radiological findings in Brazilian patients with mucolipidosis types II/III.

The present study aims to provide orientation for clinicians and radiologists to recognize the most prevalent findings leading to diagnosis in mucolipidosis from a description of the natural history of five Brazilian cases. We conducted an observational and retrospective study of five patients with clinical and radiological diagnosis of mucolipidosis. Clinical evaluation consisted of information obtained from records and including physical, neurologic, and dysmorphic evaluations. Radiologic studies consisted of complete skeletal radiographs of all patients. Enzyme assessment was performed for confirmation of the diagnosis. The five patients were referred for genetic evaluation due to disproportionate short stature with short trunk accompanied by waddling gait. Age at referral varied from 11months to 28years. The most prevalent findings were joint restriction (4/5 patients), neuropsychomotor developmental delay (3/5), coarse facies (2/5), hypertrophic cardiomyopathy (2/5), and mental retardation (1/4 patients). The most common radiological findings were anterior beaking of the vertebral bodies (5/5), shallow acetabular fossae (5/5), epiphyseal dysplasia (5/5), platyspondyly (4/5), pelvic dysplasia (4/5), decreased bone mineralization (4/5), scoliosis (3/5), wide and oar-shaped ribs (3/5), generalized epiphyseal ossification delay (3/5), and hypoplasia of basilar portions of ilea (3/5). Enzyme assessment showed α-iduronidase, α-mannosidase, β-glucuronidase, hexosaminidase A, and total hexosaminidase increased in plasma and normal glycosaminoglycans concentration. One patient was clinically classified as ML II and four patients as ML III. The follow-up of five patients showed the typical clinical and radiological findings allowing the diagnosis, thus improving clinical management and providing adequate genetic counseling. Clinicians and radiologists can take advantage of the information from this work, enhancing their differential diagnosis ability.

Genotype/Phenotype correlation with partial duplications of 6p and 6q

Partial trisomy 6p and 6q are rare and clinical features include craniofacial changes, mental retardation and developmental delay. The study aims to correlate the genotype/ phenotype of a 6p and 6q duplication carrier. MVSN, female, single daughter of nonconsanguineous and healthy young couple. From an earlier relationship, the father had a 13-year-old son. Delivered by C-section, gestation of 37 weeks. The clinical analysis revealed: microcephaly, brachycephaly, syndromic facies, prominent forehead, hyperarousalism, strabismus, short nose, anteverted nares, smooth philtrum, thin lip, upper lip tented, micrognathism, dental anomalies, low-set ears, slender fingers, nails malformation, digitiform thumb, bilateral flat foot, hypotonia and neuropsychomotor developmental delay (NPMD). In the physical examination performed at 2 years of age, weight was 7,570 Kg (&lt;3,58%), length was 74 cm (&lt;3,95%) and cephalic perimeter was 43 cm (&lt;2%). Classic cytogenetic techniques were performed (GTG banding and high resolution GTG), molecular cytogenetic (FISH) and cytogenetic (aCGH). The karyotype showed a mosaicism 47, XX, + mar [9]/46, XX [11] (ISCN, 2016). The parental karyotype was normal. The chromosomal changes found by aCGH indicate a genetic gain at chromosomal regions 6p11.2?q12 and 6q14.1?q14.3 with a size of 10.335 Mb and 10. 765 Mb, respectively. The patient presented mosaicism of a marker chromosome (sSMC) identified by the technique of FISH as coming from chromosome 6. In region 6p11.2?q12 the genes present are: PRIM2, GUSBP4, MTRNR2L9, KHDRBS2, LGSN, PTP4A1, PHF3, EYS and MCART3P. Heart defects and kidney problems were cited in the literature as being characteristic of trisomy 6p. However, patient did not present any of these phenotypic changes. The region 6q14.1?q14.3 contains more than 20 genes. The clinical signs found in patient such as: developmental delay, mental retardation, forehead prominent, short nose and thin lips has been described in other studies in the literature as characteristic of 6q trisomy. The presence of mosaicism excludes the possibility of sSMC as the sole responsible for the patient's phenotype. Our study correlates the phenotypic characteristics presented by the patient with partial trisomy 6q collaborating for family genetic counseling.

INITIAL CLINICAL PRESENTATION IN CASES OF INBORN ERRORS OF METABOLISM IN A REFERENCE CHILDREN'S HOSPITAL: STILL A DIAGNOSTIC CHALLENGE.

ABSTRACTObjective: To assess the initial clinical presentation of confirmed cases of inborn errors of metabolism (IEM) at a reference facility for pediatric care.Methods: Cross-sectional, observational and descriptive study with data collection of outpatients, from January 2009 to December 2013. Inclusion criterion: referral to IEM investigation. Exclusion criterion: prior diagnosis of IEM. Analyzed variables: identification data; status of diagnostic investigation; family history of IEM; initial clinical presentation, laboratory abnormalities related to the hypothesis of IEM. Descriptive statistical methods were used in the data analysis.Results: We included 144 patients in the study, of which 62.5% were male. The mean and median ages were, respectively, 4.3 ± 4.7 years and 2.6 years. Twelve patients (8.3%) had a confirmed diagnosis of IEM (three with aminoacidopathies, three with organic acidemias, two with urea cycle disorders and four with lysosomal storage diseases). Cognitive impairment and seizures were the initial signs and symptoms, followed by growth retardation, neuropsychomotor developmental delay, seizures and hepatomegaly. The main laboratory abnormalities in the diagnosis were hyperammonemia and metabolic acidosis.Conclusions: The diagnosis of IEM still creates challenges to the pediatric practice. In this study, we identified the following factors: difficulty to access specific laboratory tests, reduced number of experts and poor dissemination of knowledge among healthcare schools. The early diagnosis of IEM majorly impacts the treatment and prevention of sequelae and should be considered in the initial diagnostic hypotheses.

Atraso do desenvolvimento neuropsicomotor: mapa conceitual, definições, usos e limitações do termo

ObjectiveTo retrieve the origin of the term neuropsychomotor developmental delay” (NPMD), its conceptual evolution over time, and to build a conceptual map based on literature review. Data sourceA literature search was performed in the SciELO Brazil, Web of Science, Science Direct, OneFile (GALE), Pubmed (Medline), Whiley Online, and Springer databases, from January of 1940 to January of 2013, using the following keywords NPMD delay, NPMD retardation, developmental delay, and global developmental delay. A total of 71 articles were selected, which were used to build the conceptual map of the term. Data synthesisOf the 71 references, 55 were international and 16 national. The terms developmental delay and global developmental delay were the most frequently used in the international literature and, in Brazil, delayed NPMD was the most often used. The term developmental delay emerged in the mid 1940s, gaining momentum in the 1990s. In Brazil, the term delayed NPMD started to be used in the 1980s, and has been frequently cited and published in the literature. Delayed development was a characteristic of 13 morbidities described in 23 references. Regarding the type of use, 19 references were found, with seven forms of use. Among the references, 34 had definitions of the term, and 16 different concepts were identified. ConclusionsDevelopmental delay is addressed in the international and national literature under different names, various applications, and heterogeneous concepts. Internationally, ways to improve communication between professionals have been indicated, with standardized definition of the term and use in very specific situations up to the fifth year of life, which was not found in Brazilian publications.

A microduplication of 5p15.33 reveals CLPTM1L as a candidate gene for cleft lip and palate

We report a 10-year-old boy with syndromic cleft lip and palate (CLP) and neuro-psychomotor developmental delay. Oligoarray comparative genomic hybridization (aCGH) detected an approximately 300 kb interstitial microduplication at 5p15.33 encompassing 5 protein-coding genes, including TERT and CLPTM1L, and two microRNA genes. Our findings suggest that the duplicated segment predisposes for cleft lip with or without cleft palate (CL/P), or any of the other phenotypic features presented by the patient. A gene coding a similar protein (CLPMT1) has been implicated in CLP etiology both through linkage studies and by a translocation disrupting the gene, indicating the possible involvement of CLPTM1L with CL/P. This is the first report of a possible connection between CLPTM1L and CLP.

Case Report 3p partial trisomy and 13q partial monosomy with congenital malformations and psychomotor developmental delay

We examined a girl presenting neuropsychomotor developmental delay and multiple malformations including antenatal and postnatal growth retardation, congenital heart defect, and facial dysmorphisms. Cytogenetic analysis was performed on peripheral blood lymphocytes with the GTG-banding technique, which revealed an unbalanced translocation: 46,XX,der(13)(13pter→13q34::3p24→3pter)pat. Karyotype analysis of the father demonstrated a balanced translocation, 46,XY,t(3;13)(p24;q34), indicating the inheritance of the derivative chromosome 13. The mother karyotype was normal. We suggest that most of the structural malformations seen in this patient are due to the 3p trisomy, while the neuropsychomotor alterations are a consequence of both chromosome aberrations.

Intrauterine myelomeningocele repair Postnatal results and follow-up at 3.5 years of age — initial experience from a single reference service in Brazil

Present the outcomes of six cases submitted to intrauterine myelomeningocele (MMC) repair. Descriptive observational study of six children submitted to antenatal surgical repair of MMC between 26 and 27 weeks gestation. All deliveries were through cesarean section. The following neonatal variables were assessed: gestational age at delivery, birth weight, Apgar scores, need for intubation, duration of hospital stay and need for postnatal shunt procedures. After 3.5 years, the children were evaluated using the Columbia Mental Maturity Scale or Denver II tests and the Hoffer Ambulation Scale. All deliveries were preterm at a mean gestational age of 32 + 4 weeks and mean birth weight was 1,942 g. Two infants had Apgar scores <7 at 1 min and 1 at 5 min. Ventricular-peritoneal shunts were placed in two cases. All six children are alive: five have normal cognitive development and one has a neuropsychomotor developmental delay. Two children had normal leg movements, a sacral functional level and are community ambulators. Three children had upper lumbar anatomical level lesions and one had a lower thoracic level lesion at the time of fetal surgery. One child, with an L1-L2 anatomical level lesion, in noambulatory and fully dependent on a wheelchair for mobility. Antenatal surgical repair of MMC reduced the need for postnatal shunt placements. Despite preterm delivery, the cognitive development of most children at 3.5 years was normal. Antenatal surgery seemed to improve lower limb motor function in these cases.

Computed tomography and electroencephalography in evaluation of children with motor and language disorders

In order to study the utility of computed tomography (CT) scan of the head and electroencephalogram (EEG) in the evaluation of children with neuropsychomotor developmental delay as well as to evaluate possible correlations between these two testing modalities, we reviewed the head CT and EEG findings in 111 children with motor and language disorders. The children were of both sexes and were divided into three groups by age: 0-12 months, 13-48 months and greater than 48 months […] COMPUTED TOMOGRAPHY [...]