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PubMed2005

Assessment of social communication skills in preschoolers.

This paper orients the reader to social communication assessment and reviews methods for assessing social communication behavior in children from toddlerhood through the preschool years. Most standardized, normed tests of language in this age range focus on morpho-syntactic and semantic comprehension and production abilities. While social communication is perhaps one of the most important skills for peer acceptance, these skills are often overlooked in language evaluation with children. However, there are a number of caregiver questionnaires, interviews, or direct social-communication sampling methods that are available to assist clinicians or researchers in documenting social-communication skills or behaviors. Since assessment of social communication is essential in clinical work with children with an autism spectrum disorder, some of the tools described below are outgrowths of autism research or provide autism-related scores. While many children receiving social communication assessments do not have autism, the need to assess social communication skills in children with language impairment is highlighted by the growing literature documenting social and pragmatic difficulties in this population (Bishop 2000 Causes, Characteristics, Intervention, and Outcome. Hove, UK: Psychology press). Regardless of whether the measures presented herein were initially designed for children with autism or not, they will provide insights into the social communicative behaviors or tendencies in young children.

Child, Preschool↗

PubMed2026

Targeting the Microbiota-Gut-Brain Axis: Emerging Nanomedicine Approaches for Neurodegenerative Diseases.

The microbiota-gut-brain axis (MGBA) is a bidirectional relationship between the gut microbiota (GM) and the brain, where the GM affects the gastrointestinal tract (GIT) and the central nervous system (CNS), and vice versa. Microbiotas are important for several vital body processes, including metabolism, immunity, and homeostasis. The MGBA has three main pathways: the vagal nerve mechanism, the immune-related mechanism, and the neuroendocrine mechanism. GM imbalance, known as dysbiosis, affects the GIT, the brain, and the CNS. Furthermore, dysbiosis is linked to several neurological disorders such as Alzheimer's (AD), Parkinson's (PD), depression, autism spectrum disorder (ASD), and multiple sclerosis (MS). Studying MGBA gives researchers new therapeutic ideas using microbiota. Using special diets rich in fiber and probiotics, in addition to fecal microbiota transplantation (FMT), is being studied as a new therapy for MGBA. From the point of view that these therapeutic interventions maintain microbiota imbalance, which in turn will affect the brain and can relieve the neurological disorders caused by dysbiosis and MGBA.

Humans↗

PubMed2005

[Can we cure autism? From outcome to intervention].

Outcome in autism is variable but with a significant trend toward a poor prognosis and despite reports that outcome in individuals with autism may be improving secondary to early intensive interventions there is still much to be learned about the natural history and the effects of intervention in autism spectrum disorders. While there may not be a known cure for autism, there are a number of viable treatment options available. The primary models of treatment are non pharmacological interventions that include intervention models such as applied behavior analysis and developmental and structured teaching. The role of pharmacological interventions is limited to treating specific symptoms that may be interfering with a child's ability to learn or function within a particular environment. The question of whether or not we can cure autism needs to be discussed in terms of the need to overcome the as of yet poorly understood fundamental disturbance in autism and the need to develop treatment protocols specifically targeting social deficits. At the present time, it is more appropriate to speak of our quest to understand autism than it is to speak of a cure.

Autistic Disorder↗

PubMed2004

Mapping the brain in autism. A voxel-based MRI study of volumetric differences and intercorrelations in autism.

Autism is a disorder of neurodevelopment resulting in pervasive abnormalities in social interaction and communication, repetitive behaviours and restricted interests. There is evidence for functional abnormalities and metabolic dysconnectivity in 'social brain' circuitry in this condition, but its structural basis has proved difficult to establish reliably. Explanations for this include replication difficulties inherent in 'region of interest' approaches usually adopted, and variable inclusion criteria for subjects across the autism spectrum. Moreover, despite a consensus that autism probably affects widely distributed brain regions, the issue of anatomical connectivity has received little attention. Therefore, we planned a fully automated voxel-based whole brain volumetric analysis in children with autism and normal IQ. We predicted that brain structural changes would be similar to those previously shown in adults with autism spectrum disorder and that a correlation analysis would suggest structural dysconnectivity. We included 17 stringently diagnosed children with autism and 17 age-matched controls. All children had IQ >80. Using Brain Activation and Morphological Mapping (BAMM) software, we measured global brain and tissue class volumes and mapped regional grey and white matter differences across the whole brain. With the expectation that volumes of interconnected regions correlate positively, we carried out a preliminary exploration of 'connectivity' in autism by comparing the nature of inter-regional grey matter volume correlations with control. Children with autism had a significant reduction in total grey matter volume and significant increase in CSF volume. They had significant localized grey matter reductions within fronto-striatal and parietal networks similar to findings in our previous study, and additional decreases in ventral and superior temporal grey matter. White matter was reduced in the cerebellum, left internal capsule and fornices. Correlation analysis revealed significantly more numerous and more positive grey matter volumetric correlations in controls compared with children with autism. Thus, using similar diagnostic criteria and image analysis methods in otherwise healthy populations with an autistic spectrum disorder from different countries, cultures and age groups, we report a number of consistent findings. Taken together, our data suggest abnormalities in the anatomy and connectivity of limbic-striatal 'social' brain systems which may contribute to the brain metabolic differences and behavioural phenotype in autism.

Adolescent↗

PubMed2004

Cognitive and behavioral correlates of tuberous sclerosis complex.

Tuberous sclerosis complex is a multisystem disorder in which neurologic problems cause the greatest disability. High rates of mental retardation and autism spectrum disorders are associated with the diagnosis. Early-onset seizures and increased tuber burden are risk factors for cognitive impairment. Early-onset seizures, particularly infantile spasms, are risk factors for autism. Tubers within the temporal lobe and cerebellum are often mentioned as risk factors for autism, although the findings are inconsistent. Seizure control is important for developmental outcome and quality of life. Early behavioral assessment and therapeutic intervention, as well as seizure control, are the most effective means of promoting neurodevelopmental outcome.

Anticonvulsants↗

PubMed2004

Autistic spectrum disorder and the fragile X premutation.

Fragile X syndrome (FXS) is the most common inherited cause of mental retardation. It is also one of the most common identifiable causes of Autism Spectrum Disorder (ASD). Carriers of FXS are often considered to be cognitively and behaviorally unaffected. However, we report here on six individuals in the premutation range who also have ASD. A comparison is made with five subjects in the premutation range who did not receive a diagnosis of ASD. The six individuals with ASD had a range of cognitive ability levels from no impairment to moderate retardation. Discussion includes the impact of molecular variables including lowered FMR1 protein and elevated FMR1 mRNA in addition to environmental factors leading to the complex neurodevelopmental disorder of ASD.

Adult↗

PubMed2006

Rate of head growth decelerates and symptoms worsen in the second year of life in autism.

BACKGROUND: Longitudinal studies of head circumference growth in infants later diagnosed with autism are needed to understand the accelerated head growth in this disorder. METHODS: We analyzed longitudinal head circumference data from birth to 3 years in 28 children later diagnosed with autism spectrum disorder on the basis of individual growth curve analyses using hierarchical linear models. RESULTS: Head circumference Z scores relative to norms significantly increased in the autism sample from birth to 12 months, but this pattern did not persist beyond 12 months. Rather, the rate of change in head circumference from 12 to 36 months was not different from the normative sample. CONCLUSIONS: These results suggest that a period of exceptionally rapid head growth occurs during the first year of life in autism; after 12 months of age, the rate of head circumference growth decelerates relative to the rate during the first year of life. Studies of behavioral development in infants later diagnosed with autism suggest that the period of acceleration of head growth precedes and overlaps with the onset of behavioral symptoms, and the period of deceleration coincides with a period of worsening of symptoms in the second year of life.

Age Factors↗

PubMed2003

Children with autistic spectrum disorders. I: comparison of placebo and single dose of human synthetic secretin.

AIMS: To examine the effect of a single dose of human synthetic secretin (HSS) on behaviour and communication in children with autism spectrum disorder (ASD) using an objective measure of communication and social reciprocity and standardised rating scales. METHODS: Randomised, crossover, double blind, and placebo controlled trial of a single intravenous dose of human synthetic secretin (HSS) 2 CU/kg. The 62 subjects (3-8 years) were assigned to group 1 (saline placebo/HSS) or group 2 (HSS/saline placebo). Diagnosis was confirmed by ADI-R (Autism Diagnostic Interview-Revised) algorithm. Severity of symptoms was rated using the CARS (Childhood Autism Rating Scale). Outcome measures included Communication and Symbolic Behavior Scale (CSBS), Ritvo Real-life Rating Scale, weekly Global Rating Scale (GBRS) by parents and teachers, and daily log of gastrointestinal symptoms. The communication subscale of the CSBS, specifying communication function, reciprocity, and social-affective signalling was videotaped and scored by a blinded, trained observer. RESULTS: Sixty one children completed the study. After randomisation, there were no significant differences in gender, race, age, and parent and teacher GBRS and Ritvo Scale between the two groups. Compared with placebo, secretin treatment was not associated with significant improvement of CSBS standard scores from baseline to 2 or 4 weeks post-infusion. Five children showed clinical improvement in standard scores: two after HSS and three after placebo. There were no significant changes in gastrointestinal symptoms after HSS or saline placebo. CONCLUSIONS: A single dose of intravenous human secretin is not effective in changing behaviour and communication in children with ASD when compared to placebo.

Autistic Disorder↗

PubMed2005

Language cannot be reduced to biology: perspectives from neuro-developmental disorders affecting language learning.

The study of language knowledge guided by a purely biological perspective prioritizes the study of syntax. The essential process of syntax is recursion--the ability to generate an infinite array of expressions from a limited set of elements. Researchers working within the biological perspective argue that this ability is possible only because of an innately specified genetic makeup that is specific to human beings. Such a view of language knowledge may be fully justified in discussions on biolinguistics, and in evolutionary biology. However, it is grossly inadequate in understanding language-learning problems, particularly those experienced by children with neurodevelopmental disorders such as developmental dyslexia, Williams syndrome, specific language impairment and autism spectrum disorders. Specifically, syntax-centered definitions of language knowledge completely ignore certain crucial aspects of language learning and use, namely, that language is embedded in a social context; that the role of envrironmental triggering as a learning mechanism is grossly underestimated; that a considerable extent of visuo-spatial information accompanies speech in day-to-day communication; that the developmental process itself lies at the heart of knowledge acquisition; and that there is a tremendous variation in the orthographic systems associated with different languages. All these (socio-cultural) factors can influence the rate and quality of spoken and written language acquisition resulting in much variation in phenotypes associated with disorders known to have a genetic component. Delineation of such phenotypic variability requires inputs from varied disciplines such as neurobiology, neuropsychology, linguistics and communication disorders. In this paper, I discuss published research that questions cognitive modularity and emphasises the role of the environment for understanding linguistic capabilities of children with neuro-developmental disorders. The discussion pertains to two specific disorders, developmental dyslexia and Williams syndrome.

Genotype↗

PubMed2003

Deficits in attention, motor control, and perception: a brief review.

The concept of DAMP (deficits in attention, motor control, and perception) has been in clinical use in Scandinavia for about 20 years. DAMP is diagnosed on the basis of concomitant attention deficit/hyperactivity disorder and developmental coordination disorder in children who do not have severe learning disability or cerebral palsy. In clinically severe form it affects about 1.5% of the general population of school age children; another few per cent are affected by more moderate variants. Boys are overrepresented; girls are currently probably underdiagnosed. There are many comorbid problems/overlapping conditions, including conduct disorder, depression/anxiety, and academic failure. There is a strong link with autism spectrum disorders in severe DAMP. Familial factors and pre- and perinatal risk factors account for much of the variance. Psychosocial risk factors appear to increase the risk of marked psychiatric abnormality in DAMP. Outcome in early adult age was psychosocially poor in one study in almost 60% of unmedicated cases. There are effective interventions available for many of the problems encountered in DAMP.

Attention Deficit Disorder with Hyperactivity↗

PubMed2006

Proton magnetic resonance spectroscopy in developmentally delayed young boys with or without autism.

OBJECTIVE: The aim of the present study is to investigate whether brain metabolism of boys with autism spectrum disorder (ASD) is altered compared to boys with a developmental delay without autism if corrected for patient age and developmental level. STUDY DESIGN: 25 boys with ASD (with or without concurrent mental retardation) and 12 boys without ASD with mental retardation or language disorder underwent proton magnetic resonance spectroscopy. All analyses were performed with chronological age and developmental level as independent variables. RESULTS: No metabolic differences were found between boys with ASD and without ASD. CONCLUSIONS: Our findings do not replicate previous reports of differences in NAA, Cho and Cr levels in ASD.

Age Factors↗

PubMed2004

The genetics of autism.

Autism spectrum disorders (ASD) are among the most heritable of all neuropsychiatric disorders. Discovery of autism susceptibility genes has been the focus of intense research efforts over the last 10 years, and current estimates suggest that 10 to 20 different interacting genes are involved. Evidence from twin and family studies demonstrates increased risk in family members not only for autistic disorder, but also for a milder constellation of similar symptoms referred to as the broader phenotype. In addition, several genetic syndromes and chromosomal anomalies have been associated with ASD. Large family studies using linkage-analysis techniques have demonstrated several chromosomal regions thought to harbor genes related to the disorder. Finally, specific candidate genes based on function and location have been explored; these studies are reviewed here.

Autistic Disorder↗

PubMedDate not supplied

The cognitive profile of anorexia nervosa: a comparative study including a community-based sample.

A community-based sample of adolescent-onset anorexia nervosa (AN) cases (n = 51) was contrasted with an age-, sex-, and school-matched comparison group [comp] (n = 51) on the Wechsler Adult Intelligence Scale-Revised (WAIS-R) at a mean age of 21 years. There were no study dropouts. Fewer than 10% of AN cases were underweight at the time of testing. Overall, there were few differences across the two groups, even though the COMP group performed significantly better on the object assembly subtest. A small subgroup of AN cases showed autism-spectrum disorders. This subgroup tended toward test profiles similar to those observed in autism and Asperger syndrome. These findings are discussed in relation to the clinical need for subgrouping of AN cases with a view to improving treatment programs/interviews.

Adolescent↗

PubMed2003

Targeted treatments for symptom domains in child and adolescent autism.

CONTEXT: The number of people with autism spectrum disorders has dramatically increased over the past decade, and problem behaviours in autism are an increasing challenge to families, schools, physicians, and other health-care professionals. Pharmacological treatments can effectively target problem behaviours associated with autism. STARTING POINT: Recently, L Namerow and colleagues (J Dev Behav Pediatr 2003; 24: 104-08) presented preliminary data in children and adolescents with autism treated with citalopram, which suggested that selective serotonin-reuptake inhibitors are useful in the reduction of symptom domains such as repetitive behaviours and mood disorders. J McCracken and colleagues (N Engl J Med 2000; 347: 314-21) showed that the atypical antipsychotic risperidone reduced serious behavioural problems, such as tantrums, aggression, or self-injury in children with autism and in children with below-average intelligence quotients. These and other studies show how developments in study design, selection of patients, and outcome measures have allowed treatment trials in autism to progress beyond anecdotal reports and case observations, and show reduction in the severity of specific symptom domains within these disorders. WHERE NEXT? In therapeutic intervention the risk of treatment toxicity must be balanced against the benefits of improved symptom severity. The newer methods enable informed decisions about which patients will benefit from which treatments. Other symptom domains within autism and effects on development need to be evaluated in adequately designed clinical trials. Future strategies include extending treatment to children as young as the preschool years.

Adolescent↗

PubMed2004

Autism as a disorder of neural information processing: directions for research and targets for therapy.

The broad variation in phenotypes and severities within autism spectrum disorders suggests the involvement of multiple predisposing factors, interacting in complex ways with normal developmental courses and gradients. Identification of these factors, and the common developmental path into which they feed, is hampered by the large degrees of convergence from causal factors to altered brain development, and divergence from abnormal brain development into altered cognition and behaviour. Genetic, neurochemical, neuroimaging, and behavioural findings on autism, as well as studies of normal development and of genetic syndromes that share symptoms with autism, offer hypotheses as to the nature of causal factors and their possible effects on the structure and dynamics of neural systems. Such alterations in neural properties may in turn perturb activity-dependent development, giving rise to a complex behavioural syndrome many steps removed from the root causes. Animal models based on genetic, neurochemical, neurophysiological, and behavioural manipulations offer the possibility of exploring these developmental processes in detail, as do human studies addressing endophenotypes beyond the diagnosis itself.

Animals↗

PubMed2007

Trends in special education code assignment for autism: implications for prevalence estimates.

There is considerable controversy over reasons for observed increases in the prevalence of autism spectrum disorders. We examined trends in British Columbia education database coding of children with autism from 1996 to 2004. There was a significant linear increase in autism prevalence. The proportion of children identified by age 6 increased significantly from 1996 to 1999. When we calculated prevalence assuming onset prior to age 3, previously unidentified cases, particularly among girls in 1996 and 1997, accounted for substantial increases in estimated prevalence. The magnitude of under-identification decreased from 1996 to 2000, and rose slightly in 2001. Analyses of prevalence trends must take into account effects of earlier age at identification and inclusion of previously undetected cases on prevalence estimates.

Age Factors↗

PubMed2000

Behavior phenotype of FG syndrome: cognition, personality, and behavior in eleven affected boys.

In this study we examined several behavioral, personality, and cognitive characteristics of boys with FG syndrome. We confirmed high rates of attention and activity level problems, which were described previously. Nine of the 11 patients met criteria for attention deficit/hyperactivity disorder. The boys did not manifest autistic behavior, and none met criteria for an autism spectrum disorder, though their parents reported substantial repetitive behavior. The personalities of the participants often were described as friendly, good-natured, and cheerful, but they did not differ empirically on a standardized measure of personality structure from typically developing comparison children, even after controlling for the effects of IQ. Specifically, higher rates of agreeableness and extraversion were not confirmed, though these constructs do not correspond perfectly with the traits of affability and gregariousness described in earlier published case studies of FG syndrome. In terms of neuropsychological assessment, the boys had relatively less developed language, fine motor, and executive function skills, and visual-spatial abilities were a relative strength. Limitations and suggestions for future research are discussed.

Adolescent↗

PubMed2006

Fatty acid compositions of red blood cell phospholipids in children with autism.

We compared the compositions of fatty acids including n-3, n-6 polyunsaturated fatty acids, trans- and cis-monounsaturated fatty acids, and saturated fatty acids in the red blood cell membranes of 40 children with autism (20 with early onset autism and 20 with developmental regression) and age-matched, 20 typically developing controls and 20 subjects with non-autistic developmental disabilities. The main findings include increased levels of eicosenoic acid (20:1n9) and erucic acid (22:1n9) in autistic subjects with developmental regression when compared with typically developing controls. In addition, an increase in 20:2n6 and a decrease in 16:1n7t were observed in children with clinical regression compared to those with early onset autism. Our results do not provide strong evidence for the hypothesis that abnormal fatty acid metabolism plays a role in the pathogenesis of autism spectrum disorder, although they suggest some metabolic or dietary abnormalities in the regressive form of autism.

Autistic Disorder↗