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Biomedical subjects

M Rutter

Publications and source records attributed to M Rutter.

At least 91 records · Page 5Linked to original sources
PubMed1997

A family study of autism: cognitive patterns and levels in parents and siblings.

First-degree relatives of 99 autism probands and of 36 Down's syndrome controls were assessed with standardised tests of intellectual functioning, reading, and spelling. Higher mean verbal IQ scores, and discrepancies in favour of verbal scores, were characteristic of autism relatives. No consistent differences were found on performance scales, reading, and spelling tests. Among autism relatives, siblings affected with the broad phenotype of autism had significantly lower IQ scores and poorer reading and spelling performances than unaffected siblings. However, the small size of the cognitive difference and the lack of a distinctive cognitive profile indicates that standardised cognitive measures used in this study are unlikely to improve the operationalised definition of the broad phenotype of autism. The slightly superior verbal performance of relatives in the autism group might represent some form of heterozygote advantage.

Adolescent↗
PubMed1997

Implications of genetic research for child psychiatry.

OBJECTIVE: To review implications of genetic research in child psychiatry. METHOD: Key advances in quantitative and molecular genetics are noted and findings are summarized with respect to autism, attention-deficit hyperactivity disorder, oppositional defiant and conduct disorders, depression, schizophrenia, and Tourette's syndrome. CONCLUSIONS: Genetic findings will be helpful clinically in the elucidation of disordered brain processes, the understanding of nature-nurture interplay, diagnosis, genetic counselling, and pharmacotherapy.

Adolescent↗
PubMed1997

Opportunities for psychiatry from genetic findings.

BACKGROUND: The opportunities for psychiatry deriving from available or likely genetic advances are reviewed. METHOD: Clinical implications are considered in the context of both the misconceptions and benefits associated with relevant genetic findings. RESULTS: Misconceptions include that: heritability estimates have a 'true' fixed value; a high heritability means that environmental interventions will be ineffective; a high heritability within groups means that differences between groups will also be due to genes; genetic effects are determinative; 'genetic' means single abnormal genes; genes associated with disease must be bad and justify eugenic measures; gene therapy will be widely applicable; and genetic screening of the general population will be useful. The benefits include demonstrations that: both genes and environment have an ubiquitous influence; some prevailing diagnostic assumptions are mistaken; genes influence development; the effects of nature and nurture are not separate; and environmental effects tend to be person-specific. The potential value of molecular genetics lies in elucidation of causal processes as they apply to both brain systems and nature-nurture interplay; improving diagnosis and genetic counselling; and the development of improved pharmacological interventions. CONCLUSION: Advances in genetics will make a major impact on clinical psychiatry, and should bring practical benefits for both prevention and treatment.

Causality↗
PubMed1997

Retrospective reporting of childhood adversity: issues in assessing long-term recall.

Much evidence for associations between adverse experiences in childhood and personality disorder in adult life comes from retrospective accounts. This raises important questions over the reliability and validity of long-term recall. The strengths and limitations of different methods for assessing the accuracy and stability of retrospective reports are discussed. Evidence from cognitive psychology on memory and memory processes, and on the phenomenon of infantile amnesia, provides important background for assessing issues more specific to recall in studies of risk for psychopathology. Here, topics of particular concern include: memory for traumatic early experience; the effects of mood state and symptomatology on recall; recovered or false memories; and the implications of mental representations of early experience for understanding psychopathology. Current evidence suggests that while adequately reliable accounts of many early experiences can be gained using appropriate techniques, further methodological studies are needed, and investigations using retrospective methods would be wise to include corroborative evidence whenever feasible.

Adult↗
PubMed1997

Psychosocial adversities in childhood and adult psychopathology.

Numerous studies have reported statistical associations between adverse childhood experiences and psychopathology in adult life. A range of conceptual and methodological issues needs to be borne in mind in interpreting these findings. Methodological issues include implications of base rates of postulated risk and outcome measures, and the possibility of third variable effects. Conceptually, further evidence is needed on the aspects of early experience most likely to contribute to risk (acute vs chronic stressors: actively negative vs lack of positive experiences; and the implications of cognitive processing of events); the specificity of effects; possible mechanisms involved in mediating effects in childhood, and approaches to testing them: and factors involved in persistence into adult life. There are good reasons to assume that adverse early experience plays a contributory role in the genesis of personality disorder. However, at this stage, evidence is still limited on how this comes about.

Adult↗
PubMed1997

Physical mapping of the 5 Mb D9S196-D9S180 interval harboring the basal cell nevus syndrome gene and localization of six genes in this region.

The basal cell nevus syndrome (Gorlin syndrome) is characterized by multiple basal cell carcinomas and diverse developmental defects. The gene responsible for this syndrome has been mapped previously to a 2 cM interval between D9S196 and D9S 180 at 9q22.3, and very recently mutations of a candidate gene in this region--the human homolog of the Drosophila patched gene have been identified. We report here on physical mapping studies integrating a contig of yeast artificial chromosomes and bacterial artificial chromosomes with a long-range map spanning approximately 5 Mb between the recombination-determined flanking markers. Six genes have been mapped to this interval.

17-Hydroxysteroid Dehydrogenases↗
PubMed1996

Heterogeneity among juvenile antisocial behaviours: findings from the Virginia Twin Study of Adolescent Behavioural Development.

The examination of heterogeneity in antisocial behaviour was accomplished by applying latent class analytic methods to multivariate categorical data on 389 same-sex male twins, aged 11 to 16 from the Virginia Twin Study of Adolescent Behavioural Development (VTSABD). The data included multiple measures of oppositional and conduct disorder, attention deficit disorder, hyperactivity, impulsivity, reading disability and anxiety from mother, teacher, and child report from both questionnaire and interview (child and adult psychiatric assessment; CAPA). A latent four-class model provided a good fit to the data and yielded four phenotypically and aetiologically distinct latent classes: (1) a non-symptomatic class influenced by both additive genetic and shared environmental factors; (2) a hyperactivity-conduct disturbance class accounted for by both additive and non-additive genetic effects; (3) a 'pure' conduct disturbance class with a very strong shared environmental component; and (4) a multisymptomatic class explained entirely by the additive effect of the genes. Further characterization of these four latent classes by age of the child and parental psychiatric history is also shown.

Adolescent↗
PubMed1996

Autism research: prospects and priorities.

Research prospects and priorities in the field of autism are discussed with respect to (a) diagnosis, classification, and epidemiology; (b) clinical research; (c) neuropsychological research; (d) genetics; (e) structural and functional brain imaging; (f) postmortem studies; (g) other biological research; and (h) treatment research. Also, it is argued that research into autism has a priority in the broader field of developmental psychopathology because it carries the promise of throwing light on casual mechanisms that apply beyond the syndrome of autism.

Adolescent↗
PubMed1996

Autism: towards an integration of clinical, genetic, neuropsychological, and neurobiological perspectives.

Autism constitutes one of the best validated child psychiatric disorders. Empirical research has succeeded in delineating the key clinical phenomena, in demonstrating strong genetic influences on the underlying liability, and in identifying basic cognitive deficits. A range of neurobiological abnormalities has also been found, although the replicability of specific findings has not been high. An understanding of the causal processes leading to autism, and accounting for the marked variability in its manifestations, requires an integration across these different levels of enquiry. Although this is not yet possible, a partial integration provides a useful strategy for identifying key research questions, the limitations of existing hypotheses, and future research directions that are likely to prove fruitful. The research findings for each research level are critically reviewed in order to consider how to move towards an integration across levels.

Adolescent↗
PubMed1996

Mental retardation: genetic findings, clinical implications and research agenda.

The most important genetic advances in the field of mental retardation include the discovery of the novel genetic mechanism responsible for the Fragile X syndrome, and the imprinting involved in the Prader-Willi and Angelman syndromes, but there have also been advances in our understanding of the pathogenesis of Down syndrome and phenylketonuria. Genetic defects (both single gene Mendelizing disorders and cytogenetic abnormalities) are involved in a substantial proportion of cases of mild as well as severe mental retardation, indicating that the previous equating of severe mental retardation with pathology, and of mild retardation with normal variation, is a misleading over-simplication. Within the group in which no pathological cause can be detected, behaviour genetic studies indicate that genetic influences are important, but that their interplay with environmental factors, which are also important, is at present poorly understood. Research into the joint action of genetic and environmental influences in this group will be an important research area in the future.

Chromosome Aberrations↗
PubMed1996

Reading problems and antisocial behaviour: developmental trends in comorbidity.

Samples of poor and normal readers were followed through adolescence and into early adulthood to assess continuities in the comorbidity between reading difficulties and disruptive behaviour problems. Reading-disabled boys showed high rates of inattentiveness in middle childhood, but no excess of teacher-rated behaviour problems at age 14 and no elevated rates of aggression, antisocial personality disorder or officially recorded offending in early adulthood. Increased risks of juvenile offending among specifically retarded-reading boys seemed associated with poor school attendance, rather than reading difficulties per se. Reading problems were associated with some increases in disruptive behaviour in their teens in girls.

Adolescent↗
PubMed1996

The genetics of children's oral reading performance.

Measures of reading achievement and verbal ability have been shown to be heritable. Additionally, recent evidence has been suggestive of a major gene effect on reading disability and for problem reading in a sample of normal readers. We report on the etiology of individual differences in oral reading performance, the Slosson Oral Reading Test (SORT), for which biometrical analyses have not been reported in the literature previously. Oral reading performance was measured in a large population-based sample of twins of the Virginia Twin Study of Adolescent Behavioral Development. Biometrical analyses of the SORT suggested that, in both males and females, 69% of the phenotypic variation was due to heritable influences and 13% of the variation due to shared environmental effects. While the relative importance of genetic and environmental influences is equivalent for males and females, males showed greater phenotypic variability than females.

Achievement↗