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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 25-year-old woman with cerebral palsy of spastic quadriplegia and athetosis showed typical cardiac arrest encephalopathy on neuropathology. The etiology of cerebral palsy was perinatal origin including prematurity, asphyxia and hyperbilirubinemia. Ventricular premature beats had developed since about 20 years of age. Muscle tone also increased with aging and symptoms of vago-vagal reflex were occasionally observed after eating. At 25 years, cardiac arrest occurred and cardiopulmonary resucitation was done immediately. She remained unconscious with absent corneal reflex and irregular respiration. EEG or auditory brain stem response showed flat activity. She died of respiratory failure 53 days after the episode of cardiac arrest. Neuropathology showed bilaterally symmetrical necrosis in the superior colliculi, gracilis nuclei, cuneate nuclei and spinotrigeminal nuclei accompanied with severe necrosis in the cerebrum and cerebellum. These findings in this adult case of total asphyxia were compatible with those observed in total plus partial asphyxia in the neonates. This discrepancy may be due to difference in cerebral maturity. Children or young adults with athetotic type cerebral palsy have a high risk of sudden death. Sudden cardiac arrest seems to play an important role in sudden death of these patients.
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PMID:[A case of cardiac arrest encephalopathy in athetotic cerebral palsy]. 138 32

Prematurity is a factor that predisposes to strabismus. Three hundred of the 1785 children with strabismus in out patient care during the latter five years were preterm babies, showing that prematurity intervenes in 16.7% of cases in the onset of strabismus. The onset age of strabismus deviation was also earlier before the age of two in 30% of cases. Visual acuity, refraction, strabismus deviation and fixation in terms of the degree of prematurity are analyzed. Neuropsychological examination revealed neurologic disturbances in 28.2% of these children, of which 5% encephalopathy. The neurologic disturbances, frequently of polycentric origin also represent an obstacle in reestablishing binocular vision. Seven premature infants presented pseudostrabismus with abnormal kappa angle and small deviation angle due to macula ectopia.
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PMID:[Strabismus and pseudostrabismus in premature infants]. 252 88

A boy aged 2 years, born prematurely to Gipsy parents, presented with hypopigmentation severe encephalopathy with athetoid movements, bilateral ocular anomalies including cloudy corneas, iris atrophy and cataracts, as well as dental defects. Ultrastructural examination of the skin disclosed scare melanosomes. Although the neurologic and ocular anomalies might have been accounted for by his extreme prematurity, their association with hypomelanogenesis and dental defects support, in this patient the diagnosis of the oculocerebral hypopigmentation syndrome (Cross syndrome).
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PMID:Oculocerebral hypopigmentation syndrome (Cross syndrome) in a Gipsy child. 259 92

The clinical spectrum and outcome of neonatal convulsions within an obstetric hospital population were reviewed for the 5 years, 1978-82, inclusive. There were 156 convulsing neonates managed at the Mater Mothers Hospital (110 inborn, 46 outborn). The incidence of early neonatal convulsions for inborn babies was 3.0/1000 live births. Antenatal and perinatal risk factors were compared between the 156 convulsing infants and the 36,082 infants born during the same period who did not convulse. The leading risk factors for convulsions were prematurity, intra-uterine growth retardation, low 5 min Apgar score, pre-eclampsia, antepartum haemorrhage, twin pregnancy and breech presentation. The predominant seizure type was tonic in 28.6%, multifocal clonic in 27.2%, subtle in 18.4%, myoclonic in 15.0% and focal clonic in 8.8%. Mortality (31%) and long-term disability (43%) rates were high. Tonic seizures had the highest mortality and morbidity. Throughout the duration of the study period infants received increasingly thorough investigation. Causative factors were determined in 95% of convulsing infants, most frequent being hypoxic-ischaemic encephalopathy (40.3%) and cerebroventricular haemorrhage (30.5%). Follow-up data on 99 of the 107 survivors (93%) revealed severe disability in 25, moderate disability in eight and mild disability in 10. A poor long-term prognosis was associated with prolonged convulsions, tonic and multifocal clonic convulsions, convulsions due to asphyxia and cerebroventricular haemorrhage and an abnormal neurological examination at discharge.
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PMID:Clinical spectrum and outcome of neonatal convulsions. 321 7

Eleven pregnant squirrel monkeys were perorally exposed to lead during the latter two-thirds of pregnancy [mean blood lead 0.54 microgram/ml (2.61 mumol/l), range 0.39-0.82 microgram/ml (1.88-3.96 mumol/l)], at a dosing regime producing no maternal toxic symptoms. Lesions similar to lead encephalopathy and growth retardation of the fetal cerebrum were seen in some of the offspring, as well as neurological and behavioral symptoms at adult age. Cerebral lead levels in offspring (an abortion, stillborns, a sacrificed full-term fetus, and a neonatal death) were between 0.1-0.7 microgram/g. Pre- and perinatal mortality, and prematurity, was increased, and the size of the offspring at birth was reduced. The head circumference tended to be reduced postnatally. Zinc protoporphyrin in blood was determined in four of the pregnant monkeys; the mean values were between 0.58-1.05 micrograms/ml (0.93-1.68 mumol/l). These findings represent the first clearly prenatal brain damages described for experimental peroral lead exposure.
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PMID:Effects of lead exposure on pregnancy outcome and the fetal brain of squirrel monkeys. 360 68

A total of 364 selected high-risk premature and mature infants were studied prospectively to assess the relationship between fetal-newborn complications and motor and cognitive deficits identified during the first year of life. Deficits occurred in 24 per cent of the children: 14 per cent had one or more major deficit and the other 10 per cent had one or more minor deficit. Prematurity was one of the fetal-newborn complications not associated with deficits at one year. Complications that were associated with deficits included fetal hypoxia, respiratory difficulties, infection and newborn encephalopathy. There was also a significant association between fetal hypoxia, newborn respiratory complications, infection and newborn encephalopathy, which is in keeping with the concept that the first three may be mechanisms in CNS injury and subsequent deficits, while newborn encephalopathy reflects the injury and is an important predictor of such deficits.
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PMID:The contribution of fetal-newborn complications to motor and cognitive deficits. 384 Jul 53

Electroclinical aspects of the West syndrome are studied in their atypical forms: clinical and EEG characteristics, partial forms, Aicardi syndrome. Etiological investigations (especially CT scan) are necessary to distinguish the more frequent 'secondary forms' from the 'primary forms'. The etiological factors are: (i) Prenatal causes (hereditary affections, chromosome-related etiology, fetal etiology; (ii) Perinatal causes (prematurity, traumatic delivery); (iii) Postnatal causes (infectious diseases). The evolutive aspects and prognosis are different for 'primary' and 'secondary' forms. The time of commencement of the mode of therapy and its duration are important factors in relation to the prognosis of 'primary forms'. A pre-existing encephalopathy obviously leads to a very poor prognosis. A typical Lennox-Gastaut syndrome can be observed in infants. However, atypical forms are more frequent. These too have a poor prognosis because they are usually secondary to cerebral lesions.
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PMID:[Epileptic evolutive encephalopathies in infants (West tsyndromee and Lennox-Gastaut syndrom) (author's transl)]. 734

The incidence of cerebral palsy has remained constant at 2 per 1000 life births in western countries through cesarean section and electronic fetal monitoring have been applied increasingly often since the last decades. There has been a shift towards prenatal causes and consequences of early prematurity. High risk deliveries (3% of all) should be performed only in specialized centers for perinatal medicine. For low risk deliveries local hospitals are more convenient and are traditionally well accepted in Germany. Perinatal hypoxia as a cause of perinatal brain damage is rare. Documentation of clinical symptoms of hypoxic-ischemic encephalopathy is mandatory in these cases. To investigate regional risk factors of perinatal brain damage we propose to connect the data of the perinatal inquiries and of the examinations of preschool children directed by german law.
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PMID:[Causes of perinatal brain damage]. 777 50

The prevalence of cerebral palsy is around 0.2% and has remained constant during the last 30 years. Retrospective case-control studies do not show a clear correlation between perinatal asphyxia and the development of cerebral palsy. Less than 10% of all cerebral palsy cases show signs of severe asphyxia during labour and delivery as the major pathological and likely cause for the brain damage. Severe cases of birth asphyxia with multiorgan defects and signs of hypoxic-ischaemic encephalopathy have a high mortality and the risk of permanent brain damage is increased by a factor of 10 to 30. Inspite of this, 90% of the survivors show normal development. The association between perinatal asphyxia and neuromotor developmental disturbances does not provide proof of a causal connection. Intrapartal abnormalities of foetal heart rate monitoring are not specific for foetal asphyxia and show only a limited correlation with the apgar and the cord blood pH. Foetal heart rate recording with pathological changes does not imply an elevated risk of later problems with neuromotor development and the widespread use of foetal heart rate monitoring during labour and delivery did not result in a significant reduction in the frequency of cerebral palsy. In addition to malformations, various forms of antinatal pathology like prematurity, intrauterine growth retardation and congenital infections are related to the development of brain damage. In each case of birth asphyxia, additional pathology like congenital infections or malformations in addition to changes in brain structure as a result of asphyxia must be ruled out using specific diagnostic methods like ultrasound, computed tomography and magnetic resonance. Furthermore, a careful documentation of the developmental phases is of fundamental importance for a final evaluation. In otherwise unremarkable deliveries at term, four conditions must be fulfilled to postulate a causal relationship between asphyxia and the development of cerebral palsy: The asphyxia must be severe. During the early neonatal period, clinical symptoms of moderate to severe hypoxic-ischaemic encephalopathy with functional impairment of other organs must be present. The neurological symptoms must be typical for intrapartal asphyxia. Documentation of diagnostic evaluation to rule out other forms of pathology must be complete (21).
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PMID:[Significance of intrapartum asphyxia for the onset of fetal brain damage]. 833 Jul 9

The purpose of the present study is to compare risk factors of necrotizing enterocolitis (NEC) between two group: group A, newborns with the disease and group B, newborns with other diseases different from NEC, in order to know if these risk factors are more frequent or not in the first group. We assessed the clinical records of all the patients hospitalized in the Neonatal Intensive Care Unit and Neonatology Service of the La Raza General Hospital between 1987 and 1991 with the diagnosis of NEC. They were compared with 65 clinical records chosen at random of patients hospitalized in the same Unit with other diagnosis at the same time, and who were discharged by improvement or deceased. In all of them were look for known risk factors for NEC generally accepted such as: prematurity, neonatal asphyxia, poliglobulia, cyanotic congenital heart disease, patent ductus arteriosus, respiratory distress syndrome, catheterization of umbilical vessels, early feeding of elevated formula increases, exchange exchange transfusion, hypoxic ischemic encephalopathy, infection, etc. Just 25 records of the possible 50 with the diagnosis of NEC full filled inclusion criteria. There were no statistically significant difference in weight, sex, mortality and known risk factors of NEC between both groups. Were concluded that NEC is a disease of unknown etiology that should be studied more thoroughly. The known risk factors must be avoided because the patient susceptibility probably play an important role.
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PMID:[Risk factors of necrotizing enterocolitis]. 837 46


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