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PubMed1993

Parental interactions with children with and without mental retardation: behavior management, coerciveness, and positive exchange.

The in-home interactions of mothers and fathers with their school-age children were compared in families of children with mild or moderate mental retardation (n = 53) and families of children without mental retardation (n = 51). Consistent with expectations, the parents of children with mental retardation were relatively more controlling and less playful with their child. However, they also employed effective behavior management practices without resorting to coercive control strategies. Further, 24 to 51% of the variance in interaction processes were predicted by a set of risk factors common to both groups, with the status of the child as having or not having mental retardation accounting for relatively little unique variance.

Adolescent↗
PubMed2003

Implicit and explicit learning in young adults with mental retardation.

We examined intelligence-related differences in explicit and implicit learning using an artificial grammar paradigm. Young adults with and without mental retardation completed a sequence-learning and identification task. For some participants, sequences were constructed following an artificial grammar; for others, sequences were random. Explicit learning was determined by ability to learn and later identify random sequences. Implicit learning was determined by the tendency to incorrectly identify new grammatical sequences as seen before, relative to new nongrammatical sequences. Participants with mental retardation did more poorly than participants without mental retardation on explicit learning but just as well on implicit learning. Results suggest that learning of complex materials, when accomplished through implicit processing, is functionally equivalent in individuals with and without mental retardation.

Adult↗
PubMed1995

Molecular genetic analysis of mentally retarded males with features of the fragile-X syndrome.

The fragile-X[fra(X)] or Martin-Bell syndrome is the most common familial cause of mental retardation and is characterized by the presence of an Xq27.3 chromosome fragile site. Unstable DNA sequences representing large increases in the number of CGG trinucleotide DNA base repeats of the FMR-1 gene are located at the fragile site and responsible for the fra(X) syndrome. In order to identify whether cytogenetically normal yet mentally retarded males without a known cause of their retardation had expansion of the CGG repeat segment of the FMR-I gene, molecular genetic studies using Southern hybridization were performed with two DNA probes (fxa241 and Ox1.9) following digestion of genomic DNA from each patient with restriction enzymes Pstl and EcoRl/Eagl, respectively. DNA studies were performed on 20 (12.3%) out of 162 (122 white and 40 black people) cytogenetically normal mentally retarded males without a known cause of their retardation, but with high anthropometric discriminant values and/or clinical checklist scores identified previously and consistent with the fra(X) syndrome. None of the 20 males showed expansion of the CGG repeat of the FMR-1 gene detectable with the two probes used in this study. While heterogeneous single base pair substitutions, or small deletions or insertions in the FMR-I gene could exist in our patients, aberrations in other X-linked mental retardation genes, not identified to date but whose gene product can produce a phenotype similar to fra(X), either independently or in conjunction with the recently identified FMR-I protein, should be considered and are under investigation. Our study supports the idea that major FMR-I gene expansion detectable with Southern hybridization is rare in cytogenetically normal mentally retarded males, including those with physical and behavioural features seen in the fra(X) syndrome.

Adolescent↗
PubMed1989

Epilepsy and mental retardation following febrile seizures in childhood.

In an unselected group of children who were seen following an initial febrile convulsion, the frequency of subsequent afebrile seizures was 3.5% and of mental retardation 1%. The most common afebrile seizure type was generalized major (86%). About 3/4 of the children who developed afebrile seizures did so by three years and all by five years following the initial febrile seizure. The children with afebrile seizures differed from those without afebrile seizures in the frequency of neonatal abnormality, family history of mental retardation, focal initial febrile convulsions, and delay in psychomotor milestones before the initial febrile seizure. Only about 1/3 of the children who developed afebrile seizures ever had a recurrent febrile convulsion and none had complex recurrent febrile seizures. Half the children with mental retardation had histories of delay in psychomotor milestones prior to the initial febrile seizure, and no child with mental retardation had any seizure longer than five minutes. The administration of daily phenobarbital did not reduce the frequency of epilepsy, in spite of a significant reduction in the incidence of recurrent febrile seizures. There remains no evidence that the prevention of recurrent febrile convulsions significantly decreases the frequency of afebrile seizures or mental retardation.

Child↗
PubMed2006

Screening for fragile X syndrome among Brazilian mentally retarded male patients using PCR from buccal cell DNA.

Fragile X syndrome is one of the most frequent causes of mental retardation. Since the phenotype in this syndrome is quite variable, clinical diagnosis is not easy and molecular laboratory diagnosis is necessary. Usually DNA from blood cells is used in molecular tests to detect the fragile X mutation which is characterized by an unstable expansion of a CGG repeat in the fragile X mental retardation gene (FMR1). In the present study, blood and buccal cells of 53 mentally retarded patients were molecularly analyzed for FMR1 mutation by PCR. Our data revealed that DNA extraction from buccal cells is a useful noninvasive alternative in the screening of the FMR1 mutation among mentally retarded males.

Adolescent↗
PubMed2005

Positron emission tomography methods with potential for increased understanding of mental retardation and developmental disabilities.

Positron emission tomography (PET) is a technique that enables imaging of the distribution of radiolabeled tracers designed to track biochemical and molecular processes in the body after intravenous injection or inhalation. New strategies for the use of radiolabeled tracers hold potential for imaging gene expression in the brain during development and following interventions. In addition, PET may be key in identifying the physiological consequences of gene mutations associated with mental retardation. The development of high spatial resolution microPET scanners for imaging of rodents provides a means for longitudinal study of transgenic mouse models of genetic disorders associated with mental retardation. In this review, we describe PET methodology, illustrate how PET can be used to delineate biochemical changes during brain development, and provide examples of how PET has been applied to study brain glucose metabolism in Rett syndrome, serotonin synthesis in autism, and GABAA receptors in Angelman's syndrome and Prader-Willi syndrome. Future application of PET scanning in the study of mental retardation might include measurements of brain protein synthesis in fragile X syndrome and tuberous sclerosis complex, two common conditions associated with mental retardation in which cellular mechanisms involve dysregulation of protein synthesis. Mental retardation results in life-long disability, and application of new PET technologies holds promise for a better understanding of the biological underpinnings of mental retardation, with the potential to uncover new treatment options.

Autistic Disorder↗
PubMed1998

Hepatitis C prevalence in persons with mental retardation.

BACKGROUND: Hepatitis C virus (HCV) was identified in 1989 and has since been found in most of the world. Due to the lack of information about the prevalence of HCV in institutions for the mentally retarded it was decided to conduct a study in this population in Israel. METHODS: The Division for the Mentally Retarded in Israel provides service to 6,022 persons in 53 institutions. Four institutions in the central part of the country were selected for this pilot study. In connection with routine blood examinations a blood specimen was drawn to detect serologic markers for hepatitis C by microparticle enzyme immunoassay (MEIA). RESULTS: Of the 251 subjects tested (56% male), 10% had mild, 30% moderate, 29% severe, and 31% profound mental retardation. 4% were aged 11-18 years, 61% aged 19-45, 30% 46-60, and 5% over 61 years. In the four institutions, two subjects (0.8%) with antibodies to HCV were found. CONCLUSION: The prevalence of HCV in institutions for the mentally retarded (0.8%) does not differ appreciably from the general population in Israel (0.5%). This study, together with studies from the United States, Canada, England, Spain, Denmark, and Italy, appears to indicate that HCV is not a major public health problem in institutions for the mentally retarded.

Adolescent↗
PubMed1976

Electroencephalographic study of mentally retarded twins.

The EEGs of twenty-five pairs of twins, one or both of whom were mentally retarded, were studied. The concordance rate for mental retardation in monozygotic twins was higher than that in dizygotic twins. The vast majority of cases of mental retardation were considered to be caused by genotype but some exogenous causes were observed in discordant monozygotic twins. Paroxysmal discharges in the EEG especially those of centrencephalic type were suspected to be bioelectrical expressions of a transmissible cerebral susceptibility which may easily lead to intellectual deterioration by brain damage or epilepsy.

Adolescent↗
PubMed1992

Social support networks of adults with mental retardation who live at home.

The social support networks of 418 adults with mental retardation who live at home were found to be large, durable, active, and diverse in their composition. Family members predominated as members of these support networks. Differences were found in many network characteristics based on the gender and level of mental retardation of the adults. Males and those with the most severe mental retardation were found to be at risk for social isolation. Contrasts with the social support networks of adults in nonfamily settings were discussed.

Adolescent↗
PubMed1996

The Community Living Attitudes Scale, Mental Retardation Form: development and psychometric properties.

We described the development and psychometric properties of the Community Living Attitudes Scale, Mental Retardation Form (CLAS-MR), a 40-item measure based on the input of self-advocates and focused on contemporary community living philosophies. The CLAS-MR, which consists of four subscales that tap attitudes about people with mental retardation, demonstrated acceptable internal consistency, retest reliability, and construct validity with samples of 104 college students and 283 community members. Using data from a sample of 355 staff members from community agencies, we confirmed the factor structure of the measure. Given the importance of attitudes toward persons with mental retardation in policy making and community inclusion, the CLAS-MR can help chronicle the diffusion of the new paradigm of empowered community living for persons with mental retardation.

Activities of Daily Living↗
PubMed2004

Subtelomeric deletions detected in patients with idiopathic mental retardation using multiplex ligation-dependent probe amplification (MLPA).

Subtelomeric rearrangements are responsible for 5% to 10% of cases of unexplained mental retardation. Despite their clinical relevance, methods to screen for these cytogenetically invisible abnormalities on a routine base are scarce. We screened patients with idiopathic mental retardation for subtelomeric aberrations using multiplex ligation-dependent probe amplification (MLPA). This recently developed technique is based on PCR amplification of ligated probes hybridized to chromosome ends. Currently, 41 telomeres can be screened in just two multiplex reactions. Four subtelomeric rearrangements (5.3%) were detected in a group of 75 patients with mild to severe mental retardation in combination with dysmorphic features and/or a familial history of mental retardation: two terminal 1p deletions, a terminal 1q deletion, and a terminal 3p deletion. Deletions could be verified by FISH and marker analysis. In one case the MLPA indicated a terminal 21q deletion due to a 3-bp deletion at the site of the probe, giving a false-positive rate of 1.3%. This study demonstrates that MLPA is a fast and reliable screening method, potentially suitable for use in routine diagnostics.

Adolescent↗
PubMedDate not supplied

Close linkage of fragile X-mental retardation syndrome to haemophilia B and transmission through a normal male.

The fragile X-mental retardation syndrome is defined by a moderate to severe mental retardation associated with a cytogenetic marker, a fragile site localized on the long arm of the X chromosome at band Xq 27. This syndrome has recently been recognized as one of the major causes of genetically determined mental retardation, and as one of the most important X-linked diseases with respect to its frequency (analogous to that of Duchenne muscular dystrophy or of haemophilia A) and severity. In the absence of treatment, genetic screening for this disease would seem particularly important. Prenatal diagnosis is now feasible although difficult and detection of heterozygous carriers is only possible in approximately 50% of cases. The recent demonstration of genetic linkage between the glucose 6-phosphate dehydrogenase (G6PD)-colour blindness cluster (at Xq28) and the fragile X locus has suggested that the fragile site is indeed the site of the mutation. We show here that the fragile X and haemophilia B loci are closely linked, using as genetic marker a polymorphism of the coagulation factor IX gene. Our study of a large family has demonstrated transmission through a phenotypically normal male, a feature previously described in retrospective analysis of a few other fragile X pedigrees. Restriction polymorphisms associated with the factor IX gene should be useful for analysing this peculiar aspect of the genetics of the fragile X syndrome, and for genetic screening of the disease.

Adolescent↗
PubMed1991

Current developments in the understanding of mental retardation. Part I: Biological and phenomenological perspectives.

During the past decade, noteworthy advances have taken place within the field of mental retardation. The application of advanced biological techniques in such areas as molecular genetics and neuroimaging has substantially improved our ability to identify the biological factors that underlie the origin and pathogenesis of an increasing number of mental retardation syndromes. Refined genetic and psychosocial assessments have highlighted the impressive degree of heterogeneity that is present within and across many mental retardation syndromes, stimulating increasing interest and study. This, the first of a two-part review, will focus on recent developments in biological and phenomenological aspects of mental retardation.

Adolescent↗
PubMed2001

Age-related increases in motivation among children with mental retardation and MA- and CA-matched controls.

Child positive affect and task orientation in response to a series of cognitively demanding puzzle tasks were assessed at two time points separated by a 12-month interval in children with mild mental retardation and MA- and CA-matched controls (age range 1 to 5 years). At the first assessment, children with mild mental retardation exhibited mastery behavior appropriate for MA but not CA. At the second assessment, the goal-directed behavior of children with mild mental retardation was no different from that of both the MA and CA controls. Correlates of motivation were similar for children with mild mental retardation and typically developing children. Implications for the developmental study of children with mild mental retardation are discussed.

Age Factors↗
PubMed1985

Control in memory for movement cues by mentally retarded children.

The study was designed to determine the desirability of providing external prompts (1) to use a mnemonic to enhance accuracy of recall and (2) to use response 'priming' in memory for spatial location by mentally retarded persons. Two groups of 40 mentally retarded boys and girls and two groups of 40 MA-matched nonretarded children were compared for accuracy in the recall of movement on an arm-positioning task. No differences were found between mentally retarded subjects and MA-matched subjects treated under the same conditions. However, all groups were unable to make spontaneous control adjustments to accommodate the covert manipulations made just prior to recall. By providing response primes, appropriate performance adjustments were made by all groups, resulting in a significant improvement in accuracy of recall. These findings serve to reaffirm earlier reports showing remarkable similarity between the mentally retarded and MA-matched nonretarded subjects.

Adolescent↗
PubMed1983

Diagnostic overshadowing and professional experience with mentally retarded persons.

Possible associations between professional experience with mentally retarded people and diagnostic overshadowing were evaluated. In a 3 X 2 factorial experiment, psychologists at state developmental disabilities facilities (high-experience group), psychologists at state mental health facilities (moderate-experience group), and clinical graduate students (low-experience group) rated a case history of a person with schizophrenia on 11 scales of psychopathology. For approximately half of the subjects within each group, the client was mentally retarded in addition to schizophrenic; for the remaining subjects, the client had average intelligence. Professional experience was associated with diagnostic ratings but not with overshadowing. We concluded that diagnostic overshadowing is unrelated to a broad range of professional experience with retarded people.

Attitude of Health Personnel↗
PubMed1991

Assessment and diagnosis of mental illness in persons with mental retardation. Methods and measures.

The assessment and diagnosis of psychiatric disorders in individuals with mental retardation has been a neglected area of research. However, current research indicates that these individuals suffer from the same range of psychiatric disorders that is evident in those who are not mentally retarded. A model of assessment and diagnosis of mental illness in this population is presented that incorporates psychiatric as well as behavioral methods. The emphasis is on the comprehensive assessment of an individual's behavior, based on family history, self and informant clinical interviews, rating scales, direct observations, and an experimental analysis of the target behaviors. The model provides the basis for making differential diagnoses in terms of related psychiatric disorders and between psychiatric disorders and behavior problems. Depression and schizophrenia are used as illustrative disorders to describe the application of this model. Given the paucity of literature on the assessment and diagnosis of mental illness in individuals with mental retardation, a number of suggestions are made regarding future research and refinement of the model.

Adult↗
PubMed1997

A new X linked recessive syndrome of mental retardation and mild dysmorphism maps to Xq28.

Efforts to understand the genetic basis of mental retardation are greatly assisted by the identification of families with multiple relatives with mental retardation that clinical geneticists encounter in the routine practice of their profession. Here we describe a linkage study of a four generation family in which X linked recessive mental retardation (XLMR) is associated with minor dysmorphism and premature death of the affected males. Microsatellite based polymorphic loci evenly spaced over the entire X chromosome were used initially to detect linkage to Xq28. Further analysis identified a haplotype of Xq28 markers bounded proximally by locus DXS1113 and distally by DXS1108 that cosegregated with XLMR in this family. Two point lod scores > 3.0 provided strong evidence that the gene locus responsible for XLMR in this family is within this 7 Mb region of Xq28. The minor anomalies noted in some affected males were not distinctive enough to suggest a unique syndrome. None of our patients had features of the Waisman-Laxova syndrome or the PPM-X syndrome. The possibility of allelism with any of the five other non-specific XLMR syndromes (MRX3, MRX16, MRX25, MRX28, and MRX41) mapped to Xq28 could not be excluded. While the recognition of a gene responsible for this disorder needs much additional work, multiple female relatives at risk in this family benefit immediately from knowing their genotype and heterozygotes will have the opportunity to undergo prenatal diagnosis.

Adult↗