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Results for “global developmental delay”

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PubMed2002

Developmental outcome, including setback, in young children with severe visual impairment.

This study retrospectively investigated the developmental perspective of 69 children (40 males, 29 females) with 'potentially simple' congenital disorders of the peripheral visual system: development was examined in the context of degree of visual impairment. Developmental and visual assessments were carried out at 10 to 16 months (Time 1) and 27 to 54 months of age (Time 2). Participants were grouped according to (1) visual status: profound visual impairment (PVI), severe visual impairment (SVI); (2) developmental status on the Reynell-Zinkin scales. A majority of the sample showed normal development on all subscales (62% Time 1, 57% Time 2). Those with PVI were more developmentally vulnerable than SVI with a greater incidence of (1) uneven developmental profile at Time 1 (48% PVI, 16% SVI); (2) global learning difficulties at Time 2 (37% PVI, 0% SVI); (3) delay on individual subscales at Time 2 (p<0.02 PVI versus SVI); (4) deceleration (verbal comprehension 74% PVI, 24% SVI, sensorimotor understanding 70% PVI, 27% SVI); and (5) severe developmental setback (33% PVI, 7% SVI). Risk factors of visual level, age, and sex for poor developmental outcome in infants with visual impairment were established.

Child Development↗

PubMed2004

Effect of positioning on the incidence of abnormalities of muscle tone in low-risk, preterm infants.

UNLABELLED: BACKGROUND. The preterm infant is subject to the force of gravity: when its body lies pressed against the mattress on which it is placed. AIMS: The purpose of this study was to investigate short-term effects of varied post-natal lying positions in order to prevent neuromuscular and postural abnormalities. METHODS: 60 low risk preterm infants of 31-36 weeks gestational age were enrolled for this randomised clinical trial. Initially each child underwent neurological and psychomotor assessments which included tonus and reflex protocols as well as behavioral, sensory motor and postural examinations. The lying positions of the treated group were varied (back, prone, and side) using a specially designed moldable mattress that maintained the functional position of the infant's body. The control group was placed on their stomachs, (the standard lying position used in 1994) with a standard orthopaedic bolster support under their hips. All infants underwent a second round of examinations upon discharge to assess any changes in neurological and psychomotor outcomes. RESULTS: The sensory-motor skills examinations showed significant abnormalities in the control group: (1) dominance of the extensor muscles due to muscle shortening, (2) hyper abduction and flexion of the arms, and (3) global neuromuscular rigidity. Psychomotor and neurological exams of the control and treatment groups showed delayed developmental muscular acquisitions for infants in the control group. CONCLUSION: Regular changes in posture, while retaining correct functional positions, allowed maintenance of normal neuromuscular and osteo-articular function and permitted the development of spontaneous and functional motor activity in low-risk perterm infants.

Female↗

PubMed1984

Tactile aversion in infancy.

Twenty children referred for assessment of delay in gross motor development showed tactile aversion. This is a common cause of delay in motor development and may be misdiagnosed as cerebral palsy or as a global developmental retardation. In some infants feeding is a problem. Although the condition is self-limiting, many patients need orthopaedic treatment for abnormalities of foot posture when they start to walk.

Cerebral Palsy↗

PubMed2003

CHB2, a member of the SWI3 gene family, is a global regulator in Arabidopsis.

The SWI/SNF complex is an ATP-dependent chromatin remodeling complex that plays an important role in the regulation of eukaryotic gene expression. Very little is known about the function of SWI/SNF complex in plants compared with animals and yeast. SWI3 is one of the core components of the SWI/SNF chromatin remodeling complexes in yeast. We have identified a putative SWI3-like cDNA clone, CHB2 (AtSWI3B), from Arabidopsis thaliana by screening the expressed sequence tag database. CHB2 encodes a putative protein of 469 amino acids and shares 23% amino acid sequence identity and 64% similarity with the yeast SWI3. The Arabidopsis genome contains four SWI3-like genes, namely CHB1 (AtSWI3A), CHB2 (AtSWI3B), CHB3 (AtSWI3C) and CHB4 (AtSWI3D). The expression of CHB2, CHB3 and CHB4 mRNA was detected in all tissues analyzed by RT-PCR. The expression of CHB1 mRNA, however, could not be detected in the siliques, suggesting that there is differential expression among CHB genes in different Arabidopsis tissues. To investigate the role of CHB2 in plants, Arabidopsis plants were transformed with a gene construct comprising a CHB2 cDNA in the antisense orientation driven by the CaMV 35S promoter. Repression of CHB2 expression resulted in pleiotropic developmental abnormalities including abnormal seedling and leaf phenotypes, dwarfism, delayed flowering and no apical dominance, suggesting a global role for CHB2 in the regulation of gene expression. Our results indicate that CHB2 plays an essential role in plant growth and development.

Amino Acid Sequence↗

PubMed2002

Gelatinase B and TIMP-1 are regulated in a cell- and time-dependent manner in association with neuronal death and glial reactivity after global forebrain ischemia.

Matrix metalloproteinases (MMPs) belong to a large family of endopeptidases that regulate the pericellular environment through the cleavage of protein components of the extracellular matrix, membrane receptors and cytokines. MMP activity is controlled by the multifunctional tissue inhibitors of metalloproteinases (TIMPs). Proteases and their inhibitors are critically involved in developmental and pathological processes in numerous organs, including the brain. Global transient cerebral ischemia induces selective delayed neuronal death and neuroinflammation. We compared, in discrete vulnerable and resistant areas of the ischemic rat hippocampus, the kinetics and cellular distribution of gelatinase B and its principal inhibitor TIMP-1 and we assessed by in situ zymography, the net gelatinolytic activity at the cellular level. We show that gelatinases are expressed and active in neurons, suggesting that MMPs play a role in maintaining neural homeostasis. In the ischemic rat brain, expression and activity of gelatinase B, and expression of TIMP-1 are altered in a time-, region- and cell-dependent manner. Gelatinase B is induced first in reactive microglia and subsequently in reactive astrocytes. In situ, increases in gelatinase activity accompanied the progression of neuronal death and glial reactivity. Our results suggest that MMPs and TIMPs are involved in cell viability and tissue remodelling in the ischemic brain, and reinforces the idea that the MMP/TIMP system contributes both to neuronal demise and tissue repair in the context of glial reactivity.

Animals↗

PubMed1995

Developmental and nutritional status of internationally adopted children.

OBJECTIVES: To assess the relationship between developmental status of international adoptees at the time of entry into the United States and their nutritional status and concurrent medical problems. DESIGN: Prospective study. SETTING/PATIENTS: One hundred twenty-nine internationally adopted children attending the International Adoption Clinic at the Floating Hospital for Children, Boston, Mass, underwent detailed developmental assessments, anthropometric measurements, and medical examinations. RESULTS: The anthropometric measurements of the international adoptees were below the means for weight, height, and head circumference based on standards of the World Health Organization. Only 65 children (50%) were developmentally normal. Gross motor delays were identified in 43 children (33%), fine motor delays in 52 (40%), language delays in 23 (18%), cognitive delays in 21 (16%), and global delays in 18 (14%). The severity of delays were related to z scores for weight, height, and head circumference. The 36 children with medical problems had lower z scores compared with healthy children and were more likely to have delayed development. CONCLUSIONS: Careful developmental and growth screening of internationally adopted children at entry into the United States identifies adopted children at entry interventions and close follow-up. Longitudinal studies of internationally adopted children may provide evidence about the reversibility of growth and developmental delays, findings applicable to any environmentally deprived child.

Adoption↗

PubMed2006

Autism and developmental delay: a comparative clinical study in very young children using IBSE scale.

OBJECTIVE: This study improves the knowledge of early autistic symptomatology and research concerning (i) the significant differences in the behaviors of children with autistic disorder (AD) and children with a developmental delay (DD), and (ii) the influence of the cognitive delay on symptomatology. METHOD: Two groups of 20 young children (7-42 months) were compared: children with AD, and those with DD. The groups were paired by chronological and developmental age. The comparison was extended to four subgroups composed according to age (younger and older children--<24 months, >24 months) and to the global development quotient (GDQ) (the more and less delayed). Each child was evaluated with the Infant Behavior Summarized Evaluation scale (IBSE). RESULTS: For the younger AD children, significant differences affected social communication and their adaptation to the environment (intolerance to frustration, resistance to change). For the older children (>24 months), this study showed the rapid progression of the number of distinctive signs between AD and DD children according to age and/or developmental level. CONCLUSIONS: Cognitive delay has an important influence on the symptomatology at the moment of initial recognition of an autistic syndrome. This study is a complement for the fuller understanding of the nature and early diagnosis of disorders specific to autism at the earliest phases of development.

Autistic Disorder↗

PubMed2002

Clinical analysis of 1048 children with developmental delay.

BACKGROUND: Children with developmental delay (DD) have a variety of problems in developmental functions. The purposes of this study were to analyze the underlying diseases and risk factors in children with different functional delays. METHODS: We collected data on 1048 children who underwent assessments of developmental function, related diseases, and risk factors. All children were classified into 6 functional delay groups: cognitive, speech, motor, pervasive, global, and non-specific DDs. Differences in related diseases and risk factors of the 6 functional delay groups were determined. RESULTS: Most children had global (51.2%), speech (21.9%), and motor (13.9%) delays. Approximately 62.8% of children were associated with biological factors (19% with genetic defects or congenital anomalies, 16.5% with central nervous system lesions, 13.9% with prematurity/low birth body weight, and 13.4% with neonatal insult). We could not identify the risk factors in 36.6% of the children. Most children with motor delay had brain/neuromuscular diseases and were associated with risks of prematurity or low birth body weight; while most children with global delay had brain neuromuscular diseases or psychological/mental disorders and were associated with risks of genetic defects or congenital anomalies. CONCLUSION: Our findings suggest that there are heterogeneous risk factors and related diseases in children with different kinds of functional delay.

Birth Weight↗

PubMed2002

Imaging the metabolic footprint of Glut1 deficiency on the brain.

Cerebral 18F-fluorodeoxyglucose positron emission tomography in 14 patients with microcephaly, developmental delay, seizures, and mutations of the glucose transporter Glut1 (Glut1 deficiency syndrome) showed distinct abnormalities. Within a global context of diminished cortical uptake, more severe hypometabolism was found in the mesial temporal regions and thalami, accentuating a relative signal increase in the basal ganglia. In contrast, the structure of the brain appeared preserved in patients additionally investigated by magnetic resonance imaging. This metabolic footprint was relatively constant in all patients regardless of age, seizure history, or therapies and therefore constitutes a radiological signature of the disease. The full expression of the signature in the youngest patient (aged 19 months) indicates that the state of haploinsufficiency caused by Glut1 mutation leaves a permanent footprint on the nervous system from its earlier postnatal stages of development. The potential benefit of prompt diagnosis, aided by 18F-fluorodeoxyglucose positron emission tomography, and early initiation of available therapies is underscored by our results.

Adolescent↗

PubMed2002

Renal injury from valproic acid: case report and literature review.

A child with developmental delay and epilepsy developed glucosuria approximately 16 months after starting valproic acid therapy. Laboratory evaluation revealed global defects in proximal tubule function consistent with the De Toni-Debré-Fanconi syndrome. Discontinuation of valproate led to complete recovery 5 months later. Review of previously reported cases indicates that this complication is unique to children and reversible when the medication is discontinued.

Child↗

PubMed1999

Developmental progress of children with congenital heart defects requiring open heart surgery.

Recent advances for infants requiring early open heart surgery have resulted in a dramatic decline in mortality and severe morbidity. The developmental progress of these new survivors is currently being defined. Causes contributing to brain injury are multifactorial, and may involve preoperative, intraoperative, and postoperative events. Before surgery, these children often exhibit hypotonia, poor state regulation, microcephaly, and developmental delays. These findings are particularly prevalent in newborns. In the acute postoperative period, neurodevelopmental deficits continue to manifest clinically. Long-term follow-up studies indicate that subtle neurological deficits and global developmental lags are characteristic of this population. Overall, severe neurological sequelae are uncommon; however, mild to moderate developmental disabilities are prevalent. Functional limitations, academic achievements, and health-related quality of life are areas that deserve further attention.

Achievement↗

PubMed1982

The hospitalization of children with developmental disorders.

Hospitalization is a difficult experience for a normal child. The hospitalization of a developmentally disabled child can be especially traumatic, both for the child who can not understand what is happening to him and for hospital personnel who are unaccustomed to dealing with such children. This article discusses the hospitalization of children with developmental disorders using the theoretical perspective of developmental psychology. The following issues are considered: 1) Does the child's disorder represent a delayed or a deviant course of development?, 2) Is the child's deficit global, affecting all areas of functioning, or specific, limited to one area?, and 3) Does a disorder early in development necessarily predict later problems, or are children able to compensate for certain deficits? Suggestions for improving the care of children with developmental disorders in hospitals are offered based on research and clinical observations.

Child↗

PubMed1991

Neurologic outcome after electroencephalographically proven neonatal seizures.

Infants in whom neonatal seizures were confirmed by randomly recorded ictal electroencephalographic (EEG) tracings were retrospectively examined to determine their global neurologic outcome and the specific frequency of epilepsy, development delay, and cerebral palsy. Perinatal and postnatal clinical and EEG variables were also examined for their relevance to the neurologic outcome. Forty infants with EEG documented seizures of diverse etiologies were studied. The 27 survivors were followed up at a mean of 31 months. The outcome was unfavorable in 70%. The rate of epilepsy was 56%, of developmental delay 67%, and of cerebral palsy 63%. The etiology of seizures was an important factor influencing the outcome. Other clinical factors that showed a significant relationship with global or specific aspects of the neurologic outcome included the age at the onset of seizures, birth weight, and neurologic examination results. The EEG parameters that significantly predicted the neurologic outcome were interictal EEG background, increased seizure frequency, and decreased seizure duration.

Asphyxia↗

PubMed1999

Fragile X syndrome and an isodicentric X chromosome in a woman with multiple anomalies, developmental delay, and normal pubertal development.

We report on an individual with developmental delays, short stature, skeletal abnormalities, normal pubertal development, expansion of the fragile X triplet repeat, as well as an isodicentric X chromosome. S is a 19-year-old woman who presented for evaluation of developmental delay. Pregnancy was complicated by a threatened miscarriage. She was a healthy child with intellectual impairment noted in infancy. Although she had global delays, speech was noted to be disproportionately delayed with few words until age 3.5 years. Facial appearance was consistent with fragile X syndrome. Age of onset of menses was 11 years with normal breast development. A maternal male second cousin had been identified with fragile X syndrome based on DNA studies. The mother of this child (S's maternal first cousin) and the grandfather (S's maternal uncle) were both intellectually normal but were identified as carrying triplet expansions in the premutation range. S's mother had some school difficulties but was not identified as having global delays. Molecular analysis of S's fragile X alleles noted an expansion of more than 400 CGG repeats in one allele. Routine cytogenetic studies of peripheral blood noted the presence of an isodicentric X in 81of 86 cells scored. Five of 86 cells were noted to be 45,X. Cytogenetic fra(X) studies from peripheral blood showed that the structurally normal chromosome had the fragile site in approximately 16% of the cells. Analysis of maternal fragile X alleles identified an allele with an expansion to approximately 110 repeats. FMRP studies detected the expression of the protein in 24% of cells studied. To our knowledge, this is the first patient reported with an isodicentric X and fragile X syndrome. Whereas her clinical phenotype is suggestive of fragile X syndrome, her skeletal abnormalities may represent the presence of the isodicentric X. Treatment of S with 20 mg/day of Prozac improved her behavior. In the climate of cost con trol, this individual reinforces the recommendation of obtaining chromosomes on individuals with developmental delay even with a family history of fragile X syndrome.

Abnormalities, Multiple↗

PubMed2000

Gene regulation: better late than never?

A new study has found that, in Arabidopsis, the paternal copies of many genes are delayed in expression during early seed development. The distribution of the genes and nature of their products suggest that this delayed expression of paternal alleles may be a global phenomenon.

Alleles↗

PubMed2006

[What should be done when a child cannot learn to read?].

When a child faces difficulties in learning to read, clinicians should, first of all, examine cognitive functions. The actual reading level is checked using a test calibrated on normal reading development. They are thus able to differentiate between global learning disorders (related to mental deficiency or pervasive disorders) and specific reading impairment. Specific reading impairment might be a simple delay or developmental dyslexia. We described the first at-school training, as well as the criteria of speech therapy.

Child↗

PubMed2003

Increased brain levels of F2-isoprostane are an early marker of behavioral sequels in a rat model of global perinatal asphyxia.

Perinatal asphyxia is a major cause of immediate and postponed brain damage in the newborn. It may be responsible for several delayed neurologic disorders and, in this respect, early markers of brain injury would be relevant for therapeutic intervention as well as for identification of infants at high risk for developmental disabilities. Biochemical measurements (brain F2-isoprostane levels) and behavioral tests (ultrasonic vocalization pattern on postnatal days (pnd) 5, 8, and 11, spontaneous motor behaviors on pnd 7 and 12, and homing response on pnd 10) were performed in a rat model of global perinatal asphyxia in the immature neonate. Caesarean section was performed in rats and the pups, still in uterus horns, were placed into a water bath at 37 degrees C for either 10 or 20 min. Caesarean delivered pups were used as controls. Pups experiencing severe (20 min), in contrast to those undergoing the 10 min, asphyctic insult presented with detectable abnormalities including early (two hours after the insult) increase in brain F2-isoprostane (a direct marker of oxidative injury) without detectable changes in PGE2, COX-2 and iNOS levels, and delayed physical (reduced weight gain on pnd 5 and thereafter) and behavioral disturbances (alterations in ultrasound emission on pnd 11 and spontaneous motricity levels mainly). These findings suggest that increased brain F2-isoprostane levels shortly after the asphyctic insult are predictive of delayed behavioral disturbances in the newborn rat. The present 20-min asphyxia model might serve for the assessment of preventive and curative strategies to treat neurologic/behavioral disturbances associated with perinatal asphyxia.

Animals↗

PubMed2006

Global brain dysmyelination with above-average verbal skills in 18q- syndrome with a 17 Mb terminal deletion.

BACKGROUND: Patients with the karyotypic finding of a terminal deletion in the long arm of chromosome 18 (18q- syndrome) commonly display cerebral dysmyelination and developmental delay. To our knowledge, all reported cases characterized by molecular analysis who had no mental retardation as confirmed by neuropsychological testing had a chromosomal breakpoint within the two most distal bands, 18q22 or 18q23, leading to a deletion of 16 Mb or less. AIMS OF THE STUDY: It was the aim of this study to improve the karyotype-phenotype correlation in 18q- syndrome by thoroughly analyzing the deletion size and the mental and radiologic status in a 23-year-old woman with a terminal 18q deletion. We performed cytogenetic and molecular cytogenetic analysis, brain MRI, and extended neuropsychological testing. RESULTS: Molecular karyotyping revealed a 17 Mb deletion of terminal 18q with a breakpoint in 18q21.33 and no evidence for mosaicism. While brain MRI demonstrated severe global dysmyelination, the patient showed a neuropsychological pattern that allowed for normal psychosocial and job achievement. After delayed development in childhood, the patient caught up during puberty and showed normal verbal intelligence and skills at 23 years. However, visual, visual-spatial, visual-constructional, and executive functions were found to be severely impaired. CONCLUSION: Here, we present a patient with one of the largest terminal 18q deletions reported in an individual without obvious mental retardation. Our analysis extends the phenotypic spectrum for individuals with breakpoints in 18q21.33. In addition, this study highlights the fact that severe global dysmyelination may not be associated with general cognitive deficits.

Adult↗