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PubMed2005

Intravenous secretin for autism spectrum disorder.

BACKGROUND: Secretin is a gastro-intestinal hormone which has been presented as an effective treatment for autism based on anecdotal evidence. OBJECTIVES: To determine if intravenous secretin:1. improves the core features of autism (social interaction, communication and behaviour problems); 2. improves the non-core aspects of behaviour or function such as self injurious behaviour;3. improves the quality of life of affected individuals and their carers; 4. has short term and long term effects on outcome; 5. causes harm. SEARCH STRATEGY: Results of electronic searches of CENTRAL, MEDLINE, EMBASE, PsycINFO, CINAHL, ERIC, HealthStar and Sociofile (1998 - March 2005) were independently examined by two authors. Reference lists of trials and reviews were searched; experts and trialists were contacted to find unpublished studies. SELECTION CRITERIA: Randomised controlled trials of intravenous secretin comparing secretin with a placebo treatment in children or adults diagnosed with autism spectrum disorders, where at least one standardised outcome measure was reported. DATA COLLECTION AND ANALYSIS: Fourteen studies met inclusion criteria. All outcome data were continuous. Where trials used cross-over designs, analysis was conducted on results from first treatment phase, allowing combined analysis with parallel design trials. Where standardised assessment tools generated scores as outcome measures, comparisons were made between means of these scores. Where baseline means were reported, differences between treatment and control were determined to assess possible bias. Where mean change from baseline was reported, this was used in preference to post-treatment scores for meta-analyses or forest plots. As meta-analysis was possible for only one outcome (Childhood Autism Rating Scale), it was impossible to use sensitivity or subgroup analyses to assess impact of study quality, clinical differences in the intervention, or clinically relevant differences between groups, such as age or presence of gastrointestinal symptoms. MAIN RESULTS: Twenty-five established standardised outcome measures were reported to assess core features of autism, communication, behaviour, visio-spatial skills, affect and adverse events within fourteen included studies. No more than four studies used any one outcome measure similarly. Outcomes were reported between three and six weeks. RCTs of efficacy of secretin in autism have not shown improvements for core features of autism. AUTHORS' CONCLUSIONS: There is no evidence that single or multiple dose intravenous secretin is effective and as such it should not currently be recommended or administered as a treatment for autism. Further experimental assessment of secretin's effectiveness for autism can only be justified if methodological problems of existing research can be overcome.

Autistic Disorder↗

PubMed2004

Proteomic studies identified a single nucleotide polymorphism in glyoxalase I as autism susceptibility factor.

Autism is a neurodevelopmental disability characterized by deficits in verbal communications, impairments in social interactions, and repetitive behaviors. Several studies have indicated strong involvement of multigenic components in the etiology of autism. Linkage analyses and candidate gene search approaches so far have not identified any reliable susceptibility genes. We are using a proteomic approach to identify protein abnormalities due to aberrant gene expression in autopsied autism brains. In four of eight autism brains, we have found an increase in polarity (more acidic) of glyoxalase I (Glo1) by two-dimensional gel electrophoresis. To identify the molecular change resulting in the shift of Glo1 polarity, we undertook sequencing of GLO1 gene. Direct sequencing of GLO1 gene/mRNA in these brains, has identified a single nucleotide polymorphism (SNP), C419A. The SNP causes an Ala111Glu change in the protein sequence. Population genetics of GLO1 C419A SNP studied in autism (71 samples) and normal and neurological controls (49 samples) showed significantly higher frequency for the A419 (allele frequency 0.6 in autism and 0.4 in controls, one-tailed Fisher's test P < 0.0079). Biochemical measurements have revealed a 38% decrease in Glo1 enzyme activity in autism brains (one-tailed t-test P < 0.026). Western blot analysis has also shown accumulation of advanced glycation end products (AGE's) in autism brains. These data suggest that homozygosity for A419 GLO1 resulting in Glu111 is a predisposing factor in the etiology of autism.

Adolescent↗

PubMed2006

Gaze-fixation, brain activation, and amygdala volume in unaffected siblings of individuals with autism.

BACKGROUND: The broad autism phenotype includes subclinical autistic characteristics found to have a higher prevalence in unaffected family members of individuals with autism. These characteristics primarily affect the social aspects of language, communication, and human interaction. The current research focuses on possible neurobehavioral characteristics associated with the broad autism phenotype. METHODS: We used a face-processing task associated with atypical patterns of gaze fixation and brain function in autism while collecting brain functional magnetic resonance imaging (fMRI) and eye tracking in unaffected siblings of individuals with autism. RESULTS: We found robust differences in gaze fixation and brain function in response to images of human faces in unaffected siblings compared with typically developing control individuals. The siblings' gaze fixations and brain activation patterns during the face processing task were similar to that of the autism group and showed decreased gaze fixation along with diminished fusiform activation compared with the control group. Furthermore, amygdala volume in the siblings was similar to the autism group and was significantly reduced compared with the control group. CONCLUSIONS: Together, these findings provide compelling evidence for differences in social/emotional processing and underlying neural circuitry in siblings of individuals with autism, supporting the notion of unique endophenotypes associated with the broad autism phenotype.

Adolescent↗

PubMed2006

Autism and environmental genomics.

Autism spectrum disorders (ASD) are defined by behavior and diagnosed by clinical history and observation but have no biomarkers and are presumably, etiologically and biologically heterogeneous. Given brain abnormalities and high monozygotic concordance, ASDs have been framed as neurobiologically based and highly genetic, which has shaped the research agenda and in particular criteria for choosing candidate ASD genes. Genetic studies to date have not uncovered genes of strong effect, but a move toward "genetic complexity" at the neurobiological level may not suffice, as evidence of systemic abnormalities (e.g. gastrointestinal and immune), increasing rates and less than 100% monozygotic concordance support a more inclusive reframing of autism as a multisystem disorder with genetic influence and environmental contributors. We review this evidence and also use a bioinformatic approach to explore the possibility that "environmentally responsive genes" not specifically associated with the nervous system, but potentially associated with systemic changes in autism, have not hitherto received sufficient attention in autism genetics investigations. We overlapped genes from NIEHS Environmental Genome Project, the Comparative Toxicogenomics Database, and the SeattleSNPs database of genes relevant to the human immune and inflammatory response with linkage regions identified in published autism genome scans. We identified 135 genes in overlap regions, of which 56 had never previously been studied in relation to autism and 47 had functional SNPs (in coding regions). Both our review and the bioinformatics exercise support the expansion of criteria for evaluating the relevance of genes to autism risk to include genes related to systemic impact and environmental responsiveness. This review also suggests the utility of environmental genomic resources in highlighting the potential relevance of particular genes within linkage regions. Environmental responsiveness and systems impacts consistent with system-wide findings in autism are thus supported as important considerations in identifying the numerous and complex modes of gene-environment interaction in autism.

Animals↗

PubMed2000

Early development, temperament, and functional impairment in autism and fragile X syndrome.

We compared the developmental status, functional abilities, and temperament of 31 young boys with fragile X syndrome (FXS) who did not have autism, matched on chronological age, gender, and race, with 31 boys with autism but no FXS. Children with autism exhibited a more variable profile of development in comparison with a relatively flat profile for children with FXS. Children with autism were significantly more delayed in social skills and were rated by observers as exhibiting a greater degree of impairment in cognitive, communication, and social skills. On temperament ratings, both groups were slower to adapt, less persistent, and more withdrawing than the reference group. Boys with FXS were rated as more active than the referent group, whereas boys with autism were rated as less intense, more distractible, having a higher threshold for response, and less rhythmic than the reference group. A smaller three-group analysis compared boys with FXS, boys with autism, and boys with both FXS and autism. Children with both autism and FXS were substantially more delayed than children with autism or FXS alone.

Age Factors↗

PubMed2001

A family genetic study of autism associated with profound mental retardation.

We sought to determine if the family loading for either the broader autism phenotype or for cognitive impairment differed according to whether or not autism was accompanied by severe mental retardation. The sample comprised 47 probands with autism meeting ICD-10 criteria, as assessed by the Autism Diagnostic Interview and the Autism Diagnostic Observation Schedule. Family history interview and findings were compared with those for the higher IQ autism and Down syndrome samples in the Bolton et al. (1994) study. The familial loading for autism and for the broader phenotype was closely comparable to that in the study of higher IQ autism, and different from that for Down syndrome. The family loading for scholastic achievement difficulties was slightly, but significantly, higher when autism was accompanied by severe retardation.

Adolescent↗

PubMed2003

[Genetics of autism: from genome scans to candidate genes].

The autistic disorder was firstly described by Leo Kanner sixty years ago. This complex developmental disability is characterized by social and communicative impairments and repetitive and stereotyped behaviours and interests. The prevalence of autism in the general population is about 1 in 1,000, with four males affected for one female. In approximately 15% of the cases, autism is associated with known genetic disorders, such as fragile X syndrome, tuberous sclerosis or Rett syndrome. Nevertheless, a recognised medical etiology can only be identified in a minority of cases. A higher recurrence risk in families with autistic subjects (45 times greater than the prevalence in the general population) and higher concordance for autism among monozygotic (60-90%) than dizygotic (0-10%) twins argue for a genetic predisposition to idiopathic autism. The past decade has been marked by an increased interest in the genetic basis of autism, with a series of multiple independent whole genome scans and chromosomal abnormalities studies. These analyses have pointed out several candidate regions on chromosomes 2q, 7q, 6q, 15q and sex chromosomes. These regions possess candidate genes that have been screened for mutations or association with autism. However, a clear involvement of a major susceptibility gene (or genes) in autism remains far from clear. The results from linkage studies and the clear drop in the concordance rates between monozygotic and dizygotic twins suggests that the genetic aetiology of autism is certainly heterogeneous (different genes in different families) and polygenic (more than one affected gene per individual). The almost finished sequence of the human genome and the generation of haplotype maps will shed light on the inter-individual genetic variability and will certainly increase the power and reliability of association studies for complex traits, such as autism.

Autistic Disorder↗

PubMed2004

Epilepsy is not a prominent feature of primary autism.

The authors report on a series of 72 patients (57 male, 15 female; aged from 4 to 21 years) affected by autism with the aim of evaluate their experience regarding the prevalence of seizure and/or epilepsy. Patients were divided into two groups: the first includes individuals (n = 54) affected by so-called idiopathic or primary autism which was further subdivided according to the grade of mental retardation (MR) and the second (n = 18) in which a known pathological event was associated to the autism (secondary autism). According to these results in the first group 12 % of autistic patients with moderate MR (i.e., IQ > 55) suffered from seizures but in three patients (9 %) they were occasional and only in one recurrent (i.e., epileptic) (3 %). Autistic patients with severe MR (i.e., IQ < 55) suffered from seizures in 20 % of the cases: in three the episodes were recurrent (15 %) and in one occasional (5 %). In the second group in which autism was associated to other morbidities 61 % (n = 11/18) had seizures, being recurrent in 10 (55 %). According to this series, in autism the risk of epilepsy is higher compared to the general population but it does not seem to be correlated to the autism itself, but rather to the associated co-morbidities and underlying brain dysfunction (overall prevalence of epilepsy in primary autism [4/54 or 7.4 %] vs. secondary autism [10/18 or 55 %]).

Adolescent↗

PubMed2006

A genetic variant that disrupts MET transcription is associated with autism.

There is strong evidence for a genetic predisposition to autism and an intense interest in discovering heritable risk factors that disrupt gene function. Based on neurobiological findings and location within a chromosome 7q31 autism candidate gene region, we analyzed the gene encoding the pleiotropic MET receptor tyrosine kinase in a family based study of autism including 1,231 cases. MET signaling participates in neocortical and cerebellar growth and maturation, immune function, and gastrointestinal repair, consistent with reported medical complications in some children with autism. Here, we show genetic association (P = 0.0005) of a common C allele in the promoter region of the MET gene in 204 autism families. The allelic association at this MET variant was confirmed in a replication sample of 539 autism families (P = 0.001) and in the combined sample (P = 0.000005). Multiplex families, in which more than one child has autism, exhibited the strongest allelic association (P = 0.000007). In case-control analyses, the autism diagnosis relative risk was 2.27 (95% confidence interval: 1.41-3.65; P = 0.0006) for the CC genotype and 1.67 (95% confidence interval: 1.11-2.49; P = 0.012) for the CG genotype compared with the GG genotype. Functional assays showed that the C allele results in a 2-fold decrease in MET promoter activity and altered binding of specific transcription factor complexes. These data implicate reduced MET gene expression in autism susceptibility, providing evidence of a previously undescribed pathophysiological basis for this behaviorally and medically complex disorder.

Alleles↗

PubMed2005

Screening for autism in infants and preschool children with developmental delay.

OBJECTIVE: This study aimed to identify emotional and behavioural problems specific to young children with autism using the Developmental Behaviour Checklist (DBC-P) and thus evaluate the efficacy of this checklist as a screening tool for autism in children with developmental delay aged 18-48 months. METHOD: Subjects were 60 children with autism and developmental delay and 60 children with developmental delay without autism. RESULTS: Features were identified which differentiated the children with autism from those with developmental delay without autism. Analyses revealed that a 17-item version of the DBC-P performed well as a screening tool for autism, with an 'area under the curve' of 0.874, sensitivity of 0.8750, and specificity of 0.6909. CONCLUSIONS: The DBC-P offers a potential simple and inexpensive method of screening at risk populations of preschool children with developmental delay for autism, thus facilitating timely referral to scarce specialist autism diagnostic services.

Autistic Disorder↗

PubMed2005

Identification of significant association and gene-gene interaction of GABA receptor subunit genes in autism.

Autism is a common neurodevelopmental disorder with a significant genetic component. Existing research suggests that multiple genes contribute to autism and that epigenetic effects or gene-gene interactions are likely contributors to autism risk. However, these effects have not yet been identified. Gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the adult brain, has been implicated in autism etiology. Fourteen known autosomal GABA receptor subunit genes were studied to look for the genes associated with autism and their possible interactions. Single-nucleotide polymorphisms (SNPs) were screened in the following genes: GABRG1, GABRA2, GABRA4, and GABRB1 on chromosome 4p12; GABRB2, GABRA6, GABRA1, GABRG2, and GABRP on 5q34-q35.1; GABRR1 and GABRR2 on 6q15; and GABRA5, GABRB3, and GABRG3 on 15q12. Intronic and/or silent mutation SNPs within each gene were analyzed in 470 white families with autism. Initially, SNPs were used in a family-based study for allelic association analysis--with the pedigree disequilibrium test and the family-based association test--and for genotypic and haplotypic association analysis--with the genotype-pedigree disequilibrium test (geno-PDT), the association in the presence of linkage (APL) test, and the haplotype family-based association test. Next, with the use of five refined independent marker sets, extended multifactor-dimensionality reduction (EMDR) analysis was employed to identify the models with locus joint effects, and interaction was further verified by conditional logistic regression. Significant allelic association was found for markers RS1912960 (in GABRA4; P = .01) and HCV9866022 (in GABRR2; P = .04). The geno-PDT found significant genotypic association for HCV8262334 (in GABRA2), RS1912960 and RS2280073 (in GABRA4), and RS2617503 and RS12187676 (in GABRB2). Consistent with the allelic and genotypic association results, EMDR confirmed the main effect at RS1912960 (in GABRA4). EMDR also identified a significant two-locus gene-gene effect model involving RS1912960 in GABRA4 and RS2351299 in GABRB1. Further support for this two-locus model came from both the multilocus geno-PDT and the APL test, which indicated a common genotype and haplotype combination positively associated with disease. Finally, these results were also consistent with the results from the conditional logistic regression, which confirmed the interaction between GABRA4 and GABRB1 (odds ratio = 2.9 for interaction term; P = .002). Through the convergence of all analyses, we conclude that GABRA4 is involved in the etiology of autism and potentially increases autism risk through interaction with GABRB1. These results support the hypothesis that GABA receptor subunit genes are involved in autism, most likely via complex gene-gene interactions.

Autistic Disorder↗

PubMedDate not supplied

Abnormally high plasma levels of vitamin B6 in children with autism not taking supplements compared to controls not taking supplements.

BACKGROUND: There have been many studies of the effect of high-dose supplementation of vitamin B6 on children and adults with autism, with all but one reporting benefits. OBJECTIVE: The aim of this study was to investigate the biochemical basis for vitamin B6 therapy by measuring the level of total vitamin B6 in the plasma of unsupplemented children with autism spectrum disorder compared to unsupplemented control subjects. PARTICIPANTS: Children with autism spectrum disorders (n = 35, age 3-9 years) and unrelated typical children (n = 11, age 6-9 years), all from Arizona, were studied. (This includes the data from 24 children with autism from our previous study.) METHODOLOGY: A microbiologic assay was used to measure the level of total vitamin B6 (including phosphorylated and unphosphorylated forms), in a blinded fashion. RESULTS: Children with autism had a 75% higher level of total vitamin B6 than the controls (medians of 56 versus 32 ng/mL, respectively, p = 0.00002). Most of the autistic children (77%) had levels that were more than 2 standard deviations above the median value of the controls. The autistic girls (n = 5) also had elevated levels (mean of 54.6 ng/mL, median of 60 ng/mL). DISCUSSION: These results are consistent with previous studies that found that: (1) pyridoxal kinase had a very low activity in children with autism and (2) pyridoxal 5 phosphate (PLP) levels are unusually low in children with autism. Thus, it appears that the low conversion of pyridoxal and pyridoxine to PLP results in low levels of PLP, which is the active cofactor for 113 known enzymatic reactions, including the formation of many key neurotransmitters. CONCLUSIONS: Total vitamin B6 is abnormally high in autism, consistent with previous reports of an impaired pyridoxal kinase for the conversion of pyridoxine and pyridoxal to PLP. This may explain the many published studies of benefits of high-dose vitamin B6 supplementation in some children and adults with autism.

Autistic Disorder↗

PubMedDate not supplied

Psychopharmacology in autism.

Autism is a neurobiological disorder. The core clinical features of autism include impairment in social interaction, impairments in verbal and nonverbal communication, and restricted, repetitive, and stereotyped patterns of behavior, interests, and activities. Autism often has coexisting neuropsychiatric disorders, including seizure disorders, attention deficit hyperactivity disorder, affective disorders, anxiety disorder, obsessive-compulsive disorder, and Tourette disorder. No etiology-based treatment modality has been developed to cure individuals with autism. However, comprehensive intervention, including parental counseling, behavior modification, special education in a highly structured environment, sensory integration training, speech therapy, social skill training, and medication, has demonstrated significant treatment effects in many individuals with autism. Findings from preliminary studies of major neurotransmitters and other neurochemical agents strongly suggest that neurochemical factors play a major role in autism. The findings also provide the rationale for psychopharmacotherapy in individuals with autism. This article reviews studies of neurochemical systems and related psychopharmacological research in autism and related neuropsychiatric disorders. Clinical indications for pharmacotherapy are described, and uses of various medications are suggested. This article also discusses new avenues of investigation that may lead to the development of more effective medication treatments in persons with autism.

Adult↗

PubMed2006

Combining information from multiple sources in the diagnosis of autism spectrum disorders.

BACKGROUND: Standard case criteria are proposed for combined use of the Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule to diagnose autism and to define the broader category of autism spectrum disorders. METHOD: Single and combined Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule algorithms were compared to best estimate diagnoses in four samples: U.S. (n = 960) and Canadian (n = 232) participants 3 years and older, U.S. participants younger than 36 months (n = 270), and U.S. participants older than 36 months with profound mental retardation (n = 67). RESULTS: Sensitivities and specificities of 80% and higher were obtained when strict criteria for an autism diagnosis using both instruments were applied in the U.S. samples, and 75% or greater in the Canadian sample. Single-instrument criteria resulted in significant loss of specificity. Specificity was poor in the sample with profound mental retardation. Lower sensitivity and specificity were also obtained when proposed criteria for broader spectrum disorders were applied. CONCLUSIONS: The Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule make independent, additive contributions to the judgment of clinicians that result in a more consistent and rigorous application of diagnostic criteria.

Asperger Syndrome↗

PubMed2003

The pathogenesis of autism: insights from congenital blindness.

There is substantial heterogeneity in the aetiology and clinical presentation of autism. So how do we account for homogeneity in the syndrome? The answer to this question will be critical for any attempt to trace the links between brain pathology and the psychological disabilities that characterize autism. One possibility is that the source of homogeneity in autism is not to be found 'in the child', but rather in dysfunction of the system constituted by child-in-relation-to-other. We have been exploring this hypothesis through the study of congenitally blind children, among whom features of autism, and the syndrome of autism itself, are strikingly common. To justify such an approach, one needs to establish that the clinical features in blind children have qualities that are indeed 'autistic-like'. We conducted systematic observations of the social interactions of two matched groups of congenitally blind children who do not have autism, rating their social engagement, emotional tone, play and language during three sessions of free play in the school playground. The qualities of social impairment in the more disabled children were similar to those in sighted children with autism. Additional evidence came from independent ratings of the children in a different play setting: on the childhood autism rating scale (CARS), the socially impaired children had 'autistic-like' abnormalities in both social and non-social domains. If we can determine the way in which congenital blindness predisposes to features of autism, we shall be in a better position to trace the developmental pathways that lead to the syndrome in sighted children.

Autistic Disorder↗

PubMed2005

A survey of sleep problems in autism, Asperger's disorder and typically developing children.

BACKGROUND: Sleep problems are common in typically developing (TD) children and in children with autism, however, less is known about the sleep of children with Asperger's disorder (AD). The aim of this study was to compare sleep patterns of children with autism and AD to a TD group of children. METHODS: Sixty-six parents of TD children, 53 parents of children with autism, and 52 parents of children with AD completed a survey on their child's sleep patterns, the nature and severity of any sleep problems and success of any treatment attempted. RESULTS: The results showed high prevalence of sleep problems with significantly more problems reported in the autism and AD groups (TD = 50%, autism = 73%, AD = 73%), with no significant differences between groups on severity or type of sleep problem. Children with AD were significantly more likely to be sluggish and disoriented after waking and had a higher Behavioral Evaluation of Disorders of Sleep (BEDS) total score compared to the other two groups. The autism and AD groups reported significantly better treatment success for medication compared to the TD group. The autism group reported significantly better success for behavioural treatment compared to the AD group. CONCLUSIONS: In conclusion, children with AD may have more symptoms of sleep disturbance, and different types of sleep problems than children with autism. As this is the first study to compare autism and AD and to survey treatment outcomes, further research is needed to validate these findings.

Asperger Syndrome↗

PubMed2004

Event-related brain potentials reveal anomalies in temporal processing of faces in autism spectrum disorder.

BACKGROUND: Individuals with autism exhibit impairments in face recognition, and neuroimaging studies have shown that individuals with autism exhibit abnormal patterns of brain activity during face processing. The current study examined the temporal characteristics of face processing in autism and their relation to behavior. METHOD: High-density event-related brain potentials (ERPs) were recorded to images of faces, inverted faces, and objects from 9 individuals with autism spectrum disorder (15-42 years old) and 14 typical individuals (16-37 years old). RESULTS: With respect to a face-sensitive ERP component (N170), individuals with autism exhibited longer N170 latencies to faces than typical individuals but comparable latencies to objects. Typical individuals exhibited longer N170 latencies to inverted as compared to upright faces, whereas individuals with autism did not show differences in N170 latency to upright versus inverted faces. Neural speed of face processing, as reflected in N170 latency, correlated with performance on a face recognition task for individuals with autism. CONCLUSIONS: These data provide evidence for slowed neural speed of face processing in autism and highlight the role of speed of processing in face processing impairments in autism.

Adolescent↗

PubMed2005

Psychiatric disorders in parents of children with autism: a meta-analysis.

BACKGROUND: The genetic basis of autism has received great attention during the last few years. The psychiatric status of parents of persons with autism has been studied as part of the broad phenotype of autism. METHODS: In the current study we examined all studies in which psychiatric difficulties of parents of children with autism were compared to those of parents of other children, as part of the broad phenotype of autism. RESULTS: Overall, when parents of children with autism were compared to all other parents taken together, i.e., parents of typically developing children grouped together with parents of children with diagnoses other than autism, they were found to have more psychiatric difficulties, but this finding was inconsistent. Once type of comparison group (e.g., Down Syndrome, learning disabilities) and method of assessing psychiatric difficulties (e.g., self-report, clinical measures) were taken into account, different findings were yielded for the various comparison groups and methods of assessing psychiatric difficulties in parents, suggesting that parents of children with autism present more psychiatric difficulties, mostly in comparisons involving samples of parents of children with no known genetic risk (e.g., Down Syndrome). CONCLUSIONS: These findings suggest that in future studies, researchers should carefully consider the advantages and disadvantages of various comparison groups and other characteristics, such as method of assessment, gender, and level of functioning, in attempting to delineate the specificity and universality of the broad phenotype of autism.

Adult↗