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Query: UMLS:C0025362 (mental retardation)
15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinician is often held responsible for obstetric events that are suspected of being related to cerebral palsy. To review the incidence of cerebral palsy and to aid the clinician in this situation, a search of published studies was conducted. Composite rates of cerebral palsy in different birth weight infants and cerebral palsy with and without serious mental retardation were calculated. The cumulative incidence rate at the age of 5 to 7 years was 2.7 cases of cerebral palsy for 1000 birth cohorts. Approximately 36% of all cerebral palsy occurred in the infant less than 2500 gm. Serious mental retardation (intelligence quotient less than 50) accompanied cerebral palsy approximately 30% of the time for the term infant and 18% of the time when the infant was less than 2500 gm. On the basis of a past estimation that 70% of cerebral palsy is of antepartum or unknown origin, the term infant at risk for intrapartum-attributed cerebral palsy may be about 1 in 2000 term births.
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PMID:The incidence of cerebral palsy. 149 45

A pediatric neurologist analyzed the case histories of 30 4-16 year old children diagnosed with cerebellar ataxia in the pediatric neurology unit at the Royal Hospital for Sick Children in Edinburgh, Scotland to examine its clinical features, investigative findings, and etiology. Previous unfavorable events happened to 14 children (46.6%). Yet only 6 (42.8%) of these 14 children had unfavorable events of etiological significance. These previous unfavorable events occurred during the perinatal period (48%). These events in order of significance were asphyxia, prematurity, neonatal jaundice, and trauma. 66.6% of all children had an unsteady gait. The 2nd and 3rd most common signs of cerebellar ataxia were truncal ataxia (53.3%) and hypotonia (36.6%). The next most common symptom was considerable delay in reaching gross motor milestones (50%) such as not sitting until 2 years old. 23 (76.6%) of the children had dysfunctions in 1 of the cerebellar divisions. Clinical examination found dysfunctions most often in the paleocerebellum (86.6) followed by the neocerebellum (70%) and archicerebellum (56.6%). The paleocerebellum and the archicerebellum were the only divisions involved in 6 and 1 of the remaining children, respectively. The most common cause of ataxia was hydrocephalus (23.3%) followed by perinatal problems (20%). 70% of the patients also experienced other central nervous system conditions such as macrocephaly and mental retardation. 5 children had normal investigative findings, 3 of whom had cerebellar ataxia syndrome, 1 had congenital ataxic cerebral palsy, and 1 had familiar ataxia.
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PMID:Cerebellar ataxia in childhood: a review of clinical features, investigative findings and aetiology in 30 cases. 150 89

The visual acuity of 77 children (aged between 1 1/2 and eight years) with cerebral palsy and mental retardation was tested using acuity cards. Results varied by no more than one octave in 79 per cent of the cases. The median acuity of children with severe motor disabilities was lower and the variability from test to test was greater than for those with mild motor disabilities. Grouping the children roughly according to degree of mental retardation, the more retarded group tended to be more visually disabled and vary more from test to test. In general, day-to-day variability was greater than within-day inter-observer variability. The use of acuity cards to evaluate visual acuity in severely disabled and mentally retarded children, whose acuity is difficult to evaluate with conventional acuity tests, is a useful alternative method.
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PMID:Effect of mental retardation and motor disability on testing with visual acuity cards. 153 Nov 34

Three children with cerebral palsy and mental retardation showed irritability after surgical procedures. They were subsequently diagnosed as having heterotopic ossification. Heterotopic ossification developed around the hip in all cases--two after bilateral adductor releases at the operative site and the third after spinal fusion at a site unrelated to the surgery.
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PMID:Postoperative heterotopic ossification in the child with cerebral palsy: three case reports. 154 35

An institutionalized adult cerebral palsy (CP) population was studied to evaluate the orthopaedic, functional, and cardiopulmonary status of 14 residents with untreated scoliosis greater than 45 degrees as compared with 42 residents with mild or no curves. Both groups were comparable in age, sex distribution, percentage of quadriplegics, and extent of mental retardation. Patients in the scoliosis group had more orthopaedic deformities involving the pelvis and hips and needed modified wheelchairs more often than did those without curves. There were no differences in incidence of decubiti, highest functional level achieved, functional loss, oxygen saturation, or pulse.
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PMID:Untreated scoliosis in severe cerebral palsy. 157 97

We compared the neurological condition and functions at age 4 years for two cohorts of children initially treated in the neonatal intensive care units in two countries: Denmark (10) and Ireland (2). The comparisons were made in two ways: first, the more usual comparison between frequencies of cerebral palsy, mental retardation, hydrocephalus, visual and hearing loss. A second comparison was based on the items, subscales, and total scores on a neurological battery developed from the Danish data. Comparisons were made among three different birthweight groups within each country as well as between countries using analysis of variance (ANOVA). In both cohorts, significant differences were shown between two subgroups: those with birthweights less than 2300 gms and those with birthweights over 2500 gms for all subscales except the neurological ones in the Irish cohort. In the Danish cohort, significant differences were shown on all subscales among three birthweight groups: less than 1501 gms; 1501-2300 gms; and over 2500 gms. Significant differences were shown between countries for easy drawing, neurology "b", and fine motor testing.
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PMID:A comparison of neurological assessment scores from two cohorts of low-birthweight children evaluated at age four years: Dublin and Copenhagen. 160 86

The differences in the velocity and pulsatility indexes in the internal carotid artery were evaluated in 62 normal controls, 42 infants with cerebral palsy, and 22 infants with mental retardation, all within the first year of life. In the normal controls, the average maximal blood flow velocity (A/L), and the maximal end-diastolic flow velocity increased during the first year of life. Pulsatility index decreased significantly between the ages of newborn to 2 mos and 3-5 mos, and remained constant thereafter. Compared with normal controls, the average maximal blood flow velocity and the maximal end-diastolic flow velocity values were significantly reduced in infants with cerebral palsy during the first 6 months of life, while no differences in these values were observed in infants with mental retardation. There were no differences in the pulsatility index values in the 3 subject groups throughout the first year of life. Flow velocity in the internal carotid artery could reflect the status of the cerebral circulation in infants within the first year of life.
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PMID:Internal carotid arterial blood flow velocity in infants. 162 16

Swallowing dysfunction is the main cause of drooling in cerebral palsy. Medical treatment is inefficient. Surgical treatment involves neurectomy, translocation of the salivary duct or salivary gland resection. Following this, reeducation is advisable. Indications are based on the degree of drooling and on the degree of histories mental retardation. The authors present 2 case histories of drooling in patients with cerebral palsy treated by submandibular gland resection and parotid duct ligation.
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PMID:[Surgical treatment of salivary incontinence in cerebral palsy]. 166 Jan 21

Fetal ischemia or hypoxia can lead to cerebral palsy, mental retardation and epilepsy. We propose that the production of nitric oxide and oxygen radicals by neurons when ischemic or hypoxic brain is reperfused may contribute to cerebral injury. Ischemia will depolarize neuronal membranes causing the synaptic discharge of the excitatory neurotransmitter glutamate, which in turn opens the voltage-dependent, N-methyl-D-aspartic acid-specific glutamate receptor/ionophore, allowing calcium to accumulate in the neuron. Calcium in turn activates an oxygen-dependent neuronal nitric oxide synthetase, which oxidizes arginine to produce nitric oxide (.NO) when oxygen is readmitted to brain by reperfusion. Nitric oxide reacts with the oxygen radical superoxide (O2-), also produced by reperfusion, to form peroxynitrite (ONOO-). Peroxynitrite can diffuse for several micrometers before decomposing to form the powerful and cytotoxic oxidants hydroxyl radical and nitrogen dioxide. The hypothesis is consistent with available evidence on the protective action of glutamate antagonists and of oxygen radical scavengers for limiting cerebral infarction following focal ischemia.
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PMID:The double-edged role of nitric oxide in brain function and superoxide-mediated injury. 167 55

We presented the case of a 78-year-old man with mental retardation and spastic paraparesis diagnosed early in life as cerebral palsy. Six years prior to demise he had post-traumatic subdural hematoma, which was removed surgically. The neuropathological examination revealed the sequelae of the recent trauma, superimposed on the extensive old lesions. Cavitary changes in the periventricular white matter and cortical ulegyria in the border zones of the major cerebral arteries vascularization were characteristic of perinatal hypoxic-ischemic lesions. Peculiar in the ulegyria were extensive areas with numerous corpora amylacea adjacent to the areas of fibrillar and cellular gliosis. Another sequelae of involution processes was the atrophy of brain hemispheres (secondary microcephaly). The case appears to be an example of the late degenerative involution changes developing on the background of lesions originated from the perinatal period.
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PMID:Sequelae of perinatal central nervous system damage after long-term survival. 181 12


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