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Thomas W. Frazier
Cleveland Clinic Children's Hospital Center for Pediatric Behavioral Health, Cleveland, OH, USA

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Journal article
Published: 01 September 2017 in International Journal of Bipolar Disorders
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Bipolar disorder (BD) is a common disorder with high reoccurrence rate in general population. It is critical to have objective biomarkers to identify BD patients at an individual level. Neurocognitive signatures including affective Go/No-go task and Cambridge Gambling task showed the potential to distinguish BD patients from health controls as well as identify individual siblings of BD patients. Moreover, these neurocognitive signatures showed the ability to be replicated at two independent cohorts which indicates the possibility for generalization. Future studies will examine the possibility of combining neurocognitive data with other biological data to develop more accurate signatures.

ACS Style

Mon-Ju Wu; Benson Mwangi; Ives Cavalcante Passos; Isabelle E. Bauer; Bo Cao; Thomas W. Frazier; Giovana B. Zunta-Soares; Jair C. Soares. Prediction of vulnerability to bipolar disorder using multivariate neurocognitive patterns: a pilot study. International Journal of Bipolar Disorders 2017, 5, 1 -7.

AMA Style

Mon-Ju Wu, Benson Mwangi, Ives Cavalcante Passos, Isabelle E. Bauer, Bo Cao, Thomas W. Frazier, Giovana B. Zunta-Soares, Jair C. Soares. Prediction of vulnerability to bipolar disorder using multivariate neurocognitive patterns: a pilot study. International Journal of Bipolar Disorders. 2017; 5 (1):1-7.

Chicago/Turabian Style

Mon-Ju Wu; Benson Mwangi; Ives Cavalcante Passos; Isabelle E. Bauer; Bo Cao; Thomas W. Frazier; Giovana B. Zunta-Soares; Jair C. Soares. 2017. "Prediction of vulnerability to bipolar disorder using multivariate neurocognitive patterns: a pilot study." International Journal of Bipolar Disorders 5, no. 1: 1-7.

Review
Published: 11 May 2017 in Journal of the American Academy of Child & Adolescent Psychiatry
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Objective Numerous studies have identified abnormal gaze in individuals with autism. However, only some findings have been replicated, the magnitude of effects is unclear, and the pattern of gaze differences across stimuli remains poorly understood. To address these gaps, a comprehensive meta-analysis of autism eye-tracking studies was conducted. Method PubMed and a manual search of 1,132 publications were used to identify studies comparing looking behavior to social and/or nonsocial stimuli between individuals with autism and controls. Sample characteristics, eye-tracking methods, stimulus features, and regions of interest (ROIs) were coded for each comparison within each study. Multivariate mixed-effects meta-regression analyses examined the impact of study methodology, stimulus features, and ROI on effect sizes derived from comparisons using gaze-fixation metrics. Results The search yielded 122 independent studies with 1,155 comparisons. Estimated effect sizes tended to be small to medium but varied substantially across stimuli and ROIs. Overall, nonsocial ROIs yielded larger effect sizes than social ROIs; however, eye and whole-face regions from stimuli with human interaction produced the largest effects (Hedges g = 0.47 and 0.50, respectively). Studies with weaker study designs or reporting yielded larger effects, but key effects remained significant and medium in size, even for high-rigor designs. Conclusion Individuals with autism show a reliable pattern of gaze abnormalities that suggests a basic problem with selecting socially relevant versus irrelevant information for attention and that persists across ages and worsens during perception of human interactions. Aggregation of gaze abnormalities across stimuli and ROIs could yield clinically useful risk assessment and quantitative, objective outcome measurements.

ACS Style

Thomas W. Frazier; Mark Strauss; Eric W. Klingemier; Emily E. Zetzer; Antonio Y. Hardan; Charis Eng; Eric Youngstrom. A Meta-Analysis of Gaze Differences to Social and Nonsocial Information Between Individuals With and Without Autism. Journal of the American Academy of Child & Adolescent Psychiatry 2017, 56, 546 -555.

AMA Style

Thomas W. Frazier, Mark Strauss, Eric W. Klingemier, Emily E. Zetzer, Antonio Y. Hardan, Charis Eng, Eric Youngstrom. A Meta-Analysis of Gaze Differences to Social and Nonsocial Information Between Individuals With and Without Autism. Journal of the American Academy of Child & Adolescent Psychiatry. 2017; 56 (7):546-555.

Chicago/Turabian Style

Thomas W. Frazier; Mark Strauss; Eric W. Klingemier; Emily E. Zetzer; Antonio Y. Hardan; Charis Eng; Eric Youngstrom. 2017. "A Meta-Analysis of Gaze Differences to Social and Nonsocial Information Between Individuals With and Without Autism." Journal of the American Academy of Child & Adolescent Psychiatry 56, no. 7: 546-555.

Journal article
Published: 27 December 2016 in Sensors
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This paper reviews the state-of-the-art in sensing technologies that are relevant for Autism Spectrum Disorder (ASD) screening and therapy. This disorder is characterized by difficulties in social communication, social interactions, and repetitive behaviors. It is diagnosed during the first three years of life. Early and intensive interventions have been shown to improve the developmental trajectory of the affected children. The earlier the diagnosis, the sooner the intervention therapy can begin, thus, making early diagnosis an important research goal. Technological innovations have tremendous potential to assist with early diagnosis and improve intervention programs. The need for careful and methodological evaluation of such emerging technologies becomes important in order to assist not only the therapists and clinicians in their selection of suitable tools, but to also guide the developers of the technologies in improving hardware and software. In this paper, we survey the literatures on sensing technologies for ASD and we categorize them into eye trackers, movement trackers, electrodermal activity monitors, tactile sensors, vocal prosody and speech detectors, and sleep quality assessment devices. We assess their effectiveness and study their limitations. We also examine the challenges faced by this growing field that need to be addressed before these technologies can perform up to their theoretical potential.

ACS Style

John-John Cabibihan; Hifza Javed; Mohammed Aldosari; Thomas W. Frazier; Haitham Elbashir. Sensing Technologies for Autism Spectrum Disorder Screening and Intervention. Sensors 2016, 17, 46 .

AMA Style

John-John Cabibihan, Hifza Javed, Mohammed Aldosari, Thomas W. Frazier, Haitham Elbashir. Sensing Technologies for Autism Spectrum Disorder Screening and Intervention. Sensors. 2016; 17 (12):46.

Chicago/Turabian Style

John-John Cabibihan; Hifza Javed; Mohammed Aldosari; Thomas W. Frazier; Haitham Elbashir. 2016. "Sensing Technologies for Autism Spectrum Disorder Screening and Intervention." Sensors 17, no. 12: 46.

Research article
Published: 08 July 2016 in Autism
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This study investigated the psychometric properties of the Child and Family Quality of Life scale, a measure of psychosocial quality of life in those with autism and related developmental disorders. Parents of 212 children suspected of autism spectrum disorder completed the Child and Family Quality of Life prior to a diagnostic evaluation. Results indicated that the Child and Family Quality of Life measured six unique quality-of-life constructs (child, family/caregiver, financial, external support, partner relationship, and coping), had good reliability across score ranges and exhibited expected patterns of convergent validity. Caregivers of autism spectrum disorder–affected children reported reduced family quality of life prior to the time of diagnosis relative to caregivers of children with other developmental disabilities. The Child and Family Quality of Life is a brief, reliable measure for assessing psychosocial quality of life in families affected by developmental disability. This study is the first to demonstrate impairments in family quality of life early in the developmental course of autism spectrum disorder, prior to formal diagnosis. In addition to traditional child-focused intervention strategies, families with autism spectrum disorder–affected children require early, broad intervention strategies that positively impact the whole family.

ACS Style

Leslie A Markowitz; Charina Reyes; Rebecca A Embacher; Leslie L Speer; Nancy Roizen; Thomas W Frazier. Development and psychometric evaluation of a psychosocial quality-of-life questionnaire for individuals with autism and related developmental disorders. Autism 2016, 20, 832 -844.

AMA Style

Leslie A Markowitz, Charina Reyes, Rebecca A Embacher, Leslie L Speer, Nancy Roizen, Thomas W Frazier. Development and psychometric evaluation of a psychosocial quality-of-life questionnaire for individuals with autism and related developmental disorders. Autism. 2016; 20 (7):832-844.

Chicago/Turabian Style

Leslie A Markowitz; Charina Reyes; Rebecca A Embacher; Leslie L Speer; Nancy Roizen; Thomas W Frazier. 2016. "Development and psychometric evaluation of a psychosocial quality-of-life questionnaire for individuals with autism and related developmental disorders." Autism 20, no. 7: 832-844.

New research
Published: 03 February 2016 in Journal of the American Academy of Child & Adolescent Psychiatry
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Objective Abnormal eye gaze is a hallmark characteristic of autism spectrum disorder (ASD), and numerous studies have identified abnormal attention patterns in ASD. The primary aim of the present study was to create an objective, eye tracking-based autism risk index. Method In initial and replication studies, children were recruited after referral for comprehensive multidisciplinary evaluation of ASD and subsequently grouped by clinical consensus diagnosis (ASD n = 25/15, non-ASD n = 20/19 for initial/replication samples). Remote eye tracking was blinded to diagnosis and included multiple stimuli. Dwell times were recorded to each a priori–defined region of interest (ROI) and averaged across ROIs to create an autism risk index. Receiver operating characteristic curve analyses examined classification accuracy. Correlations with clinical measures evaluated whether the autism risk index was associated with autism symptom severity independent of language ability. Results In both samples, the autism risk index had high diagnostic accuracy (area under the curve [AUC] = 0.91 and 0.85, 95% CIs = 0.81–0.98 and 0.71–0.96), was strongly associated with Autism Diagnostic Observation Schedule–Second Edition (ADOS-2) severity scores (r = 0.58 and 0.59, p< .001), and not significantly correlated with language ability (r ≤| –0.28|, p > .095). Conclusion The autism risk index may be a useful quantitative and objective measure of risk for autism in at-risk settings. Future research in larger samples is needed to cross-validate these findings. If validated and scaled for clinical use, this measure could inform clinical judgment regarding ASD diagnosis and track symptom improvements.

ACS Style

Thomas W. Frazier; Eric W. Klingemier; Mary Beukemann; Leslie Speer; Leslie Markowitz; Sumit Parikh; Steven Wexberg; Kimberly Giuliano; Elaine Schulte; Carol Delahunty; Veena Ahuja; Charis Eng; Michael J. Manos; Antonio Y. Hardan; Eric A. Youngstrom; Mark S. Strauss. Development of an Objective Autism Risk Index Using Remote Eye Tracking. Journal of the American Academy of Child & Adolescent Psychiatry 2016, 55, 301 -309.

AMA Style

Thomas W. Frazier, Eric W. Klingemier, Mary Beukemann, Leslie Speer, Leslie Markowitz, Sumit Parikh, Steven Wexberg, Kimberly Giuliano, Elaine Schulte, Carol Delahunty, Veena Ahuja, Charis Eng, Michael J. Manos, Antonio Y. Hardan, Eric A. Youngstrom, Mark S. Strauss. Development of an Objective Autism Risk Index Using Remote Eye Tracking. Journal of the American Academy of Child & Adolescent Psychiatry. 2016; 55 (4):301-309.

Chicago/Turabian Style

Thomas W. Frazier; Eric W. Klingemier; Mary Beukemann; Leslie Speer; Leslie Markowitz; Sumit Parikh; Steven Wexberg; Kimberly Giuliano; Elaine Schulte; Carol Delahunty; Veena Ahuja; Charis Eng; Michael J. Manos; Antonio Y. Hardan; Eric A. Youngstrom; Mark S. Strauss. 2016. "Development of an Objective Autism Risk Index Using Remote Eye Tracking." Journal of the American Academy of Child & Adolescent Psychiatry 55, no. 4: 301-309.

Journal article
Published: 27 October 2015 in Molecular Autism
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Previous studies have demonstrated aggregation of autistic traits in undiagnosed family members of children with autism spectrum disorder (ASD), which has significant implications for ASD risk in their offspring. This study capitalizes upon a large, quantitatively characterized clinical-epidemiologic family sample to establish the extent to which family transmission pattern and sex modulate ASD trait aggregation. Data were analyzed from 5515 siblings (2657 non-ASD and 2858 ASD) included in the Interactive Autism Network. Autism symptom levels were measured using the Social Responsiveness Scale (SRS) and by computing Diagnostic and Statistical Manual of Mental Disorders-Fifth Edition (DSM-5) symptom scores based on items from the SRS and Social Communication Questionnaire. Generalized estimating equation models evaluated the influence of family incidence types (single versus multiple incidence families; male-only ASD-affected families versus families with female ASD-affected children), diagnostic group (non-ASD children with and without a history of language delay with autistic speech and ASD-affected children), and sibling sex on ASD symptom levels. Non-ASD children manifested elevated ASD symptom burden when they were members of multiple incidence families-this effect was accentuated for male children in female ASD-containing families-or when they had a history of language delay with autistic qualities of speech. In this sample, ASD-affected children from multiple incidence families had lower symptom levels than their counterparts in single incidence families. Recurrence risk for ASD was higher for children from female ASD-containing families than for children from male-only families. Sex and patterns of family transmission modulate the risk of autism symptom burden in undiagnosed siblings of ASD-affected children. Identification of these symptoms/traits and their molecular genetic causes may have significant implications for genetic counseling and for understanding inherited liabilities that confer risk for ASD in successive generations. Autism symptom elevations were more dramatic in non-ASD children from multiple incidence families and those with a history of language delay and autistic qualities of speech, identifying sub-groups at substantially greater transmission risk. Higher symptom burden and greater recurrence in children from female ASD-containing families indicate that familial aggregation patterns are further qualified by sex-specific thresholds, supportive of the notion that females require a higher burden of deleterious liability to cross into categorical ASD diagnosis.

ACS Style

Thomas W. Frazier; Eric A. Youngstrom; Antonio Y. Hardan; Stelios Georgiades; John N. Constantino; Charis Eng. Quantitative autism symptom patterns recapitulate differential mechanisms of genetic transmission in single and multiple incidence families. Molecular Autism 2015, 6, 58 .

AMA Style

Thomas W. Frazier, Eric A. Youngstrom, Antonio Y. Hardan, Stelios Georgiades, John N. Constantino, Charis Eng. Quantitative autism symptom patterns recapitulate differential mechanisms of genetic transmission in single and multiple incidence families. Molecular Autism. 2015; 6 (1):58.

Chicago/Turabian Style

Thomas W. Frazier; Eric A. Youngstrom; Antonio Y. Hardan; Stelios Georgiades; John N. Constantino; Charis Eng. 2015. "Quantitative autism symptom patterns recapitulate differential mechanisms of genetic transmission in single and multiple incidence families." Molecular Autism 6, no. 1: 58.

Journal article
Published: 01 June 2014 in Journal of the American Academy of Child & Adolescent Psychiatry
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ACS Style

Thomas W. Frazier; Stelios Georgiades; Somer L. Bishop; Antonio Y. Hardan. Dr. Frazier et al. reply:. Journal of the American Academy of Child & Adolescent Psychiatry 2014, 53, 700 -701.

AMA Style

Thomas W. Frazier, Stelios Georgiades, Somer L. Bishop, Antonio Y. Hardan. Dr. Frazier et al. reply:. Journal of the American Academy of Child & Adolescent Psychiatry. 2014; 53 (6):700-701.

Chicago/Turabian Style

Thomas W. Frazier; Stelios Georgiades; Somer L. Bishop; Antonio Y. Hardan. 2014. "Dr. Frazier et al. reply:." Journal of the American Academy of Child & Adolescent Psychiatry 53, no. 6: 700-701.

Original research
Published: 18 March 2014 in Brain and Behavior
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Background Four of the most consistently replicated variants associated with mood disorder occur in genes important for synaptic function: ANK3 (rs10994336), BDNF (rs6265), CACNA1C (rs1006737), and DGKH (rs1170191). Aims The present study examined associations between these candidates, mood disorder diagnoses, cognition, and fronto‐limbic regions implicated in affect regulation. Methods and materials Participants included 128 individuals with bipolar disorder (33% male, Mean age = 38.5), 48 with major depressive disorder (29% male, Mean age = 40.4), and 149 healthy controls (35% male, Mean age = 36.5). Genotypes were determined by 5′‐fluorogenic exonuclease assays (TaqMan®). Fronto‐limbic volumes were obtained from high resolution brain images using Freesurfer. Chi‐square analyses, bivariate correlations, and mediational models examined relationships between genetic variants, mood diagnoses, cognitive measures, and brain volumes. Results Carriers of the minor BDNF and ANK3 alleles showed nonsignificant trends toward protective association in controls relative to mood disorder patients (P = 0.047). CACNA1C minor allele carriers had larger bilateral caudate, insula, globus pallidus, frontal pole, and nucleus accumbens volumes (smallest r = 0.13, P = 0.043), and increased IQ (r = 0.18, P < 0.001). CACNA1C associations with brain volumes and IQ were independent; larger fronto‐limbic volumes did not mediate increased IQ. Other candidate variants were not significantly associated with diagnoses, cognition, or fronto‐limbic volumes. Discussion and conclusions CACNA1C may be associated with biological systems altered in mood disorder. Increases in fronto‐limbic volumes and cognitive ability associated with CACNA1C minor allele genotypes are congruent with findings in healthy samples and may be a marker for increased risk for neuropsychiatric phenotypes. Even larger multimodal studies are needed to quantify the magnitude and specificity of genetic‐imaging‐cognition‐symptom relationships.

ACS Style

Thomas W. Frazier; Eric Youngstrom; Brian A. Frankel; Giovana B. Zunta‐Soares; Marsal Sanches; Michael Escamilla; David Nielsen; Jair C. Soares. Candidate gene associations with mood disorder, cognitive vulnerability, and fronto‐limbic volumes. Brain and Behavior 2014, 4, 418 -430.

AMA Style

Thomas W. Frazier, Eric Youngstrom, Brian A. Frankel, Giovana B. Zunta‐Soares, Marsal Sanches, Michael Escamilla, David Nielsen, Jair C. Soares. Candidate gene associations with mood disorder, cognitive vulnerability, and fronto‐limbic volumes. Brain and Behavior. 2014; 4 (3):418-430.

Chicago/Turabian Style

Thomas W. Frazier; Eric Youngstrom; Brian A. Frankel; Giovana B. Zunta‐Soares; Marsal Sanches; Michael Escamilla; David Nielsen; Jair C. Soares. 2014. "Candidate gene associations with mood disorder, cognitive vulnerability, and fronto‐limbic volumes." Brain and Behavior 4, no. 3: 418-430.

Journal article
Published: 10 March 2014 in Journal of Clinical Medicine
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This report evaluates whether classification tree algorithms (CTA) may improve the identification of individuals at risk for bipolar spectrum disorders (BPSD). Analyses used the Longitudinal Assessment of Manic Symptoms (LAMS) cohort (629 youth, 148 with BPSD and 481 without BPSD). Parent ratings of mania symptoms, stressful life events, parenting stress, and parental history of mania were included as risk factors. Comparable overall accuracy was observed for CTA (75.4%) relative to logistic regression (77.6%). However, CTA showed increased sensitivity (0.28 vs. 0.18) at the expense of slightly decreased specificity and positive predictive power. The advantage of CTA algorithms for clinical decision making is demonstrated by the combinations of predictors most useful for altering the probability of BPSD. The 24% sample probability of BPSD was substantially decreased in youth with low screening and baseline parent ratings of mania, negative parental history of mania, and low levels of stressful life events (2%). High screening plus high baseline parent-rated mania nearly doubled the BPSD probability (46%). Future work will benefit from examining additional, powerful predictors, such as alternative data sources (e.g., clinician ratings, neurocognitive test data); these may increase the clinical utility of CTA models further.

ACS Style

Thomas W. Frazier; Eric A. Youngstrom; Mary A. Fristad; Christine Demeter; Boris Birmaher; Robert A. Kowatch; L. Eugene Arnold; David Axelson; Mary K. Gill; Sarah M. Horwitz; Robert L. Findling. Improving Clinical Prediction of Bipolar Spectrum Disorders in Youth. Journal of Clinical Medicine 2014, 3, 218 -232.

AMA Style

Thomas W. Frazier, Eric A. Youngstrom, Mary A. Fristad, Christine Demeter, Boris Birmaher, Robert A. Kowatch, L. Eugene Arnold, David Axelson, Mary K. Gill, Sarah M. Horwitz, Robert L. Findling. Improving Clinical Prediction of Bipolar Spectrum Disorders in Youth. Journal of Clinical Medicine. 2014; 3 (1):218-232.

Chicago/Turabian Style

Thomas W. Frazier; Eric A. Youngstrom; Mary A. Fristad; Christine Demeter; Boris Birmaher; Robert A. Kowatch; L. Eugene Arnold; David Axelson; Mary K. Gill; Sarah M. Horwitz; Robert L. Findling. 2014. "Improving Clinical Prediction of Bipolar Spectrum Disorders in Youth." Journal of Clinical Medicine 3, no. 1: 218-232.

Twin study
Published: 07 March 2014 in Journal of Autism and Developmental Disorders
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The present study examined genetic and shared environment contributions to quantitatively-measured autism symptoms and categorically-defined autism spectrum disorders (ASD). Participants included 568 twins from the Interactive Autism Network. Autism symptoms were obtained using the Social Communication Questionnaire and Social Responsiveness Scale. Categorically-defined ASD was based on clinical diagnoses. DeFries-Fulker and liability threshold models examined etiologic influences. Very high heritability was observed for extreme autism symptom levels (\( {\text{h}}_{g}^{2} = . 9 2{-} 1. 20 \)). Extreme levels of social and repetitive behavior symptoms were strongly influenced by common genetic factors. Heritability of categorically-defined ASD diagnosis was comparatively low (.21, 95 % CI 0.15–0.28). High heritability of extreme autism symptom levels confirms previous observations of strong genetic influences on autism. Future studies will require large, carefully ascertained family pedigrees and quantitative symptom measurements.

ACS Style

Thomas W. Frazier; Lee Thompson; Eric A. Youngstrom; Paul Law; Antonio Y. Hardan; Charis Eng; Nathan Morris. A Twin Study of Heritable and Shared Environmental Contributions to Autism. Journal of Autism and Developmental Disorders 2014, 44, 2013 -2025.

AMA Style

Thomas W. Frazier, Lee Thompson, Eric A. Youngstrom, Paul Law, Antonio Y. Hardan, Charis Eng, Nathan Morris. A Twin Study of Heritable and Shared Environmental Contributions to Autism. Journal of Autism and Developmental Disorders. 2014; 44 (8):2013-2025.

Chicago/Turabian Style

Thomas W. Frazier; Lee Thompson; Eric A. Youngstrom; Paul Law; Antonio Y. Hardan; Charis Eng; Nathan Morris. 2014. "A Twin Study of Heritable and Shared Environmental Contributions to Autism." Journal of Autism and Developmental Disorders 44, no. 8: 2013-2025.

Original research article
Published: 01 January 2014 in Frontiers in Genetics
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Autism spectrum disorders (ASD) are highly heritable complex neurodevelopmental disorders with a 4:1 male: female ratio. Common genetic variation could explain 40-60% of the variance in liability to autism. Because of their small effect, genome-wide association studies (GWASs) have only identified a small number of individual single-nucleotide polymorphisms (SNPs). To increase the power of GWASs in complex disorders, methods like convergent functional genomics (CFG) have emerged to extract true association signals from noise and to identify and prioritize genes from SNPs using a scoring strategy combining statistics and functional genomics. We adapted and applied this approach to analyze data from a GWAS performed on families with multiple children affected with autism from Autism Speaks Autism Genetic Resource Exchange (AGRE). We identified a set of 133 candidate markers that were localized in or close to genes with functional relevance in ASD from a discovery population (545 multiplex families); a gender specific genetic score based on these common variants explained 1% (P = 0.01 in males) and 5% (P = 8.7x10-7 in females) of genetic variance in an independent sample of multiplex families. Overall, our work demonstrates that prioritization of GWAS data based on functional genomics identified common variants associated with autism and provided additional support for a common polygenic background in autism.

ACS Style

Jerome Carayol; Gerard D. Schellenberg; Beth Dombroski; Claire Amiet; Bérengère Génin; Karine Fontaine; Francis Rousseau; Céline Vazart; David Cohen; Thomas W. Frazier; Antonio Y. Hardan; Geraldine Dawson; Thomas Rio Frio. A scoring strategy combining statistics and functional genomics supports a possible role for common polygenic variation in autism. Frontiers in Genetics 2014, 5, 1 .

AMA Style

Jerome Carayol, Gerard D. Schellenberg, Beth Dombroski, Claire Amiet, Bérengère Génin, Karine Fontaine, Francis Rousseau, Céline Vazart, David Cohen, Thomas W. Frazier, Antonio Y. Hardan, Geraldine Dawson, Thomas Rio Frio. A scoring strategy combining statistics and functional genomics supports a possible role for common polygenic variation in autism. Frontiers in Genetics. 2014; 5 ():1.

Chicago/Turabian Style

Jerome Carayol; Gerard D. Schellenberg; Beth Dombroski; Claire Amiet; Bérengère Génin; Karine Fontaine; Francis Rousseau; Céline Vazart; David Cohen; Thomas W. Frazier; Antonio Y. Hardan; Geraldine Dawson; Thomas Rio Frio. 2014. "A scoring strategy combining statistics and functional genomics supports a possible role for common polygenic variation in autism." Frontiers in Genetics 5, no. : 1.

Book chapter
Published: 01 January 2014 in Comprehensive Guide to Autism
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Irritable, aggressive behavior can present a substantial impediment to the development and current functioning of individuals with autism. This chapter presents a brief review of the history of aggression treatment in autism and focuses on recent data concerning combined behavioral and medication treatment. An assessment-based model for the selection of initial treatment approaches and revision of the initial plan is presented. This model is based on a comprehensive biopsychosocial evaluation of the individual exhibiting aggression, including medical/neurological/psychiatric evaluations, neurobehavioral assessment, and functional behavioral assessment. Case examples applying the model are provided. Finally, the importance of balancing between least intrusive and maximally effective treatment approaches is discussed, as are future directions in research focusing on improving the assessment and treatment of aggressive behavior. Autism spectrum disorders represent a set of neurodevelopmental conditions that impact relationships, learning, and daily functioning. Unfortunately, irritable, aggressive behaviors are also common in autism-affected individuals (Lecavalier. J Autism Dev Disord 36(8):1101–14; 2006), further diminishing their functioning and quality of life. The present chapter begins by defining the problem of irritable, aggressive behavior in autism and the impact of this behavior on the individual, their family, and surrounding environment. We then briefly review the history of treatment for irritable, aggressive behavior in autism, focusing on behavioral and medication interventions. After providing historical context, the most recent research findings regarding combined medication and behavioral treatment are presented. This review is followed by presentation of an iterative model for assessment-driven treatment of aggressive behavior in autism and case examples demonstrating the application of this model. Finally, we end by discussing gaps in our current knowledge and future direction for research in aggressive behavior. The chapter does not specifically address self-injurious behaviors. While many of the concepts discussed would apply to self-injurious behavior as well, because of the unique nature of these behaviors, we chose to focus exclusively on irritable, aggressive behaviors directed toward others.

ACS Style

Thomas W. Frazier; Rebecca Embacher; Allison Frazier. Reducing Aggression in ASD with Combined Medication and Behavioral Therapy. Comprehensive Guide to Autism 2014, 2317 -2332.

AMA Style

Thomas W. Frazier, Rebecca Embacher, Allison Frazier. Reducing Aggression in ASD with Combined Medication and Behavioral Therapy. Comprehensive Guide to Autism. 2014; ():2317-2332.

Chicago/Turabian Style

Thomas W. Frazier; Rebecca Embacher; Allison Frazier. 2014. "Reducing Aggression in ASD with Combined Medication and Behavioral Therapy." Comprehensive Guide to Autism , no. : 2317-2332.

New research
Published: 26 December 2013 in Journal of the American Academy of Child & Adolescent Psychiatry
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Objective To examine differences in behavioral symptoms and cognitive functioning between males and females with autism spectrum disorder (ASD). Method We analyzed data from 2,418 probands with autism (304 females and 2,114 males) included in the Simons Simplex Collection. Sex differences were evaluated across measures of autism symptoms, cognitive and motor functioning, adaptive behavior, and associated behavior problems. Measurement bias was examined using latent variable models of symptoms. Unadjusted and propensity-adjusted analyses were computed to ensure that sex differences were not due to unbalanced sampling. Moderator and mediator analyses evaluated whether sex differences were modified by clinical characteristics or were driven by cognitive ability. Results Females with ASD had greater social communication impairment, lower levels of restricted interests, lower cognitive ability, weaker adaptive skills, and greater externalizing problems relative to males. Symptom differences could not be accounted for by measurement differences, indicating that diagnostic instruments captured autism similarly in males and females. IQ reductions mediated greater social impairment and reduced adaptive behavior in females with ASD, but did not mediate reductions in restricted interests or increases in irritability. Conclusions A specific female ASD phenotype is emerging that cannot be accounted for by differential symptom measurement. The present data suggest that the relatively low proportion of high-functioning females may reflect the effect of protective biological factors or may be due to under-identification. Additional carefully accrued samples are needed to confirm the present pattern and to evaluate whether observed sex ratios in high-functioning cases are reduced if female-specific indicators of restricted interests are included.

ACS Style

Thomas W. Frazier; Stelios Georgiades; Somer L. Bishop; Antonio Y. Hardan. Behavioral and Cognitive Characteristics of Females and Males With Autism in the Simons Simplex Collection. Journal of the American Academy of Child & Adolescent Psychiatry 2013, 53, 329 -340.e3.

AMA Style

Thomas W. Frazier, Stelios Georgiades, Somer L. Bishop, Antonio Y. Hardan. Behavioral and Cognitive Characteristics of Females and Males With Autism in the Simons Simplex Collection. Journal of the American Academy of Child & Adolescent Psychiatry. 2013; 53 (3):329-340.e3.

Chicago/Turabian Style

Thomas W. Frazier; Stelios Georgiades; Somer L. Bishop; Antonio Y. Hardan. 2013. "Behavioral and Cognitive Characteristics of Females and Males With Autism in the Simons Simplex Collection." Journal of the American Academy of Child & Adolescent Psychiatry 53, no. 3: 329-340.e3.

Research article
Published: 08 October 2013 in Autism
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Demographic and clinical factors may influence assessment of autism symptoms. This study evaluated these correlates and also examined whether social communication and interaction and restricted/repetitive behavior provided unique prediction of autism spectrum disorder diagnosis. We analyzed data from 7352 siblings included in the Interactive Autism Network registry. Social communication and interaction and restricted/repetitive behavior symptoms were obtained using caregiver-reports on the Social Responsiveness Scale. Demographic and clinical correlates were covariates in regression models predicting social communication and interaction and restricted/repetitive behavior symptoms. Logistic regression and receiver operating characteristic curve analyses evaluated the incremental validity of social communication and interaction and restricted/repetitive behavior domains over and above global autism symptoms. Autism spectrum disorder diagnosis was the strongest correlate of caregiver-reported social communication and interaction and restricted/repetitive behavior symptoms. The presence of comorbid diagnoses also increased symptom levels. Social communication and interaction and restricted/repetitive behavior symptoms provided significant, but modest, incremental validity in predicting diagnosis beyond global autism symptoms. These findings suggest that autism spectrum disorder diagnosis is by far the largest determinant of quantitatively measured autism symptoms. Externalizing (attention deficit hyperactivity disorder) and internalizing (anxiety) behavior, low cognitive ability, and demographic factors may confound caregiver-report of autism symptoms, potentially necessitating a continuous norming approach to the revision of symptom measures. Social communication and interaction and restricted/repetitive behavior symptoms may provide incremental validity in the diagnosis of autism spectrum disorder.

ACS Style

Thomas W Frazier; Eric Youngstrom; Rebecca Embacher; Antonio Y Hardan; John N Constantino; Paul Law; Robert L Findling; Charis Eng. Demographic and clinical correlates of autism symptom domains and autism spectrum diagnosis. Autism 2013, 18, 571 -582.

AMA Style

Thomas W Frazier, Eric Youngstrom, Rebecca Embacher, Antonio Y Hardan, John N Constantino, Paul Law, Robert L Findling, Charis Eng. Demographic and clinical correlates of autism symptom domains and autism spectrum diagnosis. Autism. 2013; 18 (5):571-582.

Chicago/Turabian Style

Thomas W Frazier; Eric Youngstrom; Rebecca Embacher; Antonio Y Hardan; John N Constantino; Paul Law; Robert L Findling; Charis Eng. 2013. "Demographic and clinical correlates of autism symptom domains and autism spectrum diagnosis." Autism 18, no. 5: 571-582.

Journal article
Published: 22 April 2013 in Behavioural Brain Research
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Research has demonstrated the potential role of the brainstem in the pathobiology of autism. Previous studies have suggested reductions in brainstem volume and a relationship between this structure and sensory abnormalities. However, little is known regarding the developmental aspects of the brainstem across childhood and adolescence. The goal of this pilot study was to examine brainstem development via MRI volumetry using a longitudinal research design. Participants included 23 boys with autism and 23 matched controls (age range = 8–17 years), all without intellectual disability. Participants underwent structural MRI scans once at baseline and again at two-year follow-up. Brainstem volumetric measurements were performed using the BRAINS2 software package. There were no significant group differences in age, gender, handedness, and total brain volume; however, full-scale IQ was higher in controls. Autism and control groups showed different patterns of growth in brainstem volume. While whole brainstem volume remained stable in controls over the two-year period, the autism group showed increases with age reaching volumes comparable to controls by age 15 years. This increase of whole brainstem volume was primarily driven by bilateral increases in gray matter volume. Findings from this preliminary study are suggestive of developmental brainstem abnormalities in autism primarily involving gray matter structures. These findings are consistent with autism being conceptualized as a neurodevelopmental disorder with alterations in brain-growth trajectories. More longitudinal MRI studies are needed integrating longitudinal cognitive/behavioral data to confirm and elucidate the clinical significance of these atypical growth patterns.

ACS Style

Roger J. Jou; Thomas W. Frazier; Matcheri S. Keshavan; Nancy J. Minshew; Antonio Y. Hardan. A two-year longitudinal pilot MRI study of the brainstem in autism. Behavioural Brain Research 2013, 251, 163 -167.

AMA Style

Roger J. Jou, Thomas W. Frazier, Matcheri S. Keshavan, Nancy J. Minshew, Antonio Y. Hardan. A two-year longitudinal pilot MRI study of the brainstem in autism. Behavioural Brain Research. 2013; 251 ():163-167.

Chicago/Turabian Style

Roger J. Jou; Thomas W. Frazier; Matcheri S. Keshavan; Nancy J. Minshew; Antonio Y. Hardan. 2013. "A two-year longitudinal pilot MRI study of the brainstem in autism." Behavioural Brain Research 251, no. : 163-167.

Book chapter
Published: 01 January 2013 in Encyclopedia of Autism Spectrum Disorders
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Factor analysis refers to statistical methods that attempt to represent a set of correlated observed variables (questionnaire items, autism symptoms, etc.) in terms of a smaller number of unobserved...

ACS Style

Tracey Ward; Raphael Bernier; Cora Mukerji; Danielle Perszyk; James C. McPartland; Ellen Johnson; Susan Faja; Maureen Nevers; Thomas Frazier; Patricia Howlin; Sarah Savage; Thomas Zane; Traci Lanner; Michelle Myers; Ernst Vanbergeijk; Samantha Huestis; Nirit Bauminger-Zviely; Peter Doehring; Guus Voorst; Kelly Macy; Jennifer M. Kwon; Edward McNulty; S. Michael Chapman; Michael J. Crowley; Allison Bean; Susan Hyman; Lawrence David Scahill; Lorna Wing; A. Charles Catania; John Thorne; Usha Kini; Maura Moyle; Claire Plowgian; Francesca Happé; Jane Case-Smith; Lauren Schmitt; Moira Lewis; Mary Jane Weiss; Jan Van Der Rutger Gaag; Hillary Hurst; Laura Bonazinga; Diane R. Paul; Carolyn A. Doyle; Christopher J. McDougle; Kate S. Perri; Marcel Moran; Kimberly Stigler; Margaret St. John; David Hessl; Andrea Schneider; Juli Katon; Nouchine Hadjikhani; Nicole Rinehart; Peter Enticott; John Bradshaw; Mark Palmieri; Robert LaRue; John Molteni; Patricia Prelock; Ralph-Axel Müller; Shaunessy Egan; Dawn Hendricks; Katherin C. Holman; Kristen D’Eramo. Factor Analysis. Encyclopedia of Autism Spectrum Disorders 2013, 1238 -1242.

AMA Style

Tracey Ward, Raphael Bernier, Cora Mukerji, Danielle Perszyk, James C. McPartland, Ellen Johnson, Susan Faja, Maureen Nevers, Thomas Frazier, Patricia Howlin, Sarah Savage, Thomas Zane, Traci Lanner, Michelle Myers, Ernst Vanbergeijk, Samantha Huestis, Nirit Bauminger-Zviely, Peter Doehring, Guus Voorst, Kelly Macy, Jennifer M. Kwon, Edward McNulty, S. Michael Chapman, Michael J. Crowley, Allison Bean, Susan Hyman, Lawrence David Scahill, Lorna Wing, A. Charles Catania, John Thorne, Usha Kini, Maura Moyle, Claire Plowgian, Francesca Happé, Jane Case-Smith, Lauren Schmitt, Moira Lewis, Mary Jane Weiss, Jan Van Der Rutger Gaag, Hillary Hurst, Laura Bonazinga, Diane R. Paul, Carolyn A. Doyle, Christopher J. McDougle, Kate S. Perri, Marcel Moran, Kimberly Stigler, Margaret St. John, David Hessl, Andrea Schneider, Juli Katon, Nouchine Hadjikhani, Nicole Rinehart, Peter Enticott, John Bradshaw, Mark Palmieri, Robert LaRue, John Molteni, Patricia Prelock, Ralph-Axel Müller, Shaunessy Egan, Dawn Hendricks, Katherin C. Holman, Kristen D’Eramo. Factor Analysis. Encyclopedia of Autism Spectrum Disorders. 2013; ():1238-1242.

Chicago/Turabian Style

Tracey Ward; Raphael Bernier; Cora Mukerji; Danielle Perszyk; James C. McPartland; Ellen Johnson; Susan Faja; Maureen Nevers; Thomas Frazier; Patricia Howlin; Sarah Savage; Thomas Zane; Traci Lanner; Michelle Myers; Ernst Vanbergeijk; Samantha Huestis; Nirit Bauminger-Zviely; Peter Doehring; Guus Voorst; Kelly Macy; Jennifer M. Kwon; Edward McNulty; S. Michael Chapman; Michael J. Crowley; Allison Bean; Susan Hyman; Lawrence David Scahill; Lorna Wing; A. Charles Catania; John Thorne; Usha Kini; Maura Moyle; Claire Plowgian; Francesca Happé; Jane Case-Smith; Lauren Schmitt; Moira Lewis; Mary Jane Weiss; Jan Van Der Rutger Gaag; Hillary Hurst; Laura Bonazinga; Diane R. Paul; Carolyn A. Doyle; Christopher J. McDougle; Kate S. Perri; Marcel Moran; Kimberly Stigler; Margaret St. John; David Hessl; Andrea Schneider; Juli Katon; Nouchine Hadjikhani; Nicole Rinehart; Peter Enticott; John Bradshaw; Mark Palmieri; Robert LaRue; John Molteni; Patricia Prelock; Ralph-Axel Müller; Shaunessy Egan; Dawn Hendricks; Katherin C. Holman; Kristen D’Eramo. 2013. "Factor Analysis." Encyclopedia of Autism Spectrum Disorders , no. : 1238-1242.

Book chapter
Published: 01 January 2013 in Encyclopedia of Autism Spectrum Disorders
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Acallosal syndrome; Callosotomy (surgical severing); Complete agenesis; Dysgenesis (malformation); Hypogenesis (partial formation); Hypoplasia (underdevelopment); Partial agenesis The corpus callosum (CC) is the largest white matter fiber tract (also known as commissure) connecting the two hemispheres of the brain. Agenesis of the corpus callosum (AgCC) is present at birth and encompasses structural defects of the development of the corpus callosum that range from partial to complete loss of these connective fiber tracts. Primary AgCC is a complete loss of the CC without other accompanying brain changes. A rare individual diagnosed with autism or ASD is found to have AgCC. The CC is divided into seven subregions (see definition of the corpus callosum). AgCC is divided into partial (Fig. 1) and complete (Fig. 2) based on whether one or more subregions are missing (Fig. 1) or whether th

ACS Style

Thomas Frazier; Antonio Hardan. Agenesis of Corpus Callosum. Encyclopedia of Autism Spectrum Disorders 2013, 87 -90.

AMA Style

Thomas Frazier, Antonio Hardan. Agenesis of Corpus Callosum. Encyclopedia of Autism Spectrum Disorders. 2013; ():87-90.

Chicago/Turabian Style

Thomas Frazier; Antonio Hardan. 2013. "Agenesis of Corpus Callosum." Encyclopedia of Autism Spectrum Disorders , no. : 87-90.

Book chapter
Published: 01 January 2013 in Encyclopedia of Autism Spectrum Disorders
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Corpus callosum (CC) abnormalities in autism generally refer to reductions in the midsagittal size, volume, or integrity of the CC in individuals with autism spectrum disorders. Over the last few decades, case reports have been published supporting an association between partial or complete agenesis or other abnormalities of the CC and social deficits. While not all individuals with agenesis of the corpus callosum meet full DSM criteria for autism spectrum disorders, they often show behavioral, cognitive, and functional patterns reminiscent of autism, particularly individuals with complete agenesis (Paul et al., 2007) (Fig. 1).Corpus Callosum Abnormalities in Autism, Fig. 1Total corpus callosum and Witelson subdivisions. Subdivision 1: rostrum in black; subdivision 2: genu in yellow; subdivision 3: rostral body in pink; subdivision 4: anterior midbody in aqua; subdivision 5: posterior midbody in green; subdivision 6: isthmus

ACS Style

Thomas Frazier; Antonio Hardan. Corpus Callosum Abnormalities in Autism. Encyclopedia of Autism Spectrum Disorders 2013, 804 -807.

AMA Style

Thomas Frazier, Antonio Hardan. Corpus Callosum Abnormalities in Autism. Encyclopedia of Autism Spectrum Disorders. 2013; ():804-807.

Chicago/Turabian Style

Thomas Frazier; Antonio Hardan. 2013. "Corpus Callosum Abnormalities in Autism." Encyclopedia of Autism Spectrum Disorders , no. : 804-807.

Book chapter
Published: 01 January 2013 in Encyclopedia of Autism Spectrum Disorders
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Confirmatory factor analysis; Exploratory factor analysis; Factor analysis; Factor mixture modeling; Finite mixture models; Growth mixture modeling; Item response theory; Latent class analysis...

ACS Style

Moira Lewis; Courtenay Norbury; Rhiannon Luyster; Lauren Schmitt; Andrea McDuffie; Eileen Haebig; Donna S. Murray; Geralyn Timler; Thomas W Frazier; David L. Holmes; Adam Feinstein; Lisa Wiesner; Kimberly Johnson; Peter Doehring; Patricia Prelock; Michele Goyette-Ewing; Evelynne Green; Hilary Boorstein; Harriet Levin; Deborah Fein; Debra Dunn; Michael Levine; Alyse Greer; Cristan Farmer; Jane Hamilton; Cyndi Schumann; Aparna Nadig; Maura Moyle; Claire Plowgian; Jeffrey Glennon; John W. Thomas; Andrew Iskandar; Lee Marcus; Pamela Brucker; Susan Y. Bookheimer; Peter Szatmari; Svein Eikeseth; Tristram Smith; Winifred Schultz-Krohn; Vannesa T. Mueller; Lawrence David Scahill; Eva Troyb. Latent Variable Modeling. Encyclopedia of Autism Spectrum Disorders 2013, 1698 -1699.

AMA Style

Moira Lewis, Courtenay Norbury, Rhiannon Luyster, Lauren Schmitt, Andrea McDuffie, Eileen Haebig, Donna S. Murray, Geralyn Timler, Thomas W Frazier, David L. Holmes, Adam Feinstein, Lisa Wiesner, Kimberly Johnson, Peter Doehring, Patricia Prelock, Michele Goyette-Ewing, Evelynne Green, Hilary Boorstein, Harriet Levin, Deborah Fein, Debra Dunn, Michael Levine, Alyse Greer, Cristan Farmer, Jane Hamilton, Cyndi Schumann, Aparna Nadig, Maura Moyle, Claire Plowgian, Jeffrey Glennon, John W. Thomas, Andrew Iskandar, Lee Marcus, Pamela Brucker, Susan Y. Bookheimer, Peter Szatmari, Svein Eikeseth, Tristram Smith, Winifred Schultz-Krohn, Vannesa T. Mueller, Lawrence David Scahill, Eva Troyb. Latent Variable Modeling. Encyclopedia of Autism Spectrum Disorders. 2013; ():1698-1699.

Chicago/Turabian Style

Moira Lewis; Courtenay Norbury; Rhiannon Luyster; Lauren Schmitt; Andrea McDuffie; Eileen Haebig; Donna S. Murray; Geralyn Timler; Thomas W Frazier; David L. Holmes; Adam Feinstein; Lisa Wiesner; Kimberly Johnson; Peter Doehring; Patricia Prelock; Michele Goyette-Ewing; Evelynne Green; Hilary Boorstein; Harriet Levin; Deborah Fein; Debra Dunn; Michael Levine; Alyse Greer; Cristan Farmer; Jane Hamilton; Cyndi Schumann; Aparna Nadig; Maura Moyle; Claire Plowgian; Jeffrey Glennon; John W. Thomas; Andrew Iskandar; Lee Marcus; Pamela Brucker; Susan Y. Bookheimer; Peter Szatmari; Svein Eikeseth; Tristram Smith; Winifred Schultz-Krohn; Vannesa T. Mueller; Lawrence David Scahill; Eva Troyb. 2013. "Latent Variable Modeling." Encyclopedia of Autism Spectrum Disorders , no. : 1698-1699.

Original paper
Published: 18 February 2012 in Journal of Autism and Developmental Disorders
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A growing body of literature has identified size reductions of the corpus callosum (CC) in autism. However, to our knowledge, no published studies have reported on the growth of CC volumes in youth with autism. Volumes of the total CC and its sub-divisions were obtained from 23 male children with autism and 23 age- and gender-matched controls at baseline and 2-year follow-up. Persistent reductions in total CC volume were observed in participants with autism relative to controls. Only the rostral body subdivision showed a normalization of size over time. Persistent reductions are consistent with the diagnostic stability and life-long impairment observed in many individuals with autism. Multi-modal imaging studies are needed to identify specific fiber tracks contributing to CC reductions.

ACS Style

Thomas W. Frazier; Matcheri S. Keshavan; Nancy J. Minshew; Antonio Y. Hardan. A Two-Year Longitudinal MRI Study of the Corpus Callosum in Autism. Journal of Autism and Developmental Disorders 2012, 42, 2312 -2322.

AMA Style

Thomas W. Frazier, Matcheri S. Keshavan, Nancy J. Minshew, Antonio Y. Hardan. A Two-Year Longitudinal MRI Study of the Corpus Callosum in Autism. Journal of Autism and Developmental Disorders. 2012; 42 (11):2312-2322.

Chicago/Turabian Style

Thomas W. Frazier; Matcheri S. Keshavan; Nancy J. Minshew; Antonio Y. Hardan. 2012. "A Two-Year Longitudinal MRI Study of the Corpus Callosum in Autism." Journal of Autism and Developmental Disorders 42, no. 11: 2312-2322.