ACE Publications

Our Center has published more than 170 research articles on the topic of autism in leading journals such as Science, New England Journal of Medicine, Proceedings of the National Academy of Sciences, and the Journal of the American Medical Association.

Our center publishes research findings that capitalize on a wide range of research techniques and span many topics in autism. For example, our research studies examine behavior using eye tracking technology, brain imaging using magnetic resonance imaging (MRI) and genetics.


Big Data Approaches to Decomensatory Heterogeneity Across the Autism Spectrum

Lombardo, M. V., Lai, M., & Baron-Cohen, S. (2019). Big data approaches to decomposing heterogeneity across the autism spectrum. Molecular Psychiatry. doi:10.1038/s41380-018-0321-0. PDF.


Autism is a diagnostic label based on behavior. While the diagnostic criteria attempt to maximize clinical consensus, it also masks a wide degree of heterogeneity between and within individuals at multiple levels of analysis. Understanding this multi-level heterogeneity is of high clinical and translational importance. Here we present organizing principles to frame research examining multi-level heterogeneity in autism. Theoretical concepts such as ‘spectrum’ or ‘autisms’ reflect non-mutually exclusive explanations regarding continuous/dimensional or categorical/qualitative variation between and within individuals. However, common practices of small sample size studies and case–control models are suboptimal for tackling heterogeneity. Big data are an important ingredient for furthering our understanding of heterogeneity in autism. In addition to being ‘feature-rich’, big data should be both ‘broad’ (i.e., large sample size) and ‘deep’ (i.e., multiple levels of data collected on the same individuals). These characteristics increase the likelihood that the study results are more generalizable and facilitate evaluation of the utility of different models of heterogeneity. A model’s utility can be measured by its ability to explain clinically or mechanistically important phenomena, and also by explaining how variability manifests across different levels of analysis. The directionality for explaining variability across levels can be bottom-up or top-down, and should include the importance of development for characterizing changes within individuals. While progress can be made with ‘supervised’ models built upon a priori or theoretically predicted distinctions or dimensions of importance, it will become increasingly important to complement such work with unsupervised data-driven discoveries that leverage unknown and multivariate distinctions within big data. A better understanding of how to model heterogeneity between autistic people will facilitate progress towards precision medicine for symptoms that cause suffering, and person-centered support.


The ASD Living Biology: From cell proliferation to clinical phenotype 

Courchesne, E., Pramparo, T., Gazestani, V. H., Lombardo, M. V., Pierce, K., & Lewis, N. E. (2018).The ASD Living Biology: From cell proliferation to clinical phenotype. Molecular Psychiatry, 24(1), 88-107. doi:10.1038/s41380-018-0056-y PDF.


Autism spectrum disorder (ASD) has captured the attention of scientists, clinicians and the lay public because of its uncertain origins and striking and unexplained clinical heterogeneity. Here we review genetic, genomic, cellular, postmortem, animal model, and cell model evidence that shows ASD begins in the womb. This evidence leads to a new theory that ASD is a multistage, progressive disorder of brain development, spanning nearly all of prenatal life. ASD can begin as early as the 1st and 2nd trimester with disruption of cell proliferation and differentiation. It continues with disruption of neural migration, laminar disorganization, altered neuron maturation and neurite outgrowth, disruption of synaptogenesis and reduced neural network functioning. Among the most commonly reported high-confidence ASD (hcASD) genes, 94% express during prenatal life and affect these fetal processes in neocortex, amygdala, hippocampus, striatum and cerebellum. A majority of hcASD genes are pleiotropic, and affect proliferation/differentiation and/or synapse development. Proliferation and subsequent fetal stages can also be disrupted by maternal immune activation in the 1st trimester. Commonly implicated pathways, PI3K/AKT and RAS/ERK, are also pleiotropic and affect multiple fetal processes from proliferation through synapse and neural functional development. In different ASD individuals, variation in how and when these pleiotropic pathways are dysregulated, will lead to different, even opposing effects, producing prenatal as well as later neural and clinical heterogeneity. Thus, the pathogenesis of ASD is not set at one point in time and does not reside in one process, but rather is a cascade of prenatal pathogenic processes in the vast majority of ASD toddlers. Despite this new knowledge and theory that ASD biology begins in the womb, current research methods have not provided individualized information: What are the fetal processes and early-age molecular and cellular differences that underlie ASD in each individual child? Without such individualized knowledge, rapid advances in biological-based diagnostic, prognostic, and precision medicine treatments cannot occur. Missing, therefore, is what we call ASD Living Biology. This is a conceptual and paradigm shift towards a focus on the abnormal prenatal processes underlying ASD within each living individual. The concept emphasizes the specific need for foundational knowledge of a living child's development from abnormal prenatal beginnings to early clinical stages. The ASD Living Biology paradigm seeks this knowledge by linking genetic and in vitro prenatal molecular, cellular and neural measurements with in vivo post-natal molecular, neural and clinical presentation and progression in each ASD child. We review the first such study, which confirms the multistage fetal nature of ASD and provides the first in vitro fetal-stage explanation for in vivo early brain overgrowth. Within-child ASD Living Biology is a novel research concept we coin here that advocates the integration of in vitro prenatal and in vivo early post-natal information to generate individualized and group-level explanations, clinically useful prognoses, and precision medicine approaches that are truly beneficial for the individual infant and toddler with ASD.

The Geometric Preference Subtype in ASD: Identifying a Consistent, Early-Emerging Phenomenon Through Eye Tracking

Moore, A., Wozniak, M., Yousef, A., Barnes, C. C., Cha, D., Courchesne, E., & Pierce, K. (2018). The geometric preference subtype in ASD: identifying a consistent, early-emerging phenomenon through eye tracking. Molecular Autism, 9, 19. PMID: 29581878. PDF.


BACKGROUND:The wide range of ability and disability in ASD creates a need for tools that parse the phenotypic heterogeneity into meaningful subtypes. Using eye tracking, our past studies revealed that when presented with social and geometric images, a subset of ASD toddlers preferred viewing geometric images, and these toddlers also had greater symptom severity than ASD toddlers with greater social attention. This study tests whether this "GeoPref test" effect would generalize across different social stimuli.

METHODS:Two hundred and twenty-seven toddlers (76 ASD) watched a 90-s video, the Complex Social GeoPref test, of dynamic geometric images paired with social images of children interacting and moving. Proportion of visual fixation time and number of saccades per second to both images were calculated. To allow for cross-paradigm comparisons, a subset of 126 toddlers also participated in the original GeoPref test. Measures of cognitive and social functioning (MSEL, ADOS, VABS) were collected and related to eye tracking data. To examine utility as a diagnostic indicator to detect ASD toddlers, validation statistics (e.g., sensitivity, specificity, ROC, AUC) were calculated for the Complex Social GeoPref test alone and when combined with the original GeoPref test. 

RESULTS: ASD toddlers spent a significantly greater amount of time viewing geometric images than any other diagnostic group. Fixation patterns from ASD toddlers who participated in both tests revealed a significant correlation, supporting the idea that these tests identify a phenotypically meaningful ASD subgroup. Combined use of both original and Complex Social GeoPref tests identified a subgroup of about 1 in 3 ASD toddlers from the "GeoPref" subtype (sensitivity 35%, specificity 94%, AUC 0.75.) Replicating our previous studies, more time looking at geometric images was associated with significantly greater ADOS symptom severity.

CONCLUSIONS: Regardless of the complexity of the social images used (low in the original GeoPref test vs high in the new Complex Social GeoPref test), eye tracking of toddlers can accurately identify a specific ASD "GeoPref" subtype with elevated symptom severity. The GeoPref tests are predictive of ASD at the individual subject level and thus potentially useful for various clinical applications (e.g., early identification, prognosis, or development of subtype-specific treatments).



Rethinking the Idea of Late Autism Spectrum Disorder Onset

Bacon, E. C., Courchesne, E., Barnes, C. C., Cha, D., Pence, S., Schreibman, L., Stahmer, A. & Pierce, K. (2017). Rethinking the idea of late autism spectrum disorder onset. Development and psychopathology, 1-17. PMID: 28803559.


A common theory of autism spectrum disorder (ASD) symptom onset includes toddlers who do not display symptoms until well after age 2, which are termed late-onset ASD cases. Objectives were to analyze differences in clinical phenotype between toddlers identified as ASD at initial evaluations (early diagnosed) versus those initially considered nonspectrum, then later identified as ASD (late diagnosed). Two hundred seventy-three toddlers recruited from the general population based on a failed developmental screening form or parent or physician concerns were followed longitudinally from 12 months and identified as early- and late-diagnosed cases of ASD, language delayed, or typically developing. Toddlers completed common standardized assessments and experimental eye-tracking and observational measures every 9-12 months until age 3. Longitudinal performance on standardized assessments and experimental tests from initial evaluations were compared. Delay in social communication skills was seen in both ASD groups at early-age initial assessment, including increased preference for nonsocial stimuli, increased stereotypic play, reduced exploration, and use of gestures. On standardized psychometric assessments, early-diagnosed toddlers showed more impairment initially while late-diagnosed toddlers showed a slowing in language acquisition. Similar social communication impairments were present at very early ages in both early-detected ASD and so-called late-onset ASD. Data indicate ASD is present whether detected or not by current methods, and development of more sensitive tools is needed.

Toddlers Later Diagnosed with Autism Exhibit Structural Abnormalities in Temporal, Frontal, and Occipital Corpus Callosum Fibers

Fingher, N., Dinstein, I., Ben-Shachar, M., Haar, S., Dale, A. M., Eyler, L., Pierce, K., Dale, A. & Courchesne, E. (2017). Toddlers later diagnosed with autism exhibit multiple structural abnormalities in temporal corpus callosum fibers. Cortex, 97, 291-305. PMID: 28202133.


Interhemispheric functional connectivity abnormalities are often reported in autism and it is thus not surprising that structural defects of the corpus callosum (CC) are consistently found using both traditional MRI and DTI techniques. Past DTI studies however, have subdivided the CC into 2 or 3 segments without regard for where fibers may project to within the cortex, thus placing limitations on our ability to understand the nature, timing and neurobehavioral impact of early CC abnormalities in autism. Leveraging a unique cohort of 97 toddlers (68 autism; 29 typical) we utilized a novel technique that identified seven CC tracts according to their cortical projections. Results revealed that younger (<2.5 years old), but not older toddlers with autism exhibited abnormally low mean, radial, and axial diffusivity values in the CC tracts connecting the occipital lobes and the temporal lobes. Fractional anisotropy and the cross sectional area of the temporal CC tract were significantly larger in young toddlers with autism. These findings indicate that water diffusion is more restricted and unidirectional in the temporal CC tract of young toddlers who develop autism. Such results may be explained by a potential overabundance of small caliber axons generated by excessive prenatal neural proliferation as proposed by previous genetic, animal model, and postmortem studies of autism. Furthermore, early diffusion measures in the temporal CC tract of the young toddlers were correlated with outcome measures of autism severity at later ages. These findings regarding the potential nature, timing, and location of early CC abnormalities in autism add to accumulating evidence, which suggests that altered inter-hemispheric connectivity, particularly across the temporal lobes, is a hallmark of the disorder.

Heirarchical Cortical Transcriptome Disorganization in Autism

Lombardo, M. V., Courchesne, E., Lewis, N. E., & Pramparo, T. (2017). Hierarchical cortical transcriptome disorganization in autism. Molecular autism, 8(1), 29. PMID: 28649314. PDF


BACKGROUND: Autism spectrum disorders (ASD) are etiologically heterogeneous and complex. Functional genomics work has begun to identify a diverse array of dysregulated transcriptomic programs (e.g., synaptic, immune, cell cycle, DNA damage, WNT signaling, cortical patterning and differentiation) potentially involved in ASD brain abnormalities during childhood and adulthood. However, it remains unclear whether such diverse dysregulated pathways are independent of each other or instead reflect coordinated hierarchical systems-level pathology.

METHODS: Two ASD cortical transcriptome datasets were re-analyzed using consensus weighted gene co-expression network analysis (WGCNA) to identify common co-expression modules across datasets. Linear mixed-effect models and Bayesian replication statistics were used to identify replicable differentially expressed modules. Eigengene network analysis was then utilized to identify between-group differences in how co-expression modules interact and cluster into hierarchical meta-modular organization. Protein-protein interaction analyses were also used to determine whether dysregulated co-expression modules show enhanced interactions. RESULTS: We find replicable evidence for 10 gene co-expression modules that are differentially expressed in ASD cortex. Rather than being independent non-interacting sources of pathology, these dysregulated co-expression modules work in synergy and physically interact at the protein level. These systems-level transcriptional signals are characterized by downregulation of synaptic processes coordinated with upregulation of immune/inflammation, response to other organism, catabolism, viral processes, translation, protein targeting and localization, cell proliferation, and vasculature development. Hierarchical organization of meta-modules (clusters of highly correlated modules) is also highly affected in ASD.

CONCLUSIONS: These findings highlight that dysregulation of the ASD cortical transcriptome is characterized by the dysregulation of multiple coordinated transcriptional programs producing synergistic systems-level effects that cannot be fully appreciated by studying the individual component biological processes in isolation.

Maternal Immune Activation Dysregulation of the Fetal Brain Transcriptome and Relevance to the Pathophysiology of Autism Spectrum Disorder

Lombardo, M. V., Moon, H. M., Su, J., Palmer, T. D., Courchesne, E., & Pramparo, T. (2017). Maternal immune activation dysregulation of the fetal brain transcriptome and relevance to the pathophysiology of autism spectrum disorder. Molecular psychiatry. PMID: 28322282.


Maternal immune activation (MIA) via infection during pregnancy is known to increase risk for autism spectrum disorder (ASD). However, it is unclear how MIA disrupts fetal brain gene expression in ways that may explain this increased risk. Here we examine how MIA dysregulates rat fetal brain gene expression (at a time point analogous to the end of the first trimester of human gestation) in ways relevant to ASD-associated pathophysiology. MIA downregulates expression of ASD-associated genes, with the largest enrichments in genes known to harbor rare highly penetrant mutations. MIA also downregulates expression of many genes also known to be persistently downregulated in the ASD cortex later in life and which are canonically known for roles in affecting prenatally late developmental processes at the synapse. Transcriptional and translational programs that are downstream targets of highly ASD-penetrant FMR1 and CHD8 genes are also heavily affected by MIA. MIA strongly upregulates expression of a large number of genes involved in translation initiation, cell cycle, DNA damage and proteolysis processes that affect multiple key neural developmental functions. Upregulation of translation initiation is common to and preserved in gene network structure with the ASD cortical transcriptome throughout life and has downstream impact on cell cycle processes. The cap-dependent translation initiation gene, EIF4E, is one of the most MIA-dysregulated of all ASD-associated genes and targeted network analyses demonstrate prominent MIA-induced transcriptional dysregulation of mTOR and EIF4E-dependent signaling. This dysregulation of translation initiation via alteration of the Tsc2–mTor–Eif4e axis was further validated across MIA rodent models. MIA may confer increased risk for ASD by dysregulating key aspects of fetal brain gene expression that are highly relevant to pathophysiology affecting ASD.


To Screen or Not to Screen for ASD Universally is Not the Question: Why the Task Force Got it Wrong

Pierce K, Courchesne E, Bacon E.  To Screen or Not to Screen for ASD Universally is Not the Question: Why the Task Force Got it Wrong. The Journal of pediatrics. 2016;176:182-194. doi:10.1016/j.jpeds.2016.06.004. PDF.


There is widespread agreement across the American Academy of Pediatrics (AAP), expert panels, parents, and autism advocacy organizations, as well as the US Department of Health and Human Services Interagency Autism Coordinating Committee that early identification and intervention for toddlers with autism spectrum disorder (ASD) is a high public health priority and that universal early screening in pediatric populations is an essential tool for early ASD risk detection. The AAP guidelines to implement universal early screening for autism1 as standard of care is one of the most positive and successful public health policies ever created for children affected by autism. Indeed, such a policy has led to the regular detection and treatment of autism by the second birthday in cities with systematic screening programs. Early screening by pediatricians is becoming commonplace in the US and is objectively successful. Studies show that using standardized screening tools is the most accurate approach to early at-risk autism detection, even compared with pediatrician judgment and surveillance. Private and public resources and research have together resulted in the development of early screening approaches that, when implemented, can detect ASD 2-3 years sooner than the national average of 4 years of age. Implementing ASD screening as standard-of-care is particularly important for children from low socioeconomic status and minority backgrounds who are consistently overlooked and underdetected and as a result, have a later age of first diagnosis and delayed access to services relative to other children. Early detection importantly allows for intervention to begin earlier, which is considered essential to achieving the best outcomes. Research suggests that individuals with positive outcomes, including gains in IQ, adaptive skills, and reduction in ASD core symptoms, as well as those with optimal outcomes who no longer meet criteria for ASD over time, are more likely to have been identified and treated before 3 years of age. In the midst of this major accomplishment and advance over the past when children with ASD commonly went undetected and untreated for years across childhood, the US Preventive Services Task Force (USPSTF) released its recommendations about early universal screening for ASD. Earlier this year, the USPSTF (referred to here as “Task Force”) released a report on ASD screening that stated: “Current evidence is insufficient to assess the balance of benefits and harms of screening for ASD in young children for whom no concerns of ASD have been raised by their parents or a clinician.” In essence, the Task Force failed to recommend universal screening for ASD in the general pediatric population because it claims there is insufficient evidence of its benefits (but later admits its “harms” are minimal).

Diffusion Tensor Imaging Provides Evidence of Possible Axonal Overconnectivity in Frontal Lobes in Autism Spectrum Disorder Toddlers

Solso, S., Xu, R., Proudfoot, J., Hagler, D. J., Campbell, K., Venkatraman, V., ... & Eyler, L. (2016). Diffusion tensor imaging provides evidence of possible axonal overconnectivity in frontal lobes in autism spectrum disorder toddlers. Biological psychiatry, 79(8), 676-684. PMID: 26300272. PDF.


Theories of brain abnormality in autism spectrum disorder (ASD) have focused on underconnectivity as an explanation for social, language, and behavioral deficits but are based mainly on studies of older autistic children and adults.

In 94 ASD and typical toddlers ages 1 to 4 years, we examined the microstructure (indexed by fractional anisotropy) and volume of axon pathways using in vivo diffusion tensor imaging of fronto-frontal, fronto-temporal, fronto-striatal, and fronto-amygdala axon pathways, as well as posterior contrast tracts. Differences between ASD and typical toddlers in the nature of the relationship of age to these measures were tested.

Frontal tracts in ASD toddlers displayed abnormal age-related changes with greater fractional anisotropy and volume than normal at younger ages but an overall slower than typical apparent rate of continued development across the span of years. Posterior cortical contrast tracts had few significant abnormalities.

Frontal fiber tracts displayed deviant early development and age-related changes that could underlie impaired brain functioning and impact social and communication behaviors in ASD.


journal cover Eye Tracking Reveals Abnormal Visual Preference for Geometric Images as an Early Biomarker of an Autism Spectrum Disorder Subtype Associated with Increased Symptom Severity

Pierce K, Marinero S, Hazin R, McKenna B, Barnes C, Malige A. Eye Tracking Reveals Abnormal Visual Preference for Geometric Images as an Early Biomarker of an Autism Spectrum Disorder Subtype Associated with Increased Symptom Severity. Biological Psychiatry. 2015 Apr 11. doi:                    10.1016/j.biopsych.2015.03.032. PDF.


Results of a study published  on April 11, 2015 in Biological Psychiatry by Karen Pierce and colleagues contained 444 subjects sampled from the general population and is the largest eye tracking study of ASD to date.  The study explores the question of eye gaze patterns as a valid biomarker of ASD and concludes that yes, eye tracking can identify a meaningful subgroup on the spectrum.

Data also shows that an individual toddler’s eye tracking profile can have prognostic value in that those with heightened visual attention towards dynamic geometric images tended to be more severely symptomatic.   This has implications regarding how we approach the diagnosis of ASD and potentially what treatments we prescribe. Specificity and positive predictive value of the “Geo Pref Test” were considerably high (98% and 90% respectively), making it a very strong biomarker finding.

The study does more than identify a robust biomarker of ASD, it, for the first time, opens the possibility that the early identification of ASD can move beyond purely clinical observation techniques and into more objective, biologically based approaches.

Prediction of Autism by translation and Immune/Inflammation Coexpressed Genes in Toddlers From Pediatric Community.

Pramparo T, Pierce K, Lombardo MV, et al. Prediction of Autism by Translation and Immune/Inflammation Coexpressed Genes in Toddlers From Pediatric Community Practices. 
JAMA Psychiatry. Published online March 04, 2015. doi:10.1001/jamapsychiatry.2014.300  PDF. 


The identification of genomic signatures that aid early identification of individuals at risk for autism spectrum disorder (ASD) in the toddler period remains a major challenge because of the genetic and phenotypic heterogeneity of the disorder. Generally, ASD is not diagnosed before the fourth to fifth birthday.

To apply a functional genomic approach to identify a biologically relevant signature with promising performance in the diagnostic classification of infants and toddlers with ASD.

Proof-of-principle study of leukocyte RNA expression levels from 2 independent cohorts of children aged 1 to 4 years (142 discovery participants and 73 replication participants) using Illumina microarrays. Coexpression analysis of differentially expressed genes between Discovery ASD and control toddlers were used to define gene modules and eigengenes used in a diagnostic classification analysis. Independent validation of the classifier performance was tested on the replication cohort. Pathway enrichment and protein-protein interaction analyses were used to confirm biological relevance of the functional networks in the classifier. Participant recruitment occurred in general pediatric clinics and community settings. Male infants and toddlers (age range, 1-4 years) were enrolled in the study. Recruitment criteria followed the 1-Year Well-Baby Check-Up Approach. Diagnostic judgment followed DSM-IV-TR and Autism Diagnostic Observation Schedule criteria for autism. Participants with ASD were compared with control groups composed of typically developing toddlers as well as toddlers with global developmental or language delay.

Logistic regression and receiver operating characteristic curve analysis were used in a classification test to establish the accuracy, specificity, and sensitivity of the module-based classifier.

Our signature of differentially coexpressed genes was enriched in translation and immune/inflammation functions and produced 83% accuracy. In an independent test with approximately half of the sample and a different microarray, the diagnostic classification of ASD vs control samples was 75% accurate. Consistent with its ASD specificity, our signature did not distinguish toddlers with global developmental or language delay from typically developing toddlers (62% accuracy).

This proof-of-principle study demonstrated that genomic biomarkers with very good sensitivity and specificity for boys with ASD in general pediatric settings can be identified. It also showed that a blood-based clinical test for at-risk male infants and toddlers could be refined and routinely implemented in pediatric diagnostic settings.

Different Functional Neural Substrates for Good and Poor Language Outcome in Autism.

Lombardo, M., Pierce, K., Eyler, L., Barnes, C, Ahrens-Barbeau, C., Solso, S., Campbell, K., & Courchesne, E. (2015). Different functional neural substrates for good and poor language outcome in autism. Neuron, 86(2), 567-577. PDF.


Autism (ASD) is vastly heterogeneous, particularly in early language development. While ASD language trajectories in the first years of life are highly unstable, by early childhood these trajectories stabilize and are predictive of longer-term outcome. Early neural substrates that predict/precede such outcomes are largely unknown, but could have considerable translational and clinical impact. Pre-diagnosis fMRI response to speech in ASD toddlers with relatively good language outcome was highly similar to non-ASD comparison groups and robustly recruited language-sensitive superior temporal cortices. In contrast, language-sensitive superior temporal cortices were hypoactive in ASD toddlers with poor language outcome. Brain-behavioral relationships were atypically reversed in ASD, and a multimodal combination of pre-diagnostic clinical behavioral measures and speech-related fMRI response showed the most promise as an ASD prognosis classifier. Thus, before ASD diagnoses and outcome become clinically clear, distinct functional neuroimaging phenotypes are already present that can shed insight on an ASD toddler’s later outcome.



PubMed ArticleMeasuring Outcomes in an Early Intervention Program for Young Children with Autism Spectrum Disorder:  Use of a Curriculum-Based Assessment.

Bacon, L., Dufek, S., Schreibman, L. Stahmer, A., Pierce, K. and Courchesne, E. (2014). Measuring Outcomes in an Early Intervention Program for Young Children with Autism Spectrum Disorder: Use of a Curriculum-Based Assessment. Autism Research and Treatment.  PMID: 24711926, PMCID: PMC3966353. PDF.


Measuring progress of children with autism spectrum disorder (ASD) during intervention programs is a challenge faced by researchers and clinicians. Typically, standardized assessments of child development are used within research settings to measure the effects of early intervention programs. However, the use of standardized assessments is not without limitations, including lack of sensitivity of some assessments to measure small or slow progress, testing constraints that may affect the child's performance, and the lack of information provided by the assessments that can be used to guide treatment planning. The utility of a curriculum-based assessment is discussed in comparison to the use of standardized assessments to measure child functioning and progress throughout an early intervention program for toddlers with risk for ASD. Scores derived from the curriculum-based assessment were positively correlated with standardized assessments, captured progress masked by standardized assessments, and early scores were predictive of later outcomes. These results support the use of a curriculum-based assessment as an additional and appropriate method for measuring child progress in an early intervention program. Further benefits of the use of curriculum-based measures for use within community settings are discussed.


NewEngland JM logo Patches of Disorganization in the Neocortex of Children with Autism

Rich Stoner, Maggie L. Chow, Maureen P. Boyle, Susan M. Sunkin, Peter R. Mouton, Subhojit Roy, Anthony Wynshaw-Boris, Sophia A. Colamarino, Ed S. Lein, and Eric Courchesne. Patches of Disorganization in the Neocortex of Children with  Autism.N  Engl J Med. 2014 Mar 27; 370:1209-19. DOI: 10.1056/NEJMoa1307491. PDF.



Autism involves early brain overgrowth and dysfunction, which is most strongly evident in the prefrontal cortex. As assessed on pathological analysis, an excess of neurons in the prefrontal cortex among children with autism signals a disturbance in prenatal development and may be concomitant with abnormal cell type and laminar development.

To systematically examine neocortical architecture during the early years after the onset of autism, we used RNA in situ hybridization with a panel of layer- and cell-type–specific molecular markers to phenotype cortical microstructure. We assayed markers for neurons and glia, along with genes that have been implicated in the risk of autism, in prefrontal, temporal, and occipital neocortical tissue from postmortem samples obtained from children with autism and unaffected children between the ages of 2 and 15 years.

We observed focal patches of abnormal laminar cytoarchitecture and cortical disorganization of neurons, but not glia, in prefrontal and temporal cortical tissue from 10 of 11 children with autism and from 1 of 11 unaffected children. We observed heterogeneity between cases with respect to cell types that were most abnormal in the patches and the layers that were most affected by the pathological features. No cortical layer was uniformly spared, with the clearest signs of abnormal expression in layers 4 and 5. Three-dimensional reconstruction of layer markers confirmed the focal geometry and size of patches.

In this small, explorative study, we found focal disruption of cortical laminar architecture in the cortexes of a majority of young children with autism. Our data support a probable dysregulation of layer formation and layer-specific neuronal differentiation at prenatal developmental stages. (Funded by the Simons Foundation and others.)


Blood-based Gene Expression Signatures of Infants and Toddlers with Autism

Glatt SJ, Tsuang MT, Winn M, Chandler SD, Collins M, Lopez L, Weinfeld M, Carter C, Schork N, Pierce K, Courchesne E. Blood-based gene expression signatures of infants and toddlers with autism. J Am Acad Child Adolesc Psychiatry. 2012 Sep;51(9):934-44.e2. doi: 10.1016/j.jaac.2012.07.007. Epub 2012 Aug 2. PDF. 

Abnormal microglial-neuronal spatial organization in the dorsolateral prefrontal cortex in autism

Morgan JT, Chana G, Abramson I, Semendeferi K, Courchesne E, Everall IP. Abnormal microglial-neuronal spatial organization in the dorsolateral prefrontal cortex in autism. Brain Res. 2012 May 25;1456:72-81. doi: 10.1016/j.brainres.2012.03.036. Epub 2012 Mar 23.

PLoS Genetics

Chow ML, Pramparo T, Winn ME, Barnes CC, Li HR, Weiss L, Fan JB, Murray S,    April C, Belinson H, Fu XD, Wynshaw-Boris A, Schork NJ, Courchesne E. Age-dependent brain gene expression and copy number anomalies in autism suggest distinct pathological processes at young versus mature ages. PLoS Genet. 2012;8(3):e1002592.doi: 10.1371/journal.pgen.1002592. Epub 2012 Mar 22.

Chow ML, Winn ME, Li HR, April C, Wynshaw-Boris A, Fan JB, Fu XD,           Courchesne E, Schork NJ. Preprocessing and Quality Control Strategies for Illumina DASL Assay-Based Brain Gene Expression Studies with Semi-Degraded Samples. Front Genet. 2012;3:11. doi: 10.3389/fgene.2012.00011.

Eyler LT, Pierce K, Courchesne E. A failure of left temporal cortex to specialize for language is an early emerging and fundamental property of autism. Brain. 2012 Mar;135(Pt 3):949-60. doi: 10.1093/brain/awr364. Epub 2012 Feb 20.


Courchesne E, Mouton PR, Calhoun ME, Semendeferi K, Ahrens-Barbeau C, Hallet MJ, Barnes CC, Pierce K. Neuron number and size in prefrontal cortex of children with autism. JAMA. 2011 Nov 9;306(18):2001-10. PubMed PMID: 22068992.

Chow ML, Li HR, Winn ME, April C, Barnes CC, Wynshaw-Boris A, Fan JB, Fu XD, Courchesne E, Schork NJ. Genome-wide expression assay comparison across frozen and fixed postmortem brain tissue samples. BMC Genomics. 2011 Sep 10;12:449. PubMed PMID: 21906392; PubMed Central PMCID: PMC3179967.

Pierce, K., Carter, C., Weinfeld, M., Desmond, J., Hazin, R., Bjork, R., Gallagher, N. Detecting, studying, and treating autism early: the one-year well-baby check-up approach. Journal of Pediatrics, 158:5, 2011.

Pierce, K., Conant, D., Hazin, R., Desmond, J., & Stoner, R. A preference for geometric patterns early in life as a risk factor for autism. Archives of General Psychiatry. 68(1):101-9, 2011.

Courchesne, E., Campbell, K., Solso, S. Brain growth across the life span in autism: Age-specific changes in anatomical pathology. Brain Research, 1380:138-45, 2011

Delahanty, R.J., Kang, J.Q., Brune, C.W., Kistner, E.O., Courchesne, E., Cox, N.J., Cook, E.H. Jr, Macdonald, R.L., Sutcliffe, J.S. Maternal transmission of a rare GABRB3 signal peptide variant is associated with autism. Molecular Psychiatry. 16(1):86-96, 2011

Pierce, K. Early functional brain development in autism and the promise of sleep fMRI. Brain Research, 1380:162-74, 2011


Morgan, J.T., Chana, G., Pardo, C.A., Achim, C., Semendeferi, K., Buckwalter, J., Courchesne, E., Everall, I.P. Microglial Activation and Increased Microglial Density Observed in the Dorsolateral Prefrontal Cortex in Autism. Biological Psychiatry, 15;68(4):368-376, 2010.

Schumann, C.M., Bloss, C.S., Barnes, C.C., Wideman, G.M., Carper, R.A., Akshoomoff, N., Pierce, K., Hagler, D., Schork, N., Lord, C., Courchesne, E. Longitudinal magnetic resonance imaging study of cortical development through early childhood in autism. Journal of Neuroscience, 30(12):4419-27, 2010.


Luyster, R., Gotham, K., Guthrie, W., Coffing, M., Petrak, R., DiLavore, P., Pierce, K., Bishop, S., Esler, A., Hus, V., Richler, J., Risi, S., and Lord, C. Autism Diagnostic Observation Schedule Toddler Module: A new module of a standardized diagnostic measure for autism spectrum disorders. Journal Autism Developmental Disorders. 39(9)1305-1320, 2009.

Schumann, C., Barnes, C., Lord, C., Courchesne, E. Amygdala Enlargement in Toddlers with Autism Related to Severity of Social and Communication Impairments. Biological Psychiatry, 66(10):942-949, 2009,

Pierce, K., Glatt, S., Liptak, G.S. & McIntyre (2009). The Power and Promise of Identifying Autism Early: Insights From the Search for Clinical and Biological Markers, Annals of Clinical Psychiatry. 21(3):132-47, 2009.

Delahanty, R.J., Kang, J.Q., Brune, C.W., Kistner, E.O., Courchesne, E., Cox, N.J., Cook, E.H. Jr, Macdonald, R.L., Sutcliffe, J.S. Maternal transmission of a rare GABRB3 signal peptide variant is associated with autism. Molecular Psychiatry. 2009 Nov 24. [Epub ahead of print]


Morgan, J., Chana, G., Buckwalter, J., Courchesne, E., Everall, I. Increased Iba-1 positive microglial cell density in the autistic brain. Biological Psychiatry, 63(7):197S-197S, 2008

Pierce, K. & Redcay, E. (2008). Fusiform activity in children with an ASD is a matter of “who.” Biological Psychiatry, 64(7):552-60, 2008.

Redcay, E., Haist, F., Courchesne, E. Functional neuroimaging of speech perception during pivotal period in language acquisition. Developmental Science, 11(2):237-52, 2008.

Kim, S., Brune, C., Kistner, E., Christian, S., Courchesne, E., Cox, N., Cook, E. Transmission disequilibrium testing of the chromosome 15q11-q13 region in autism. American Journal of Medical Genetics Neuropsychiatry, 147B(7):1116-25, 2008.

Kleinhans, N., Muller, R., Cohen, D., Courchesne, E. Atypical functional lateralization of language in autism spectrum disorders. Brain Research, 1221:115-125, 2008

Redcay E, Courchesne E. Deviant functional magnetic resonance imaging patterns of brain activity to speech in 2-3 year old children with an autism spectrum disorder. Biological Psychiatry, 64(7):589-98, 2008.


Gaffrey, M.S., Kleinhans, N.M., Haist, F., Akshoomoff, N., Campbell, A., Courchesne, E., Muller, R.A. A typical participation of visual cortex during word processing in autism: An fMRI study of semantic decision. Neuropsychologia, 45(8):1672-84, 2007. Epub 2007 Jan 16.

Belmonte, M.K., Mazziotta, J.C., Minshew, N.J., Evans, A.C., Courchesne, E., Dager, S.R., Bookheimer, S.Y., Aylward, E.H., Amaral, D.G., Cantor, R.M., Chugani, D.C., Dale, A.M., Davatzikos, C., Gerig, G., Herbert, M.R., Lainhart, J.E., Murphy, D.G., Piven, J., Reiss, A.L., Schultz, R.T., Zeffiro, T.A., Levi-Pearl, S., Lajonchere, C., Colamarino, S.A. Offering to Share: How to Put Heads Together in Autism Neuroimaging. Journal of Autism Developmental Disorders, 38(1):2-13, 2008.

Kennedy, D.P., Semendeferi, K., Courchesne, E. No reduction of spindle neuron number in frontoinsular cortex in autism. Brain Cognition. 64(2):124-9, 2007. 2007 Mar 10; [Epub ahead of print]

Bloss, C.S., Courchesne, E. MRI Neuroanatomy in Young Girls With Autism: A Preliminary Study. Journal of the American Academy of Child and Adolescent Psychiatry, 46(4):515-523, 2007.

Redcay, E., Kennedy, D., Courchesne, E. fMRI during natural sleep as a method to study brain function during early childhood. Neuroimage, 38(4):696-707, 2007.

Brune, C.W., Kim, S.J., Hanna, G.L., Courchesne, E., Lord, C., Leventhal BL, et al. Family-Based Association Testing of OCD-associated SNPs of SLC1A1 in an autism sample. Autism Research 1(2):108-13, 2007.

Courchesne, E., Pierce, K., Schumann, C.M., Redcay, E., Buckwalter, J.A., Kennedy, D.P. and Morgan, J. Mapping early brain development in autism. Neuron, 56(2):399-413, 2007.


Kennedy, D.P., Redcay, E., Courchesne, E. Failing to deactivate: resting functional abnormalities in autism. Proceedings of the National Academy of Sciences U S A, 103(21):8275-80, 2006. Epub 2006 May 15.

DiCicco-Bloom, E., Lord, C., Zwaigenbaum, L., Courchesne, E., Dager, S.R., Schmitz, C., Schultz, R.T., Crawley, J., Young, L.J. The developmental neurobiology of autism spectrum disorder. Journal of Neuroscience, 26(26):6897-906, 2006. Review.

Buxhoeveden, D.P., Semendeferi, K., Buckwalter, J., Schenker, N., Switzer, R., Courchesne, E. Reduced minicolumns in the frontal cortex of patients with autism. Neuropathology and Applied Neurobiology, 32(5):483-91, 2006.

Akshoomoff, N., Farid, N., Courchesne, E., Haas, R. Abnormalities on the Neurological Examination and EEG in Young Children with Pervasive Developmental Disorders. Journal of Autism Developmental Disorders, 37(5):887-93, 2006.


Carper, R.A. and Courchesne, E. Localized enlargement of the frontal cortex in early autism. Biological Psychiatry, 57:126-133, 2005.

Haist, F., Adamo, M., Westerfield, M., Courchesne, E., Townsend, J. The functional neuroanatomy of spatial attention in autism spectrum disorder. Developmental Neuropsychology, 27(3):425-58, 2005.

Courchesne, E. Pierce, K. Why the frontal cortex in autism might be talking only to itself: local over-connectivity but long-distance disconnection. Current Opinion in Neurobiology, 15(2):225-30, 2005.

Teder-Salejarvi, W.A., Pierce, K.L., Courchesne, E., Hillyard, S.A. Auditory spatial localization and attention deficits in autistic adults. Brain Research and Cognitive Brain Research, 23(2-3):221-34, 2005.

Courchesne, E., Pierce, K. Brain overgrowth in autism during a critical time in development: implications for frontal pyramidal neuron and interneuron development and connectivity. International Journal of Developmental Neuroscience, 23(2-3):153-70, 2005.

Kemmotsu, N., Villabos, M.E., Gaffrey, M.S., Courchesne, E., Muller, R.A. Activity and functional connectivity of inferior frontal cortex associated with response conflict. Brain Research and Cognitive Brain Research, 24(2):335-42, 2005

Redcay, E., and Courchesne, E. When is the brain enlarged in autism? A meta-analysis of all brain size reports. Biol. Psychiatry,;58(1):1-9, 2005.

Courchesne, E., Redcay, E., Morgan, J.T., Kennedy, D.P. Autism at the beginning: Microstructural and growth abnormalities underlying the cognitive and behavioral phenotype of autism. Development and Psychopathology, 17(3):577-97, 2005. Review


Pierce, K., Haist, F., Sedaghat, F., & Courchesne, E., 2004. The brain response to personally familiar faces in autism: findings of fusiform activity and beyond. Brain, 2004 127(Pt 12):2703-16.

Akshoomoff, N., Lord, C., Lincoln, A.J., Courchesne, R.Y., Carper, R.A., Townsend, J., Courchesne, E. Outcome classification of preschool children with autism spectrum disorders using MRI brain measures. Journal of the American Academy of Child Adolescent Psychiatry, 43(3):349-357, 2004.

Allen, G., Muller, R-A., Courchesne, E. Cerebellar function in autism: fMRI activation during a simple motor task. Biological Psychiatry (2004), 56:269-78, 2004.

Makeig, S., Delorme, A, Westerfield, M., Jung, T.-P., Townsend, J., Courchesne, E., Sejnowski, T.J. Electroencephalographic brain dynamics following manually responded visual targets. Public Library of Science Biology. 2(6):E176. Epub June 15, 2004.

Courchesne, E., Redcay, E., Kennedy, D.P. The autistic brain: birth through adulthood. Current Opinion in Neurobiology, 17:489-96, 2004.

Belmonte, M.K., Cook, Jr., E.H., Anderson, G.M., Rubenstein, J.L.R., Greenough, W.T., Beckel-Mitchner, A., Courchesne, E., Boulanger, L.M., Powell, S.B., Levitt, P.R., Perry, E.K., Jiang, Y.H., DeLorey, T.M., Tierney, E. Autism as a disorder of neural information processing: directions for research and targets for therapy. Molecular Psychiatry, online publication 23 March 2004, 1-18.

Courchesne, E. Brain development in autism: Early overgrowth followed by premature arrest of growth. Mental Retardation and Developmental Disabilities Research Reviews, 10:106-11, 2004.


Muller, R-A., Kleinhans, N., Kemmotsu, N., Pierce, K., Courchesne, E. Abnormal variability and distribution of functional maps in autism: an fMRI study of visuomotor learning. American Journal of Psychiatry, 160(10):1847-62, 2003.

Allen, G. And Courchesne, E. Differential effects of developmental cerebellar abnormality on cognitive and motor functions in the cerebellum: An fMRI study of autism. American Journal of Psychiatry, 160(2):262-273, 2003.

Courchesne, E., Bartholomeusz, H.H., Karns, C.M., Townsend, J. MRI evidence of increased brain size in young children but not adults with autism. Biological Psychiatry, Accepted Pending Revision 4/4/03.

Courchesne, E., Carper, R., Akshoomoff, N. Evidence of brain overgrowth in the first year of life in autism. Journal of the American Medical Association, 290(3):337-344, 2003.

Muller, R.A., Kleinhans, N., Courchesne, E. Linguistic theory and neuroimaging evidence: an fMRI study of Broca’s area in lexical semantics. Neuropsychologia. 41(9):1199-207, 2003.


Makeig, S, Westerfield, M, Jung, T-P, Enghoff, S, Townsend, J, Courchesne, E, Sejnowski, TJ. Dynamic brain sources of visual evoked responses. Science, 295(5555), 690-694, 2002.

Carper, R.A., Moses, P., Tigue, Z.D., Courchesne, E. Cerebral lobes in autism: Early hyperplasia and abnormal age effects. NeuroImage, 16:1038-51, 2002.

Akshoomoff, N., Pierce, K., Courchesne, E. The neurobiological basis of autism from a developmental perspective. Development and Psychopathology, 14:613-634, 2002.

Bartholomeusz, H.H., Courchesne, E., and Karns, C. Relationship between head circumference and brain volume in healthy normal children and adults. Neuropediatrics, 33:239-41, 2002.

Kim, S.J., Herzing, L.B., Veenstra-VanderWeele, J., Lord, C., Courchesne, R., Leventhal, B.L., Ledbetter, D.H., Courchesne, E., Cook, Jr., E.H. Mutation screening and transmission disequilibrium study of ATP10C in autism. American Journal of Medical Genetics, 114(2):137-43, 2002.

Muller, R.A., Kleinhans, N., Pierce, K., Kemmotsu, N., Courchesne, E. Functional MRI of motor sequence acquisition: effects of learning stage and performance. Cognitive Brain Research, 14(2):277-93, 2002.

Jones, W., Hesselink, J., Courchesne, E., Duncan, T., Matsuda, K., Bellugi, U. Cerebellar abnormalities in infants and toddlers with Williams syndrome. Developmental Medicine and Child Neurology, 44(10):688-94, 2002.

Courchesne, E. Abnormal early brain development in autism. Molecular Psychiatry, 7:S21-S23, 2002.

Müller, R.-A., Pierce, K., Kleinhans, N., Kemmotsu, N. & Courchesne, E. Functional MRI of motor sequence learning: effects of learning stage and performance. Cognitive Brain Research, 14:277-293, 2002.

Kim, S-J., Young, L. J., Gonen, D, , Veenstra-Vanderweele, J., Courchesne, R.Y., Courchesne, E., Lord, C., Leventhal, B.L., Cook, Jr., E.H., Insel, T.R. Transmission disequilibrium testing of arginine vasopressin receptor 1A (AVPR1A) polymorphisms in Autism. Molecular Psychiatry, 7:502-507, 2002.

Veenstra-VanderWeele, J., Kim, S-J, Lord, C., Courchesne, R., Akshoomoff, N., Leventhal, B.L., Courchesne, E., and Cook, E.H. Transmission disequilibrium studies of the serotonin 5-HT2A receptor gene (HTR2A) in autism. American Journal of Medical Genetics (Neuropsychiatric Genetics) 114:277-283, 2002.

Bartholomeusz, H.H., Courchesne, E., Karns, C. Relationship between head circumference and brain volume in healthy normal children and adults. Neuropediatrics, 33:239-241, 2002.

Courchesne, E. and Pierce, K. Autism. In V.S. Ramachandran (Editor), Encyclopedia of the Human Brain, Volume 1, Academic Press, San Diego, CA, 2002.

Pierce, K. And Courchesne, E. Autism. Encyclopedia of Cognitive Science MacMillan, Hampshire UK, L. Nadel (editor), pp.278-283, 2002,


Pierce, K., Muller, R.A., Ambrose, J., Allen, G., Courchesne, E. Face processing occurs outside the fusiform ‘face area’ in autism: Evidence from functional MRI. Brain, 124:2059-2073, 2001.

Allen, G. And Courchesne, E. Attention function and dysfunction in autism. Frontiers in Bioscience, 6:d105-119, 2001.

Kim, S-J, Cox, N., Courchesne, R., Lord, C., Corsello, C., Akshoomoff, N., Guter, S., Leventhal, B.L., Courchesne, E., and Cook, E.H. Transmission disequilibrium mapping at the serotonin transporter gene (SLC6A4) region in autistic disorder. Molecular Psychiatry. 7:278-288, 2001.

Jung, T.P., Makeig, S., Westerfield, M., Townsend, J., Courchesne, E., Sejnowski, T.J. Analysis and visualization of single-trial event-related potentials. Human Brain Mapping, 14(3):166-85, 2001.

Courchesne, E., Karns, C., Davis, H.R., Ziccardi, R., Tigue, Z., Pierce, K., Moses, P., Chisum, H.J., Lord, C., Lincoln, A.J., Pizzo, S., Schreibman, L., Haas, R.H., Akshoomoff, N., Courchesne, R.Y. Unusual brain growth patterns in early life in patients with autistic disorder: An MRI study. Neurology, 57:245-254, 2001.

Muller, R-A., Pierce, K., Ambrose, J.B., Allen, G., Courchesne, E. Atypical patterns of cerebral motor activation in autism: a functional magnetic resonance study. Biological Psychiatry, 49:665-676, 2001.

Pierce, K., Courchesne, E. Evidence for a cerebellar role in reduced exploration and stereotyped behavior in autism. Biological Psychiatry, 49:655-664, 2001.

Saitoh, O., Karns, C., Courchesne, E. Development of the hippocampal formation from 2 to 42 years: MRI evidence of smaller area dentata in autism. Brain, 124:1317-1324, 2001.

Moses, P., Courchesne, E., Stiles, J., Trauner, D., Egaas, B., Edwards, E. Regional size reduction in the Human corpus callosum following pre- and perinatal brain injury. Cerebral Cortex, 10:1200-1210, 2000.

Townsend, J., Westerfield, M., Leaver, E., Makeig, S., Jung, T-P., Pierce, K., Courchesne, E. Event-related brain response abnormalities in autism: evidence for impaired cerebello-frontal spatial attention networks. Cognitive Brain Research, 11(1), 127-145. 2001.

Muller, R-A., Kleinhans, N., Courchesne, E. Broca’s area and the discrimination of frequency transitions: a functional MRI study. Brain and Language, 76:70-76, 2001.

Juul-Dam, N., Townsend, J., Courchesne, E. Prenatal, perinatal, and neonatal factors in autism, PDD-NOS, and the general population. Pediatrics, 107(4):e63, 2001.


Courchesne, E. And Pierce, K. An inside look at the neurobiology, etiology, and future research of autism. Advocate, pp.18-22, 2000.

Jung, T-P., Makeig, S., Westerfield, M., Townsend, J., Courchesne, E., Sejnowski, T.J. Removal of eye activity artifacts from visual event-related potentials in normal and clinical subjects. Clinical Neurophysiology, 111:1745-1758, 2000.

Courchesne, E., Chisum, H.J., Townsend, J., Cowles, A., Covington, J., Egaas, B., Harwood, M., Hinds, S., Press, G.A. Normal brain development and aging: Quantitative analysis at in vivo MR imaging in healthy volunteers. Radiology, 216:672-682, 2000.

Jung, T-P., Makeig, S., Westerfield, M., Townsend, J., Courchesne, E., and Sejnowski, T.J. Blind source separation of single-trial event-related potentials in a visual spatial attention task. IEEE Transactions on Biomedical Engineering. In press, 2000.

Carper, R.A. and Courchesne, E. Inverse correlation between frontal lobe and cerebellum sizes in children with autism. Brain, 123:836-844, 2000.

Graf, W.D., Marin-Garcia, J., Gao, H.G., Pizzo, S., Naviaux, R.K., Markusic, B.S., Barshop, B.A., Courchesne, E., Haas, R.H. Autism associated with the mtDNA G8363A tRNAlys mutation. Journal of Child Neurology, 15:357-361, 2000.

Pierce, K. and Courchesne, E. Exploring the neurofunctional organization of face processing in autism. Archives of General Psychiatry, 57:344-345, 2000.


Ciesielski, K.T., Courchesne, E. and Elmasian, R. Effects of focused selective attention tasks on event-related potentials in autistic and normal individuals. Electroencephalography and Clinical Neurophysiology, 75:207-220, 1990.

Lincoln, A.J., Courchesne, E., and Elmasian, R. Considerations for the study of event-related brain potentials and developmental psychopathology. In: A. Rothenberger (Ed.), Brain and Behavior in Child Psychiatry. Springer-Verlag: New York, pp. 16-33, 1990.

Grillon, C., Courchesne, E., Ameli, R., Geyer, M.A. and Braff, D.L. Increased distractibility in schizophrenic patients: Electrophysiologic and behavioral evidence. Archives of General Psychiatry, 47:171-179, 1990.

Grillon, C., Courchesne, E., Ameli, R., Elmasian, R. and Braff, D. Effects of rare non-target stimuli on brain electrophysiological activity and performance. International Journal of Psychophysiology, 9:257-267, 1990.

Press, G.A., Murakami, J.W., Courchesne, E., Grafe, M. and Hesselink, J.R. The cerebellum: 3. Anatomic-MR correlation in the coronal plane. American Journal of Roentgenology, 154(3):593-602, 1990 the coronal plane. American Journal of Neuroradiology, 11:41-50, 1990. (Also published in the March 1990 issue of American Journal of Roentgenology.)

Courchesne, E., Akshoomoff, N.A. and Townsend, J. Recent advances in autism. Current Opinions in Pediatrics, 2:685-693,1990.

Grillon, C., Ameli, R., Courchesne, E. and Braff, D.L. Effects of task relevance and attention on P3 in schizophrenic patients. Schizophrenia Research, 4:11-21, 1991.

Courchesne, E. Neuroanatomic imaging in autism. Pediatrics, 87:781-790, 1991.

Hsu, M., Yeung-Courchesne, R., Courchesne, E. and Press, G.A. Absence of magnetic resonance imaging evidence of pontine abnormality in infantile autism. Archives of Neurology, 48:1160-1163, 1991.

Epstein, C.J., Korenberg, J.R., Annerén, G., Antonarakis, S.E., Aymé, S., Courchesne, E., Epstein, L.B., Fowler, A., Groner, Y., Huret, J.L., Kemper, T.L., Lott, I.T., Lubin, B.H., Magenis, E., Opitz, J.M., Patterson, D., Priest, J.H., Pueschel, S.M., Rapoport, S.I., Sinet, P.-M., Tanzi, R.E. and de la Cruz, F. Protocols to establish genotype-phenotype correlations in Down syndrome. American Journal of Human Genetics, 49:207-235, 1991.

Courchesne, E. Autism. In: E. Peschel, R. Peschel, C.W. Howe and J.W. Howe (Eds.), Neurobiological Disorders in Children & Adolescents: A Guide to Research & Policy on Schizophrenia, Bipolar Disorder, Autism & More for Professionals & Families. Jossey-Bass: San Francisco, 1992.

Murakami, J.W., Courchesne, E., Haas, R.H., Press, G.A. and Yeung-Courchesne, R. Cerebellar and cerebral abnormalities in Rett syndrome: A quantitative MR analysis. American Journal of Roentgenology, 159:177-183, 1992.

Press, G.A. and Courchesne, E. Atlas of cerebellar hemispheres and vermis. In: L.A. Hyman and V.C. Hinck (Eds.), Clinical Brain Imaging: Normal Structure and Functional Anatomy. Mosby Yearbook Publishers Inc., pp. 251-279, 1992.

Press, G.A. and Courchesne, E. Cerebellar hemispheres and vermis. In: L.A. Hyman and V.C. Hinck (Eds.), Clinical Brain Imaging: Normal Structure and Functional Anatomy. Mosby Yearbook Publishers Inc., pp. 281-286, 1992.

Akshoomoff, N.A., Courchesne, E., Press, G.A. and Iragui, V. Contribution of the cerebellum to neuropsychological functioning: Evidence from a case of cerebellar degenerative disorder. Neuropsychologia, 30:315-328, 1992.

Akshoomoff, N.A. and Courchesne, E. A new role for the cerebellum in cognitive operations. Behavioral Neuroscience, 106:731-738, 1992.

Courchesne, E., Akshoomoff, N.A. and Townsend, J. Recent advances in autism. In: H. Naruse and E.M. Ornitz (Eds.), Neurobiology of Infantile Autism. Elsevier Science Publishers B.V., pp. 111-128, 1992.

Lincoln, A.J., Dickstein, P., Courchesne, E., Elmasian, R. and Tallal, P. Auditory processing abilities in non-retarded adolescents and young adults with developmental receptive language disorder and autism. Brain and Language, 43:613-622, 1992.

Clark, V.P., Courchesne, E. and Grafe, M. In vivo myeloarchitectonic analysis of human striate and extrastriate cortex using magnetic resonance imaging. Cerebral Cortex, 2:417-424, 1992.

Courchesne, E., Press, G.A. and Yeung-Courchesne, R. Parietal lobe abnormalities detected with MR in patients with infantile autism. American Journal of Roentgenology, 160:387-393, 1993.

Lincoln, A.J., Courchesne, E., Harms, L. and Allen, M. Contextual probability evaluation in autistic, receptive developmental language disorder, and control children: Event-related potential evidence. Journal of Autism and Developmental Disorders, 23:37-58, 1993.

Courchesne, E., Townsend, J.P., Akshoomoff, N.A., Yeung-Courchesne, R., Press, G.A., Murakami, J.W., Lincoln, A.J., James, H.E., Saitoh, O., Egaas, B., Haas, R.H., and Schreibman, L. A new finding: Impairment in shifting attention in autistic and cerebellar patients. In: S.H. Broman and J. Grafman (Eds.), Atypical Cognitive Deficits in Developmental Disorders: Implications for Brain Function. Lawrence Erlbaum: New Jersey, pp. 101-137, 1994.

Courchesne, E., Saitoh, O., Yeung-Courchesne, R., Press, G.A. Lincoln, A.J., Haas, R.H. and Schreibman, L. Abnormality of cerebellar vermian lobules VI and VII in patients with infantile autism: Identification of hypoplastic and hyperplastic subgroups with MR imaging. American Journal of Roentgenology, 162:123-130, 1994.

Courchesne, E., Townsend, J. and Saitoh, O. The brain in infantile autism: Posterior fossa structures are abnormal. Neurology, 44:214-223, 1994.

Courchesne, E., Yeung-Courchesne, R. and Egaas, B. Methodology in neuroanatomic measurement. Neurology, 44:203-208, 1994.

Courchesne, E., Saitoh, O., Townsend, J.P., Yeung-Courchesne, R.,Press, G.A., Lincoln, A.J., Haas, R.H. and Schreibman, L. Cerebellar hypoplasia and hyperplasia in infantile autism. The Lancet, 343:63-64, 1994.

Courchesne, E., Townsend, J. and Chase, C. Neurodevelopmental principles guide research on developmental psychopathologies. In: D. Cicchetti and D. Cohen (Eds.), A Manual of Developmental Psychopathology, New York: John Wiley, pp. 195-226, 1994.

Townsend, J. and Courchesne, E. Parietal damage and narrow “spotlight” spatial attention. Journal of Cognitive Neuroscience, 6:220-232, 1994.72.

Akshoomoff, N.A. and Courchesne, E. ERP evidence for a shifting attention deficit in patients with damage to the cerebellum. Journal of Cognitive Neuroscience, 6:388-399, 1994.

Courchesne, E., Chisum, H. and Townsend, J. Neural activity-dependent brain changes in development: Implications for psychopathology. Development and Psychopathology, 6:697-722, 1994.

Courchesne, E., Chisum, H. and Townsend, J. Neural activity-dependent brain changes in development: Implications for psychopathology. Development and Psychopathology, 6:697-722, 1994.

Courchesne, E., Townsend, J., Akshoomoff, N.A., Saitoh, O., Yeung-Courchesne, R., Lincoln, A.J., James, H.E., Haas, R.H., Schreibman, L. and Lau, L. Impairment in shifting attention in autistic and cerebellar patients. Behavioral Neuroscience, 108:848-865, 1994.

Saitoh, O., Courchesne, E., Egaas, B., Lincoln, A.J. and Schreibman, L. Cross-sectional area of the posterior hippocampus in autistic patients with cerebellar and corpus callosum abnormalities. Neurology, 45:317-324, 1995.

Courchesne, E., Akshoomoff, N.A., Townsend, J. and Saitoh, O. A model system for the study of attention and the cerebellum: Infantile autism. In: G. Karmos, M. Molnar, V. Csépe, I. Czigler, and J.E. Desmedt (Eds.), Perspectives of Event-Related Potentials Research (EEG Suppl. 44), Amsterdam: Elsevier Science B.V., pp. 315-325, 1995.

Egaas, B., Courchesne, E. and Saitoh, O. Reduced size of corpus callosum in autism. Archives of Neurology, 52:794-801, 1995.

Courchesne, E. New evidence of cerebellar and brainstem hypoplasia in autistic infants, children and adolescents: The MR imaging study by Hashimoto and colleagues. Journal of Autism and Developmental Disorders, 25:19-22, 1995.

Belmonte, M., Egaas, B., Townsend, J. and Courchesne, E. NMR intensity of corpus callosum differs with age but not with diagnosis of autism. NeuroReport, 6:1253-1256, 1995.

Lincoln, A.J., Courchesne, E., Harms, L. and Allen, M. Sensory modulation of auditory stimuli in children with autism and receptive developmental language disorder: Event-related brain potential evidence. Journal of Autism and Developmental Disorders, 25:521-539, 1995.

Courchesne, E. Infantile autism. Part 1: MR imaging abnormalities and their neurobehavioral correlates. International Pediatrics, 10:141-154, 1995.

Courchesne, E. Infantile autism. Part 2: A new neurodevelopmental model. International Pediatrics, 10:155-165, 1995.

Townsend, J., Courchesne, E. and Egaas, B. Slowed orienting of covert visual-spatial attention in autism: Specific deficits associated with cerebellar and parietal abnormality. Development and Psychopathology, 8:563-584, 1996.

Townsend, J., Singer Harris, N. and Courchesne, E. Visual attention abnormalities in autism: Delayed orienting to location. Journal of the International Neuropsychological Society, 2:541-550, 1996.

Haas, R.H., Townsend, J., Courchesne, E., Lincoln, A.J., Schreibman, L. and Yeung-Courchesne, R. Neurologic abnormalities in infantile autism. Journal of Child Neurology, 11:84-92, 1996.

Courchesne, E. Brain: early sensory experience on neural structural development. In: S. Parker (Ed. in Chief), 1997 McGraw-Hill Yearbook of Science and Technology, supplement to Encyclopedia of Science and Technology. McGraw-Hill Inc.: New York, pp. 57-58, 1997.

Courchesne, E. and Plante, E. Measurement and analysis issues in neurodevelopmental MR imaging. In: R.W. Thatcher, G.R. Lyon, J. Rumsey and N. Krasnegor (Eds.), Developmental Neuroimaging: Mapping the Development of Brain and Behavior. Academic Press: New York, pp. 43-65, 1997.

Courchesne, E. Brainstem, cerebellar and limbic neuroanatomical abnormalities in autism. Current Opinion in Neurobiology, 7:269-278, 1997.

Yeung-Courchesne, R. and Courchesne, E. From impasse to insight in autism research: From behavioral symptoms to biological explanations. Development and Psychopathology, 9:389-419, 1997.

Allen, G., Buxton, R.B., Wong, E.C. and Courchesne, E. Attentional activation of the cerebellum independent of motor involvement. Science, 275:1940-1943, 1997.

Courchesne, E. Prediction and preparation: Anticipatory role of the cerebellum in diverse neurobehavioral functions. Behavioral and Brain Sciences, 20:248-249, 1997.

Courchesne, E. and Allen, G. Prediction and preparation, fundamental functions of the cerebellum. Learning and Memory, 4:1-35, 1997.

Akshoomoff, N.A., Courchesne, E. and Townsend, J. Attention coordination and anticipatory control. In: J.D. Schmahmann (Ed.), The Cerebellum and Cognition, International Review of Neurobiology, Vol. 41. Academic Press: San Diego, pp. 575-598, 1997.

Cook, Jr., E.H., Lindgren, V., Leventhal, B.L., Courchesne, R., Lincoln, A., Shulman, C., Lord, C. and Courchesne, E. Autism or atypical autism in maternally but not paternally derived proximal 15q duplication. American Journal of Human Genetics, 60:928-934, 1997.

Cook, Jr., E.H., Courchesne, R., Lord, C., Cox , N., Yan, S., Lincoln, A., Haas, R., Courchesne, E. and Leventhal, B.L. Evidence of linkage between the serotonin transporter and autistic disorder. Molecular Psychiatry, 2:247-250, 1997.

Allen, G. and Courchesne, E. The cerebellum and non-motor function: Clinical implications. Molecular Psychiatry, 3:207-210, 1998.

Saitoh, O. and Courchesne, E. MRI study of the brain in autism. Psychiatry and Clinical Neurosciences, 52:S219-S222, 1997.

Lincoln, A., Courchesne, E., Allen, M., Hanson, E. and Ene, Michaela. Neurobiology of asperger syndrome: Seven case studies and quantitative magnetic resonance imaging findings. In: E. Schopler, G. Mesibov and Kunce (Eds.) Asperger Syndrome or High Functioning Autism? New York: Plenum Press, 1998.

Cook. Jr., E.H., Courchesne, R.Y., Cox, N.J., Lord, C., Gonen, D., Guter, S.J., Lincoln, A., Nix, K., Haas, R., Leventhal, B.L. and Courchesne, E. Linkage disequilibrium mapping with 15q11-13 markers in autistic disorder. The American Journal of Human Genetics, 62:1077-1083, 1998.

Courchesne, E. and Yeung-Courchesne, R, and Pierce, K. Biological and behavioral heterogeneity in autism: Role of pleiotropy and epigenesis. In: S.H. Broman and J.M. Fletcher (Eds.) The Changing Nervous System: Neurobehavioral Consequences of Early Brain Disorders. New York: Oxford University Press, pp. 292-338, 1999.

Müller, R.-A. and Courchesne, E. The duplicity of plasticity: A conceptual approach to the study of early lesions and developmental disorders. In: M. Ernst and J. Rumsey (Eds.) The Foundation and Future of Functional Neuroimaging in Child Psychiatry, New York: Cambridge University Press, 1998.

Müller, R.-A., Courchesne, E. and Allen, G. The cerebellum: So much more. Science, 282:879 880, 1998. (Letter)

Courchesne, E. An MRI study of autism: The cerebellum revisited. Neurology, 52:1106, 1999.

Harris, N.S., Courchesne, E., Townsend, J., Carper, R.A. and Lord, C. Neuroanatomic contributions to slowed orienting of attention in children with autism. Cognitive Brain Research, 8:61-71, 1999.

Courchesne, E., Müller, R.-A. and Saitoh, O. Brain weight in autism: Normal in the majority of cases, megalencephalic in rare cases. Neurology, 52:1057-1059. 1999.

Makeig, S., Westerfield, M., Jung, T-P, Covington, J., Townsend, J., Sejnowski, T. and Courchesne, E. Functionally independent components of late positive event-related potential during visual spatial attention. Journal of Neuroscience, 19(7), 2665-80, 1999.

Townsend, J., Courchesne, E., Covington, J., Westerfield, M., Harris, N.S., Lyden, P., Lowry, T.P. and Press, G.A. Spatial attention deficits in patients with acquired or developmental cerebellar abnormality. Journal of Neuroscience,19(13):5632-5643, 1999.

Jung, T-P, Makeig, S., Westerfield, M., Townsend, J., Courchesne, E., and Sejnowski, T.J. Analyzing and visualizing single-trial event-related potentials. Advances in Neural Information Processing Systems, 11:118-124, 1999.

Makeig, S., Westerfield, M., Townsend, J., Jung, T-P., Courchesne, E., and Sejnowski, T.J. Functionally independent components of early event-related potentials in a visual spatial attention task. Philosophical Transactions: Biological Sciences, 354:(1387):1135-1144, 1999.

Jung, T-P., Makeig, S., Westerfield, M., Townsend, J., Courchesne, E., and Sejnowski, T.J. Independent component analysis of single-trial event-related potentials. 1St Int’l Workshop on Independent Component Analysis and Signal Separation, 173-178, 1999.

Lassig, J.P., Vachirasomtoon, K., Hartzell, K., Leventhal, M., Courchesne, E., Courchesne, R., Lord, C., Leventhal, B.L., Cook, Jr., E.H. Physical mapping of the serotonin 5-HT7 receptor gene (HTR7) to chromosome 10 and pseudogene (HTR7P) to chromosome 12, and testing of linkage disequilibrium between HTR7 and autistic disorder. American Journal of Medical Genetics (Neuropsychiatric Genetics), 88:472-475, 1999.


Woods, D.L., Courchesne, E., Hillyard, S.A. and Galambos, R. Split-second recovery of the P3 component in multiple decision tasks. In: H.H. Kornhuber and L. Deecke (Eds.). Progress in Brain Research. Vol. 54: Motivation, Motor and Sensory Processes of the Brain. Elsevier/North-Holland Biomedical Press: Amsterdam, pp. 322-330, 1980.

Woods, D.L., Hillyard, S.A., Courchesne, E. and Galambos, R. Electrophysiological signs of split-second decision making. Science. 207:655-657, 1980.

Woods, D.L., Courchesne, E., Hillyard, S.A. and Galambos, R. Recovery cycles of event-related potentials in multipledetection tasks. Electroencephalography and Clinical Neurophysiology, 50:335-347, 1980.

Courchesne, E., Ganz, L. and Norcia, A.M. Event-related brain potentials to human faces in infants. Child Development, 52:804-811, 1981.

Courchesne, E. Cognitive components of the event-related brain potential: Changes associated with development. In: A.W.K. Gaillard and W. Ritter (Eds.), Tutorials in Event-Related Potential Research: Endogenous Components. North-Holland Publishing Co.: Amsterdam, pp. 329-344, 1983.

Kurtzberg, D., Vaughan, Jr., H.G., Courchesne, E., Friedman, D., Harter, M.R. and Putnam, L.E. Developmental aspects of event-related potentials. In: R. Karrer, J. Cohen and P. Tueting (Eds.), Brain and Information Event-related Potentials, Vol. 425. The New York Academy of Sciences: New York, pp. 300-318, 1984.

Courchesne, E., Kilman, B.A., Galambos, R. and Lincoln, A.L. Autism: Processing of novel auditory information assessed by event-related brain potentials. Electroencephalography and Clinical Neurophysiology. 59:238-248, 1984.

Courchesne, E. A critical review of the use of ERP’s for studying developmental psychopathologies. Center for Studies of Child and Adolescent Psychopathology, Clinical Research Branch, National Institutes of Mental Health, 1984.

Courchesne, E., Lincoln, A.J., Kilman, B.A. and Galambos, R. Event-related brain potential correlates of the processing of novel visual and auditory information in autism. Journal of Autism and Develop mental Disorders, 15:55-76, 1985.

Lincoln, A.J., Courchesne, E., Kilman, B.A. and Galambos R. Neuropsychological correlates of information-processing by children with Down syndrome. Journal of Mental Deficiency, 89:403-414, 1985.

Courchesne, E., Courchesne, R.Y., Hicks, G. and Lincoln, A.J. Functioning of the brain-stem auditory pathway in non-retarded autistic individuals. Electroencephalography and Clinical Neurophysiology, 61:491-501, 1985.

Woods, D.L. and Courchesne, E. The recovery functions of auditory event-related potentials during split-second discriminations. Electroencephalography and Clinical Neurophysiology, 65:304-15, 1986. Electroencephalography and Clinical Neurophysiology, 65:304-315, 1986.

Woods, D.L. and Courchesne, E. Event-related potentials during split-second auditory and visual decision making. In: W.C. McCallum, R. Zappoli and F. Denoth (Eds.), Cerebral Psychophysiology: Studies in Event-Related Potentials, (EEG Suppl. 39), 152-154, 1986.

Courchesne, E. A neurophysiological view of autism. In: E. Schopler and G.B. Mesibov (Eds.), Neurobiological Issues in Autism. Plenum Press: New York, pp. 285-324, 1987.

Courchesne, E., Elmasian, R. and Yeung-Courchesne, R. Electrophysiological correlates of cognitive processing: P3b and Nc, basic, clinical, and developmental research. In: A.M. Halliday, S.R. Butler and R. Paul (Eds.), A Textbook of Clinical Neurophysiology, John Wiley and Sons Ltd.: Sussex, pp. 645-676, 1987.

Courchesne, E., Hesselink, J.R., Jernigan, T.L. and Yeung-Courchesne, R. Abnormal neuroanatomy in a nonretarded person with autism: Unusual findings with magnetic resonance imaging. Archives of Neurology, 44:335-341, 1987.

Courchesne, E. and Yeung-Courchesne, R. Event-related brain potentials. In: M. Rutter, A. Hussain Tuma and I.S. Lann (Eds.), Assessment and Diagnosis in Child Psychopathology. Guilford Press: New York, pp. 264-299, 1987.

Woods, D.L. and Courchesne, E. Intersubject variability elucidates the cerebral generators and psychological correlates of ERPs. In: R. Johnson, Jr., J.W. Rohrbaugh and R. Parasuraman (Eds.), Current Trends in Event-Related Potential Research (EEG Suppl. 40) Elsevier Science Publishers B.V.: New York, pp. 293-299, 1987.

Ameli, R., Courchesne, E., Lincoln, A., Kaufman, A.S. and Grillon, C. Visual memory processes in high-functioning individuals with autism. Journal of Autism and Developmental Disorders, 18:601-615, 1988.

Adams, J., Courchesne, E., Elmasian, R. and Lincoln, A. Increased amplitude of the auditory P2 and P3b components in adolescents with developmental dysphasia. In: R. Johnson, Jr., R. Parasuraman and J.W. Rohrbaugh (Eds.), Current Trends in Event-Related Potential Research (EEG Suppl. 40). Elsevier Science Publishers B.V.: New York, pp. 577-583, 1987.

Lincoln, A.J., Courchesne, E., Kilman, B.A., Elmasian, R. and Allen, M. A study of intellectual abilities in high-functioning people with autism. Journal of Autism and Developmental Disorders, 18:505-524, 1988.

Courchesne, E. Physioanatomical considerations in Down syndrome. In: L. Nadel (Ed.), The Psychobiology of Down Syndrome. MIT Press: Cambridge, MA, pp. 291-313, 1988.

Lincoln, A.J., Courchesne, E., Elmasian, R. Hypothesis testing with principal components analysis: The dissociation of P3b and Nc. In: R. Johnson, Jr., J.W. Rohrbaugh and R. Parasuraman (Eds.), Current Trends in Event-Related Potential Research (EEG Suppl. 40) Elsevier Science Publishers B.V.: New York, pp. 211-219, 1987.

Courchesne, E. Cerebellar changes in autism. In: J. Swann and A. Messer (Eds.), Disorders of the Developing Nervous System: Changing Views on Their Origins, Diagnoses and Treatments. Alan R. Liss, Inc.: New York, pp. 93-109, 1988.

Courchesne, E., Yeung-Courchesne, R., Press, G.A., Hesselink, J.R. and Jernigan, T.L. Hypoplasia of cerebellar vermal lobules VI and VII in autism. The New England Journal of Medicine, 318:1349-1354, 1988.

Courchesne, E. Chronology of postnatal human brain development: Event-related potential, positron emission tomography, myelinogenesis, and synaptogenesis studies. In: J.W. Rohrbaugh, R. Parasuraman and R. Johnson (Eds.), Event-Related Brain Potentials: Basic Issues and Applications. Oxford Press: New York, pp. 210-241, 1990.

Courchesne, E. Neuroanatomical systems involved in infantile autism: The implications of cerebellar abnormalities. In: G. Dawson (Ed.), Autism: New Perspectives on Diagnosis, Nature and Treatment. The Guilford Press: New York, pp. 119-143, 1989.

Courchesne, E., Press, G.A., Murakami, J., Berthoty, D., Grafe, M., Wiley, C.A. and Hesselink, J.R. The cerebellum in sagittal plane-- Anatomic-MR correlation: 1. The vermis. American Journal of Neuroradiology, 10:659-665, 1989. (Also published in the October 1989 issue of American Journal of Roentgenology.)

Press, G.A., Murakami, J., Courchesne, E., Berthoty, D.P., Grafe, M., Wiley, C.A. and Hesselink, J.R. The cerebellum in sagittal plane--Anatomic-MR correlation: 2. The cerebellar hemispheres. American Journal of Neuroradiology, 10:667-676, 1989. (Also published in the October 1989 issue of American Journal of Roentgenology.)

Murakami, J.W., Courchesne, E., Press, G.A., Yeung-Courchesne, R. and Hesselink, J.R. Reduced cerebellar hemisphere size and its relationship to vermal hypoplasia in autism. Archives of Neurology, 46:689-694, 1989.

Courchesne, E., Lincoln, A.J., Yeung-Courchesne, R., Elmasian, R. and Grillon, C. Pathophysiologic findings in non-retarded autism and receptive developmental language disorder. Journal of Autism and Developmental Disorders, 19:1-17, 1989.

Grillon, C., Courchesne, E. and Akshoomoff, N. Brainstem and middle latency auditory evoked potentials in autism and developmental language disorder. Journal of Autism and Developmental Disorders, 19:255-269, 1989.

Akshoomoff, N., Courchesne, E., Yeung-Courchesne, R. and Costello, J. Brainstem auditory evoked potentials in receptive developmental language disorder. Brain and Language, 37:409-418, 1989.1970s

Courchesne, E. and Barlow, G.W. Effect of isolation on components of aggressive and other behavior in the hermit crab, Pagurus samuelis. Z. vergl. Physiologie. 75:32-48, 1971.

Courchesne, E., Hillyard, S.A. and Galambos, R. Stimulus novelty, task relevance and the visual evoked potential in man. Electroencephalography and Clinical Neurophysiology, 39:131-143, 1975.

Hillyard, S.A., Courchesne, E., Krausz, H.I. and Picton, T.W. Scalp topography of the P3 wave in different auditory decision tasks. In: W.C. McCallum and J.R. Knott (Eds.). The Responsive Brain. The Proceedings of the Third International Congress on Event-Related Slow Potentials of the Brain. John Wright and Sons Ltd.: Bristol, pp. 81-87, 1976.

Courchesne, E. Event-related brain potentials: Comparison between children and adults. Science. 197:589-592, 1977.

Courchesne, E., Hillyard, S.A. and Courchesne, R.Y. P3 waves to the discrimination of targets in homogeneous and heterogeneous stimulus sequences. Psychophysiology, 14:590-597, 1977.

Courchesne, E. Neurophysiological correlates of cognitive development: Changes in long-latency event-related potentials from childhood to adulthood. Electroencephalography and Clinical Neurophysiology, 45:468-482, 1978.

Courchesne, E. Changes in P3 waves in event repetition: Long-term effects on scalp distribution and amplitude. Electroencephalography and Clinical Neurophysiology, 45:754-766, 1978.

Courchesne, E., Courchesne, R.Y. and Hillyard, S.A. The effect of stimulus deviation on P3 waves to easily recognized stimuli. Neuropsychologia, 16:189-199, 1978.

Courchesne, E. From infancy to adulthood: The neurophysiological correlates of cognition. In: J.E. Desmedt (Ed.), Progress in Clinical Neurophysiology. Volume 6: Cognitive Components in Event-Related Cerebral Potentials. Karger Publishing: New York, pp. 224-242, 1979.

Campbell, K.B., Courchesne, E., Picton, T.W. and Squires, K.C. Evoked potential correlates of human information processing. Biological Psychology, 8:45-68, 1979.