Dyskinetic and dystonic cerebral palsy and birth

Foley, John J.

doi:10.1111/j.1651-2227.1992.tb12079.x

Cited by 25 publications

(11 citation statements)

References 26 publications

(11 reference statements)

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“…3 With mounting uncertainty about the importance of external perinatal influences, CP is increasingly regarded as a group of sporadic disorders of unknown aetiology.' 4 Similarly affected relatives are uncommon in the families of patients with CP.5 Excluding ataxic CP (which is frequently inherited) any genetic contribution to CP is thought to be small,6 although more likely if there are symmetrical physical signs.7 One hypothesis which might explain isolated cases of spastic or athetoid CP is fresh dominant genetic mutation. In autosomal dominant conditions where biological fitness is reduced, that is, affected subjects are less likely to reproduce (which seems likely in CP), some cases must arise by mutation assuming that there is genetic equilibrium between a constant mutation rate and the effects of natural selection.8 If affected subjects rarely have children, the genetic basis of the condition may not be apparent.…”

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confidence: 99%

Parental age, genetic mutation, and cerebral palsy.

Fletcher

Foley

1993

Journal of Medical Genetics

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Parental age and birth order were studied in 251 patients with cerebral palsy. No parental age or birth order effects were observed in spastic quadriplegia or diplegia, but a paternal age effect was detected in those with athetoid/ dystonic cerebral palsy and congenital hemiplegia. These observations indicate that some cases of athetoid/dystonic or hemiplegic cerebral palsy might arise by fresh dominant genetic mutation. (J7 Med Genet 1993;30:44-6) MethodsAll cases were ascertained from the records of the Cheyne Centre for Spastic Children, London. All had been referred from general practitioners or paediatricians in south-east England and were seen and examined personally by one of the authors (JF) between 1955 and 1986. CP was defined as above, low birth weight (LBW) as < 2500 g, and prematurity as birth before 37 weeks' gestation.Cases with recognisable syndromes or malformations, genetic or metabolic disorders, kernicterus, other identifiable causes for the motor disorder (including postnatal factors), similarly affected relatives, ataxic CP, or asymmetrical quadriplegia were excluded.The records of 532 cases were examined. Of these, 172 had spastic diplegia (65% preterm, 69% LBW), 102 had congenital hemiplegia (23% preterm, 20% LBW), 104 had symmetrical spastic quadriplegia (26% preterm, 35% LBW), and 154 had athetoid/dystonic CP (14% preterm, 19% LBW). Sibship size, birth order, parental ages at the time of birth, and date of birth were recorded. Of the 532 cases, 399 were born in the UK to parents whose ages had been recorded; 251 of these were born between 1961 and 1983 which is the period for which the Registrar General has published annual mean parental ages for the UK population.'0 Methods of birth order and parental age analysis were those described by Emery.11 Birth order was analysed using the method of Haldane and Smith. 12 For each case, the observed birth order is recorded and the expected birth order and its variance (assuming no birth order effect) calculated from the sibship size and published tables." In each group of cases, the standard error of the difference between the sums of the observed and expected birth orders is the square root of the sum of the variances. Parental ages at the time of birth of each case were compared with mean UK population maternal and paternal ages for the corresponding year using paired t tests. For each group of cases, mean differences between observed and expected values of paternal age (dp), maternal age (dn)j and birth order (db) were calculated.As dp, dm) and db are mutually dependent variables, a method based on regression analysis was used to compare any statistically significant value of one with that predicted by the observed values of the other two."I 13 The difference between observed and predicted values is d,-b12 d2, where di is the mean increase in one of the three variables (dp, dm3 or db), d2 is the mean increase in one of the other two, and b12 is a regression coefficient given by s1r12/s2 44

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Parental age, genetic mutation, and cerebral palsy.

Fletcher

Foley

1993

Journal of Medical Genetics

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“…Ekstrapiramidni tip CP ili diskinetički sindrom obično se javlja kod terminske djece. U većini slučajeva uzrok je teška akutna perinatalna asfiksija koja se u novorođenačko doba prezentuje kao encefalopatija s hipotonijom (11). Miješani oblik CP sadrži osobine spasticiteta i diskinezije.…”

Section: Uvodunclassified

Uticaj Antiepileptičke Terapije Na Elektroencefalografske Nalaze Kod Djece Sa Cerebralnom Paralizom

Serdar¹,

Simic²

2018

SCEPED

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Epilepsija dodatno komplikuje teško hronično stanje cerebralne paralize.Vezu između ova dva stanja predstavlja lezija mozga koja je u njihovoj etiološkoj osnovi.Pojava epilepsije na izvjestan način predstavlja indeks težine izraženosti cerebralneparalize i oštećenje mozga je obično veće kod djece sa cerebralnom paralizom i epilepsijom.Elektroencefalografija je najvažnija metoda u dijagnostikovanju epilepsije, kojaje često pridružena kod djece sa cerebralnom paralizom.

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“…Przekop et al suggests that “choreoathetosis” may be a better term to use to describe the athetotic movements observed in children, to distinguish it from athetosis in adults characterized by slow writhing, often in the fingers or toes. Athetosis in infants is characterized by “slow continuous writhing movements that prevent maintenance of a stable posture” [34], as defined by the 2008 Taskforce on Childhood Movement Disorders, whereas dystonia is more defined by hypertonic postures [6,34,37]. Shapiro has observed that infants with CP related to kernicterus rarely present initially with fixed postures or contractures.…”

Section: Classification Of Movement Disorders Due To Bilirubin Toxmentioning

confidence: 99%

Movement disorders due to bilirubin toxicity

Rose

Vassar

2015

Seminars in Fetal and Neonatal Medicine

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Summary Advances in the care of neonatal hyperbilirubinemia have decreased the incidence of kernicterus. However, neonatal exposure to high levels of bilirubin continues to cause severe motor symptoms and cerebral palsy (CP). Exposure to moderate levels of unconjugated bilirubin may also cause damage to the developing central nervous system, specifically the basal ganglia and cerebellum. Brain lesions identified using magnetic resonance imaging following extreme hyperbilirubinemia have been linked to dyskinetic CP. Newer imaging techniques, such as diffusion tensor imaging or single-photon emission computed tomography, allow quantification of more subtle white matter injury following presumed exposure to unbound bilirubin, and may explain more subtle movement disorders. New categories of bilirubin-induced neurologic dysfunction, either independently or characterized by subtle bilirubin encephalopathy, following moderate hyperbilirubinemia have been implicated in long-term motor function. Further research is needed to identify subtle impairments resulting from moderate to severe neonatal hyperbilirubinemia, understand the influence of perinatal risk factors on bilirubin toxicity, and develop neuroprotective treatment strategies to prevent movement disorders due to bilirubin toxicity.

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Dyskinetic and dystonic cerebral palsy and birth

Cited by 25 publications

References 26 publications

Parental age, genetic mutation, and cerebral palsy.

Parental age, genetic mutation, and cerebral palsy.

Uticaj Antiepileptičke Terapije Na Elektroencefalografske Nalaze Kod Djece Sa Cerebralnom Paralizom

Movement disorders due to bilirubin toxicity

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