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PubMed2001

Non-significance of early speech delay in children with autism and normal intelligence and implications for DSM-IV Asperger's disorder.

According to the DSM-IV, children with Asperger's disorder do not have significant cognitive or speech delays, whereas children with autistic disorder may or may not. In our study, children with normal intelligence who had clinical diagnoses of autism or Asperger syndrome were divided into two groups: those with and without a significant speech delay. The purpose was to determine if clinically meaningful differences existed between the two groups that would support absence of speech delay as a DSM-IV criterion for Asperger's disorder. No significant differences were found between the 23 children with a speech delay and the 24 children without a speech delay on any of the 71 variables analyzed, including autistic symptoms and expressive language. Results suggest that early speech delay may be irrelevant to later functioning in children who have normal intelligence and clinical diagnoses of autism or Asperger syndrome and that speech delay as a DSM-IV distinction between Asperger's disorder and autism may not be justified.

Autistic Disorder↗

PubMed1997

[Coincidence of epilepsy and Asperger syndrome. Case report and review].

Asperger syndrome is an autistic disorder and was first described by Hans Asperger in 1944 without further acceptance in the literature over almost four decades. Following several publications in the 1980s, for the disorder became more widely known and was first introduced into ICD-10 and DSM-IV as a new diagnosis in 1988 and 1994, respectively. The etiology is unknown. We present a female patient with typical features of Asperger syndrome, suffering also from epilepsy and internal medical disorders. The associated diseases, diagnostic criteria and possible therapeutic options are discussed.

Adolescent↗

PubMed1999

The neuroanatomy of autism: a voxel-based whole brain analysis of structural scans.

Autism is a biological disorder which affects social cognition, and understanding brain abnormalities of the former will elucidate the brain basis of the latter. We report structural MRI data on 15 high-functioning individuals with autistic disorder. A voxel-based whole brain analysis identified grey matter differences in an amygdala centered system relative to 15 age- and IQ-matched controls. Decreases of grey matter were found in anterior parts of this system (right paracingulate sulcus, left inferior frontal gyrus). Increases were found in posterior parts (amygdala/peri-amygdaloid cortex, middle temporal gyrus, inferior temporal gyrus), and in regions of the cerebellum. These structures are implicated in social cognition by animal, imaging and histopathological studies. This study therefore provides converging evidence of the physiological basis of social cognition.

Adult↗

PubMed1990

A controlled crossover trial of fenfluramine in autism.

We report a 12 month double-blind randomized crossover trial of fenfluramine in 20 children with the syndrome of autism. On active drug most of the children lost weight and blood serotonin levels fell by an average of 60%. There was a fall in urinary dopamine (DA) and noradrenaline (NA) levels and increased excretion of homovanillic acid (HVA). Some of the children showed improvement in tests of cognitive and language function, although the results did not achieve overall statistical significance. Event-related brain potentials (ERPs) were obtained in seven subjects on an auditory choice reaction time task. Side effects of the drug included irritability and lethargy. Fenfluramine may have a limited place in the management of some patients with autistic disorder.

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↗

PubMed2001

Neurological presentation of three patients with 22q11 deletion (CATCH 22 syndrome).

Chromosome 22q11 deletion (CATCH 22 syndrome or velocardiofacial syndrome) is one of the most frequent chromosomal syndromes. Neurological features other than cognitive disorders are probably the least-described part of the expanding phenotype of the 22q11 deletion. We report the neurological features of three unrelated children with a de novo deletion: one patient with an autistic disorder, a second patient with hypocalcaemic neonatal seizures and unusual persistent epileptic focus at electroencephalographic follow-up, and a third patient with atypical absence epilepsy. These observations enlarge the clinical and neurological spectrum of the 22q11 deletion. Awareness of such cases is necessary, and a diagnosis of the 22q11 deletion should be suspected in children with common neurological features associated with severe or mild dysmorphism. Diagnosis of the 22q11 deletion should be confirmed by fluorescence in situ hybridization analysis associated with standard chromosomal analysis.

Abnormalities, Multiple↗

PubMed2000

Cerebellar abnormalities in mental illness. A study on Purkinje cell density in schizophrenic men.

The linear Purkinje cell density in the cerebellar vermis was investigated in a small cohort of adult onset schizophrenic men with well-documented hippocampal abnormalities. There were no differences in comparison with age-matched controls. This negative finding indicates that vermian abnormalities undoubtedly seen in some schizophrenic patients may constitute a subsyndrome, possibly related to autistic disorders in which cerebellar abnormalities are well corroborated.

Adult↗

PubMed2002

Open-label study of olanzapine in children with pervasive developmental disorder.

The effects of olanzapine on the symptomatology of children with pervasive developmental disorder with emphasis on problems of communication and the safety of the drug were investigated in a 3-month open-label, open-dosage study. Participating in the study were 25 children age 6 to 16 years with a diagnosis of either autistic disorder or pervasive developmental disorder not otherwise specified. Psychometric measures included the Clinical Global Impression of Severity/Improvement, the Aberrant Behavior Checklist, and the TARGET (a checklist of five target symptoms). Communication skills were assessed during behavioral analysis of a playroom session. Safety measures included clinical chemistry variables, electrocardiography, the SimpsonAngus Neurological Rating Scale, the Barnes Akathisia Scale, and vital signs. Twenty-three children completed the study and showed significant improvement on three subscales of the Aberrant Behavior Checklist (Irritability, Hyperactivity, and Excessive Speech) and the TARGET. The final mean dose was 10.7 mg/day. Several aspects of communication were also improved after olanzapine treatment. However, only three children were considered responders in terms of the Clinical Global Impression of Severity/Improvement scores. The most important adverse events were weight gain, increased appetite, and loss of strength. Three children showed extrapyramidal symptoms that disappeared after the dose was lowered. Thus, while olanzapine was a relatively safe medication in children, its clinical relevance in children with pervasive developmental disorder may be limited.

Adolescent↗

PubMed2006

Brief report: "the autism epidemic". The registered prevalence of autism in a Swedish urban area.

The objective of this study was to establish rates of diagnosed autism spectrum disorders (ASDs) in a circumscribed geographical region. The total population born in 1977-1994, living in Göteborg Sweden in 2001, was screened for ASD in registers of the Child Neuropsychiatry Clinic. The minimum registered rate of autistic disorder was 20.5 in 10,000. Other ASDs were 32.9 in 10,000, including 9.2 in 10,000 with Asperger syndrome. Males predominated. In the youngest group (7-12 years), 1.23% had a registered diagnosis of ASD. There was an increase in the rate of diagnosed registered ASD over time; the cause was not determined. The increase tended to level off in the younger age cohort, perhaps due to Asperger syndrome cases missed in screening.

Asperger Syndrome↗

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↗

PubMed2002

Gender identity problems in autistic children.

Several psychiatric and behavioural problems have been described in children with autism. The aim of this case report is to discuss the developmental pattern of cross-gender behaviour in children with autistic disorder. Two boys are described with high functioning autism, followed for about 4 years, who showed persistent gender identity problems.

Autistic Disorder↗

PubMed2005

The Autism Genome Project: goals and strategies.

Autism is a complex neurodevelopmental disorder with a broad spectrum of symptoms and varying severity. Currently, no biological diagnosis exists. Although there has been a significant increase in autism genetics research recently, validated susceptibility genes for the most common, sporadic forms of autistic disorder, as well as familial autism, have yet to be identified. The identification of autism-susceptibility genes will not only assist in the identification and/or development of better medications that can help improve the health and neurodevelopment of children with autism, but will also allow for better perinatal diagnosis. The Autism Genome Project (AGP) is a large-scale, collaborative genetics research project initiated by the National Alliance for Autism Research and the National Institutes of Health, and is aimed at sifting through the human genome in search of autism-susceptibility genes. Phase I of the AGP will consist of genome-wide scans utilizing both SNP array and microsatellite technologies. Linkage analysis will subsequently be performed on approximately 1500 pedigrees as will downstream fine-mapping and sequencing of the critical linkage intervals. Ultimately, the vision will be to identify the exact nucleotide variants within genes which give rise to predisposition. The AGP intends to move the field of autism clinical management forward by answering questions about the causal mechanisms underlying the pathophysiology of autism. From this knowledge, therapeutic targets for drug treatments, and ultimately, a newborn screening diagnostic that would allow for early intervention, can begin to be developed.

Autistic Disorder↗

PubMed2003

The symptoms of autism spectrum disorders in adolescence and adulthood.

This article describes the symptoms of autism spectrum disorders (ASD) manifested by 405 individuals between the ages of 10 and 53 years, all of whom had an ASD diagnosis. Data were collected using the Autism Diagnostic Interview-Revised (ADI-R) to assess the pattern of autism symptoms in adolescence and adulthood. Findings include that although virtually all sample members met the criteria for Autistic Disorder earlier in their childhood, just over half (54.8%) would have met autism criteria if current scores were used to complete the diagnostic algorithm; that adolescents were more likely to improve in the Reciprocal Social Interaction domain than the adults, whereas the adults were more likely to improve in the Restricted, Repetitive Behaviors and Interests domain, and there were no differences in severity of symptoms between cohorts in the Communication domain; and that individual symptoms showed unique trajectories, with greatest symptom abatement between lifetime and current ADI-R ratings for speaking in at least three-word phrases and the least symptom improvement for having friendships. Findings were interpreted in the context of life course development, reformulations of diagnostic criteria, and changing service contexts for individuals with autism spectrum disorders.

Adolescent↗

PubMed2005

Interaction and imitation deficits from infancy to 4 years of age in children with autism: a pilot study based on videotapes.

The present study investigated the influence of developmental level on interaction and imitation in infants and young children with autism on the basis of family videos and filmed consultation. The sample comprised 18 children with autism divided into groups according to their developmental quotient (DQ>50 and DQ<50). A quantitative evaluation was performed on video observations at four periods (10-12 months, 16-18 months, 24-26 months, after 4 years) using scales appropriate for the evaluation of interaction and imitation impairments. The findings showed that, at a very early age, infants later diagnosed as having autistic disorder show different intensities of interaction and imitation deficits according to developmental level.

Autistic Disorder↗

PubMed2005

Lack of evidence for association between the serotonin transporter gene (SLC6A4) polymorphisms and autism in the Chinese trios.

Serotonin regulates several aspects of brain development, and it is involved in a range of behaviors frequently disturbed in autistic disorder. The serotonin transporter is a critical component of the serotonergic system. The serotonin transporter gene (SLC6A4) is of special interest given the nature of the biological findings and the reported effects of selective serotonin reuptake inhibitors of autistic symptoms. So far the genetics researches of the SLC6A4 gene have given conflicting results. The aim of study was to investigate the association between the SLC6A4 gene and autism in the Chinese Han population. The present study was conducted with the detection of three single nucleotide polymorphisms (SNP(S)) located within the SLC6A4 gene by using the polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) analysis. We performed a family-based association study of these polymorphisms in 175 Chinese Han family trios. Linkage disequilibrium (LD) measurement (D') analysis showed the presence of LD between markers across the locus. No significant evidence of association was found at any of the markers detected by using the transmission disequilibrium test (TDT) and haplotype analyses in all samples and male samples. Our findings suggest that it is unlikely that DNA variations in the SLC6A4 gene play a significant role in the genetic predisposition to autism in the Chinese Han population or that allelic heterogeneity at the SLC6A4 loci dilutes potential disease-allele association.

Asian People↗

PubMed1995

[Infantile autism in France in 1994].

The author tries, in is own, name to translate the French position on early child autism. This position can be expressed through a few acceptable points for the majority of French professionals, obviously without any idea of a consensus. The concept of a plurifactorial determinism and the psychopathological view of the disorder which is not thought of in France as susceptible to be reduced to a handicap of a primarily cognitive nature are therefore underlined. Thus the importance of a unified multidimensional therapeutic approach that considers the different consequences of the illness without forgetting its fundamentally interactive nature ("autistic-making process"). Today, the psychoanalytic approach tends to concentrate on the analysis of secondary factors of upholding and on the significance given in the after-thought by the autistic disorders within the family group. This opens the way to a collaboration between specialists of the different disciplines that are involved, including those who work in the field of neuroscience.

Autistic Disorder↗

PubMed1989

Clinical effect of buspirone in autistic children.

Buspirone is a novel antianxiety agent with no chemical similarity to other psychotropic medications. Pharmacological effects include inhibition of serotonin neurons, decrease of striatal levels of serotonin and metabolites, and reduction in serotonin binding sites. Buspirone also has effects on dopamine, norepinephrine, and the GABA systems. To pursue an antiserotonergic treatment rationale for autistic disorder, an open-blind 4-week trial comparing buspirone to fenfluramine or methylphenidate was conducted. Hyperactivity was a target symptom in three children with improvement noted in two with buspirone. Behavioral toxicity was encountered in one of two autistic subjects treated with methylphenidate and very mild improvement in another subject on fenfluramine. An autistic child with obsessive ideation was unchanged. No adverse reaction to buspirone was encountered. Further investigation in a double-blind trial of buspirone is warranted for treatment of symptoms of autism, especially aggression and hyperactivity.

Autistic Disorder↗

PubMed1995

Low serum tryptophan to large neutral amino acids ratio in idiopathic infantile autism.

The serum tryptophan to large neutral amino acids ratio (Try/LNAA) is considered a reliable marker of tryptophan availability for brain serotonin synthesis. A dysfunction of brain serotonergic activity has been postulated to exist in autistic disorder and supported by recent studies. On this basis, we determined the serum amino acids levels in 40 children with idiopathic infantile autism as well as in 46 control children. A significantly lower serum Try/LNAA ratio was observed in the autistic subjects compared to the normal controls. In 14 autistic children (35%) this ratio was 2 SD below the mean value obtained in the control group. These results suggest that a low brain tryptophan availability due to a low serum Try/LNAA ratio could be one of the possible mechanisms involved in the alteration of serotonergic function in autism.

Adolescent↗