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PubMed1989

Suprasellar arachnoid cysts: management by cyst wall resection.

Five children with ventricular dilatation (4 boys, 1 girl) had features seen on computer tomographic scan that were consistent with suprasellar arachnoid cysts. All children were investigated with a CT ventriculogram and/or CT cisternogram, and no communication with the cyst was demonstrated. Three children were seen in the 1st year of life and the remaining 2 children were between 1 and 5 years of age. Hydrocephalus and developmental delay were the most common presenting features, followed by visual disturbance, squint, or ataxia. Direct surgical decompression was performed in all 5 patients to avoid long-term placement of a ventriculoperitoneal shunt. A temporary shunt was placed in 2 children because of high intracranial pressure. Direct partial excision of the cyst wall to allow long-term drainage into the basal cisterns or ventricular system was successful in all children. The presence of subdural collections postoperatively required temporary shunting in 2 children. After follow-up for between 10 and 22 months no clinical endocrinological sequelae have been detected, but 2 children have raised serum prolactin levels. Three children are developmentally delayed; one of these has regained some skills since surgery. Direct surgical decompression of suprasellar arachnoid cysts to avoid long-term shunt placement is the preferred method of surgical treatment for this condition.

Arachnoid↗
PubMed2002

Additional patient with del(12)(q21.2q22): further evidence for a candidate region for cardio-facio-cutaneous syndrome?

Cardio-facio-cutaneous (CFC) syndrome is characterized by a distinct facial appearance, cardiac defects, ectodermal anomalies and developmental delay. Recently, we reported a 19-month-old girl with phenotypic manifestations consistent with the CFC syndrome who had an interstitial deletion of the long arm of chromosome 12, del(12)(q21.2q22), implicating a possible locus for CFC syndrome. Here, we report an additional patient with a cytogenetically identical interstitial deletion: 47,XYY,del(12)(q21.2q22). To further characterize this deletion we used microarray-based comparative genomic hybridization (array CGH). Array CGH confirmed both the deletion and the second Y chromosome. The deletion on chromosome 12q spanned at least 14 Mb as indicated by the positions on the genome sequence of the 4 BAC clones included in the deletion. While the proband did not have the classic features of CFC, he had some dysmorphic craniofacial characteristics, ectodermal anomalies and moderate developmental delay which were suggestive of CFC syndrome; however, this patient did not have classical CFC. The phenotypic differences between the two del(12)(q21.2q22) patients may be due to variability in the expression of the syndrome, or this deletion may present as a syndrome with overlapping features. Alternatively, the phenotypic differences may result from discordance at the molecular level, which may yield a critical minimal region of deletion for CFC. The region 12q21.2 --> q22 remains a possible candidate region for CFC syndrome. Additional characterization of these and other CFC patients may confirm and further refine this candidate region.

Abnormalities, Multiple↗
PubMed2001

Micro syndrome in Muslim Pakistan children.

OBJECTIVE: To date, Micro syndrome has been reported in only three children from one family. We describe an additional 14 children from 11 families. DESIGN: Retrospective case series. PARTICIPANTS: Fourteen children from 11 families attending one of five British hospitals. MAIN OUTCOME MEASURES: The following features were documented: pre- and postoperative eye findings, electrophysiologic analysis, systemic abnormalities, development, neuroimaging, genealogy, geographic origin of family. RESULTS: We expand and modify the description of ocular and electrophysiologic findings in Micro syndrome. The eye findings of microphakia, microphthalmos, characteristic lens opacity, and atonic pupils were the presenting feature in all infants and were the most reliable diagnostic signs in the immediate postnatal period. Cortical visual impairment, microcephaly, and developmental delay were not always detectable initially; they developed in all children by 6 months of age. Microgenitalia were a useful diagnostic clue in affected males only. Therefore, eye features were more consistently useful in determining diagnosis than dysmorphology or brain imaging. The families of all the children originate from the Muslim population of Northern Pakistan. Inheritance is likely to be autosomal recessive. CONCLUSIONS: Micro syndrome usually presents to the ophthalmologist, who may be able to make the diagnosis on the basis of characteristic eye findings combined with ethnic origin. Initially, the nature and severity of nonophthalmic features are not apparent. Early diagnosis of the underlying condition is important to guide management of the cataracts, glaucoma, and developmental delay. It is helpful for the family and medical staff to be aware of the low level of vision that develops despite optimal ophthalmic intervention. Genetic counseling extending into the wider family is particularly important in view of the high rate of consanguinity.

Adolescent↗
PubMed1995

Prenatal diagnosis of 45,X/46,XX mosaicism and 45,X: implications for postnatal outcome.

The prognosis for 45,X/46,XX mosaicism diagnosed prenatally has yet to be established. We report our experience with 12 patients in whom prenatal diagnosis of 45,X/46,XX mosaicism was detected by amniocentesis for advanced maternal age or decreased maternal serum alpha-feto protein and compared them with 41 45,X/46,XX patients diagnosed postnatally. The girls in the prenatal group range in age from 3 mo to 10 years. All have had normal linear growth. Four had structural anomalies including: ASD (n = 1); ptosis and esotropia (n = 1); labial fusion (n = 1); and urogenital sinus, dysplastic kidneys, and hydrometrocolpos (n = 1). Gonadotropins were measured in seven; one had elevated luteinizing hormone/FSH at 3 mo of age. One has developmental delay and seizures as well as ophthalmologic abnormalities. None would have warranted karyotyping for clinical suspicion of Turner syndrome. The prevalence of 45,X/46,XX mosaicism is 10-fold higher among amniocenteses than in series of postnatally diagnosed individuals with Turner syndrome, which suggests that most individuals with this karyotype escape detection and that an ascertainment bias exists toward those with clinically evident abnormalities. The phenomenon of a milder phenotype for the prenatal group is similar to that observed for 45,X/46,XY diagnosed prenatally. Prenatal counseling for 45,X/46,XX in the absence of such ultrasound abnormalities as hydrops fetalis should take into account the expectation of a milder phenotype (except, possibly, with respect to developmental delay) than that of patients ascertained postnatally. The same does not hold true for 45,x diagnosed prenatally.

Amniocentesis↗
PubMed2006

The moral judgment of juvenile delinquents: a meta-analysis.

A meta-analysis of 50 studies was conducted to investigate whether juvenile delinquents use lower levels of moral judgment than their nondelinquent age-mates and, if so, what factors may influence or moderate the developmental delay. The results show a lower stage of moral judgment for juvenile delinquents (d=.76). Effect sizes were large for comparisons involving male offenders, late adolescents, delinquents with low intelligence, and incarcerated delinquents. The largest effect sizes were found for period of incarceration and comparisons involving juvenile delinquents with psychopathic disorder. Production instead of recognition measures, dilemma-free assessment methods, and non-blind scoring procedures yielded relatively large effect sizes, whereas effect sizes were medium for comparisons involving delinquents with average intelligence, non-incarcerated delinquents, female offenders, as well as early and middle adolescents. Psychopathic disorder and institutionalization were identified as unique moderators of the link between moral judgment and juvenile delinquency. It is concluded that developmentally delayed moral judgment is strongly associated with juvenile delinquency, even after controlling for socioeconomic status, gender, age and intelligence.

Adolescent↗
PubMed2003

The clinical syndrome of creatine transporter deficiency.

To describe the clinical, spectroscopic and neuropsychological features of the first family diagnosed with a defect in the creatine transporter. Proton Magnetic Resonance Spectroscopy (MRS) indicated an absence of creatine and phosphocreatine in the brain of a male patient characterized by developmental delay, mild epilepsy and severe expressive language impairment. Subsequent genetic testing revealed a defect in the X-linked creatine transporter (SLC6A8/CT1), with a hemizygous mutation in the patient and a heterozygous mutation for the female carriers. Magnetic resonance imaging and spectroscopy examinations were performed on a 1.5T clinical MR Scanner. Neuropsychological examinations were performed on the index patient and maternal relatives. Preliminary spectroscopy results indicate the disorder prevents transport of creatine and phosphocreatine in the brain of the affected male. However, the skeletal muscle demonstrates the presence of creatine and phosphocreatine which correlates clinically with normal structure and function. Female carriers demonstrated impairments in confrontational naming and verbal memory assessments. This new neurological syndrome is associated with developmental delay, mild epilepsy, severe language impairment. MR Spectroscopy is a non-invasive method for obtaining a preliminary diagnosis of this disorder. Muscle creatine uptake may be normal in this disorder.

Adult↗
PubMed2002

Detecting rearrangements in children using subtelomeric FISH and SKY.

The etiology of mental retardation (MR), often presenting as developmental delay in childhood, is unknown in approximately one-half of cases. G-banding is the standard method for investigating those suspected of having a chromosomal etiology; however, detection of structural abnormalities is limited by the size and pattern of the G-bands involved. Rearrangements involving subtelomeric regions have been shown to cause MR and this has generated interest in investigating the prevalence of these rearrangements using telomere-specific probes. In addition, because cryptic interchromosomal rearrangements may not be small or confined to chromosomal ends, spectral karyotyping (SKY) using chromosome-specific painting probes may be of value. We report here a study using these two FISH-based techniques in 50 children with idiopathic MR or developmental delay and normal GTG-banded karyotypes. Our objective was to assess the prevalence of cryptic rearrangements in this population using subtelomeric FISH and SKY. Three rearrangements were detected by subtelomeric FISH: a derivative 5 from a maternal t(5;21); a recombinant 11 from a paternal pericentric inversion; and a 2q deletion that was also present in the mother. Only the derivative 5 was detected by SKY. SKY did not detect any interstitial interchromosomal rearrangement. The prevalence of clinically significant cryptic rearrangements by subtelomeric FISH and SKY was thus 4% (95% confidence interval 0.5-13.7) and 2% (95% CI 0.05-10.7), respectively. This study supports the view that G-banding does not detect all clinically significant chromosomal abnormalities and that subtelomeric FISH and SKY can detect some of these abnormalities.

Adolescent↗
PubMed1994

Blood serum levels of PCDFs and PCBs in Yu-Cheng children peri-natally exposed to a toxic rice oil.

Children secondarily exposed through their mothers to a toxic rice oil containing PCDFs and PCBs in the Yu-cheng incident have shown developmental delay even a decade after the incident. Forty-five serum samples were collected from these children in February 1991 ad small amounts analyzed for their contaminant content using sample enrichment and isotope dilution mass spectrometry. In about one-half the samples, detectable levels of PCDFs and PCBs could still be determined with average values for 2, 3, 4, 7, 8-PnCDF and 1, 2, 3, 4, 7, 8-HxCDF of 300 and 620 ng/kg serum lipid, respectively. The mean of the total PCBs on a whole weight basis was 7.5 micrograms/kg. These concentrations of PCDFs and PCBs are still 10 to 25 times higher than those from a matched control population. Although the serum levels did not correlate with developmental delays, those for the two PCDFs but not the total PCBs correlated with duration of breast feeding indicative of postnatal exposure. The results of this study suggest that estimation of past prenatal exposure of children to PCDFs is best carried out using current mother and not current child blood concentrations.

Adult↗
PubMed1986

Analysis of environmental determinants of aggression and disruption in mentally retarded children.

This study evaluated methods for empirically identifying environmental determinants of aggressive and disruptive behavior in three developmentally delayed children. A variety of sessions conducted on an inpatient treatment unit were designed to stimulate contingencies maintaining aggression and disruption in the subjects' natural environments. The basic analog conditions included: instructional demands, contingent social disapproval, and structured play. In addition, variations of the three basic conditions were developed based on informal observation and parental reports of naturally occurring contingencies. Results showed considerable variability both between and within subjects. However, for each subject a specific analog condition was shown to produce relatively higher rates of aberrant behavior. Subsequently, behavioral treatments based on assessment results were successfully implemented with two of the subjects. Results are discussed in terms of the importance and practical limitations of conducting systematic assessment of aberrant repertoires in developmentally delayed clients.

Adolescent↗
PubMedDate not supplied

Prevalence of dental caries in an adult population with mental disabilities in Spain.

The objective of this study was to analyze the prevalence of dental caries and the possible influence of extraoral factors in a group of adults with a mild to moderate degree of developmental delay. A total of 166 subjects ranging in age from 20 to 40 years were examined. All subjects were institutionalized, and 70.4% (n = 117) participated in a preventive program designed by the educators of the center. This consisted of weekly fluoride mouthrinses (0.2%) and control of dental plaque by toothbrushing with a fluoride toothpaste. The mean DMFT index for the whole sample was 5.97. Subjects in the oldest age group had the highest DMFT index and the lowest filled component. There were no significant differences in the DMFT index and its components between the subjects who received a weekly fluoride mouthrinse (n = 117) and those who did not (n = 49). Comparison of subjects who had cerebral palsy, Down Syndrome, and idiopathic developmental delay (n = 157) found a significantly lower DMFT index (p < 0.05) in the persons with Down Syndrome compared with the other special-needs groups. Other factors which could influence the results-such as fluoride use, oral hygiene, and administration of benzodiazepines-were also analyzed. An analysis of the results revealed a moderately high prevalence of caries in the whole sample that was lower than that in a national survey. This could be attributed to strict dietary control of sugar in the study population.

Adult↗
PubMed1998

[Brain magnetic resonance imaging findings in two cases of Hunter's syndrome].

Magnetic resonance (MR) imaging findings in two cases of Hunter's syndrome [mucopolysaccharidosis (MPS) type II A] are reported. The first case is a 15-year-old boy in whom the diagnosis of Hunter's syndrome was made at 2 years of age on the basis of increased glycosaminoglycans in the urine, developmental delay, characteristic faces, joint contraction, family histories, and radiological characteristics including oar-like deformed ribs and dysplasia of lumbar vertebrae. MR images showed marked enlargement of the lateral ventricles and third ventricle. The cerebral cortical sulci were diffusely dilated. Abnormal intensity lesions in the lateral part of the lentiform nucleus, the subcortex of the insula, the pons, and the right thalamus were seen. Diffuse hyperintensity throughout the periventricular white matter is also seen on T2-weighted images. The second case is a 3-year-old boy, born at immature delivery. At 2 months of age, he was admitted to a pediatric department because of liver dysfunction, inguinal hernias and umbilical hernia. The diagnosis of Hunter's syndrome was made by developmental delay, gargoylism, joint contraction, kyphosis, and biochemical investigation of urine. Urinary glycosaminoglycans significantly increased. Skeletal radiography showed dysplasia of the lumbar vertebrae and acetabulum. T1-weighted MR images demonstrated numerous hypointense spots in the corpus callosum and the cerebral white matter, presumably suggesting large perivascular spaces. Multiple cystic changes appeared to be hyperintense on T2-weighted images. Numerous linear hyperintense lesions were visible in the corona radiata. Patchy areas of hyperintense areas were seen, more prominent in the parietal lobes. Neuropathological examinations in cases of Hunter's syndrome have previously shown marked dilatation of ventricular system, large perivascular spaces secondary to mucopolysaccharide storage, demyelination and gliosis in the white matter and so forth. MR findings correlated well with previously reported neuropathological findings. MR study is not only useful for diagnosing Hunter's syndrome but also helpful to follow the pathological status.

Adolescent↗
PubMed2005

Cardiofaciocutaneous syndrome (CFC) with congenital peripheral neuropathy and nonorganic malnutrition: an autopsy study.

Many phenotypic manifestations have been reported in cardiofaciocutaneous (CFC) syndrome, but none, to date, are pathognomonic or obligatory. Previous histopathological studies reported findings in skin and hair; no autopsy studies have been published. We report the clinical and autopsy findings of a 7-year-old boy with severe CFC syndrome and malnutrition of psychosocial origin. Manifestations of CFC, reported previously, included macrocephaly and macrosomia at birth; short stature; hypotonia; global developmental delays; dry, sparse thin curly hair; sparse eyebrows and eyelashes; dilated cerebral ventricles; high cranial vault; bitemporal constriction; supraorbital ridge hypoplasia; hypertelorism; ptosis; exophthalmos; depressed nasal bridge; anteverted nostrils; low-set, posteriorly-rotated, large, thick ears; decayed, dysplastic teeth; strabismus; hyperelastic skin; wrinkled palms; keratosis pilaris atrophicans faciei; ulerythema ophryogenes; hyperkeratosis; gastroesophageal reflux; and tracheobronchomalacia. Additional findings, not previously reported, include islet cell hyperplasia, lymphoid depletion, thymic atrophy and congenital hypertrophy of peripheral nerves with onion bulb formations. Although the islet cell hyperplasia, lymphoid depletion, and thymic atrophy are nonspecific findings that may be associated with either CFC or malnutrition, the onion bulb hypertrophy is specific for a demyelinating-remyelinating neuropathy. These findings implicate congenital peripheral neuropathy in the pathogenesis of the developmental delays, feeding difficulties, respiratory difficulties, ptosis and short stature in this case. Additional studies of other cases of CFC are needed.

Abnormalities, Multiple↗
PubMed2004

Reduced growth hormone secretion prolongs puberty but does not delay the developmental increase in luteinizing hormone in the absence of gonadal negative feedback.

Previous studies have shown that the growth hormone (GH) axis is important for timing the later stages of puberty in female monkeys. However, it is not clear whether these growth-related signals are important for the initiation of puberty and early pubertal events. The present study, using female rhesus monkeys, used two approaches to answer this question. Experiment 1 tested the hypothesis that reduced GH secretion would blunt the rise in nocturnal LH secretion in young (17 mo; n = 7) but not older adolescent ovariectomized females (29 mo; n = 6). Reduced GH secretion was induced by treating females with the sustained release somatostatin analogue formulation, Sandostatin LAR (625 microg/kg). Morning (0900-0930 h) and evening (2200-2230 h) concentrations of bioactive LH were higher in older adolescent compared to young adolescent females. However, diurnal concentrations were not affected by the inhibition of GH secretion in either age group when compared to the placebo-treated, control condition. Experiment 2 tested the hypothesis that reduced GH secretion induced in young juvenile females would delay the initial increase in nocturnal LH secretion and subsequent early signs of puberty. In order to examine this hypothesis, puberty in control females (n = 7) was compared to those in which puberty had been experimentally arrested until a late adolescent age (29 mo) by the use of a depot GnRH analogue, Lupron (750 microg kg(-1) mo(-1); n = 7). Once the analogue treatment was discontinued, the progression of puberty was compared to a group treated in a similar fashion but made GH deficient by continuous treatment with Sandostatin LAR (n = 6). Puberty occurred as expected in control females with the initial rise in evening LH at 21 mo, menarche at 22 mo, and first ovulation at 30 mo. As expected, Lupron arrested reproductive maturation, but elevations in morning and evening LH and menarche occurred within 2 mo of the cessation of Lupron in both Lupron and Lupron-GH-suppressed females. In contrast, first ovulation was delayed significantly in the Lupron-GH-suppressed females (41 mo) compared to the Lupron-only females (36 mo). These data indicate that within this experimental model, reduced GH secretion does not perturb the early stages of puberty but supports previous observations that the GH axis is important for timing the later stages of puberty and attainment of fertility. Taken together, the data indicate that factors that reduce GH secretion may have a deleterious effect on the completion of puberty.

Animals↗
PubMed1996

Maternal uniparental isodisomy of human chromosome 14 associated with a paternal t(13q14q) and precocious puberty.

Cytogenetic and molecular investigation of a boy with precocious puberty and motor developmental delay revealed a 45,XY,t(14q14q) or i(14q) karyotype with no paternal chromosome 14 contribution. VNTR analysis of loci on four other chromosomes excluded non-paternity with greater than 99% confidence. Results of VNTR and CA repeat analyses of ten loci along the entire length of chromosome 14 were consistent with homozygosity at all loci, suggesting that the chromosomal rearrangement was a maternal isochromosome for 14q. As the proband's father had a balanced Robertsonian translocation, t(13q14q), we suggest that the origin of the maternal uniparental disomy (UPD) was fertilization by a nullisomy 14 sperm with formation of the isochromosome in the early embryo. Also, the proband has several clinical features in common with six previously reported liveborn cases of maternal UPD 14: hypotonia and motor developmental delay, mild dysmorphic facial features, low birth weight and growth abnormalities, and, more specifically, precocious puberty among the four cases old enough to assess. The emergence of a syndrome associated with maternal UPD 14 suggests the possibility of genomic imprinting of regions of chromosome 14, especially a gene involved in the onset of puberty.

Adolescent↗
PubMed2005

Early regression in social communication in autism spectrum disorders: a CPEA Study.

In a multisite study of 351 children with autism spectrum disorders, 21 children with developmental delays, and 31 children with typical development, this study used caregiver interviews (i.e., the Autism Diagnostic Interview-Revised) at the time of entry into other research projects and follow-up telephone interviews designed for this project to describe the children's early acquisition and loss of social-communication milestones. Children who had used words spontaneously and meaningfully and then stopped talking were described by their caregivers as showing more gestures, greater participation in social games, and better receptive language before the loss and fewer of these skills after the loss than other children with autism spectrum disorders. A significant minority of children with autism without word loss showed a very similar pattern of loss of social-communication skills, a pattern not observed in the children with developmental delays or typical development.

Age Factors↗
PubMed1997

Angelman's syndrome: clinical and electroencephalographic findings.

Angelman's syndrome is a rare genetic disorder characterized by developmental delay, craniofacial abnormalities, ataxia, paroxysmal laughter, and seizures. The diagnosis is suspected in infants who have the characteristic clinical features and electroencephalographic (EEG) abnormalities and is confirmed by the genetic identification of a maternally derived 15q11-13 deletion. We report on 3 patients with genetically confirmed Angelman's syndrome who had the characteristic clinical and EEG features. The EEGs demonstrated high-amplitude 2- to 3-Hz delta activity, with intermittent spike-and-slow-wave discharges maximal in the occipital region in 2 patients and generalized sharp-and-slow-wave discharges, occipital spikes, and electrographic status epilepticus during slow-wave sleep in the other patient. The findings of generalized high-amplitude delta slowing and occipital spike-and-wave discharges, facilitated by eye closure, in children with developmental delay and seizures suggest the diagnosis of Angelman's syndrome and should lead to genetic testing.

Angelman Syndrome↗
PubMed2006

Moderate iron deficiency in infancy: biology and behavior in young rats.

Iron deficiency anemia in early childhood is associated with developmental delays and perhaps, irreversible alterations in neurological functioning. The goals were to determine if dietary induced gestational and lactational iron deficiency alters brain monoamine metabolism and behaviors dependent on that neurotransmitter system. Young pregnant rats were provided iron deficient or control diets from early in gestation through to weaning of pups and brain iron concentration, regional monoamine variables and achievement of specific developmental milestones were determined throughout lactation. Despite anemia during lactation, most brain iron concentrations did not fall significantly until P25, and well after significant changes in monoamine levels, transporter levels, and D2R density changed in terminal fields. The changes in D2R density were far smaller than previously observed models that utilized severe dietary restriction during lactation or after weaning. Iron deficient pups had normal birth weight, but were delayed in the attainment of a number of milestones (bar holding, vibrissae-evoked forelimb placing). This approach of iron deficiency in utero and during lactation sufficient to cause moderate anemia but not stunt growth demonstrates that monaminergic metabolism changes occur prior to profound declines in brain iron concentration and is associated with developmental delays. Similar developmental delays in iron deficient human infants suggest to us that alterations in iron status during this developmental period likely affects developing brain monaminergic systems in these infants.

Age Factors↗
PubMed2006

Mutational and genotype-phenotype correlation analyses in 28 Polish patients with Cornelia de Lange syndrome.

Cornelia de Lange syndrome (CdLS) is a multisystem congenital anomaly disorder characterized by prenatal and postnatal growth retardation, developmental delay, distinctive facial dysmorphism, limb malformations, and multiple organ defects. Mutations in the NIPBL gene have been discovered recently as a major etiology for this syndrome, and were detected in 27-56% of patients. Two groups have found significant differences in the severity or penetrance of some phenotypes between mutation positive and mutation negative patients. Different clinical features have also been described among patients with missense versus truncating mutations. In this study, we identified 13 NIPBL mutations in 28 unrelated Polish CdLS patients (46.4%), 11 were novel. Mutation positive patients were more severely affected in comparison to mutation negative individuals with respect to weight, height, and mean head circumference at birth, facial dysmorphism and speech impairment. Analyses of combined data from this and the two previous studies revealed that the degree of growth, developmental delay and limb defects showed significant differences between patients with and without mutations and between patients with missense and truncating mutations, whereas only a portion of these features differed significantly in any individual study. Furthermore, bioinformatic analyses of the NIPBL protein revealed several novel domains, which may give further clues about potential functions of this protein.

Adolescent↗