Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The improved survival of extremely premature infants has generated intense interest in the quality of life of the survivors. This review focuses on the major long-term complications of prematurity (developmental disability, retinopathy of prematurity, chronic lung disease) and concludes with an overview of the broader spectrum of morbidity. Severe impairment (cerebral palsy, mental retardation, retrolental fibroplasia, severe chronic lung disease) fortunately occurs in a small proportion of survivors. However, the prevalence of the lesser morbidities (minimal cerebral dysfunction/learning disability, poor growth, postneonatal illnesses, rehospitalization) is less clearly defined. These problems all have an impact on families, and on medical and educational services.
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PMID:Medical complications of prematurity. 293 64

The frequency of the developmental dysfunction and specific learning disabilities were assessed in the retrospective study in the group of 56 school-aged twins. The relationships between genetic, perinatal and social factors and learning disability were also determined. It was found that 12.5% of twins had learning disabilities. The most common neurodevelopmental dysfunction were language disorders, poor graphomotor fluency and poor fine motor dexterity. It was also found that educational difficulty were associated with prematurity, low Apgar scores, neonatal complications and familial predisposition.
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PMID:Neurodevelopmental dysfunction and specific learning disabilities in school-aged twins. 1091 65

Twins are at greater risk of death and severe morbidity than singletons which is in excess of that attributable to their greater prematurity. Monozygous, specifically monochorionic, twins are at greater risk than dichorionic twins. The major morbidity is neurological impairment usually presenting as cerebral palsy or severe learning disability and frequently, but not always, associated with fetal death of a co-twin. The likely pathogenesis of the neurological impairment is ischaemia attributable to haemodynamic imbalance via placental vascular anastomoses. In addition to the neurological impairment, congenital cardiac, renal, intestinal and other anomalies are more common but discordant in monozygous twins. It has been hypothesized that cerebral palsy and other neurological impairment in apparently singleton infants is attributable to early loss of a twin, the 'vanishing' twin phenomenon. It is also postulated that other congenital anomalies in singletons may be attributable to the same phenomenon.
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PMID:Neurological outcome in twins. 1223 46

The objective of this study was to investigate the background and associated factors in a representative group of young males with Asperger syndrome (AS) presenting at a specialized autism clinic. One hundred males aged 5 years 6 months to 24 years 6 months, with a mean age of 11 years 4 months (SD 3y 10mo), who had a clinical diagnosis of AS were included in the study. An in-depth review of their medical records and neuropsychological test data was performed. There was a high rate (51%) of non-verbal learning disability (defined as Verbal IQ more than 15 points higher than Performance IQ), but otherwise there was little or no support for the notion of right-hemisphere brain dysfunction being at the core of the syndrome. There was a very high rate of close relatives with autism spectrum problems, but also high rates of prenatal and perinatal problems, including prematurity and postmaturity. In comparison with general population data, those with AS very often had a combination of genetic and prenatal and perinatal risk factors. Non-verbal learning disability test results applied in about half the group. There was a subgroup of individuals with AS who had macrocephalus. However, there was no support for an association of AS with low body mass index.
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PMID:One hundred males with Asperger syndrome: a clinical study of background and associated factors. 1547 68

Developmental dyscalculia is a specific learning disability affecting the normal acquisition of arithmetic skills. Genetic, neurobiologic, and epidemiologic evidence indicates that dyscalculia, like other learning disabilities, is a brain-based disorder. However, poor teaching and environmental deprivation have also been implicated in its etiology. Because the neural network of both hemispheres comprises the substrate of normal arithmetic skills, dyscalculia can result from dysfunction of either hemisphere, although the left parietotemporal area is of particular significance. The prevalence of developmental dyscalculia is 5 to 6% in the school-aged population and is as common in girls as in boys. Dyscalculia can occur as a consequence of prematurity and low birthweight and is frequently encountered in a variety of neurologic disorders, such as attention-deficit hyperactivity disorder (ADHD), developmental language disorder, epilepsy, and fragile X syndrome. Developmental dyscalculia has proven to be a persisting learning disability, at least for the short term, in about half of affected preteen pupils. Educational interventions for dyscalculia range from rote learning of arithmetic facts to developing strategies for solving arithmetic exercises. The long-term prognosis of dyscalculia and the role of remediation in its outcome are yet to be determined.
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PMID:Developmental dyscalculia. 1555 92

Approximately 6% of school-aged children have math difficulties (MD). A neurogenetic etiology has been suggested due to the presence of MD in some genetic syndromes such as 22q11.2DS. However, the contribution of 22q11.2DS to the MD phenotype has not yet been investigated. This is the first population-based study measuring the frequency of 22q11.2DS among school children with MD. Children (1,564) were identified in the schools through a screening test for language and math. Of these children, 152 (82 with MD and 70 controls) were selected for intelligence, general neuropsychological, and math cognitive assessments and for 22q11.2 microdeletion screening using MLPA. One child in the MD group had a 22q11.2 deletion spanning the LCR22-4 to LCR22-5 interval. This child was an 11-year-old girl with subtle anomalies, normal intelligence, MD attributable to number sense deficit, and difficulties in social interactions. Only 19 patients have been reported with this deletion. Upon reviewing these reports, we were able to characterize a new syndrome, 22q11.2 DS (LCR22-4 to LCR22-5), characterized by prematurity; pre- and postnatal growth restriction; apparent hypotelorism, short/upslanting palpebral fissures; hypoplastic nasal alae; pointed chin and nose; posteriorly rotated ears; congenital heart defects; skeletal abnormalities; developmental delay, particularly compromising the speech; learning disability (including MD, in one child); intellectual disability; and behavioral problems. These results suggest that 22q11.2 DS (LCR22-4 to LCR22-5) may be one of the genetic causes of MD.
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PMID:Are 22q11.2 distal deletions associated with math difficulties? 2498 30