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PubMed2007

Quantitative temporal lobe differences: autism distinguished from controls using classification and regression tree analysis.

The temporal lobe is thought to be abnormal in autism, yet standard volumetric analyses are often unrevealing when age, sex, IQ, and head size are controlled. Quantification of temporal lobe structures were obtained in male subjects with autism and controls, where subjects with head circumference (HC) defined macrocephaly were excluded, so that volume differences were not just related to the higher prevalence of macrocephaly in autism. Various statistical methods were applied to the analysis including a classification and regression tree (CART) method, a non-parametric technique that helps define patterns of relationships that may be meaningful in distinguishing temporal lobe differences between subjects with autism and age and IQ matched controls. Subjects with autism were also compared to a separate control group with reading disorder (RD), with the prediction that the temporal lobe morphometric analysis of the reading disorder controls would be more similar to that of the autism group. The CART method yielded a high specificity in classifying autism subjects from controls based on the relationship between the volume of the left fusiform gyrus (LFG) gray and white matter, the right temporal stem (RTS) and the right inferior temporal gyrus gray matter (RITG-GM). Reading disordered individuals were more similar to subjects with autism. Simple size differences did not distinguish the groups. These findings demonstrate different relationships within temporal lobe structures that distinguish subjects with autism from controls. Results are discussed in terms of pathological connectivity within the temporal lobe as it relates to autism.

Adolescent↗

PubMed2006

Auditory characteristics of children with autism.

OBJECTIVES: The objectives of this study were (1) to describe the auditory characteristics of children with autism relative to those of typically developing children and (2) to describe the test-retest reliability of behavioral auditory test measures with this population of children with autism. DESIGN: Audiometric data were obtained from 22 children diagnosed with autism and 22 of their typically developing peers. The audiologic test battery consisted of behavioral measures (i.e., visual reinforcement audiometry, tangible reinforcement operant conditioning audiometry, and conditioned play audiometry) and physiological measures (auditory brain stem response audiometry, distortion product otoacoustic emissions, and acoustic reflexes). RESULTS: Children with autism had physiologic test results equivalent to their typically developing counterparts. That is, no differences in auditory brain stem response audiometry, distortion product otoacoustic emissions, or acoustic reflex results were noted between the children with autism and typically developing children. However, behavioral measures revealed that about half of the children diagnosed with autism presented pure-tone averages outside of normal limits (i.e., >20 dB HL), although their response thresholds to speech were within normal limits. All behavioral test results were within normal limits (i.e., </=20 dB HL) for the typically developing children. In addition, test-retest variability was typically 15 dB or greater for children with autism as compared with variability of 10 dB or less for most of the typically developing children. CONCLUSIONS: Children with autism demonstrated essentially equivalent results on a battery of physiological auditory tests as those obtained from typically developing children. However, on average, behavioral responses of children with autism were elevated and less reliable relative to those of typically developing children. Furthermore, approximately half of the children with autism demonstrated behavioral pure-tone averages outside of the normal hearing range (i.e., >20 dB HL) despite having normal to near-normal hearing sensitivity as determined by other audiometric measures.

Acoustic Impedance Tests↗

PubMed2005

Effects of familial risk factors and place of birth on the risk of autism: a nationwide register-based study.

BACKGROUND: The etiology of autism is unknown. A strong genetic component has been detected but non-genetic factors may also be involved in the etiology. METHODS: We used data from the Danish Psychiatric Central Register and the Danish Civil Registration System to study some risk factors of autism, including place of birth, parental place of birth, parental age, family history of psychiatric disorders, and paternal identity. RESULTS: A total of 943,664 children younger than ten years were followed from 1994 to 2001; of those, 818 children developed autism. The highest risks of autism were found in siblings of children with autism, or Asperger's syndrome and other pervasive developmental disorders (PDDs), with relative risks of 22 and 13, respectively. The relative risk of autism in the child was about twice as high if the mother had been diagnosed with a psychiatric disorder. The risk of autism was associated with increasing degree of urbanisation of the child's place of birth and with increasing paternal, but not maternal, age. An increased relative risk of 1.4 was found if the mother was born outside Europe, and in children of parents who were born in different countries. CONCLUSIONS: The highest risk of autism was found in families with a history of autism, or Asperger's syndrome and other PDDs in siblings, supporting the commonly accepted knowledge that genetic factors are involved in the etiology of autism.

Asperger Syndrome↗

PubMed2001

Autism and the school nurse.

Until recently, treatment for children with autism involved housing them in hospitals for the developmentally disabled. Today, more states are returning children with autism to their home communities, and more parents are choosing or are being required to keep their children with autism in their homes. Laws were developed to ensure that children with autism receive some form of education, often through the local school system. School nurses, who may not have experience working with children with autism, may feel uncertain about how to provide support for the child with autism. Approximately 300,000 persons in the United States have autism or display autistic behaviors. About one-third are under age 21. People with autism come from all socioeconomic classes. Males are four times more likely to be affected by autism than females. People with autism can be expected to live a normal lifespan.

Adolescent↗

PubMed2002

Relation of childhood gastrointestinal disorders to autism: nested case-control study using data from the UK General Practice Research Database.

OBJECTIVES: To assess whether children with autism are more likely to have a history of gastrointestinal disorders than children without autism. DESIGN: Nested case-control study. SETTING: UK General Practice Research Database. SUBJECTS: Children born after 1 January 1988 and registered with the General Practice Research Database within 6 months of birth. OUTCOME MEASURES: Chronic inflammation of the gastrointestinal tract, coeliac disease, food intolerance, and recurrent gastrointestinal symptoms recorded by the general practitioner. RESULTS: 9 of 96 (9%) children with a diagnosis of autism (cases) and 41 of 449 (9%) children without autism (matched controls) had a history of gastrointestinal disorders before the index date (the date of first recorded diagnosis of autism in the cases and the same date for controls). The estimated odds ratio for a history of gastrointestinal disorders among children with autism compared with children without autism was 1.0 (95% confidence interval 0.5 to 2.2). CONCLUSIONS: No evidence was found that children with autism were more likely than children without autism to have had defined gastrointestinal disorders at any time before their diagnosis of autism.

Autistic Disorder↗

PubMed1998

The effect of semantic and emotional context on written recall for verbal language in high functioning adults with autism spectrum disorder.

OBJECTIVE: Several deficits have been proposed to account for cognitive impairment in autism including an inability to comprehend the perspectives of others ("theory of mind"), an inability to process emotional information, and difficulty drawing together diverse information in context ("central coherence"). Because context (central coherence) and emotion can influence memory, a study was designed to show if autism spectrum disorder was associated with impaired utilisation of context and emotion in recall; and if impairments in theory of mind processing would influence recall in autism spectrum disorder. METHODS: Ten high functioning subjects with autism spectrum disorder and 13 age and IQ matched controls were tested using recall tests. In the first coherence memory test, subjects listened to a series of word lists that were in varying degrees of syntactic and semantic (coherent) order and were asked to recall the words. In the second coherence memory test, subjects listened to stories consisting of sentences that were, or were not, in logical (coherent) order. In the emotional memory test, the subjects listened to sentences that were highly emotional or non-emotional. In the theory of mind test, the subjects listened to stories requiring varying levels of understanding of the perspectives of others. RESULTS: There were no significant differences between groups in recall of coherent versus incoherent word lists, nor was there a significant difference between groups in recall of coherent versus incoherent stories. However, the control subjects recalled more of the emotional than non-emotional sentences, whereas the autism spectrum disorder group did not show such a difference. No significant difference existed in recall of stories requiring varying levels of understanding of the perspectives of others among subjects with autism spectrum disorder, and subjects with autism spectrum disorder did not differ from control subjects in the influence of theory of mind content on story recall. CONCLUSION: The study shows that memory in high functioning adults with autism spectrum disorder is facilitated by emotional content to a lesser degree than it is facilitated by coherence. Therefore, impairments in emotional processing cannot be considered as simply an effect of the "weak central coherence" theory in autism spectrum disorder. Whereas the reasons for this emotional deficit are unknown, evidence of abnormalities of the limbic structures in autism spectrum disorder may provide an anatomical explanation.

Adult↗

PubMed1995

Autism and associated behavioral disorders: pharmacotherapeutic intervention.

OBJECTIVE: To review the literature on autism and pervasive developmental disorders (PDDs) as well as their respective pharmacotherapies. DATA SOURCES: An Index Medicus, MEDLINE, and bibliographic search of the literature pertaining to autism, PDDs, and respective treatments. STUDY SELECTION: Because of the paucity of literature on the treatment of autism and PDDs, the selection of reported data for this review included both controlled and uncontrolled studies, as well as case reports and any other information reported in the literature on the treatment of these disorders. DATA SYNTHESIS: Autism and PDDs are severe developmental disabilities defined by behavioral criteria. These disorders are lifelong in nature and present in varying severity of clinical manifestations. Behavioral manifestations of patients with autism include core deficits in social interaction, communication, and imaginative activities, with a restricted repertoire of activities and interests. The present understanding of the neurochemical basis of the disorder is limited. The role of pharmacotherapy in the management of autism and PDDs is to ameliorate behavioral symptoms that interfere with the patient's ability to participate in educational, social, work, and family systems. Agents that have shown positive clinical effects in the treatment of children with autism and PDDs are reviewed in this article. CONCLUSIONS: Autism is a complex developmental disorder representing a heterogeneous group of individuals with similar symptomatologies and multiple biologic etiologies. Present pharmacotherapeutic intervention seeks to resolve behavioral symptoms. Treatment of autism and PDDs requires appropriate delineation of the behaviors and neurobiologic disorders associated with each patient. No single therapeutic agent, or combination thereof, is appropriate for the treatment of all children and adults with autism or PDDs.

Autistic Disorder↗

PubMed2002

Effects of age on brain volume and head circumference in autism.

OBJECTIVE: To determine whether brain volume, as assessed on MRI scans, differs between individuals with autism and control subjects, and whether such differences are affected by age. BACKGROUND: Previous studies have found increased brain weight, head circumference, and MRI brain volume in children with autism. However, studies of brain size in adults with autism have yielded conflicting results. The authors hypothesize that enlargement of the brain may be a feature of brain development during early childhood in autism that normalizes with maturational processes. METHODS: The authors measured total brain volumes from 1.5-mm coronal MRI scans in 67 non-mentally retarded children and adults with autism and 83 healthy community volunteers, ranging in age from 8 to 46 years. Head circumference was also measured. Groups did not differ on age, sex, verbal IQ, or socioeconomic status. RESULTS: Brain volumes were significantly larger for children with autism 12 years old and younger compared with normally developing children, when controlling for height. Brain volumes for individuals older than age 12 did not differ between the autism and control groups. Head circumference was increased in both younger and older groups of subjects with autism, suggesting that those subjects older than age 12 had increased brain volumes as children. CONCLUSIONS: Brain development in autism follows an abnormal pattern, with accelerated growth in early life that results in brain enlargement in childhood. Brain volume in adolescents and adults with autism is, however, normal, and appears to be due to a slight decrease in brain volume for these individuals at the same time that normal children are experiencing a slight increase.

Adolescent↗

PubMed2004

Linguistic and cognitive functioning and autism symptoms in young children with fragile X syndrome.

Linguistic and cognitive profiles were examined in 18 children with autism and 18 children with fragile X syndrome (mean ages = 34 months). State-of-the-art diagnostic procedures for autism symptom identification were administered. Eight children with fragile X met criteria for autism. Comparison of linguistic and cognitive profiles (autism, fragile X without autism, fragile X with autism) revealed that children with fragile X (with autism) were more impaired in nonverbal cognition and expressive language. Receptive language was a relative strength for children with fragile X (without autism). There were no differences in receptive language in children with autism, regardless of fragile X status. Low receptive language may be a marker for autism symptoms in young children with fragile X.

Autistic Disorder↗

PubMed2001

No evidence for a new variant of measles-mumps-rubella-induced autism.

OBJECTIVE: A link has been postulated between measles-mumps-rubella (MMR) vaccine and a form of autism that is a combination of developmental regression and gastrointestinal symptoms that occur shortly after immunization. This hypothesis has involved 3 separate claims: 1) that there is new phenotype of autism involving regression and gastrointestinal symptoms, 2) that this new variant is responsible for the alleged rise of autism rates, and 3) that this phenotype is associated with biological findings suggestive of the persistence of measles infection. We tested the first of these claims. If this new "autistic enterocolitis" syndrome had some validity, then 1 or several of the following 6 predictions should be supported by empirical data: 1) childhood disintegrative disorder has become more frequent, 2) the mean age of first parental concern for autistic children who are exposed to MMR is closer to the mean immunization age than in children who are not exposed to MMR, 3) regression in the development of children with autism has become more common in MMR-vaccinated children, 4) the age of onset for autistic children with regression clusters around the MMR immunization date and is different from that of autistic children without regression, 5) children with regressive autism have distinct symptom and severity profiles, and 6) regressive autism is associated with gastrointestinal symptoms and/or inflammatory bowel disorder. METHODS: Three samples were used. Epidemiologic data on 96 children (95 immunized with MMR at a median age of 13.5 months) who were born between 1992 and 1995 and had a pervasive developmental disorder diagnosis as reported in a recent UK survey (post-MMR sample) were compared with data from 2 previous clinical samples (1 pre-MMR [n = 98] and 1 post-MMR [n = 68]) of autistic patients. All patients were assessed with the standardized Autism Diagnostic Interview (ADI), allowing rigorous comparison of age at first parental concerns and rates of regression across samples. Reliability was excellent on ADI scores, age of parental concern, and developmental regression. Furthermore, data on bowel symptoms and disorders were available in the epidemiologic survey from both pediatric and parental sources, and immunization dates were obtained from computerized records. RESULTS: The prevalence of childhood disintegrative disorder was 0.6/10 000 (95% confidence interval: 0.02-3.6/10 000); this very low rate is consistent with previous estimates and is not suggestive of an increased frequency of this form of pervasive developmental disorder in samples of children who are immunized with MMR. There was no difference in the mean age at first parental concern between the 2 samples exposed to MMR (19.3 and 19.2 months) and the pre-MMR sample (19.5 months). Thus, MMR immunization was not associated with a shift toward an earlier age for first parental concerns. Similarly, the rate of developmental regression reported in the post-MMR sample (15.6%) was not different from that in the pre-MMR sample (18.4%); therefore, there was no suggestion that regression in the developmental course of autism had increased in frequency since MMR was introduced. In the epidemiologic sample, the subset of autistic children with regression had no other developmental or clinical characteristics, which would have argued for a specific, etiologically distinct phenotype. Parents of autistic children with developmental regression detected the first symptoms at a very similar age (19.8 months) to those of autistic children without regression (19.3 months). Moreover, the mean intervals from MMR immunization to parental recognition of autistic symptoms were comparable in autistic children with or without regression (248 vs 272 days; not significant). In the epidemiologic sample, gastrointestinal symptoms were reported in 18.8% of children. Constipation was the most common symptom (9.4%), and no inflammatory bowel disorder was reported. Furthermore, there was no association between developmental regression and gastrointestinal symptoms (odds ratio: 0.63; 95% confidence interval: 0.06-3.2; not significant), and only 2.1% of the sample experienced both problems, a rate that did not exceed chance expectations. CONCLUSIONS: No evidence was found to support a distinct syndrome of MMR-induced autism or of "autistic enterocolitis." These results add to the recent accumulation of large-scale epidemiologic studies that all failed to support an association between MMR and autism at population level. When combined, the current findings do not argue for changes in current immunization programs and recommendations.

Age of Onset↗

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↗

PubMed2006

Selective serotonin reuptake inhibitors in autism: a review of efficacy and tolerability.

BACKGROUND: Awareness of the impact and prevalence of autism spectrum disorders has significantly increased in recent years. Given the dearth of reliable interventions, there is great interest in demonstrating efficacy of the various treatment options. A growing body of evidence links autism spectrum disorders to abnormalities in serotonin function, and the selective serotonin reuptake inhibitors (SSRIs) have been utilized to target various symptoms of the disorders. This article reviews the available data on the efficacy and tolerability of SSRIs in individuals with autism spectrum disorders. Objectives for future research in this area will also be suggested. DATA SOURCES AND STUDY SELECTION: The entire PubMed database including MEDLINE (1966-July 2005) was searched for English-language biomedical articles. Search terms included autism, autism spectrum disorder, citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, pervasive developmental disorder, selective serotonin reuptake inhibitors, and sertraline. All clinical trials evaluating treatment outcomes associated with the use of SSRIs in managing symptoms of autism that were identified in the search were reviewed. All randomized controlled trials and open-label trials were included in this review. Case reports and case series were excluded. DATA SYNTHESIS: We identified 3 randomized controlled trials and 10 open-label trials or retrospective chart reviews on the use of SSRIs in autism and autism spectrum disorders. The SSRIs that have been studied in autism spectrum disorders are citalopram, escitalopram, fluoxetine, fluvoxamine, and sertraline. Most studies demonstrate significant improvement in global functioning and in symptoms associated with anxiety and repetitive behaviors. While side effects were generally considered to be mild, increased activation and agitation occurred in some subjects. CONCLUSIONS: Although SSRIs may demonstrate therapeutic benefit in autism spectrum disorders, methodological weaknesses of many of the clinical trials suggest the need for additional randomized controlled trials. Furthermore, given the increased awareness of the dangers associated with SSRI-induced activation and agitation, the presence of these side effects in the autistic population warrants closer attention to dosage, titration, and subject selection issues.

Adolescent↗

PubMed1998

The puzzle of autism: an ophthalmologic contribution.

PURPOSE: A previous study of 86 thalidomide-affected subjects with ophthalmic manifestations revealed the unexpected finding of autism in 4 of the 5 severely retarded individuals. The subjects had anomalies associated with an early gestational effect of thalidomide, including facial nerve palsy and incomitant strabismus. Because autism has been observed in a few cases of Möbius sequence (Möbius syndrome), a condition characterized by involvement of the sixth and seventh cranial nerves, the similarity to early thalidomide embryopathy suggested a relation between cranial nerve involvement and autism. The present study was undertaken to further evaluate the association of autism with patients manifesting findings of Möbius syndrome. METHODS: A prospective study of 25 Swedish patients with Möbius sequence was conducted. The patients had a complete multidisciplinary evaluation, including ophthalmologic and psychiatric examinations and standard testing for autism. Findings associated with autism were compared with the ocular and systemic anomalies of the 4 thalidomide-affected subjects. RESULTS: In the Möbius group 6 patients had autism, achieving the criteria for autism according to all the diagnostic manuals that were used. One patient showed autistic-like conditions meeting fewer numbers of the criteria. A few were too young to be meeting evaluated. Incomitant strabismus ranging from primary abduction defects alone to a horizontal gaze paresis pattern was noted in these patients, in addition to characteristic findings of seventh nerve paresis. Aberrant lacrimation was observed in many cases, especially often associated with autism. CONCLUSION: The common group of anomalies noted in both cases of thalidomide embryopathy and Möbius sequence suggests that brain-stem damage probably early in embryogenesis can sometimes be associated with autism.

Abnormalities, Drug-Induced↗

PubMed1999

Autism spectrum disorders at 20 and 42 months of age: stability of clinical and ADI-R diagnosis.

The association between, and stability of, clinical diagnosis and diagnosis derived from the Autism Diagnostic Interview-Revised (ADI-R; Lord, Rutter, & Le Couteur, 1994) was examined in a sample of prospectively identified children with childhood autism and other pervasive developmental disorders assessed at the age of 20 months and 42 months. Clinical diagnosis of autism was stable, with all children diagnosed with childhood autism at age 20 months receiving a diagnosis of childhood autism or a related pervasive developmental disorder (PDD) at age 42 months. Clinical diagnosis of childhood autism was also reasonably sensitive, with all children who went on to receive a clinical diagnosis of childhood autism at 42 months being identified as having autism or PDD at 20 months. However, clinical diagnosis for PDD and Asperger's syndrome lacked sensitivity at 20 months, with several children who subsequently received these diagnoses at 42 months receiving diagnoses of language disorder or general developmental delay, as well as in two cases being considered clinically normal, at the earlier timepoint. The ADI-R was found to have good specificity but poor sensitivity at detecting childhood autism at 20 months; however, the stability of diagnosis from 20 to 42 months was good. In addition, the ADI-R at age 20 months was not sensitive to the detection of related PDDs or Asperger's syndrome. The continuity and discontinuity between behavioural abnormalities identified at both timepoints in the three domains of impairment in autism was examined, both in children who met final clinical criteria for an autistic spectrum disorder, and for children with language disorder who did not, as well as for a small sample of typically developing children.

Autistic Disorder↗

PubMed2000

Story-telling ability in children with autism or Asperger syndrome: a window into the imagination.

BACKGROUND: Autism spectrum conditions are diagnosed on the basis of impaired imagination. The present study used a totally free story-telling method to assess if narratives produced by children with autism or Asperger Syndrome (AS) contained fewer imaginative events. METHOD: In Condition 1, children were offered an imaginary theme and asked to elaborate a story. In Condition 2, they were offered a reality-based theme with the same instructions. Comparison groups included 13 children with autism, 14 children with AS, 15 children with moderate learning difficulties (MLD), and 14 normally developing children. The non-autistic controls had a verbal mental age (VMA) either equivalent or lower than the autism and AS groups. RESULTS: Both the children with autism and AS were less likely to introduce imaginary elements into their stories in Condition 2, though the children with AS were more able to produce imaginative narratives than children with autism in Condition 1. CONCLUSIONS: This study provides experimental evidence for imaginative impairments in story-telling in children with autism spectrum conditions. These are discussed in terms of two cognitive theories: executive dysfunction and theory of mind. LIMITATIONS: In this study it was not possible to match the children with autism and AS with each other on VMA, as the children with autism were not as high-functioning. Future research could examine VMA matched groups of autism and AS.

Asperger Syndrome↗

PubMed2024

Convergence on CaMK4: A Key Modulator of Autism-Associated Signaling Pathways in Neurons.

Although the precise underlying cause(s) of autism spectrum disorder remain unclear, more than 1000 rare genetic variations are associated with the condition. For many people living with profound autism, this genetic heterogeneity has impeded the identification of common biological targets for therapy development for core and comorbid traits that include significant impairments in social communication and repetitive and restricted behaviors. A substantial number of genes associated with autism encode proteins involved in signal transduction and synaptic transmission that are critical for brain development and function. CAMK4 is an emerging risk gene for autism spectrum disorder that encodes the CaMK4 (calcium/calmodulin-dependent protein kinase 4) enzyme. CaMK4 is a key component of a Ca2+-activated signaling pathway that regulates neurodevelopment and synaptic plasticity. In this review, we discuss 3 genetic variants of CAMK4 found in individuals with hyperkinetic movement disorder and comorbid neurological symptoms including autism spectrum disorder that are likely pathogenic with monogenic effect. We also comment on 4 other genetic variations in CAMK4 that show associations with autism spectrum disorder, as well as 12 examples of autism-associated variations in other genes that impact CaMK4 signaling pathways. Finally, we highlight 3 environmental risk factors that impact CaMK4 signaling based on studies of preclinical models of autism and/or clinical cohorts. Overall, we review molecular, genetic, physiological, and environmental evidence that suggest that defects in the CaMK4 signaling pathway may play an important role in a common autism pathogenesis network across numerous patient groups, and we propose CaMK4 as a potential therapeutic target.

Humans↗

PubMed2003

Analysis of prevalence trends of autism spectrum disorder in Minnesota.

BACKGROUND: Alarming increases in the prevalence of autism spectrum disorder have been reported recently in the United States and Europe. OBJECTIVES: To quantify and characterize prevalence trends over time in autism spectrum disorder in Minnesota. METHODS: We conducted an age-period-birth cohort analysis of special educational disability data from the Minnesota Department of Children, Families & Learning from the 1981-1982 through the 2001-2002 school years. RESULTS: Prevalence rates of autism spectrum disorder rose substantially over time within single-age groups and increased from year to year within birth cohorts. Autism spectrum disorder prevalence among children aged 6 to 11 years increased from 3 per 10 000 in 1991-1992 to 52 per 10 000 in 2001-2002. All other special educational disability categories also increased during this period, except for mild mental handicap, which decreased slightly from 24 per 10 000 to 23 per 10 000. We found that federal and state administrative changes favoring identification of autism spectrum disorders corresponded in time with the increasing rates. CONCLUSIONS: We observed dramatic increases in the prevalence of autism spectrum disorder as a primary special educational disability starting in the 1991-1992 school year, and the trends show no sign of abatement. We found no corresponding decrease in any special educational disability category to suggest diagnostic substitution as an explanation for the autism trends in Minnesota. We could not assess changes in actual disease incidence with these data, but federal and state administrative changes in policy and law favoring better identification and reporting of autism are likely contributing factors to the prevalence increases and may imply that autism spectrum disorder has been underdiagnosed in the past.

Adolescent↗

PubMed2005

Magnetic resonance imaging and head circumference study of brain size in autism: birth through age 2 years.

CONTEXT: While the neuroanatomical basis of autism is not yet known, evidence suggests that brain enlargement may be characteristic of this disorder. Inferences about the timing of brain enlargement have recently come from studies of head circumference (HC). OBJECTIVES: To examine brain volume and HC in individuals with autism as compared with control individuals. DESIGN: A cross-sectional study of brain volume was conducted at the first time point in an ongoing longitudinal magnetic resonance imaging study of brain development in autism. Retrospective longitudinal HC measurements were gathered from medical records on a larger sample of individuals with autism and local control individuals. SETTING: Clinical research center. PARTICIPANTS: The magnetic resonance imaging study included 51 children with autism and 25 control children between 18 and 35 months of age (the latter included both developmentally delayed and typically developing children). Retrospective, longitudinal HC data were examined from birth to age 3 years in 113 children with autism and 189 local control children. MAIN OUTCOME MEASURES: Cerebral cortical (including cortical lobes) and cerebellar gray and white matter magnetic resonance imaging brain volumes as well as retrospective HC data from medical records were studied. RESULTS: Significant enlargement was detected in cerebral cortical volumes but not cerebellar volumes in individuals with autism. Enlargement was present in both white and gray matter, and it was generalized throughout the cerebral cortex. Head circumference appears normal at birth, with a significantly increased rate of HC growth appearing to begin around 12 months of age. CONCLUSIONS: Generalized enlargement of gray and white matter cerebral volumes, but not cerebellar volumes, are present at 2 years of age in autism. Indirect evidence suggests that this increased rate of brain growth in autism may have its onset postnatally in the latter part of the first year of life.

Age Factors↗